Đang tải... (xem toàn văn)
(BQ) Part 2 book Guyton and hall textbook of medical physiology has contents: Respiration; aviation, space, and deep sea diving physiology; gastrointestinal physiology; metabolism and temperature regulation; sports physiology,.... and other contents.
CHAPTER 8 The main functions of respiration are to provide oxygen to the tissues and remove carbon dioxide The four major components of respiration are (1) pulmonary ventilation, which means the inflow and outflow of air between the atmosphere and the lung alveoli; (2) diffusion of oxygen (O2) and carbon dioxide (CO2) between the alveoli and the blood; (3) transport of oxygen and carbon dioxide in the blood and body fluids to and from the body’s tissue cells; and (4) regulation of ventilation and other facets of respi ration This chapter is a discussion of pulmonary ven tilation, and the subsequent five chapters cover other respiratory functions plus the physiology of special respi ratory abnormalities MECHANICS OF PULMONARY VENTILATION MUSCLES THAT CAUSE LUNG EXPANSION AND CONTRACTION The lungs can be expanded and contracted in two ways: (1) by downward and upward movement of the dia phragm to lengthen or shorten the chest cavity, and (2) by elevation and depression of the ribs to increase and decrease the anteroposterior diameter of the chest cavity Figure 38-1 shows these two methods Normal quiet breathing is accomplished almost entirely by the first method, that is, by movement of the dia phragm During inspiration, contraction of the diaphragm pulls the lower surfaces of the lungs downward Then, during expiration, the diaphragm simply relaxes, and the elastic recoil of the lungs, chest wall, and abdominal struc tures compresses the lungs and expels the air During heavy breathing, however, the elastic forces are not pow erful enough to cause the necessary rapid expiration, so extra force is achieved mainly by contraction of the abdominal muscles, which pushes the abdominal con tents upward against the bottom of the diaphragm, thereby compressing the lungs The second method for expanding the lungs is to raise the rib cage Raising the rib cage expands the lungs because, in the natural resting position, the ribs slant downward, as shown on the left side of Figure 38-1, thus allowing the sternum to fall backward toward the vertebral column When the rib cage is elevated, however, the ribs project almost directly forward, so the sternum also moves forward, away from the spine, making the anteroposterior thickness of the chest about 20 percent greater during maximum inspiration than during expira tion Therefore, all the muscles that elevate the chest cage are classified as muscles of inspiration, and the muscles that depress the chest cage are classified as muscles of expiration The most important muscles that raise the rib cage are the external intercostals, but others that help are the (1) sternocleidomastoid muscles, which lift upward on the sternum; (2) anterior serrati, which lift many of the ribs; and (3) scaleni, which lift the first two ribs The muscles that pull the rib cage downward during expiration are mainly (1) the abdominal recti, which have the powerful effect of pulling downward on the lower ribs at the same time that they and other abdominal muscles also compress the abdominal contents upward against the diaphragm, and (2) the internal intercostals Figure 38-1 also shows the mechanism by which the external and internal intercostals act to cause inspiration and expiration To the left, the ribs during expiration are angled downward, and the external intercostals are elon gated forward and downward As they contract, they pull the upper ribs forward in relation to the lower ribs, which causes leverage on the ribs to raise them upward, thereby causing inspiration The internal intercostals function exactly in the opposite manner, functioning as expiratory muscles because they angle between the ribs in the oppo site direction and cause opposite leverage PRESSURES THAT CAUSE THE MOVEMENT OF AIR IN AND OUT OF THE LUNGS The lung is an elastic structure that collapses like a balloon and expels all its air through the trachea whenever there is no force to keep it inflated Also, there are no attach ments between the lung and the walls of the chest cage, except where it is suspended at its hilum from the mediastinum, the middle section of the chest cavity Instead, the lung “floats” in the thoracic cavity, surrounded by a thin layer of pleural fluid that lubricates movement of the 497 UNIT VII Pulmonary Ventilation Unit VII Respiration EXPIRATION INSPIRATION Increased vertical diameter Elevated rib cage Increased AP diameter External intercostals contracted Internal intercostals relaxed Diaphragmatic contraction Abdominals contracted lungs within the cavity Further, continual suction of excess fluid into lymphatic channels maintains a slight suction between the visceral surface of the lung pleura and the parietal pleural surface of the thoracic cavity Therefore, the lungs are held to the thoracic wall as if glued there, except that they are well lubricated and can slide freely as the chest expands and contracts Volume change (liters) Figure 38-1. Contraction and expansion of the thoracic cage during expiration and inspiration, demonstrating diaphragmatic contraction, function of the intercostal muscles, and elevation and depression of the rib cage AP, anteroposterior Alveolar Pressure—The Air Pressure Inside the Lung Alveoli. When the glottis is open and no air is flowing into or out of the lungs, the pressures in all parts of the respiratory tree, all the way to the alveoli, are equal to atmospheric pressure, which is considered to be zero ref erence pressure in the airways—that is, centimeters of water pressure To cause inward flow of air into the 498 0.25 Alveolar pressure +2 Pleural Pressure and Its Changes during Respiration. Pressure (cm H2O) Pleural pressure is the pressure of the fluid in the thin space between the lung pleura and the chest wall pleura As noted earlier, this pressure is normally a slight suction, which means a slightly negative pressure The normal pleural pressure at the beginning of inspiration is about −5 centimeters of water, which is the amount of suction required to hold the lungs open to their resting level During normal inspiration, expansion of the chest cage pulls outward on the lungs with greater force and creates more negative pressure, to an average of about −7.5 cen timeters of water These relationships between pleural pressure and changing lung volume are demonstrated in Figure 38-2, showing in the lower panel the increasing negativity of the pleural pressure from −5 to −7.5 during inspiration and in the upper panel an increase in lung volume of 0.5 liter Then, during expiration, the events are essentially reversed Lung volume 0.50 –2 Transpulmonary pressure –4 –6 Pleural pressure –8 Inspiration Expiration Figure 38-2. Changes in lung volume, alveolar pressure, pleural pressure, and transpulmonary pressure during normal breathing alveoli during inspiration, the pressure in the alveoli must fall to a value slightly below atmospheric pressure (below 0) The second curve (labeled “alveolar pressure”) of Figure 38-2 demonstrates that during normal inspira tion, alveolar pressure decreases to about −1 centimeters of water This slight negative pressure is enough to pull 0.5 liter of air into the lungs in the seconds required for normal quiet inspiration During expiration, alveolar pressure rises to about +1 centimeter of water, which forces the 0.5 liter of Lung volume change (liters) 0.50 Expiration 0.25 Inspiration Saline-filled 0.50 Expiration 0.25 Inspiration 0 –4 –5 Pleural pressure (cm H2O) –6 Figure 38-3. Compliance diagram in a healthy person This diagram shows changes in lung volume during changes in transpulmonary pressure (alveolar pressure minus pleural pressure) inspired air out of the lungs during the to seconds of expiration Transpulmonary Pressure—The Difference between Alveolar and Pleural Pressures. Note in Figure 37-2 that the transpulmonary pressure is the pressure differ ence between that in the alveoli and that on the outer surfaces of the lungs (pleural pressure), and it is a measure of the elastic forces in the lungs that tend to collapse the lungs at each instant of respiration, called the recoil pressure Compliance of the Lungs The extent to which the lungs will expand for each unit increase in transpulmonary pressure (if enough time is allowed to reach equilibrium) is called the lung compliance The total compliance of both lungs together in the normal adult human averages about 200 milliliters of air per centimeter of water transpulmonary pressure That is, every time the transpulmonary pressure increases cen timeter of water, the lung volume, after 10 to 20 seconds, will expand 200 milliliters Compliance Diagram of the Lungs. Figure 38-3 is a diagram relating lung volume changes to changes in pleural pressure, which, in turn, alters transpulmonary pressure Note that the relation is different for inspiration and expiration Each curve is recorded by changing the pleural pressure in small steps and allowing the lung volume to come to a steady level between successive steps The two curves are called, respectively, the inspiratory compliance curve and the expiratory compliance curve, and the entire diagram is called the compliance diagram of the lungs The characteristics of the compliance diagram are determined by the elastic forces of the lungs These forces can be divided into two parts: (1) elastic forces of the lung Air-filled UNIT VII Lung volume change (liters) Chapter 38 Pulmonary Ventilation –2 –4 –6 Pleural pressure (cm H2O) –8 Figure 38-4. Comparison of the compliance diagrams of saline-filled and air-filled lungs when the alveolar pressure is maintained at atmospheric pressure (0 cm H2O) and pleural pressure is changed in order to change the transpulmonary pressure tissue and (2) elastic forces caused by surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces The elastic forces of the lung tissue are determined mainly by elastin and collagen fibers interwoven among the lung parenchyma In deflated lungs, these fibers are in an elastically contracted and kinked state; then, when the lungs expand, the fibers become stretched and unkinked, thereby elongating and exerting even more elastic force The elastic forces caused by surface tension are much more complex The significance of surface tension is shown in Figure 38-4, which compares the compliance diagram of the lungs when filled with saline solution and when filled with air When the lungs are filled with air, there is an interface between the alveolar fluid and the air in the alveoli In lungs filled with saline solution, there is no air-fluid interface, and therefore, the surface tension effect is not present; only tissue elastic forces are opera tive in the lung filled with saline solution Note that transpleural pressures required to expand air-filled lungs are about three times as great as those required to expand lungs filled with saline solution Thus, one can conclude that the tissue elastic forces tending to cause collapse of the air-filled lung represent only about one third of the total lung elasticity, whereas the fluid-air surface tension forces in the alveoli represent about two thirds The fluid-air surface tension elastic forces of the lungs also increase tremendously when the substance called surfactant is not present in the alveolar fluid Surfactant, Surface Tension, and Collapse of the Alveoli Principle of Surface Tension. When water forms a surface with air, the water molecules on the surface of the water have an especially strong attraction for one another As a result, the water surface is always attempting to contract This is what holds raindrops together—a tight 499 Unit VII Respiration contractile membrane of water molecules around the entire surface of the raindrop Now let us reverse these principles and see what happens on the inner surfaces of the alveoli Here, the water surface is also attempting to contract This tends to force air out of the alveoli through the bronchi and, in doing so, causes the alveoli to try to collapse The net effect is to cause an elastic contractile force of the entire lungs, which is called the surface tension elastic force Surfactant and Its Effect on Surface Tension. Surfac tant is a surface active agent in water, which means that it greatly reduces the surface tension of water It is secreted by special surfactant-secreting epithelial cells called type II alveolar epithelial cells, which constitute about 10 percent of the surface area of the alveoli These cells are granular, containing lipid inclusions that are secreted in the surfactant into the alveoli Surfactant is a complex mixture of several phospholip ids, proteins, and ions The most important components are the phospholipid dipalmitoyl phosphatidylcholine, surfactant apoproteins, and calcium ions The dipalmitoyl phosphatidylcholine and several less important phospho lipids are responsible for reducing the surface tension They perform this function by not dissolving uniformly in the fluid lining the alveolar surface Instead, part of the molecule dissolves while the remainder spreads over the surface of the water in the alveoli This surface has from one twelfth to one half the surface tension of a pure water surface In quantitative terms, the surface tension of different water fluids is approximately the following: pure water, 72 dynes/cm; normal fluids lining the alveoli but without surfactant, 50 dynes/cm; normal fluids lining the alveoli and with normal amounts of surfactant included, between and 30 dynes/cm Pressure in Occluded Alveoli Caused by Surface Tension. If the air passages leading from the alveoli of the lungs are blocked, the surface tension in the alveoli tends to collapse the alveoli This collapse creates positive pres sure in the alveoli, attempting to push the air out The amount of pressure generated in this way in an alveolus can be calculated from the following formula: Pressure = × Surface tension Radius of alveolus For the average-sized alveolus with a radius of about 100 micrometers and lined with normal surfactant, this calculates to be about centimeters of water pressure (3 mm Hg) If the alveoli were lined with pure water without any surfactant, the pressure would calculate to be about 18 centimeters of water pressure—4.5 times as great Thus, one sees the importance of surfactant in reducing alveolar surface tension and therefore also reduc ing the effort required by the respiratory muscles to expand the lungs 500 Effect of Alveolar Radius on the Pressure Caused by Surface Tension. Note from the preceding formula that the pressure generated as a result of surface tension in the alveoli is inversely affected by the radius of the alveolus, which means that the smaller the alveolus, the greater the alveolar pressure caused by the surface tension Thus, when the alveoli have half the normal radius (50 instead of 100 micrometers), the pressures noted earlier are doubled This phenomenon is especially significant in small prema ture babies, many of whom have alveoli with radii less than one quarter that of an adult person Further, surfactant does not normally begin to be secreted into the alveoli until between the sixth and seventh months of gestation, and in some cases, even later Therefore, many premature babies have little or no surfactant in the alveoli when they are born, and their lungs have an extreme tendency to collapse, sometimes as great as six to eight times that in a normal adult person This situation causes the condition called respiratory distress syndrome of the newborn It is fatal if not treated with strong measures, especially properly applied continuous positive pressure breathing EFFECT OF THE THORACIC CAGE ON LUNG EXPANSIBILITY Thus far, we have discussed the expansibility of the lungs alone, without considering the thoracic cage The thoracic cage has its own elastic and viscous characteristics, similar to those of the lungs; even if the lungs were not present in the thorax, muscular effort would still be required to expand the thoracic cage Compliance of the Thorax and the Lungs Together The compliance of the entire pulmonary system (the lungs and thoracic cage together) is measured while expanding the lungs of a totally relaxed or paralyzed subject To measure compliance, air is forced into the lungs a little at a time while recording lung pressures and volumes To inflate this total pulmonary system, almost twice as much pressure as is required to inflate the same lungs after removal from the chest cage is necessary Therefore, the compliance of the combined lung-thorax system is almost exactly one half that of the lungs alone— 110 milliliters of volume per centimeter of water pressure for the combined system, compared with 200 ml/cm for the lungs alone Furthermore, when the lungs are expanded to high volumes or compressed to low volumes, the limitations of the chest become extreme When near these limits, the compliance of the combined lung-thorax system can be less than one fifth that of the lungs alone “Work” of Breathing We have already pointed out that during normal quiet breathing, all respiratory muscle contraction occurs during Chapter 38 Pulmonary Ventilation PULMONARY VOLUMES AND CAPACITIES Floating drum Recording drum Counterbalancing weight Figure 38-5. A spirometer To the left in Figure 38-6 are listed four pulmonary lung volumes that, when added together, equal the maximum volume to which the lungs can be expanded The signifi cance of each of these volumes is the following: The tidal volume is the volume of air inspired or expired with each normal breath; it amounts to about 500 milliliters in the average adult male The inspiratory reserve volume is the extra volume of air that can be inspired over and above the normal tidal volume when the person inspires with full force; it is usually equal to about 3000 milliliters The expiratory reserve volume is the maximum extra volume of air that can be expired by forceful expiration after the end of a normal tidal expiration; this volume normally amounts to about 1100 milliliters The residual volume is the volume of air remaining in the lungs after the most forceful expiration; this volume averages about 1200 milliliters Mouthpiece In describing events in the pulmonary cycle, it is some times desirable to consider two or more of the volumes together Such combinations are called pulmonary capacities To the right in Figure 38-6 are listed the important pulmonary capacities, which can be described as follows: The inspiratory capacity equals the tidal volume plus the inspiratory reserve volume This capacity is the amount of air (about 3500 milliliters) a person can breathe in, beginning at the normal expiratory level and distending the lungs to the maximum amount 6000 5000 Lung volume (ml) Pulmonary ventilation can be studied by recording the volume movement of air into and out of the lungs, a method called spirometry A typical basic spirometer is shown in Figure 38-5 It consists of a drum inverted over a chamber of water, with the drum counterbalanced by a weight In the drum is a breathing gas, usually air or oxygen; a tube connects the mouth with the gas chamber When one breathes into and out of the chamber, the drum rises and falls, and an appropriate recording is made on a moving sheet of paper Figure 38-6 shows a spirogram indicating changes in lung volume under different conditions of breathing For ease in describing the events of pulmonary ventilation, the air in the lungs has been subdivided in this diagram into four volumes and four capacities, which are the Water Pulmonary Volumes Pulmonary Capacities RECORDING CHANGES IN PULMONARY VOLUME—SPIROMETRY Oxygen chamber average for a young adult man Table 38-1 summarizes the average pulmonary volumes and capacities 4000 1000 Vital Total lung capacity capacity Tidal volume 3000 2000 Inspiratory capacity Inspiratory reserve volume Functional residual capacity Expiratory reserve volume Residual volume Time Figure 38-6. A diagram showing respiratory excursions during normal breathing and during maximal inspiration and maximal expiration 501 UNIT VII inspiration; expiration is almost entirely a passive process caused by elastic recoil of the lungs and chest cage Thus, under resting conditions, the respiratory muscles normally perform “work” to cause inspiration but not to cause expiration The work of inspiration can be divided into three frac tions: (1) that required to expand the lungs against the lung and chest elastic forces, called compliance work or elastic work; (2) that required to overcome the viscosity of the lung and chest wall structures, called tissue resistance work; and (3) that required to overcome airway resistance to move ment of air into the lungs, called airway resistance work Energy Required for Respiration. During normal quiet respiration, only to percent of the total energy expended by the body is required for pulmonary ventilation However, during heavy exercise, the amount of energy required can increase as much as 50-fold, especially if the person has any degree of increased airway resistance or decreased pulmo nary compliance Therefore, one of the major limitations on the intensity of exercise that can be performed is the person’s ability to provide enough muscle energy for the respiratory process alone Unit VII Respiration Table 38-1 Average Pulmonary Volumes and Capacities for a Healthy, Young Adult Man Pulmonary Volumes and Capacities Normal Values (ml) Table 38-2 Abbreviations and Symbols for Pulmonary Function VT Tidal volume FRC Functional residual capacity 500 ERV Expiratory reserve volume Inspiratory reserve volume 3000 RV Residual volume Expiratory volume 1100 IC Inspiratory capacity Residual volume 1200 IRV Inspiratory reserve volume TLC Total lung capacity Volumes Tidal volume Capacities Inspiratory capacity 3500 VC Vital capacity Functional residual capacity 2300 Raw Vital capacity 4600 Resistance of the airways to flow of air into the lung Total lung capacity 5800 C Compliance VD Volume of dead space gas VA Volume of alveolar gas VI Inspired volume of ventilation per minute The functional residual capacity equals the expiratory reserve volume plus the residual volume This capacity is the amount of air that remains in the lungs at the end of normal expiration (about 2300 milliliters) The vital capacity equals the inspiratory reserve volume plus the tidal volume plus the expiratory reserve volume This capacity is the maximum amount of air a person can expel from the lungs after first filling the lungs to their maximum extent and then expiring to the maximum extent (about 4600 milliliters) The total lung capacity is the maximum volume to which the lungs can be expanded with the greatest possible effort (about 5800 milliliters); it is equal to the vital capacity plus the residual volume All pulmonary volumes and capacities are usually about 20 to 25 percent less in women than in men, and they are greater in large and athletic people than in small and asthenic people ABBREVIATIONS AND SYMBOLS USED IN PULMONARY FUNCTION STUDIES Spirometry is only one of many measurement procedures that the pulmonary physician uses daily Many of these measurement procedures depend heavily on mathemati cal computations To simplify these calculations, as well as the presentation of pulmonary function data, several abbreviations and symbols have become standardized The more important of these are given in Table 38-2 Using these symbols, we present here a few simple alge braic exercises showing some of the interrelations among the pulmonary volumes and capacities; the student should think through and verify these interrelations VC = IRV + V T + ERV VC = IC + ERV TLC = VC + RV TLC = IC + FRC FRC = ERV + RV 502 VE Expired volume of ventilation per minute VS Shunt flow VA Alveolar ventilation per minute VO Rate of oxygen uptake per minute VCO2 Amount of carbon dioxide eliminated per minute VCO Rate of carbon monoxide uptake per minute DLO2 Diffusing capacity of the lungs for oxygen DLCO Diffusing capacity of the lungs for carbon monoxide PB Atmospheric pressure Palv Alveolar pressure Ppl Pleural pressure PO2 Partial pressure of oxygen PCO2 Partial pressure of carbon dioxide PN2 Partial pressure of nitrogen PaO2 Partial pressure of oxygen in arterial blood PaCO2 Partial pressure of carbon dioxide in arterial blood PAO2 Partial pressure of oxygen in alveolar gas PACO2 Partial pressure of carbon dioxide in alveolar gas PAH2O Partial pressure of water in alveolar gas R Respiratory exchange ratio Q Cardiac output CaO2 Concentration of oxygen in arterial blood CvO2 Concentration of oxygen in mixed venous blood SO2 Percentage saturation of hemoglobin with oxygen SaO2 Percentage saturation of hemoglobin with oxygen in arterial blood DETERMINATION OF FUNCTIONAL RESIDUAL CAPACITY, RESIDUAL VOLUME, AND TOTAL LUNG CAPACITY—HELIUM DILUTION METHOD The functional residual capacity (FRC), which is the volume of air that remains in the lungs at the end of each Chapter 38 Pulmonary Ventilation MINUTE RESPIRATORY VOLUME EQUALS RESPIRATORY RATE TIMES TIDAL VOLUME The minute respiratory volume is the total amount of new air moved into the respiratory passages each minute and is equal to the tidal volume times the respiratory rate per minute The normal tidal volume is about 500 milliliters, and the normal respiratory rate is about 12 breaths per minute Therefore, the minute respiratory volume averages about 6 L/min A person can live for a short period with a minute respiratory volume as low as 1.5 L/min and a respiratory rate of only to breaths per minute The respiratory rate occasionally rises to 40 to 50 per minute, and the tidal volume can become as great as the vital capacity, about 4600 milliliters in a young adult man This can give a minute respiratory volume greater than 200 L/min, or more than 30 times normal Most people cannot sustain more than one half to two thirds of these values for longer than minute Some of the air a person breathes never reaches the gas exchange areas but simply fills respiratory passages where gas exchange does not occur, such as the nose, pharynx, and trachea This air is called dead space air because it is not useful for gas exchange On expiration, the air in the dead space is expired first, before any of the air from the alveoli reaches the atmosphere Therefore, the dead space is very dis advantageous for removing the expiratory gases from the lungs Measurement of the Dead Space Volume. A simple method for measuring dead space volume is demonstrated by the graph in Figure 38-7 In making this measurement, the subject suddenly takes a deep breath of 100 percent O2, which fills the entire dead space with pure O2 Some oxygen also mixes with the alveolar air but does not completely replace this air Then the person expires through a rapidly recording nitrogen meter, which makes the record shown in the figure The first portion of the expired air comes from the dead space regions of the respiratory passageways, where the air has been completely replaced by O2 Therefore, in the early part of the record, only O2 appears, and the nitrogen concentration is zero Then, when alveolar air begins to reach the nitrogen meter, the nitrogen concentra tion rises rapidly, because alveolar air containing large amounts of nitrogen begins to mix with the dead space air After still more air has been expired, all the dead space air 80 60 40 20 gen concentration tro Reco rded ni RV = FRC − ERV and TLC = FRC + IC “DEAD SPACE” AND ITS EFFECT ON ALVEOLAR VENTILATION Inspiration of pure oxygen where FRC is functional residual capacity, CiHe is initial concentration of helium in the spirometer, CfHe is final concentration of helium in the spirometer, and ViSpir is initial volume of the spirometer Once the FRC has been determined, the residual volume (RV) can be determined by subtracting expiratory reserve volume (ERV), as measured by normal spirome try, from the FRC Also, the total lung capacity (TLC) can be determined by adding the inspiratory capacity (IC) to the FRC That is, The ultimate importance of pulmonary ventilation is to continually renew the air in the gas exchange areas of the lungs, where air is in proximity to the pulmonary blood These areas include the alveoli, alveolar sacs, alveolar ducts, and respiratory bronchioles The rate at which new air reaches these areas is called alveolar ventilation Percent nitrogen Ci FRC = He − 1 ViSpir CfHe ALVEOLAR VENTILATION 0 100 200 300 400 500 Air expired (ml) Figure 38-7. A record of the changes in nitrogen concentration in the expired air after a single previous inspiration of pure oxygen This record can be used to calculate dead space, as discussed in the text 503 UNIT VII normal expiration, is important to lung function Because its value changes markedly in some types of pulmonary disease, it is often desirable to measure this capacity The spirometer cannot be used in a direct way to measure the FRC because the air in the residual volume of the lungs cannot be expired into the spirometer, and this volume constitutes about one half of the FRC To measure FRC, the spirometer must be used in an indirect manner, usually by means of a helium dilution method, as follows A spirometer of known volume is filled with air mixed with helium at a known concentration Before breathing from the spirometer, the person expires normally At the end of this expiration, the remaining volume in the lungs is equal to the FRC At this point, the subject immediately begins to breathe from the spirometer, and the gases of the spirometer mix with the gases of the lungs As a result, the helium becomes diluted by the FRC gases, and the volume of the FRC can be calculated from the degree of dilution of the helium, using the following formula: Unit VII Respiration has been washed from the passages and only alveolar air remains Therefore, the recorded nitrogen concentration reaches a plateau level equal to its concentration in the alveoli, as shown to the right in the figure With a little thought, the student can see that the gray area represents the air that has no nitrogen in it; this area is a measure of the volume of dead space air For exact quantification, the following equation is used: VD = Gray area × VE Pink area + Gray area where VD is dead space air and VE is the total volume of expired air Let us assume, for instance, that the gray area on the graph is 30 square centimeters, the pink area is 70 square centimeters, and the total volume expired is 500 milliliters The dead space would be 30 × 500 = 150 ml 30 + 70 Normal Dead Space Volume. The normal dead space air in a young adult man is about 150 milliliters Dead space air increases slightly with age Anatomical Versus Physiological Dead Space. The method just described for measuring the dead space mea sures the volume of all the space of the respiratory system other than the alveoli and their other closely related gas exchange areas; this space is called the anatomic dead space On occasion, some of the alveoli are nonfunctional or only partially functional because of absent or poor blood flow through the adjacent pulmonary capillaries Therefore, from a functional point of view, these alveoli must also be considered dead space When the alveolar dead space is included in the total measurement of dead space, this is called the physiological dead space, in contradistinction to the anatomical dead space In a normal person, the ana tomical and physiological dead spaces are nearly equal because all alveoli are functional in the normal lung, but in a person with partially functional or nonfunctional alveoli in some parts of the lungs, the physiological dead space may be as much as 10 times the volume of the anatomical dead space, or to liters These problems are discussed further in Chapter 40 in relation to pulmonary gaseous exchange and in Chapter 43 in relation to certain pulmo nary diseases RATE OF ALVEOLAR VENTILATION Alveolar ventilation per minute is the total volume of new air entering the alveoli and adjacent gas exchange areas each minute It is equal to the respiratory rate times the amount of new air that enters these areas with each breath VA = Freq × ( VT − VD ) where V A is the volume of alveolar ventilation per minute, Freq is the frequency of respiration per minute, VT is the tidal volume, and VD is the physiologic dead space volume Thus, with a normal tidal volume of 500 milliliters, a normal dead space of 150 milliliters, and a respiratory rate 504 of 12 breaths per minute, alveolar ventilation equals 12 × (500 − 150), or 4200 ml/min Alveolar ventilation is one of the major factors deter mining the concentrations of oxygen and carbon dioxide in the alveoli Therefore, almost all discussions of gaseous exchange in the following chapters on the respiratory system emphasize alveolar ventilation Functions of the Respiratory Passageways Trachea, Bronchi, and Bronchioles Figure 38-8 highlights the respiratory passageways The air is distributed to the lungs by way of the trachea, bronchi, and bronchioles One of the most important challenges in the respiratory passageways is to keep them open and allow easy passage of air to and from the alveoli To keep the trachea from collapsing, multiple cartilage rings extend about five sixths of the way around the trachea In the walls of the bronchi, less extensive curved cartilage plates also maintain a rea sonable amount of rigidity yet allow sufficient motion for the lungs to expand and contract These plates become progressively less extensive in the later generations of bronchi and are gone in the bronchioles, which usually have diameters less than 1.5 millimeters The bronchioles are not prevented from collapsing by the rigidity of their walls Instead, they are kept expanded mainly by the same transpulmonary pressures that expand the alveoli That is, as the alveoli enlarge, the bronchioles also enlarge, but not as much Muscular Wall of the Bronchi and Bronchioles and Its Control. In all areas of the trachea and bronchi not occu pied by cartilage plates, the walls are composed mainly of smooth muscle Also, the walls of the bronchioles are almost entirely smooth muscle, with the exception of the most terminal bronchiole, called the respiratory bronchiole, which is mainly pulmonary epithelium and underlying fibrous tissue plus a few smooth muscle fibers Many obstructive diseases of the lung result from narrowing of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle Resistance to Airflow in the Bronchial Tree. Under normal respiratory conditions, air flows through the respi ratory passageways so easily that less than centimeter of water pressure gradient from the alveoli to the atmosphere is sufficient to cause enough airflow for quiet breathing The greatest amount of resistance to airflow occurs not in the minute air passages of the terminal bronchioles but in some of the larger bronchioles and bronchi near the trachea The reason for this high resistance is that there are relatively few of these larger bronchi in comparison with the approximately 65,000 parallel terminal bronchi oles, through each of which only a minute amount of air must pass In some disease conditions, the smaller bronchioles play a far greater role in determining airflow resistance because of their small size and because they are easily occluded by (1) muscle contraction in their walls, (2) edema occurring in the walls, or (3) mucus collecting in the lumens of the bronchioles Chapter 38 Pulmonary Ventilation Conchae Pharynx Epiglottis Glottis Larynx, vocal cords Trachea O2 O2 O2 CO2 CO2 UNIT VII CO2 Alveolus Pulmonary capillary Esophagus Pulmonary arteries Pulmonary veins Alveoli Figure 38-8. Respiratory passages Nervous and Local Control of the Bronchiolar Musculature—“Sympathetic” Dilation of the Bronchioles. Direct control of the bronchioles by sympathetic nerve fibers is relatively weak because few of these fibers pene trate to the central portions of the lung However, the bron chial tree is very much exposed to norepinephrine and epinephrine released into the blood by sympathetic stimu lation of the adrenal gland medullae Both these hormones, especially epinephrine because of its greater stimulation of beta-adrenergic receptors, cause dilation of the bronchial tree Parasympathetic Constriction of the Bronchioles. A few parasympathetic nerve fibers derived from the vagus nerves penetrate the lung parenchyma These nerves secrete acetylcholine and, when activated, cause mild to moderate constriction of the bronchioles When a disease process such as asthma has already caused some bronchio lar constriction, superimposed parasympathetic nervous stimulation often worsens the condition When this situa tion occurs, administration of drugs that block the effects of acetylcholine, such as atropine, can sometimes relax the respiratory passages enough to relieve the obstruction Sometimes the parasympathetic nerves are also acti vated by reflexes that originate in the lungs Most of these reflexes begin with irritation of the epithelial membrane of the respiratory passageways, initiated by noxious gases, dust, cigarette smoke, or bronchial infection Also, a bron chiolar constrictor reflex often occurs when microemboli occlude small pulmonary arteries Local Secretory Factors May Cause Bronchiolar Con striction. Several substances formed in the lungs are often quite active in causing bronchiolar constriction Two of the most important of these are histamine and slow reactive substance of anaphylaxis Both of these substances are released in the lung tissues by mast cells during allergic reactions, especially those caused by pollen in the air Therefore, they play key roles in causing the airway obstruc tion that occurs in allergic asthma; this is especially true of the slow reactive substance of anaphylaxis The same irritants that cause parasympathetic constric tor reflexes of the airways—smoke, dust, sulfur dioxide, and some of the acidic elements in smog—may also act directly on the lung tissues to initiate local, non-nervous reactions that cause obstructive constriction of the airways Mucus Lining the Respiratory Passageways, and Action of Cilia to Clear the Passageways All the respiratory passages, from the nose to the terminal bronchioles, are kept moist by a layer of mucus that coats the entire surface The mucus is secreted partly by indi vidual mucous goblet cells in the epithelial lining of the passages and partly by small submucosal glands In addi tion to keeping the surfaces moist, the mucus traps small particles out of the inspired air and keeps most of these particles from ever reaching the alveoli The mucus is removed from the passages in the following manner The entire surface of the respiratory passages, both in the nose and in the lower passages down as far as the 505 Unit VII Respiration terminal bronchioles, is lined with ciliated epithelium, with about 200 cilia on each epithelial cell These cilia beat con tinually at a rate of 10 to 20 times per second by the mecha nism explained in Chapter 2, and the direction of their “power stroke” is always toward the pharynx That is, the cilia in the lungs beat upward, whereas those in the nose beat downward This continual beating causes the coat of mucus to flow slowly, at a velocity of a few millimeters per minute, toward the pharynx Then the mucus and its entrapped particles are either swallowed or coughed to the exterior Cough Reflex The bronchi and trachea are so sensitive to light touch that slight amounts of foreign matter or other causes of irrita tion initiate the cough reflex The larynx and carina (i.e., the point where the trachea divides into the bronchi) are especially sensitive, and the terminal bronchioles and even the alveoli are sensitive to corrosive chemical stimuli such as sulfur dioxide gas or chlorine gas Afferent nerve impulses pass from the respiratory passages mainly through the vagus nerves to the medulla of the brain There, an automatic sequence of events is triggered by the neuronal circuits of the medulla, causing the following effect First, up to 2.5 liters of air are rapidly inspired Second, the epiglottis closes, and the vocal cords shut tightly to entrap the air within the lungs Third, the abdominal muscles contract forcefully, pushing against the diaphragm while other expiratory muscles, such as the internal inter costals, also contract forcefully Consequently, the pressure in the lungs rises rapidly to as much as 100 mm Hg or more Fourth, the vocal cords and the epiglottis suddenly open widely, so that air under this high pressure in the lungs explodes outward Indeed, sometimes this air is expelled at velocities ranging from 75 to 100 miles per hour Importantly, the strong compression of the lungs collapses the bronchi and trachea by causing their noncartilaginous parts to invaginate inward, so the exploding air actually passes through bronchial and tracheal slits The rapidly moving air usually carries with it any foreign matter that is present in the bronchi or trachea Sneeze Reflex The sneeze reflex is very much like the cough reflex, except that it applies to the nasal passageways instead of the lower respiratory passages The initiating stimulus of the sneeze reflex is irritation in the nasal passageways; the afferent impulses pass in the fifth cranial nerve to the medulla, where the reflex is triggered A series of reactions similar to those for the cough reflex takes place, but the uvula is depressed, so large amounts of air pass rapidly through the nose, thus helping to clear the nasal passages of foreign matter Normal Respiratory Functions of the Nose As air passes through the nose, three distinct normal respi ratory functions are performed by the nasal cavities: (1) the air is warmed by the extensive surfaces of the conchae and septum, a total area of about 160 square centimeters (see Figure 38-8); (2) the air is almost completely humidified even before it passes beyond the nose; and (3) the air is 506 partially filtered These functions together are called the air conditioning function of the upper respiratory passageways Ordinarily, the temperature of the inspired air rises to within 1°F of body temperature and to within to percent of full saturation with water vapor before it reaches the trachea When a person breathes air through a tube directly into the trachea (as through a tracheostomy), the cooling and especially the drying effect in the lower lung can lead to serious lung crusting and infection Filtration Function of the Nose. The hairs at the entrance to the nostrils are important for filtering out large particles Much more important, though, is the removal of particles by turbulent precipitation That is, the air passing through the nasal passageways hits many obstructing vanes: the conchae (also called turbinates, because they cause turbulence of the air); the septum; and the pharyn geal wall Each time air hits one of these obstructions, it must change its direction of movement The particles sus pended in the air, having far more mass and momentum than air, cannot change their direction of travel as rapidly as the air can Therefore, they continue forward, striking the surfaces of the obstructions, and are entrapped in the mucous coating and transported by the cilia to the pharynx to be swallowed Size of Particles Entrapped in the Respiratory Passages. The nasal turbulence mechanism for removing particles from air is so effective that almost no particles larger than micrometers in diameter enter the lungs through the nose This size is smaller than the size of red blood cells Of the remaining particles, many that are between and micrometers settle in the smaller bronchioles as a result of gravitational precipitation For instance, terminal bron chiolar disease is common in coal miners because of settled dust particles Some of the still smaller particles (smaller than micrometer in diameter) diffuse against the walls of the alveoli and adhere to the alveolar fluid However, many particles smaller than 0.5 micrometer in diameter remain suspended in the alveolar air and are expelled by expiration For instance, the particles of cigarette smoke are about 0.3 micrometer Almost none of these particles are precipi tated in the respiratory passageways before they reach the alveoli Unfortunately, up to one third of them precipi tate in the alveoli by the diffusion process, with the balance remaining suspended and expelled in the expired air Many of the particles that become entrapped in the alveoli are removed by alveolar macrophages, as explained in Chapter 34, and others are carried away by the lung lymphatics An excess of particles can cause growth of fibrous tissue in the alveolar septa, leading to permanent debility Vocalization Speech involves not only the respiratory system but also (1) specific speech nervous control centers in the cerebral cortex, which are discussed in Chapter 58; (2) respiratory control centers of the brain; and (3) the articulation and resonance structures of the mouth and nasal cavities Speech is composed of two mechanical functions: (1) phonation, which is achieved by the larynx, and (2) articulation, which is achieved by the structures of the mouth Chapter 84 Fetal and Neonatal Physiology Salmaso N, Jablonska B, Scafidi J, et al: Neurobiology of premature brain injury Nat Neurosci 17:341, 2014 Sferruzzi-Perri AN, Vaughan OR, Forhead AJ, Fowden AL: Hormonal and nutritional drivers of intrauterine growth Curr Opin Clin Nutr Metab Care 16:298, 2013 Sulemanji M, Vakili K: Neonatal renal physiology Semin Pediatr Surg 22:195, 2013 1081 UNIT XIV Muglia LJ, Katz M: The enigma of spontaneous preterm birth N Engl J Med 362:529, 2010 Osol G, Mandala M: Maternal uterine vascular remodeling during pregnancy Physiology (Bethesda) 24:58, 2009 Palinski W: Effect of maternal cardiovascular conditions and risk factors on offspring cardiovascular disease Circulation 129:2066, 2014 Raju TN: Developmental physiology of late and moderate prematurity Semin Fetal Neonatal Med 17:126, 2012 CHAPTER 5 There are few stresses to which the body is exposed that approach the extreme stresses of heavy exercise In fact, if some of the extremes of exercise were continued for even moderately prolonged periods, they might be lethal Therefore, sports physiology is mainly a discussion of the ultimate limits to which several of the bodily mechanisms can be stressed To give one simple example: In a person who has extremely high fever approaching the level of lethality, the body metabolism increases to about 100 percent above normal By comparison, the metabolism of the body during a marathon race may increase to 2000 percent above normal Female and Male Athletes Most of the quantitative data that are given in this chapter are for the young male athlete, not because it is desirable to know only these values, but because it is only in male athletes that relatively complete measurements have been made However, for measurements that have been made in the female athlete, similar basic physiological principles apply, except for quantitative differences caused by differences in body size, body composition, and the presence or absence of the male sex hormone testosterone In general, most quantitative values for women—such as muscle strength, pulmonary ventilation, and cardiac output, all of which are related mainly to the muscle mass—vary between two thirds and three quarters of the values recorded in men, although there are many exceptions to this generalization When measured in terms of strength per square centimeter of cross-sectional area, the female muscle can achieve almost exactly the same maximal force of contraction as that of the male muscle—between and 4 kg/cm2 Therefore, most of the difference in total muscle performance lies in the extra percentage of the male body that is muscle, which is caused partly by endocrine differences that we will discuss later The performance capabilities of the female versus male athlete are illustrated by the relative running speeds for a marathon race In a comparison, the top female performer had a running speed that was 11 percent less than that of the top male performer For other events, however, women have at times held records faster than men—for instance, for the two-way swim across the English Channel, for which the availability of extra fat seems to be an advantage for heat insulation, buoyancy, and extra long-term energy Testosterone secreted by the male testes has a powerful anabolic effect in causing greatly increased deposition of protein everywhere in the body, but especially in the muscles In fact, even a male who participates in very little sports activity but who nevertheless has a normal level of testosterone will have muscles that grow about 40 percent larger than those of a comparable female without the testosterone The female sex hormone estrogen probably also accounts for some of the difference between female and male performance, although not nearly so much as testosterone Estrogen increases the deposition of fat in the female, especially in the breasts, hips, and subcutaneous tissue At least partly for this reason, the average nonathletic female has about 27 percent body fat composition, in contrast to the nonathletic male, who has about 15 percent This increased body fat composition is a detriment to the highest levels of athletic performance in events in which performance depends on speed or on the ratio of total body muscle strength to body weight Muscles in Exercise Strength, Power, and Endurance of Muscles The final common determinant of success in athletic events is what the muscles can for you—that is, what strength they can give when it is needed, what power they can achieve in the performance of work, and how long they can continue their activity The strength of a muscle is determined mainly by its size, with a maximal contractile force between and 4 kg/cm2 of muscle cross-sectional area Thus, a man who is well supplied with testosterone or who has enlarged his muscles through an exercise training program will have correspondingly increased muscle strength To give an example of muscle strength, a world-class weight lifter might have a quadriceps muscle with a crosssectional area as great as 150 square centimeters This measurement would translate into a maximal contractile strength of 525 kilograms (or 1155 pounds), with all this force applied to the patellar tendon Therefore, one can readily understand how it is possible for this tendon at times to be ruptured or actually to be avulsed from its insertion into the tibia below the knee Also, when such forces occur in tendons that span a joint, similar forces are applied to the surfaces of the joint or sometimes to ligaments spanning the joints, thus accounting for such 1085 UNIT XV Sports Physiology Unit XV Sports Physiology happenings as displaced cartilages, compression fractures about the joint, and torn ligaments The holding strength of muscles is about 40 percent greater than the contractile strength That is, if a muscle is already contracted and a force then attempts to stretch out the muscle, as occurs when landing after a jump, this action requires about 40 percent more force than can be achieved by a shortening contraction Therefore, the force of 525 kilograms previously calculated for the patellar tendon during muscle contraction becomes 735 kilograms (1617 pounds) during holding contractions, which further compounds the problems of the tendons, joints, and ligaments It can also lead to internal tearing in the muscle In fact, forceful stretching of a maximally contracted muscle is one of the surest ways to create the highest degree of muscle soreness Mechanical work performed by a muscle is the amount of force applied by the muscle multiplied by the distance over which the force is applied The power of muscle contraction is different from muscle strength because power is a measure of the total amount of work that the muscle performs in a unit period of time Power is therefore determined not only by the strength of muscle contraction but also by its distance of contraction and the number of times that it contracts each minute Muscle power is generally measured in kilogram meters (kg-m) per minute That is, a muscle that can lift kilogram weight to a height of meter or that can move some object laterally against a force of kilogram for a distance of meter in minute is said to have a power of 1 kg-m/min The maximal power achievable by all the muscles in the body of a highly trained athlete with all the muscles working together is approximately the following: glycogen in muscles than does a person who consumes either a mixed diet or a high-fat diet Therefore, endurance is enhanced by a high-carbohydrate diet When athletes run at speeds typical for the marathon race, their endurance (as measured by the time that they can sustain the race until complete exhaustion) is approximately the following: Minutes High-carbohydrate diet 240 Mixed diet 120 High-fat diet 85 The corresponding amounts of glycogen stored in the muscle before the race started explain these differences The amounts stored are approximately the following: g/kg Muscle High-carbohydrate diet 40 Mixed diet 20 High-fat diet Muscle Metabolic Systems in Exercise kg-m/min The same basic metabolic systems are present in muscle as in other parts of the body; these systems are discussed in detail in Chapters 68 through 74 However, special quantitative measures of the activities of three metabolic systems are exceedingly important in understanding the limits of physical activity These systems are (1) the phosphocreatinecreatine system, (2) the glycogen–lactic acid system, and (3) the aerobic system Adenosine Triphosphate. The source of energy actually used to cause muscle contraction is adenosine triphosphate (ATP), which has the following basic formula: First to 10 seconds 7000 Adenosine-PO3 ~ PO3 ~ PO3− Next minute 4000 Next 30 minutes 1700 The bonds attaching the last two phosphate radicals to the molecule, designated by the symbol ~, are high-energy phosphate bonds Each of these bonds stores 7300 calories of energy per mole of ATP under standard conditions (and even slightly more than this under the physical conditions in the body, which is discussed in detail in Chapter 68) Therefore, when one phosphate radical is removed, more than 7300 calories of energy are released to energize the muscle contractile process Then, when the second phosphate radical is removed, still another 7300 calories become available Removal of the first phosphate converts the ATP into adenosine diphosphate (ADP), and removal of the second converts this ADP into adenosine monophosphate (AMP) The amount of ATP present in the muscles, even in a well-trained athlete, is sufficient to sustain maximal muscle power for only about seconds, which might be enough for one half of a 50-meter dash Therefore, except for a few seconds at a time, it is essential that new ATP be formed continuously, even during the performance of short athletic events Figure 85-1 shows the overall metabolic system, demonstrating the breakdown of ATP first to ADP and then to AMP, with the release of energy to the muscles for contraction The left-hand side of the figure shows the Thus, it is clear that a person has the capability of extreme power surges for short periods, such as during a 100-meter dash that is completed entirely within 10 seconds, whereas for long-term endurance events, the power output of the muscles is only one fourth as great as during the initial power surge This does not mean that one’s athletic performance is four times as great during the initial power surge as it is for the next 30 minutes, because the efficiency for translation of muscle power output into athletic performance is often much less during rapid activity than during less rapid but sustained activity Thus, the velocity of the 100-meter dash is only 1.75 times as great as the velocity of a 30-minute race, despite the fourfold difference in short-term versus long-term muscle power capability Another measure of muscle performance is endurance Endurance, to a great extent, depends on the nutritive support for the muscle—more than anything else, it depends on the amount of glycogen that has been stored in the muscle before the period of exercise A person who consumes a high-carbohydrate diet stores far more 1086 Chapter 85 Sports Physiology Creatine + PO3− II Glycogen Lactic acid III Glucose Fatty acids Amino acids three metabolic systems that provide a continuous supply of ATP in the muscle fibers Phosphocreatine-Creatine System Phosphocreatine (also called creatine phosphate) is another chemical compound that has a high-energy phosphate bond, with the following formula: Creatine ~ PO3− Phosphocreatine can decompose to creatine and phosphate ion, as shown in Figure 85-1, and in doing so releases large amounts of energy In fact, the high-energy phosphate bond of phosphocreatine has more energy than the bond of ATP: 10,300 calories per mole compared with 7300 for the ATP bond Therefore, phosphocreatine can easily provide enough energy to reconstitute the high-energy bond of ATP Furthermore, most muscle cells have two to four times as much phosphocreatine as ATP A special characteristic of energy transfer from phosphocreatine to ATP is that it occurs within a small fraction of a second Therefore, all the energy stored in muscle phosphocreatine is almost instantaneously available for muscle contraction, just as is the energy stored in ATP The combined amounts of cell ATP and cell phosphocreatine are called the phosphagen energy system These substances together can provide maximal muscle power for to 10 seconds, almost enough for the 100-meter run Thus, the energy from the phosphagen system is used for maximal short bursts of muscle power Glycogen–Lactic Acid System. The stored glycogen in muscle can be split into glucose, and the glucose can then be used for energy The initial stage of this process, called glycolysis, occurs without use of oxygen and, therefore, is said to be anaerobic metabolism (see Chapter 68) During glycolysis, each glucose molecule is split into two pyruvic acid molecules, and energy is released to form four ATP molecules for each original glucose molecule, as explained in Chapter 68 Ordinarily, the pyruvic acid then enters the mitochondria of muscle cells and reacts with oxygen to form still many more ATP molecules However, when there is insufficient oxygen for this second stage (the oxidative stage) of glucose metabolism to occur, most of the pyruvic acid then is converted into lactic acid, which diffuses out of the muscle cells into the interstitial fluid and blood Therefore, much of the muscle glycogen is transformed to lactic acid, but in doing so, considerable amounts of ATP are formed entirely without consumption of oxygen + O2 CO2 + H2O + Urea ATP Energy for muscle contraction ADP AMP Another characteristic of the glycogen–lactic acid system is that it can form ATP molecules about 2.5 times as rapidly as can the oxidative mechanism of mitochondria Therefore, when large amounts of ATP are required for short to moderate periods of muscle contraction, this anaerobic glycolysis mechanism can be used as a rapid source of energy However, it is only about one half as rapid as the phosphagen system Under optimal conditions, the glycogen–lactic acid system can provide 1.3 to 1.6 minutes of maximal muscle activity in addition to the to 10 seconds provided by the phosphagen system, although at somewhat reduced muscle power Aerobic System. The aerobic system is the oxidation of foodstuffs in the mitochondria to provide energy That is, as shown to the left in Figure 85-1, glucose, fatty acids, and amino acids from the foodstuffs—after some intermediate processing—combine with oxygen to release tremendous amounts of energy that are used to convert AMP and ADP into ATP, as discussed in Chapter 68 In comparing this aerobic mechanism of energy supply with the glycogen–lactic acid system and the phosphagen system, the relative maximal rates of power generation in terms of moles of ATP generation per minute are the following: Moles of ATP/min Phosphagen system Glycogen–lactic acid system 2.5 Aerobic system When comparing the same systems for endurance, the relative values are the following: Time Phosphagen system 8-10 seconds Glycogen–lactic acid system 1.3-1.6 minutes Aerobic system Unlimited time (as long as nutrients last) Thus, one can readily see that the phosphagen system is used by the muscle for power surges of a few seconds and the aerobic system is required for prolonged athletic activity In between is the glycogen–lactic acid system, which is especially important for providing extra power during such intermediate races as 200- to 800-meter runs What Types of Sports Use Which Energy Systems? By considering the vigor of a sports activity and its duration, 1087 UNIT XV Figure 85-1. Important metabolic systems that supply energy for muscle contraction I Phosphocreatine Phosphagen System, Almost Entirely 100-meter dash Jumping Weight lifting Diving Football dashes Baseball triple Phosphagen and Glycogen–Lactic Acid Systems 200-meter dash Basketball Ice hockey dashes Glycogen–lactic acid system, mainly 400-meter dash 100-meter swim Tennis Soccer Alactacid oxygen debt = 3.5 liters Exercise Table 85-1 Energy Systems Used in Various Sports Rate of oxygen uptake (L/min) Unit XV Sports Physiology Lactic acid oxygen debt = liters 12 16 20 24 28 32 36 40 44 Minutes Figure 85-2. Rate of oxygen uptake by the lungs during maximal exercise for minutes and then for about 40 minutes after the exercise is over This figure demonstrates the principle of oxygen debt Glycogen–Lactic Acid and Aerobic Systems 800-meter dash 200-meter swim 1500-meter skating Boxing 2000-meter rowing 1500-meter run 1-mile run 400-meter swim Aerobic System 10,000-meter skating Cross-country skiing Marathon run (26.2 miles, 42.2 kilometers) Jogging one can estimate closely which of the energy systems is used for each activity Various approximations are presented in Table 85-1 Recovery of the Muscle Metabolic Systems After Exercise. In the same way that the energy from phospho- creatine can be used to reconstitute ATP, energy from the glycogen–lactic acid system can be used to reconstitute both phosphocreatine and ATP Energy from the oxidative metabolism of the aerobic system can then be used to reconstitute all the other systems—the ATP, phosphocreatine, and glycogen–lactic acid systems Reconstitution of the lactic acid system means mainly the removal of the excess lactic acid that has accumulated in the body fluids Removal of the excess lactic acid is especially important because lactic acid causes extreme fatigue When adequate amounts of energy are available from oxidative metabolism, removal of lactic acid is achieved in two ways: (1) A small portion of it is converted back into pyruvic acid and then metabolized oxidatively by the body tissues, and (2) the remaining lactic acid is reconverted into glucose mainly in the liver, and the glucose in turn is used to replenish the glycogen stores of the muscles Recovery of the Aerobic System After Exercise. Even during the early stages of heavy exercise, a portion of one’s aerobic energy capability is depleted This depletion results from two effects: (1) the so-called oxygen debt and (2) depletion of the glycogen stores of the muscles 1088 Oxygen Debt. The body normally contains about liters of stored oxygen that can be used for aerobic metabolism even without breathing any new oxygen This stored oxygen consists of the following: (1) 0.5 liter in the air of the lungs, (2) 0.25 liter dissolved in the body fluids, (3) liter combined with the hemoglobin of the blood, and (4) 0.3 liter stored in the muscle fibers, combined mainly with myoglobin, an oxygen-binding chemical similar to hemoglobin In heavy exercise, almost all this stored oxygen is used within a minute or so for aerobic metabolism Then, after the exercise is over, this stored oxygen must be replenished by breathing extra amounts of oxygen over and above the normal requirements In addition, about liters more oxygen must be consumed to reconstitute both the phosphagen system and the lactic acid system All this extra oxygen that must be “repaid,” about 11.5 liters, is called the oxygen debt Figure 85-2 shows this principle of oxygen debt During the first minutes, as depicted in the figure, the person exercises heavily, and the rate of oxygen uptake increases more than 15-fold Then, even after the exercise is over, the oxygen uptake still remains above normal; at first it is very high while the body is reconstituting the phosphagen system and repaying the stored oxygen portion of the oxygen debt, and then it is still above normal although at a lower level for another 40 minutes while the lactic acid is removed The early portion of the oxygen debt is called the alactacid oxygen debt and amounts to about 3.5 liters The latter portion is called the lactic acid oxygen debt and amounts to about liters Recovery of Muscle Glycogen. Recovery from exhaustive muscle glycogen depletion is not a simple matter This process often requires days, rather than the seconds, minutes, or hours required for recovery of the phosphagen and lactic acid metabolic systems Figure 85-3 shows this recovery process under three conditions: first, in people who consume a high-carbohydrate diet; second, in people who consume a high-fat, high-protein diet; and third, in people who consume no food Note that for persons who consume a high-carbohydrate diet, full recovery occurs in about days Conversely, people who consume a high-fat, 24 20 High-carbohydrate diet 16 12 No food Fat and protein diet 0 10 20 30 40 50 Hours of recovery days Figure 85-3. The effect of diet on the rate of muscle glycogen replenishment after prolonged exercise (Modified from Fox EL: Sports Physiology Philadelphia: Saunders College Publishing, 1979.) High-carbohydrate diet 25 75 50 25 50 Mixed diet 10 20 40 75 Exhaustion High-fat diet Percent fat usage Percent carbohydrate usage 100 100 Seconds Minutes Hours Duration of exercise Figure 85-4. The effect of duration of exercise, as well as type of diet, on relative percentages of carbohydrate or fat used for energy by muscles (Data from Fox EL: Sports Physiology Philadelphia: Saunders College Publishing, 1979.) high-protein diet or no food at all show very little recovery even after as long as days The messages of this com parison are (1) it is important for athletes to consume a high-carbohydrate diet before a grueling athletic event and (2) athletes should not participate in exhaustive exercise during the 48 hours preceding the event Nutrients Used During Muscle Activity In addition to the use of a large amount of carbohydrates by the muscles during exercise, especially during the early stages of exercise, muscles use large amounts of fat for energy in the form of fatty acids and acetoacetic acid (see Chapter 69), as well as (to a much less extent) proteins in the form of amino acids In fact, even under the best conditions, in endurance athletic events that last longer than to hours, the glycogen stores of the muscle become almost totally depleted and are of little further use for energizing muscle contraction Instead, the muscle now depends on energy from other sources, mainly from fats Figure 85-4 shows the approximate relative usage of carbohydrates and fat for energy during prolonged Percent increase in strength hours of exercise Resistive training 30 25 20 UNIT XV Muscle glycogen content (g/kg muscle) Chapter 85 Sports Physiology 15 10 No-load training 0 Weeks of training 10 Figure 85-5. Approximate effect of optimal resistive exercise training on increase in muscle strength over a training period of 10 weeks exhaustive exercise under three dietary conditions: a highcarbohydrate diet, a mixed diet, and a high-fat diet Note that most of the energy is derived from carbohydrates during the first few seconds or minutes of the exercise, but at the time of exhaustion, as much as 60 to 85 percent of the energy is being derived from fats rather than carbohydrates Not all the energy from carbohydrates comes from the stored muscle glycogen In fact, almost as much glycogen is stored in the liver as in the muscles, and this glycogen can be released into the blood in the form of glucose and then taken up by the muscles as an energy source In addition, glucose solutions given to an athlete to drink during the course of an athletic event can provide as much as 30 to 40 percent of the energy required during prolonged events such as marathon races Therefore, if muscle glycogen and blood glucose are available, they are the energy nutrients of choice for intense muscle activity Even so, for a long-term endurance event, one can expect fat to supply more than 50 percent of the required energy after about the first to hours Effect of Athletic Training on Muscles and Muscle Performance Importance of Maximal Resistance Training. One of the cardinal principles of muscle development during athletic training is the following: Muscles that function under no load, even if they are exercised for hours on end, increase little in strength At the other extreme, muscles that contract at more than 50 percent maximal force of contraction will develop strength rapidly even if the contractions are performed only a few times each day Using this principle, experiments on muscle building have shown that six nearly maximal muscle contractions performed in three sets days a week give approximately optimal increase in muscle strength without producing chronic muscle fatigue The upper curve in Figure 85-5 shows the approximate percentage increase in strength that can be achieved in a previously untrained young person by this resistive training program, demonstrating that the muscle strength increases about 30 percent during the first to weeks but almost plateaus after that time Along with this increase in strength is an approximately equal percentage increase in muscle mass, which is called muscle hypertrophy 1089 Unit XV Sports Physiology In old age, many people become so sedentary that their muscles atrophy tremendously In these instances, however, muscle training may increase muscle strength more than 100 percent Muscle Hypertrophy. The average size of a person’s muscles is determined to a great extent by heredity plus the level of testosterone secretion, which, in men, causes considerably larger muscles than in women With training, however, the muscles can become hypertrophied perhaps an additional 30 to 60 percent Most of this hypertrophy results from increased diameter of the muscle fibers rather than increased numbers of fibers However, a very few greatly enlarged muscle fibers are believed to split down the middle along their entire length to form entirely new fibers, thus increasing the number of fibers slightly The changes that occur inside the hypertrophied muscle fibers include (1) increased numbers of myofibrils, proportionate to the degree of hypertrophy; (2) up to 120 percent increase in mitochondrial enzymes; (3) as much as 60 to 80 percent increase in the components of the phosphagen metabolic system, including both ATP and phosphocreatine; (4) as much as 50 percent increase in stored glycogen; and (5) as much as 75 to 100 percent increase in stored triglyceride (fat) Because of all these changes, the capabilities of both the anaerobic and the aerobic metabolic systems are increased, especially increasing the maximum oxidation rate and efficiency of the oxidative metabolic system as much as 45 percent Fast-Twitch and Slow-Twitch Muscle Fibers. In the human being, all muscles have varying percentages of fast-twitch and slow-twitch muscle fibers For instance, the gastrocnemius muscle has a higher preponderance of fast-twitch fibers, which gives it the capability of forceful and rapid contraction of the type used in jumping In contrast, the soleus muscle has a higher preponderance of slow-twitch muscle fibers and therefore is used to a greater extent for prolonged lower leg muscle activity The basic differences between the fast-twitch and the slow-twitch fibers are the following: Fast-twitch fibers are about twice as large in diameter compared with slow-twitch fibers The enzymes that promote rapid release of energy from the phosphagen and glycogen–lactic acid energy systems are two to three times as active in fast-twitch fibers as in slow-twitch fibers, thus making the maximal power that can be achieved for very short periods by fast-twitch fibers about twice as great as that of slow-twitch fibers Slow-twitch fibers are mainly organized for endurance, especially for generation of aerobic energy They have far more mitochondria than the fasttwitch fibers In addition, they contain considerably more myoglobin, a hemoglobin-like protein that combines with oxygen within the muscle fiber; the extra myoglobin increases the rate of diffusion of oxygen throughout the fiber by shuttling oxygen from one molecule of myoglobin to the next In addition, the enzymes of the aerobic metabolic system are considerably more active in slow-twitch fibers than in fast-twitch fibers 1090 The number of capillaries is greater in the vicinity of slow-twitch fibers than in the vicinity of fast-twitch fibers In summary, fast-twitch fibers can deliver extreme amounts of power for a few seconds to a minute or so Conversely, slow-twitch fibers provide endurance, delivering prolonged strength of contraction over many minutes to hours Hereditary Differences Among Athletes for FastTwitch Versus Slow-Twitch Muscle Fibers. Some people have considerably more fast-twitch than slow-twitch fibers, and others have more slow-twitch fibers; this factor could determine to some extent the athletic capabilities of different individuals Athletic training has not been shown to change the relative proportions of fast-twitch and slowtwitch fibers, however much an athlete might want to develop one type of athletic prowess over another Instead, the relative proportions of fast-twitch and slow-twitch fibers seem to be determined almost entirely by genetic inheritance, which in turn helps determine which area of athletics is most suited to each person: some people appear to be born to be marathoners, whereas others are born to be sprinters and jumpers For example, the following values are recorded percentages of fast-twitch versus slow-twitch fiber in the quadriceps muscles of different types of athletes: Fast-Twitch Slow-Twitch Marathoners 18 82 Swimmers 26 74 Average male 55 45 Weight lifters 55 45 Sprinters 63 37 Jumpers 63 37 Respiration in Exercise Although one’s respiratory ability is of relatively little concern in the performance of sprint types of athletics, it is critical for maximal performance in endurance athletics Oxygen Consumption and Pulmonary Ventilation in Exercise. Normal oxygen consumption for a young man at rest is about 250 ml/min However, under maximal conditions, this consumption can be increased to approximately the following average levels: ml/min Untrained average male 3600 Athletically trained average male 4000 Male marathon runner 5100 Figure 85-6 shows the relation between oxygen consumption and total pulmonary ventilation at different levels of exercise As would be expected, there is a linear relation Both oxygen consumption and total pulmonary ventila tion increase about 20-fold between the resting state and maximal intensity of exercise in the well-trained athlete Limits of Pulmonary Ventilation. How severely we stress our respiratory systems during exercise? This Chapter 85 Sports Physiology 110 100 80 60 40 Moderate exercise 20 0 Severe exercise 1.0 2.0 3.0 4.0 O2 consumption (L/min) Figure 85-6. Effect of exercise on oxygen consumption and ventilatory rate (Modified from Gray JS: Pulmonary Ventilation and Its Physiological Regulation Springfield, Ill: Charles C Thomas, 1950.) • Vo2max (L/min) 3.8 3.6 3.4 Training frequency = days/wk = days/wk = days/wk 3.2 3.0 2.8 percent Furthermore, the frequency of training, whether two times or five times per week, had little effect on the increase in VO2max Yet, as pointed out earlier, the VO2 max of a marathoner is about 45 percent greater than that of an untrained person Part of this greater VO2max of the marathoner probably is genetically determined; that is, people who have greater chest sizes in relation to body size and stronger respiratory muscles select themselves to become marathoners However, it is also likely that many years of training increase the marathoner’s VO2max by values considerably greater than the 10 percent that has been recorded in short-term experiments such as that in Figure 85-7 Oxygen-Diffusing Capacity of Athletes. The oxygendiffusing capacity is a measure of the rate at which oxygen can diffuse from the pulmonary alveoli into the blood This capacity is expressed in terms of milliliters of oxygen that will diffuse each minute for each millimeter of mercury difference between alveolar partial pressure of oxygen and pulmonary blood oxygen pressure That is, if the partial pressure of oxygen in the alveoli is 91 mm Hg and the oxygen pressure in the blood is 90 mm Hg, the amount of oxygen that diffuses through the respiratory membrane each minute is equal to the diffusing capacity The follow ing values are measured values for different diffusing capacities: ml/min 10 Weeks of training 12 14 Figure 85-7. Increase in VO2 max over a period of to 13 weeks of athletic training (Modified from Fox EL: Sports Physiology Philadelphia: Saunders College Publishing, 1979.) question can be answered by the following comparison for a normal young man: L/min Pulmonary ventilation at maximal exercise 100-110 Maximal breathing capacity 150-170 Thus, the maximal breathing capacity is about 50 percent greater than the actual pulmonary ventilation during maximal exercise This difference provides an element of safety for athletes, giving them extra ventilation that can be called on in such conditions as (1) exercise at high altitudes, (2) exercise under very hot conditions, and (3) abnormalities in the respiratory system The important point is that the respiratory system is not normally the most limiting factor in the delivery of oxygen to the muscles during maximal muscle aerobic metabolism We shall see shortly that the ability of the heart to pump blood to the muscles is usually a greater limiting factor Effect of Training on VO2max. The abbreviation for the rate of oxygen usage under maximal aerobic metabolism is VO2 max Figure 85-7 shows the progressive effect of athletic training on VO2max recorded in a group of subjects beginning at the level of no training and then while pursuing the training program for to 13 weeks In this study, it is surprising that the VO2max increased only about 10 Nonathlete at rest 23 Nonathlete during maximal exercise 48 Speed skater during maximal exercise 64 Swimmer during maximal exercise 71 Oarsman during maximal exercise 80 The most startling fact about these results is the severalfold increase in diffusing capacity between the resting state and the state of maximal exercise This finding results mainly from the fact that blood flow through many of the pulmonary capillaries is sluggish or even dormant in the resting state, whereas in maximal exercise, increased blood flow through the lungs causes all the pulmonary capillaries to be perfused at their maximal rates, thus providing a far greater surface area through which oxygen can diffuse into the pulmonary capillary blood It is also clear from these values that athletes who require greater amounts of oxygen per minute have higher diffusing capacities Is this the case because people with naturally greater diffusing capacities choose these types of sports, or is it because something about the training procedures increases the diffusing capacity? The answer is not known, but it is very likely that training, particularly endurance training, does play an important role Blood Gases During Exercise. Because of the great usage of oxygen by the muscles in exercise, one would expect the oxygen pressure of the arterial blood to decrease markedly during strenuous athletics and the carbon dioxide pressure of the venous blood to increase far above normal However, this normally is not the case Both of these values remain nearly normal, demonstrating the extreme ability 1091 UNIT XV Total ventilation (L/min) 120 of the respiratory system to provide adequate aeration of the blood even during heavy exercise This demonstrates another important point: The blood gases not always have to become abnormal for respiration to be stimulated in exercise Instead, respiration is stimulated mainly by neurogenic mechanisms during exercise, as discussed in Chapter 42 Part of this stimulation results from direct stimulation of the respiratory center by the same nervous signals that are transmitted from the brain to the muscles to cause the exercise An additional part is believed to result from sensory signals transmitted into the respiratory center from the contracting muscles and moving joints All this extra nervous stimulation of respiration is normally sufficient to provide almost exactly the necessary increase in pulmonary ventilation required to keep the blood respiratory gases—the oxygen and the carbon dioxide—very near to normal Effect of Smoking on Pulmonary Ventilation in Exercise. It is widely known that smoking can decrease an athlete’s “wind.” This is true for many reasons First, one effect of nicotine is constriction of the terminal bronchioles of the lungs, which increases the resistance of airflow into and out of the lungs Second, the irritating effects of the smoke cause increased fluid secretion into the bronchial tree, as well as some swelling of the epithelial linings Third, nicotine paralyzes the cilia on the surfaces of the respiratory epithelial cells that normally beat continuously to remove excess fluids and foreign particles from the respiratory passageways As a result, much debris accumulates in the passageways and adds further to the difficulty of breathing After putting all these factors together, even a light smoker often feels respiratory strain during maximal exercise, and the level of performance may be reduced Much more severe are the effects of chronic smoking There are few chronic smokers in whom some degree of emphysema does not develop In this disease, the following mechanisms occur: (1) chronic bronchitis, (2) obstruction of many of the terminal bronchioles, and (3) destruction of many alveolar walls In persons with severe emphysema, as much as four fifths of the respiratory membrane can be destroyed; then even the slightest exercise can cause respiratory distress In fact, many such patients cannot even perform the simple feat of walking across the floor of a single room without gasping for breath Cardiovascular System in Exercise Muscle Blood Flow. A key requirement of cardiovascular function in exercise is to deliver the required oxygen and other nutrients to the exercising muscles For this purpose, the muscle blood flow increases drastically during exercise Figure 85-8 shows a recording of muscle blood flow in the calf of a person for a period of minutes during moderately strong intermittent contractions Note not only the great increase in flow—about 13-fold—but also the flow decrease during each muscle contraction Two points can be made from this study: The actual contractile process itself temporarily decreases muscle blood flow because the contracting skeletal muscle compresses the intramuscular blood vessels; therefore, strong tonic muscle contractions 1092 Calf blood flow (100 mL/min) Unit XV Sports Physiology Rhythmic exercise 40 20 10 16 18 Minutes Figure 85-8. Effects of muscle exercise on blood flow in the calf of a leg during strong rhythmical contraction The blood flow was much less during contraction than between contractions (Modified from Barcroft J, Dornhorst AC: The blood flow through the human calf during rhythmic exercise, J Physiol 109:402, 1949.) can cause rapid muscle fatigue because of lack of delivery of enough oxygen and other nutrients during the continuous contraction The blood flow to muscles during exercise increases markedly The following comparison shows the maximal increase in blood flow that can occur in a well-trained athlete ml/100 g Muscle/min Resting blood flow Blood flow during maximal exercise 3.6 90 Thus, muscle blood flow can increase a maximum of about 25-fold during the most strenuous exercise Almost one half this increase in flow results from intramuscular vasodilation caused by the direct effects of increased muscle metabolism, as explained in Chapter 21 The remaining increase results from multiple factors, the most important of which is probably the moderate increase in arterial blood pressure that occurs in exercise, which is usually about a 30 percent increase The increase in pressure not only forces more blood through the blood vessels but also stretches the walls of the arterioles and further reduces the vascular resistance Therefore, a 30 percent increase in blood pressure can often more than double the blood flow, which multiplies the great increase in flow already caused by the metabolic vasodilation at least another twofold Work Output, Oxygen Consumption, and Cardiac Output During Exercise. Figure 85-9 shows the inter relations among work output, oxygen consumption, and cardiac output during exercise It is not surprising that all these factors are directly related to one another, as shown by the linear functions, because the muscle work output increases oxygen consumption, and increased oxygen consumption in turn dilates the muscle blood vessels, thus increasing venous return and cardiac output Typical cardiac outputs at several levels of exercise are as follows: 20 15 10 nd ut a C n yge ex ind ca utp co ia ard c rdia n ptio m nsu co Ox 0 200 400 600 800 1000120014001600 Work output during exercise (kg-m/min) Figure 85-9. Relation between cardiac output and work output (solid line) and between oxygen consumption and work output (dashed line) during different levels of exercise The different colored dots and squares show data derived from different studies in humans (Modified from Guyton AC, Jones CE, Coleman TB: Circulatory Physiology: Cardiac Output and Its Regulation Philadelphia: WB Saunders, 1973.) L/min Cardiac output in a young man at rest 5.5 Maximal cardiac output during exercise in a young untrained man 23 Maximal cardiac output during exercise in an average male marathoner 30 Thus, the normal untrained person can increase cardiac output a little over fourfold, and the well-trained athlete can increase output about sixfold (Individual marathoners have been clocked at cardiac outputs as great as 35 to 40 L/ min, or seven to eight times normal resting output.) Effect of Training on Heart Hypertrophy and on Cardiac Output. From the foregoing data, it is clear that marathoners can achieve maximal cardiac outputs that are about 40 percent greater than those achieved by untrained persons This results mainly from the fact that the heart chambers of marathoners enlarge about 40 percent; along with this enlargement of the chambers, the heart mass also increases 40 percent or more Therefore, not only the skeletal muscles hypertrophy during athletic training, but so does the heart However, heart enlargement and increased pumping capacity occur almost entirely in the endurance types, not in the sprint types, of athletic training Even though the heart of the marathoner is considerably larger than that of the normal person, resting cardiac output is almost exactly the same as that in a normal person However, this normal cardiac output is achieved by a large stroke volume at a reduced heart rate Table 85-2 compares stroke volume and heart rate in the untrained person and the marathoner Thus, the heart-pumping effectiveness of each heartbeat is 40 to 50 percent greater in the highly trained athlete than in the untrained person, but there is a corresponding decrease in the heart rate at rest Role of Stroke Volume and Heart Rate in Increasing the Cardiac Output. Figure 85-10 shows the approximate changes in stroke volume and heart rate as the cardiac output increases from its resting level of about 5.5 L/min to 30 L/min in the marathon runner The stroke volume Stroke Volume (ml) Heart Rate (beats/min) Resting Nonathlete Marathoner 75 105 75 50 Maximum Nonathlete Marathoner 110 162 195 185 190 170 Stroke volume 165 150 130 150 110 135 90 Heart rate 120 70 105 Heart rate (beats/min) 25 Table 85-2 Comparison of Cardiac Function Between Marathoner and Nonathlete Stroke volume (ml/beat) 10 Cardiac output (L/min) 15 30 50 10 15 20 25 Cardiac output (L/min) 30 Figure 85-10. Approximate stroke volume output and heart rate at different levels of cardiac output in a marathon athlete increases from 105 to 162 milliliters, an increase of about 50 percent, whereas the heart rate increases from 50 to 185 beats/min, an increase of 270 percent Therefore, the heart rate increase by far accounts for a greater proportion of the increase in cardiac output than does the increase in stroke volume during sustained strenuous exercise The stroke volume normally reaches its maximum by the time the cardiac output has increased only halfway to its maximum Any further increase in cardiac output must occur by increasing the heart rate Relation of Cardiovascular Performance to VO2max. During maximal exercise, both the heart rate and stroke volume are increased to about 95 percent of their maximal levels Because the cardiac output is equal to stroke volume times heart rate, one finds that the cardiac output is about 90 percent of the maximum that the person can achieve, which is in contrast to about 65 percent of maximum for pulmonary ventilation Therefore, one can readily see that the cardiovascular system is normally much more limiting on VO2max than is the respiratory system, because oxygen utilization by the body can never be more than the rate at which the cardiovascular system can transport oxygen to the tissues For this reason, it is frequently stated that the level of athletic performance that can be achieved by the marathoner mainly depends on the performance capability of his or her heart, because this is the most limiting link in the delivery of adequate oxygen to the exercising muscles Therefore, the 40 percent greater cardiac output that the marathoner can achieve over the average untrained male is 1093 UNIT XV Cardiac index (L/min/m2) 35 Oxygen consumption (L/min) Chapter 85 Sports Physiology Unit XV Sports Physiology probably the single most important physiological benefit of the marathoner’s training program Effect of Heart Disease and Old Age on Athletic Performance. Because of the critical limitation that the cardiovascular system places on maximal performance in endurance athletics, one can readily understand that any type of heart disease that reduces maximal cardiac output will cause an almost corresponding decrease in achievable total body muscle power Therefore, a person with congestive heart failure frequently has difficulty achieving even the muscle power required to climb out of bed, much less to walk across the floor The maximal cardiac output of older people also decreases considerably; there is as much as a 50 percent decrease between ages 18 and 80 years Also, there is even more of a decrease in maximal breathing capacity For these reasons, as well as because of reduced skeletal muscle mass, the maximal achievable muscle power is greatly reduced in old age Body Heat in Exercise Almost all the energy released by the body’s metabolism of nutrients is eventually converted into body heat This applies even to the energy that causes muscle contraction for the following reasons: First, the maximal efficiency for conversion of nutrient energy into muscle work, even under the best of conditions, is only 20 to 25 percent; the remainder of the nutrient energy is converted into heat during the course of the intracellular chemical reactions Second, almost all the energy that does go into creating muscle work still becomes body heat because all but a small portion of this energy is used for (1) overcoming viscous resistance to the movement of the muscles and joints, (2) overcoming the friction of the blood flowing through the blood vessels, and (3) other, similar effects, all of which convert the muscle contractile energy into heat Now, recognizing that the oxygen consumption by the body can increase as much as 20-fold in the well-trained athlete and that the amount of heat liberated in the body is almost exactly proportional to the oxygen consumption (as discussed in Chapter 73), one quickly realizes that tremendous amounts of heat are injected into the internal body tissues when performing endurance athletic events Next, with a vast rate of heat flow into the body, on a very hot and humid day that prevents the sweating mechanism from eliminating the heat, an intolerable and even lethal condition called heatstroke can easily develop in the athlete Heatstroke. During endurance athletics, even under normal environmental conditions, the body temperature often rises from its normal level of 98.6°F to 102°F or 103°F (37°C to 40°C) With very hot and humid conditions or excess clothing, the body temperature can easily rise to 106°F to 108°F (41°C to 42°C) At this level, the elevated temperature becomes destructive to tissue cells, especially the brain cells When this phenomenon occurs, multiple symptoms begin to appear, including extreme weakness, exhaustion, headache, dizziness, nausea, profuse sweating, confusion, staggering gait, collapse, and unconsciousness This entire complex is called heatstroke, and failure to treat it immediately can lead to death In fact, even though 1094 the person has stopped exercising, the temperature does not easily decrease by itself, partly because at these high temperatures, the temperature-regulating mechanism often fails (see Chapter 74) A second reason is that in heatstroke, the very high body temperature approximately doubles the rates of all intracellular chemical reactions, thus liberating still more heat The treatment of heatstroke is to reduce the body temperature as rapidly as possible The most practical way to reduce the body temperature is to remove all clothing, maintain a spray of cool water on all surfaces of the body or continually sponge the body, and blow air over the body with a fan Experiments have shown that this treatment can reduce the temperature either as rapidly or almost as rapidly as any other procedure, although some physicians prefer total immersion of the body in water containing a mush of crushed ice if available Body Fluids and Salt in Exercise As much as a 5- to 10-pound weight loss has been recorded in athletes in a period of hour during endurance athletic events under hot and humid conditions Essentially all this weight loss results from loss of sweat Loss of enough sweat to decrease body weight only percent can significantly diminish a person’s performance, and a to 10 percent rapid decrease in weight can often be serious, leading to muscle cramps, nausea, and other effects Therefore, it is essential to replace fluid as it is lost Replacement of Sodium Chloride and Potassium. Sweat contains a large amount of sodium chloride, for which reason it has long been stated that all athletes should take salt (sodium chloride) tablets when performing exercise on hot and humid days However, overuse of salt tablets has often done as much harm as good Furthermore, if an athlete becomes acclimatized to the heat by progressive increase in athletic exposure over a period of to weeks rather than performing maximal athletic feats on the first day, the sweat glands also become acclimatized, so the amount of salt lost in the sweat becomes only a small fraction of that lost before acclimatization This sweat gland acclimatization results mainly from increased aldosterone secretion by the adrenal cortex The aldosterone in turn has a direct effect on the sweat glands, increasing reabsorption of sodium chloride from the sweat before the sweat issues forth from the sweat gland tubules onto the surface of the skin Once the athlete is acclimatized, only rarely salt supplements need to be considered during athletic events Exercise-associated hyponatremia (low plasma sodium concentration) can sometimes occur after sustained physical exertion In fact, severe hyponatremia can be an important cause of fatalities in endurance athletes As noted in Chapter 25, severe hyponatremia can cause tissue edema, especially in the brain, which can be lethal In persons who experience life-threatening hyponatremia after heavy exercise, the main cause is not simply the loss of sodium due to sweating; instead, the hyponatremia is often due to ingestion of hypotonic fluid (water or sports drinks that usually have a sodium concentration of less than 18 mmol/L) in excess of sweat, urine, and insensible (mainly respiratory) fluid losses This excess fluid consumption can be Chapter 85 Sports Physiology Drugs and Athletes Without belaboring this issue, let us list some of the effects of drugs in athletics First, some persons believe that caffeine increases athletic performance In one experiment performed by a marathon runner, running time for the marathon was improved by percent through judicious use of caffeine in amounts similar to those found in one to three cups of coffee Yet experiments by other investigators have failed to confirm any advantage, thus leaving this issue in doubt Second, use of male sex hormones (androgens) or other anabolic steroids to increase muscle strength undoubtedly can increase athletic performance under some conditions, especially in women and even in men However, anabolic steroids also greatly increase the risk of cardiovascular disease because they often cause hypertension, decreased high-density blood lipoproteins, and increased low-density lipoproteins, all of which promote heart attacks and strokes In men, any type of male sex hormone preparation also leads to decreased testicular function, including both decreased formation of sperm and decreased secretion of the person’s own natural testosterone, with residual effects sometimes lasting at least for many months and perhaps indefinitely In a woman, even more significant effects such as facial hair, a bass voice, ruddy skin, and cessation of menses can occur because she is not normally adapted to the male sex hormone Other drugs, such as amphetamines and cocaine, have been reputed to increase athletic performance It is equally true that overuse of these drugs can lead to deterioration of performance Furthermore, experiments have failed to prove the value of these drugs except as a psychic stimulant Some athletes have been known to die during athletic events because of interaction between such drugs and the norepinephrine and epinephrine released by the sympathetic nervous system during exercise One of the possible causes of death under these conditions is overexcitability of the heart, leading to ventricular fibrillation, which is lethal within seconds Body Fitness Prolongs Life Multiple studies have shown that people who maintain appropriate body fitness, using judicious regimens of exercise and weight control, have the additional benefit of prolonged life Especially between the ages of 50 and 70 years, studies have shown mortality to be three times less in the most fit people than in the least fit people Why does body fitness prolong life? The following reasons are some of the most important Body fitness and weight control greatly reduce cardiovascular disease This results from (1) maintenance of moderately lower blood pressure and (2) reduced blood cholesterol and low-density lipoprotein along with increased high-density lipoprotein As pointed out earlier, these changes all work together to reduce the number of heart attacks, brain strokes, and kidney disease The athletically fit person has more bodily reserves to call on when he or she does become sick For instance, an 80-year-old nonfit person may have a respiratory system that limits oxygen delivery to the tissues to no more than 1 L/min; this means a respiratory reserve of no more than threefold to fourfold However, an athletically fit old person may have twice as much reserve This extra reserve is especially important in preserving life when the older person experiences conditions such as pneumonia that can rapidly require all available respiratory reserve In addition, the ability to increase cardiac output in times of need (the “cardiac reserve”) is often 50 percent greater in the athletically fit old person than in the nonfit person Exercise and overall body fitness also reduce the risk for several chronic metabolic disorders associated with obesity such as insulin resistance and type diabetes Moderate exercise, even in the absence of significant weight loss, has been shown to improve insulin sensitivity and reduce, or in some cases eliminate, the need for insulin treatment in patients with type diabetes Improved body fitness also reduces the risk for several types of cancers, including breast, prostate, and colon cancer Much of the beneficial effects of exercise may be related to a reduction in obesity However, studies in animals used in experiments and in humans have also shown that regular exercise reduces the risk for many chronic diseases through mechanisms that are incompletely understood but are, at least to some extent, independent of weight loss or decreased adiposity Bibliography Allen DG, Lamb GD, Westerblad H: Skeletal muscle fatigue: cellular mechanisms Physiol Rev 88:287, 2008 Booth FW, Laye MJ, Roberts MD: Lifetime sedentary living accelerates some aspects of secondary aging J Appl Physiol 111:1497, 2011 Casey DP, Joyner MJ: Compensatory vasodilatation during hypoxic exercise: mechanisms responsible for matching oxygen supply to demand J Physiol 590:6321, 2012 González-Alonso J: Human thermoregulation and the cardiovascular system Exp Physiol 97:340, 2012 Joyner MJ, Green DJ: Exercise protects the cardiovascular system: effects beyond traditional risk factors J Physiol 587:5551, 2009 Kent-Braun JA, Fitts RH, Christie A: Skeletal muscle fatigue Compr Physiol 2:997, 2012 Lavie CJ, McAuley PA, Church TS, et al: Obesity and cardiovascular diseases: implications regarding fitness, fatness, and severity in the obesity paradox J Am Coll Cardiol 63:1345, 2014 Powers SK, Jackson MJ: Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production Physiol Rev 88:1243, 2008 1095 UNIT XV driven by thirst but also may be due to conditioned behavior that is based on recommendations to drink fluid during exercise to avoid dehydration Copious supplies of water are also generally available in marathons, triathlons, and other endurance athletic events Experience by military units exposed to heavy exercise in the desert has demonstrated still another electrolyte problem—the loss of potassium Potassium loss results partly from the increased secretion of aldosterone during heat acclimatization, which increases the loss of potassium in the urine, as well as in the sweat As a consequence of these findings, some of the supplemental fluids for athletics contain properly proportioned amounts of potassium along with sodium, usually in the form of fruit juices Unit XV Sports Physiology Powers SK, Smuder AJ, Kavazis AN, Quindry JC: Mechanisms of exercise-induced cardioprotection Physiology (Bethesda) 29:27, 2014 Rosner MH: Exercise-associated hyponatremia Semin Nephrol 29: 271, 2009 Sandri M: Signaling in muscle atrophy and hypertrophy Physiology (Bethesda) 23:160, 2008 Schiaffino S, Dyar KA, Ciciliot S, et al: Mechanisms regulating skeletal muscle growth and atrophy FEBS J 280:4294, 2013 1096 Seals DR, Edward F: Adolph Distinguished Lecture: the remarkable anti-aging effects of aerobic exercise on systemic arteries J Appl Physiol 117:425, 2014 Thompson D, Karpe F, Lafontan M, Frayn K: Physical activity and exercise in the regulation of human adipose tissue physiology Physiol Rev 92:157, 2012 MISSING Normal Values for Selected Common Laboratory Measurements Average (“Normal” Value) Range Comment/Unit of Measure Sodium (Na+) 142 mmol/L 135-145 mmol/L mmol/L = Millimoles per liter Potassium (K+) 4.2 mmol/L 3.5-5.3 mmol/L Chloride (Cl−) 106 mmol/L 98-108 mmol/L Anion gap 12 mEq/L 7-16 mEq/L Bicarbonate (HCO3−) 24 mmol/L 22-29 mmol/L Hydrogen ion (H+) 40 nmol/L 30-50 nmol/L pH, arterial 7.4 7.25-7.45 Substance Electrolytes mEq/L = milliequivalents per liter Anion gap = Na+ − Cl− − HCO3− nmmol/L = nanomoles per liter pH, venous 7.37 7.32-7.42 Calcium ion (Ca++) 5.0 mg/dL 4.65-5.28 mg/dL Calcium, total 10.0 mg/dL 8.5-10.5 mg/dL Magnesium ion (Mg++) 0.8 mEq/L 0.6-1.1 mEq/L Magnesium, total 1.8 mEq/L 1.3-2.4 mEq/L Phosphate, total 3.5 mg/dL 2.5-4.5 mg/dL In plasma, HPO4= is ~1.05 mmol/L and H2PO4− is 0.26 mmol/L 4.5 g/dL mg/dL = milligrams/deciliter Average normal value can also be expressed as approximately 1.2 mmol/L or 2.4 mEq/L Nonelectrolyte Blood Chemistries 3.5-5.5 g/dL g/dL = grams per deciliter Alkaline phosphatase M: 38-126 U/L F: 70-230 U/L U/L = units per liter Bilirubin, total 0.2-1.0 mg/dL Albumin Bilirubin, conjugated 0-0.2 mg/dL Blood urea nitrogen (BUN) 14 mg/dL 10-26 mg/dL Creatinine 1.0 mg/dL 0.6-1.3 mg/dL Glucose 90 mg/dL 70-115 mg/dL Osmolarity 282 mOsm/L 275-300 mOsm/L Protein, total 7.0 g/dL 6.0-8.0 g/dL Uric acid Varies depending on muscle mass, age, and sex mOsm/L = milliosmoles per liter Osmolality is expresses as mOsm/kg of water M: 3.0-7.4 mg/dL F: 2.1-6.3 mg/dL Blood Gases O2 sat, arterial 98% 95%-99% Percentage of hemoglobin molecules saturated with oxygen PO2, arterial 90 mm Hg 80-100 mm Hg PO2 = partial pressure of oxygen in millimeters of mercury PO2, venous 40 mm Hg 25-40 mm Hg PCO2, arterial 40 mm Hg 35-45 mm Hg PCO2, venous 45 mm Hg 41-51 mm Hg Hematocrit (Hct) M: 42% F: 38% M: 39%-49% F: 35%-45% Hemoglobin (Hgb) M: 15 g/dL F: 14 g/dL M: 13.5-17.5 g/dL F: 12-16g/dL Red blood cells (RBCs) M: 5.5 ì 108/àL F: 4.7 ì 108/àL 4.3-5.7 ì 108/àL 4.3-5.7 ì 108/àL Number of cells per microliter of blood Mean corpuscular (RBC) volume (MCV) 90 fl PCO2 = partial pressure of carbon dioxide in millimeters of mercury Hematology 80-100 fl fl = femtoliters Prothrombin time (PT) 10-14 seconds Time required for the plasma to clot during a special test Platelets 150-450 ì 103/àL White blood cells, total Neutrophils Lymphocytes Monocytes Eosinophils Basophils 4.5-11.0 ì 103/àL 57%-67% 23%-33% 3%-7% 1%-3% 0%-1% Lipids Total cholesterol 35 mg/dL Triglycerides M: 40-160 mg/dL F: 35-135 mg/dL This table is not an exhaustive list of common laboratory values Most of these values are approximate reference values used by the University of Mississippi Medical Center Clinical Laboratories; normal ranges may vary among different clinical laboratories Average “normal” values and units of measure may also differ slightly from those cited in the Guyton and Hall Textbook of Medical Physiology, 13th edition For example, electrolytes are often reported in milliequivalents per liter (mEq/L), a measure of electrical charge of an electrolyte, or in millimoles per liter F, female; M, male ... Alveolar partial pressure of CO2 (mm Hg) 150 125 800 ml CO2/min 100 75 50 Expired Air Is a Combination of Dead Space Air and Alveolar Air Normal alveolar PCO2 A 25 20 0 ml CO2/min 0 10 15 20 25 30... the rate of absorption of O2 into the blood and (2) the rate of entry of new O2 into the lungs by the ventilatory process Figure 40-4 shows the effect of alveolar ventilation and rate of O2 absorption... alveolar partial pressure of O2 (PO2) One curve represents O2 absorption at a rate of 25 0 ml/min, and the other curve represents a rate of 1000 ml/min At a normal ventilatory rate of 4 .2 L/min and