Physiology of Sport and Exercise PDF

Chapter 11 Adaptations to Aerobic and Anaerobic Training 660 661 In this chapter and in the web study guide Adaptations to Aerobic Training Endurance: Muscular Versus Cardiorespiratory Evaluating Cardiorespiratory Endurance Capacity Cardiovascular Adaptations to Training Respiratory Adaptations to T...

Chapter 11 Adaptations to Aerobic and Anaerobic Training 660 661 In this chapter and in the web study guide Adaptations to Aerobic Training Endurance: Muscular Versus Cardiorespiratory Evaluating Cardiorespiratory Endurance Capacity Cardiovascular Adaptations to Training Respiratory Adaptations to Training Adaptations in Muscle Metabolic Adaptations to Training Integrated Adaptations to Chronic Endurance Exercise What Limits Aerobic Power and Endurance Performance? Long-Term Improvement in Aerobic Power and Cardiorespiratory Endurance Factors Affecting an Individual’s Response to Aerobic Training Cardiorespiratory Endurance in Nonendurance Sports Video 11.1 presents Ben Levine on the significance of O2max for sport performance. Audio for figure 11.7 describes the increases in total blood volume and plasma volume with endurance training. Activity 11.1 Adaptations reviews the cardiovascular, respiratory, and metabolic responses to training. Audio for figure 11.13 describes a twin study on the effect of heredity on O2max. Activity 11.2 Individual Response considers the factors affecting individual response to training. Activity 11.3 Aerobic Training explores adaptations in response to aerobic training by applying them to real-life situations. 662 Adaptations to Anaerobic Training Changes in Anaerobic Power and Anaerobic Capacity Adaptations in Muscle With Anaerobic Training Adaptations in the Energy Systems Activity 11.4 Anaerobic Training explores adaptations in response to anaerobic training by applying them to real-life situations. Video 11.2 Presents Stephen Piazza on what makes a good sprinter. Adaptations to High-Intensity Interval Training Specificity of Training and Cross-Training In Closing Activity 11.5 Putting It All Together reviews all concepts related to adaptations to aerobic and anaerobic training. On October 9, 2010, the Ironman World Championships were held in Kona, on the Big Island of Hawaii, for the 34th time. Some 1,800 triathletes swam 2.4 mi (3.9 km) through tough ocean waves, biked 112 mi (180 km) through hot lava fields, then ran 26.2 mi (42 km) in temperatures reaching into the 90s. Chris McCormack completed this grueling event in 8 h, 10 min, and 37 s to win the championship for the second time in 4 years. In the women’s division, Mirinda Carfrae earned her first Ironman title, finishing the course in 8:58:36—a rare women’s sub-9 h performance. How are these athletes able to compete in this race? While there is little doubt that they are genetically gifted with a high O2max, rigorous training is also required specifically to develop their cardiorespiratory endurance capacities. During a single bout of aerobic exercise, the human body precisely adjusts its cardiovascular and respiratory function to meet the energy and oxygen demands of actively contracting muscle. When these systems are challenged repeatedly, as happens with regular exercise training, they adapt in ways that allow the body to improve O2max and overall endurance performance. Aerobic training, or cardiorespiratory endurance training, improves cardiac function and peripheral blood flow and enhances the capacity of the muscle fibers to generate greater amounts of adenosine triphosphate (ATP). In this chapter, we examine adaptations in cardiovascular and respiratory function in response to endurance training and how such adaptations improve an athlete’s endurance capacity and performance. Additionally, we examine adaptations to anaerobic training. Anaerobic training improves anaerobic metabolism; short-term, high-intensity exercise capacity; tolerance for acid–base imbalances; and in some cases, muscle strength. Both aerobic and 663 anaerobic training induce a variety of adaptations that benefit exercise and sport performance. The effects of training on cardiovascular and respiratory, or aerobic, endurance is well known to endurance athletes like distance runners, cyclists, cross-country skiers, and swimmers but is often ignored by other types of athletes. Training programs for many nonendurance athletes often ignore the aerobic endurance component. This is understandable, because for maximum improvement in performance, training should be highly specific to the particular sport or activity in which the athlete participates, and endurance is frequently not recognized as important to nonendurance activities. The reasoning is, why waste valuable training time if the result is not improved performance? The problem with this reasoning is that most nonendurance sports do indeed have an endurance, or aerobic, component. For example, in football, players and coaches might fail to recognize the importance of cardiorespiratory endurance as part of the total training program. From all outward appearances, American football is an anaerobic, or burst-type, activity consisting of repeated bouts of high-intensity work of short duration. Seldom does a run exceed 40 to 60 yd (37-55 m), and even this is usually followed by a substantial rest interval. The need for endurance may not be readily apparent. What athletes and coaches might fail to consider is that this burst-type activity must be repeated many times during the game. With a higher aerobic endurance capacity, an athlete could maintain the quality of each burst activity throughout the game and would still be relatively “fresh” (have less drop-off in performance, fewer feelings of fatigue) during the fourth quarter. A parallel question arises concerning the importance of including resistance training as a part of the total training program for sports that do not demand high levels of strength, or high-intensity sprint training for sports that do not require speed or high anaerobic capacities. Yet athletes in almost all endurance sports are doing some resistance training to increase, or at least maintain, basic strength levels, as well as some sprint training to facilitate their ability to sustain speed when needed (e.g., sprinting to the finish line at the end of a marathon). Chapters 9 and 14 cover the principles of training for sport performance—the “how,” “when,” and “how much” questions about training. The focus here is on those physiological changes that occur within the body systems when aerobic or anaerobic exercise is repeated regularly to induce a training response. 664 Adaptations to Aerobic Training Improvements in endurance that accompany regular (e.g., daily, every other day) aerobic training, such as running, cycling, or swimming, result from multiple adaptations to the training stimuli. Some adaptations occur within the muscles themselves, promoting more efficient utilization of oxygen and fuel substrates. Still other important changes occur in the cardiovascular system, improving circulation to and within the muscles. Pulmonary adaptations, as will be noted later, occur to a lesser extent. Endurance: Muscular Versus Cardiorespiratory Endurance is a term that refers to two separate but related concepts: muscular endurance and cardiorespiratory endurance. Each makes a unique contribution to athletic performance, and each differs in its importance to different athletes. For sprinters, endurance is the quality that allows them to sustain a high speed over the full distance of, for example, a 100 m or 200 m dash. This component of fitness is termed muscular endurance, the ability of a single muscle or muscle group to maintain highintensity, repetitive, or static contractions. This type of endurance is also exemplified by a weightlifter doing multiple repetitions, a boxer, or a wrestler. The exercise or activity can be rhythmic and repetitive in nature, such as multiple repetitions of the bench press for the weightlifter and jabbing for the boxer. Or the activity can be more static, such as a sustained muscle action when a wrestler attempts to pin an opponent. In either case, the resulting fatigue is confined to a specific muscle group, and the activity’s duration is usually no more than 1 or 2 min. Muscular endurance is highly related to muscular strength and to anaerobic power development. While muscular endurance is specific to individual muscles or muscle groups, cardiorespiratory endurance relates to the ability to sustain prolonged, dynamic whole-body exercise using large muscle groups. Cardiorespiratory endurance is related to the development of the cardiovascular and respiratory systems’ ability to maintain oxygen delivery to working muscles during prolonged exercise, as well as the muscles’ ability to use energy aerobically (discussed in chapters 2 and 5). This is why the terms cardiorespiratory endurance and aerobic endurance are sometimes used synonymously. Evaluating Cardiorespiratory Endurance Capacity Studying the effects of training on endurance requires an objective, repeatable means of measuring an individual’s cardiorespiratory endurance capacity. In that way, the exercise scientist, coach, or athlete can monitor improvements as physiological adaptations occur during the training program. Maximal Endurance Capacity: O2max 665 Most exercise scientists regard O2max, sometimes called maximal aerobic power or maximal aerobic capacity, as the best objective laboratory measure of cardiorespiratory endurance. Recall from chapter 5 that O2max is defined as the highest rate of oxygen consumption attainable during maximal or exhaustive exercise. O2max as defined by the Fick equation is determined by maximal cardiac output (delivery of oxygen and blood flow to working muscles) and the maximal (a- )O2 difference (the ability of the active muscles to extract and use the oxygen). As exercise intensity increases, oxygen consumption eventually either plateaus or decreases slightly even with further increases in workload, indicating that a true maximal O2 has been achieved. With endurance training, more oxygen can be delivered to, and used by, active muscles than in an untrained state. Previously untrained subjects demonstrate average increases in O2max of 15% to 20% after a 20-week training program. These improvements allow individuals to perform endurance activities at a higher intensity, improving their performance potential. Figure 11.1 illustrates the increase in O2max after 12 months of aerobic training in a previously untrained individual. In this example, O2max increased by about 30%. Note that the O2 “cost” of running at a certain submaximal intensity (referred to as running economy) did not change, but higher running speeds could be attained after training. 666 Figure 11.1 Changes in O2max with 12 months of endurance training. O2max increased from 44 to 57 ml · kg−1 · min−1, a 30% increase. Peak speed during the treadmill test increased from 13 km/h (8 mph) to 16 km/h (~10 mph). Video 11.1 Presents Ben Levine on the significance of 667 O2max for sport performance. / 00:00 Submaximal Endurance Capacity In addition to increasing maximal endurance capacity, endurance training also increases submaximal endurance capacity, which is much more difficult to evaluate. A lower steadystate heart rate at the same submaximal exercise intensity is one physiological variable that can be used to objectively quantify the effect of training. Additionally, exercise scientists have used performance measures to quantify submaximal endurance capacity. For example, one test used to determine submaximal endurance capacity is the average peak absolute power output a person can maintain over a fixed period of time on a cycle ergometer. For running, the average peak speed or velocity a person can maintain during a set period of time would be a similar type of test. Generally, these tests last 30 min to an hour. Submaximal endurance capacity is more closely related to actual competitive endurance performance than O2max and is likely determined by both O2max and the lactate threshold—the point at which lactate begins to appear at a disproportionate rate in the blood (see chapter 5). With endurance training, submaximal endurance capacity increases. Cardiovascular Adaptations to Training Multiple cardiovascular adaptations occur in response to exercise training, including changes in the following: 668 Heart size Stroke volume Heart rate Cardiac output Blood flow Blood pressure Blood volume To fully understand adaptations in these variables, it is important to review how these components relate to oxygen transport. Oxygen Transport System Cardiorespiratory endurance is related to the cardiovascular and respiratory systems’ ability to deliver sufficient oxygen to meet the needs of metabolically active tissues. Recall from chapter 8 that the ability of the cardiovascular and respiratory systems to deliver oxygen to active tissues is defined by the Fick equation, which states that wholebody oxygen consumption is determined by both the delivery of oxygen via blood flow (cardiac output) and the amount of oxygen extracted by the tissues, the (a- )O2 difference. The product of cardiac output and the (a- )O2 difference determines the rate at which oxygen is being consumed: O2 = Stroke volume × Heart rate × (a- )O2 diff and O2max = Maximal stroke volume × Maximal heart rate × Maximal (a- )O2 diff Because maximal heart rate (HRmax) either stays the same or decreases slightly with training, increases in O2 max depend on adaptations in maximal stroke volume and maximal (a- )O2 difference. The oxygen demand of exercising muscles increases with increasing exercise intensity. Aerobic endurance depends on the cardiorespiratory system’s ability to deliver sufficient oxygen to these active tissues to meet their heightened demands for oxygen for oxidative metabolism. As maximal levels of exercise are achieved, heart size, blood flow, blood pressure, and blood volume can all potentially limit the maximal ability to transport oxygen. Endurance training elicits numerous changes in these components of the oxygen transport system that enable it to function more effectively. Heart Size 669 The measurement of heart size has been of interest to cardiologists for years because a hypertrophied, or enlarged, heart is typically a pathological condition indicating the presence of cardiovascular disease. Clinicians and scientists commonly use echocardiography to accurately measure the size of the heart and its chambers. Echocardiography involves the technique of ultrasound, which uses high-frequency sound waves directed through the chest wall to the heart. These sound waves are emitted from a transducer placed on the chest; and once they contact the various structures of the heart, they rebound back to a sensor, which is able to capture the deflected sound waves and provide a moving picture of the heart. A trained physician or technician can visualize the size of the heart’s chambers, thicknesses of its walls, and heart valve action. There are several forms of echocardiography: M-mode echocardiography, which provides a onedimensional view of the heart; two-dimensional echocardiography; and Doppler echocardiography, which is used more often to measure blood flow through large arteries. As an adaptation to the increased work demand, cardiac muscle mass and ventricular volume increase with training. Cardiac muscle, like skeletal muscle, undergoes morphological adaptations as a result of chronic endurance training. At one time, cardiac hypertrophy induced by exercise—“athlete’s heart,” as it was called—was viewed with concern because experts incorrectly believed that enlargement of the heart always reflected a pathological state, as sometimes occurs with severe hypertension. Training-induced cardiac hypertrophy, on the other hand, is now recognized as a normal adaptation to chronic endurance training. The left ventricle, as discussed in chapter 6, does the most work and thus undergoes the greatest adaptation in response to endurance training. The type of ventricular adaptation depends on the type of exercise training performed. For example, during resistance training, the left ventricle must contract against increased afterload from the systemic circulation. From chapter 8 we learned that blood pressure during resistance exercise can exceed 480/350 mmHg. This presents a considerable resistance that must be overcome by the left ventricle. To overcome this high afterload, the heart muscle compensates by increasing left ventricular wall thickness, thereby increasing its contractility. Thus, the increase in its muscle mass is in direct response to repeated exposure to the increased afterload with resistance training. However, there is little change in ventricular volume. With endurance training, left ventricular chamber size increases. This allows for increased left ventricular filling and consequently an increase in stroke volume. The increase in left ventricular dimensions is largely attributable to a training-induced increase in plasma volume (discussed later in this chapter) that increases left ventricular enddiastolic volume (increased preload). In concert with this, a decrease in heart rate at rest caused by increased parasympathetic tone, and during exercise at the same rate of work, allows a longer diastolic filling period. The increases in plasma volume and diastolic filling time increase left ventricular chamber size at the end of diastole. This effect of endurance training on the left ventricle is often called a volume loading effect. It was originally hypothesized that this increase in left ventricular dimensions was the only change in the left ventricle caused by endurance training. Additional research has 670 revealed that, similar to what happens in resistance training, myocardial wall thickness increases with endurance training. Highly trained endurance athletes (competitive crosscountry skiers, endurance cyclists, and long-distance runners) have greater left ventricular masses than non–endurance-trained men and women. Furthermore, left ventricular mass is highly correlated with O2max. Fagard11 conducted the most extensive review of the existing research literature in 1996, focusing on long-distance runners (135 athletes and 173 controls), cyclists (69 athletes and 65 controls), and strength athletes (178 athletes, including weight- and powerlifters, bodybuilders, wrestlers, throwers, and bobsledders, and 105 controls). For each group, the athletes were matched by age and body size with a group of sedentary control subjects. For each group of runners, cyclists, and strength athletes, the internal diameter of the left ventricle (LVID, an index of chamber size) and the total left ventricular mass (LVM) were greater in the athletes compared with their age- and sized-matched controls (figure 11.2). Thus, data from this review support the hypothesis that both left ventricular chamber size and wall thickness increase with endurance training. 671 Figure 11.2 Percentage differences in heart size of three groups of athletes (runners, cyclists, and strength athletes) compared with their age- and size-matched sedentary controls (0%). Percentage differences are presented for left ventricular internal diameter (LVID), mean wall thickness (MWT), and left ventricular mass (LVM). Data are from Fagard 1996. Most studies of heart size changes with training have been cross-sectional, comparing trained individuals with sedentary, untrained individuals. Certainly a portion of the differences that we see in figure 11.2 can be attributed to genetics, not training. However, a number of longitudinal studies have followed individuals from an untrained state to a trained state, and others have followed individuals from a trained state to an untrained state. These studies have reported increases in heart size with training and decreases with detraining. Therefore, training does bring about changes, but they are likely not as large as the differences shown in figure 11.2. In Review Cardiorespiratory endurance (also called maximal aerobic power) refers to the ability to perform prolonged, dynamic exercise using a large muscle mass. O2max—the highest rate of oxygen consumption obtainable during maximal or exhaustive exercise—is the best single measure of cardiorespiratory endurance. Cardiac output, the product of heart rate and stroke volume, represents how much blood leaves the heart each minute, whereas (a- )O2 difference is a measure of how 672 much oxygen is extracted from the blood by the tissues. According to the Fick equation, the product of these values is the rate of oxygen consumption: O2 = stroke volume × heart rate × (a- )O2 difference. Of the chambers of the heart, the left ventricle adapts the most in response to endurance training. With endurance training, the internal dimensions of the left ventricle increase, mostly in response to an increase in ventricular filling secondary to an increase in plasma volume. Left ventricular wall thickness and mass also increase with endurance training, allowing for a greater force of contraction. Stroke Volume Stroke volume at rest is substantially higher after an endurance training program than it is before training. This endurance training–induced increase is also seen at a given submaximal exercise intensity and at maximal exercise. This increase is illustrated in figure 11.3, which shows the changes in stroke volume of a subject who exercised at increasing intensities up to a maximal intensity before and after a 6-month endurance training program. Typical values for stroke volume at rest and during maximal exercise in untrained, trained, and highly trained athletes are listed in table 11.1. The wide range of stroke volume values for any given cell within this table is largely attributable to differences in body size. Larger people typically have larger hearts and a greater blood volume, and thus higher stroke volumes—an important point when one is comparing stroke volumes of different people. 673 Figure 11.3 Changes in stroke volume with endurance training during walking, jogging, and running on a treadmill at increasing velocities. 674 After aerobic training, the left ventricle fills more completely during diastole. Plasma volume expands with training, which allows for more blood to enter the ventricle during diastole, increasing end-diastolic volume (EDV). The heart rate of a trained heart is also lower at rest and at the same absolute exercise intensity than that of an untrained heart, allowing more time for the increased diastolic filling. More blood entering the ventricle increases the stretch on the ventricular walls; by the Frank-Starling mechanism (see chapter 8), this results in an increased force of contraction. The thickness of the posterior and septal walls of the left ventricle also increases slightly with endurance training. Increased ventricular muscle mass results in increased contractile force, in turn causing a lower end-systolic volume (ESV). The decrease in ESV is facilitated by the decrease in peripheral resistance that occurs with training. Increased contractility resulting from an increase in left ventricular thickness and greater diastolic filling (Frank-Starling mechanism), coupled with the reduction in systemic peripheral resistance, increases the ejection fraction [equal to (EDV − ESV) / EDV] in the trained heart. More blood enters the left ventricle, and a greater percentage of what enters is forced out with each contraction, resulting in an increase in stroke volume. Adaptations in stroke volume during endurance training are illustrated by a study in which older men trained aerobically for 1 year.9 Their cardiovascular function was evaluated before and after training. The subjects performed running, treadmill, and cycle ergometer exercise for 1 h each day, 4 days per week. They exercised at intensities of 60% to 80% of O2max, with brief bouts of exercise exceeding 90% of O2max. End-diastolic volume increased at rest and throughout submaximal exercise. The ejection fraction increased, which was associated with a decreased ESV, suggesting increased contractility of the left ventricle. O2max increased by 23%, a substantial improvement in endurance. It is clear that central stroke volume adaptations occur with endurance training, but there are also peripheral adaptations that contribute to the increase in O2max, at least in middle-aged exercisers. This was demonstrated in a unique longitudinal study involving both exercise training and a bed rest deconditioning model.22 Five 20-year-old men were tested (baseline values), placed on bed rest for 20 days (deconditioning), and then trained for 60 days, starting immediately at the conclusion of bed rest. These same five men were restudied 30 years later at the age of 50; they were tested at baseline in a relatively sedentary state and after 6 months of endurance training. The average percentage increases in O2max were similar for the subjects at age 20 (18%) and at age 50 (14%). However, the 675 increase in O2max at age 20 was explained by increases in both maximal cardiac output and maximal (a- )O2 difference; at age 50, the increase was explained primarily by an increase in (a- )O2 difference, while maximal cardiac output was unchanged. Maximal stroke volume was increased after training at both age 20 and age 50 but to a lesser degree at age 50 (+16 ml/beat at age 20 vs. +8 ml/beat at age 50). To summarize, increased left ventricular dimensions, reduced systemic peripheral resistance, and a greater blood volume account for the increases in resting, submaximal, and maximal stroke volume after an endurance training program. In Review Following endurance training, stroke volume (SV) is increased at rest and during submaximal and maximal exercise. A major factor leading to the SV increase is an increased EDV caused by an increase in plasma volume and a greater diastolic filling time secondary to a lower heart rate. Another contributing factor to increased SV is an increased left ventricular force of contraction. This is caused by hypertrophy of the cardiac muscle and increased ventricular stretch resulting from an increase in diastolic filling (increased preload), leading to greater elastic recoil (Frank-Starling mechanism). Reduced systemic vascular resistance (decreased afterload) also contributes to the increased volume of blood pumped from the left ventricle with each beat. Heart Rate Aerobic training has a major impact on heart rate at rest, during submaximal exercise, and during the postexercise recovery period. The effect of aerobic training on maximal heart rate is rather negligible. Resting Heart Rate Resting heart rate decreases markedly as a result of endurance training. Some studies have shown that a sedentary individual with an initial resting heart rate of 80 beats/min can decrease resting heart rate by approximately 1 beat/min with each week of aerobic training, at least for the first few weeks. After 10 weeks of moderate endurance training, resting heart rate can decrease from 80 to 70 beats/min or lower. On the other hand, well-controlled studies with large numbers of subjects have shown much smaller decreases in resting heart rate, that is, fewer than 5 beats/min following up to 20 weeks of aerobic training. Recall from chapter 6 that bradycardia is a term indicating a heart rate of fewer than 60 beats/min. In untrained individuals, bradycardia can be the result of abnormal cardiac 676 function or heart disease. However, highly conditioned endurance athletes often have resting heart rates lower than 40 beats/min, and some have values lower than 30 beats/min. Therefore, it is necessary to differentiate between training-induced bradycardia, which is a normal response to endurance training, and pathological bradycardia, which can be cause for concern. Research Perspective 11.1 Resting Bradycardia in Athletes The low resting heart rate (HR) of well-trained endurance athletes is most often attributed to an elevated parasympathetic (vagal) tone. However, a recent review of the available evidence casts doubt on this mechanism.6 The two alternative explanations for the resting bradycardia of athletes are a diminished sympathetic tone and a lower intrinsic heart rate. Recall from chapter 6 that the intrinsic heart rate is the rate of sinoatrial (SA) node firing in the absence of any neural or hormonal input. In studies that have blocked parasympathetic activity to the heart using the drug atropine, there is still a significant resting bradycardia in athletes. In fact, the difference in HR after parasympathetic blockade is greater than the difference in the normal HR, suggesting that the bradycardia is not the result of elevated vagal tone. Other studies have blocked both branches of the autonomic nervous system, that is, used a complete autonomic blockade. The HR after complete autonomic blockade is a measure of the intrinsic HR. In studies showing a lowered resting HR after endurance training, the bradycardia persists after complete autonomic blockade. Thus, the resting bradycardia seen in athletes is at least partially, and perhaps completely, the result of a decreased intrinsic HR. A decreased intrinsic HR can result from a remodeling of the SA node. The SA node serves as the pacemaker of the heart due to properties of ion channels and Ca2+-handling proteins in the SA node cells. Changes in these properties cause the well-known bradycardias associated with SA node disease, heart failure, atrial fibrillation, and even aging itself. In fact, the age-associated decrease in resting HR has been attributed to a downregulation of ryanodine receptors (see chapter 6) that are involved in Ca2+ flux. If these mechanisms are involved in bradycardias associated with these other processes and diseases, it is likely that they are involved in training-induced bradycardia as well. Submaximal Heart Rate During submaximal exercise, aerobic training results in a lower heart rate at any given absolute exercise intensity. This is illustrated in figure 11.4, which shows the heart rate of an individual exercising on a treadmill before and after training. At each walking or running speed, the posttraining heart rate is lower than the heart rate before training. The 677 training-induced decrease in heart rate is typically greater at higher intensities. 678 Figure 11.4 Endurance training–induced changes in heart rate during progressive walking, jogging, and running on a treadmill at increasing speeds. While maintaining a cardiac output appropriate to meet the needs of working muscle, a trained heart performs less work (lower heart rate, higher stroke volume) than an untrained heart at the same absolute workload. Maximum Heart Rate A person’s maximal heart rate (HRmax) tends to be stable and typically remains relatively unchanged after endurance training. However, several studies have suggested that for people whose untrained HRmax values exceed 180 beats/min, HRmax might be slightly lower after training. Also, highly conditioned endurance athletes often have lower HRmax values than untrained individuals of the same age, although this is not always the case. Athletes over 60 years old sometimes have higher HRmax values than untrained people of the same age. Interactions Between Heart Rate and Stroke Volume 679 During exercise, the product of heart rate and stroke volume provides a cardiac output appropriate to the intensity of the activity being performed. At maximal or near-maximal intensities, heart rate may change to provide the optimal combination of heart rate and stroke volume to maximize cardiac output. If heart rate is too fast, diastolic filling time is reduced, and stroke volume might be compromised. For example, if HRmax is 180 beats/min, the heart beats three times per second. Each cardiac cycle thus lasts for only 0.33 s. Diastole is as short as 0.15 s or less. This fast heart rate allows very little time for the ventricles to fill. As a consequence, stroke volume may decrease at high heart rates when filling time is compromised. However, if the heart rate slows, the ventricles have longer to fill. This has been proposed as one reason highly trained endurance athletes tend to have lower HRmax values: Their hearts have adapted to training by drastically increasing their stroke volumes, so lower HRmax values can provide optimal cardiac output. Which comes first? Does increased stroke volume result in a decreased heart rate, or does a lower heart rate result in an increased stroke volume? This question remains unanswered. In either case, the combination of increased stroke volume and decreased heart rate is a more efficient way for the heart to meet the metabolic demands of the exercising body. The heart expends less energy by contracting less often but more forcefully than it would if contraction frequency were increased. Reciprocal changes in heart rate and stroke volume in response to training share a common goal: to allow the heart to pump the maximal amount of oxygenated blood at the lowest energy cost. Heart Rate Recovery During exercise, as discussed in chapter 6, heart rate must increase to increase cardiac output to meet the blood flow demands of active muscles. When the exercise bout is finished, heart rate does not instantly return to its resting level. Instead, it remains elevated for a while, slowly returning to its resting rate. The time it takes for heart rate to return to its resting rate is called the heart rate recovery period. After endurance training, as shown in figure 11.5, heart rate returns to its resting level much more quickly after an exercise bout than it does before training. This is true after both submaximal and maximal exercise. 680 Figure 11.5 Changes in heart rate during recovery after a 4 min, all-out bout of exercise before and after endurance training. Because the heart rate recovery period is shorter after endurance training, this measurement has been proposed as an indirect index of cardiorespiratory fitness. In general, a more fit person recovers faster after a standardized rate of work than a less fit person, so this measure may have some utility in field settings when more direct measures of endurance capacity are not possible or feasible. However, factors other than training can also affect heart rate recovery time. For example, an elevated core temperature or an enhanced sympathetic nervous system response can prolong heart rate elevation. The heart rate recovery curve is a useful tool for tracking a person’s progress during a training program. But because of the potential influence of other factors, it should not be used to compare individuals. Cardiac Output We have looked at the effects of training on the two components of cardiac output: stroke volume and heart rate. While stroke volume increases with training, heart rate 681 generally decreases at rest and during exercise at a given absolute intensity. Because the magnitude of these reciprocal changes is similar, cardiac output at rest and during submaximal exercise at a given exercise intensity does not change much following endurance training. In fact, cardiac output can decrease slightly. This is likely the result of an increase in the (a- )O2 difference (reflecting greater oxygen extraction by the tissues) or a decrease in the rate of oxygen consumption (reflecting an increased mechanical efficiency). Generally, cardiac output matches the oxygen consumption required for any given intensity of effort. Maximal cardiac output, however, increases considerably in response to aerobic training, as seen in figure 11.6, and is largely responsible for the increase in O2max. This increase in cardiac output must result from an increase in maximal stroke volume, because HRmax changes little, if any. Maximal cardiac output ranges from 14 to 20 L/min in untrained individuals and from 25 to 35 L/min in trained individuals, and can be 40 L/min or more in highly conditioned endurance athletes. These absolute values, however, are greatly influenced by body size. 682 Figure 11.6 Changes in cardiac output with endurance training during walking, then jogging, and finally running on a treadmill as velocity increases. In Review Resting heart rate decreases as a result of endurance training. In a sedentary person, the decrease is typically about 1 beat/min per week during the initial weeks of training, but smaller decreases have been reported. Highly trained endurance athletes may have resting heart rates of 40 beats/min or lower. Heart rate during submaximal exercise is also lower, with larger decreases seen at higher exercise intensities. Maximal heart rate either remains unchanged or decreases slightly with training. Heart rate during the recovery period decreases more rapidly after training, making it an indirect but convenient way of tracking the adaptations that occur with training. However, this value is not useful for comparing fitness levels of different people. Cardiac output at rest and at submaximal levels of exercise remains unchanged (or may decrease slightly) after endurance training. Cardiac output during maximal exercise increases considerably and is largely 683 responsible for the increase in O2max. The increased maximal cardiac output is the result of the substantial increase in maximal stroke volume, made possible by training-induced changes in cardiac structure and function. Blood Flow Active muscles need considerably more oxygen and fuel substrates than inactive ones. To meet these increased needs, more blood must be delivered to these muscles during exercise. With endurance training, the cardiovascular system adapts to increase blood flow to exercising muscles to meet their higher demand for oxygen and metabolic substrates. Four factors account for this enhanced blood flow to muscle following training: Increased capillarization Greater recruitment of existing capillaries More effective blood flow redistribution from inactive regions Increased total blood volume To permit increased blood flow, new capillaries develop in trained muscles. This allows the blood flowing into skeletal muscle from arterioles to more fully perfuse the active fibers. This increase in capillaries usually is expressed as an increase in the number of capillaries per muscle fiber, or the capillary-to-fiber ratio. Table 11.2 illustrates the differences in capillary-to-fiber ratios between well-trained and untrained men, both before and after exercise.14 684 In all tissues, including muscle, not all capillaries are open at any given time. In addition to new capillarization, existing capillaries in trained muscles can be recruited and open to flow, which also increases blood flow to muscle fibers. The increase in new capillaries with endurance training and increased capillary recruitment combine to increase the cross-sectional area for exchange between the vascular system and the metabolically active muscle fibers. Because endurance training also increases blood volume, shifting more blood into the capillaries will not severely compromise venous return. A more effective redistribution of cardiac output also can increase blood flow to the active muscles. Blood flow is directed to the active musculature and shunted away from areas that do not need high flow. Blood flow can increase to the more active fibers even within a specific muscle group. Armstrong and Laughlin1 first demonstrated that endurance-trained rats could redistribute blood flow to their most active tissues during exercise better than untrained rats could. The total blood flow to the exercising hindlimbs did not differ between the trained and untrained rats. However, the trained rats distributed more of their blood to the most oxidative muscle fibers, effectively redistributing the blood flow away from the glycolytic muscle fibers. These findings are difficult to replicate in humans because of measurement challenges, as well as the fact that human skeletal muscle is a mosaic with mixed fiber types among individual muscles. Finally, the body’s total blood volume increases with endurance training, providing more blood to meet the body’s many blood flow needs during endurance activity. The mechanisms responsible for this are discussed later in this chapter. Blood Pressure Resting blood pressure does not change significantly in healthy subjects in response to endurance training, but some studies have shown modest reductions after training in borderline or moderately hypertensive individuals. In hypertensive subjects, reductions in both systolic and diastolic blood pressure of approximately 6 to 7 mmHg may result. The mechanisms underlying this reduction are unknown. Following endurance training, blood pressure is reduced at a given submaximal exercise intensity; but at maximal exercise capacity, systolic blood pressure is increased and diastolic pressure is decreased. Although resistance exercise can cause large transient increases in both systolic and 685 diastolic blood pressure during lifting of heavy weights, chronic exposure to these high pressures does not elevate resting blood pressure. Hypertension is not common in competitive weightlifters or in strength and power athletes. In fact, a few studies have even shown that resistance training may lower resting systolic blood pressure. Blood Volume Endurance training increases total blood volume, and this effect is larger at higher training intensities. Furthermore, the effect occurs rapidly. This increased blood volume results primarily from an increase in plasma volume, but there is also an increase in the volume of red blood cells. The time course and mechanism for the increase of each of these components of blood are quite different. Plasma Volume The increase in plasma volume with training is thought to result from two mechanisms. The first mechanism, which has two phases, results in increases in plasma proteins, particularly albumin. Recall from chapter 8 that plasma proteins are the major driver of oncotic pressure in the vasculature. As plasma protein concentration increases, so does oncotic pressure, and fluid is reabsorbed from the interstitial fluid into the blood vessels. During an intense bout of exercise, proteins leave the vascular space and move into the interstitial space. They are then returned in greater amounts through the lymph system. It is likely that the first phase of rapid plasma volume increase is the result of the increased plasma albumin, which is noted within the first hour of recovery from the first training bout. In the second phase, protein synthesis is turned on (upregulated) by repeated exercise, and new proteins are formed. With the second mechanism, exercise increases the release of antidiuretic hormone and aldosterone, hormones that cause reabsorption of water and sodium in the kidneys, which increases blood plasma. That increased fluid is kept in the vascular space by the oncotic pressure exerted by the proteins. Nearly all of the increase in blood volume during the first 2 weeks of training can be explained by the increase in plasma volume. Red Blood Cells An increase in red blood cell volume with endurance training also contributes to the overall increase in blood volume, but this is an inconsistent finding. Although the actual number of red blood cells may increase, the hematocrit—the ratio of the red blood cell volume to the total blood volume—may actually decrease. Figure 11.7 illustrates this apparent paradox. Notice that the hematocrit is reduced even though there has been a slight increase in red blood cells. A trained athlete’s hematocrit can decrease to such an extent that the athlete appears to be anemic on the basis of a relatively low concentration of red cells and hemoglobin (“pseudoanemia”). 686 Figure 11.7 00:00 / 00:00 Increases in total blood volume and plasma volume occur with endurance training. Note that although the hematocrit (percentage of red blood cells) decreased from 44% to 42%, the total volume of red blood cells increased by 10%. The increased ratio of plasma to cells resulting from a greater increase in the fluid portion reduces the blood’s viscosity, or thickness. Reduced viscosity may aid the smooth flow of blood through the blood vessels, particularly through the smaller vessels such as the capillaries. One of the physiological benefits of decreasing blood viscosity is that it enhances oxygen delivery to the active muscle mass. Both the total amount (absolute values) of hemoglobin and the total number of red blood cells are typically elevated in highly trained athletes, although these values relative to total blood volume are below normal. This ensures that the blood has more than ample oxygen-carrying capacity. The turnover rate of red blood cells also may be higher with 687 intense training. In Review Blood flow to active muscle is increased by endurance training. Increased muscle blood flow results from four factors: 1. Increased capillarization 2. Greater opening of existing capillaries (capillary recruitment) 3. More effective blood flow distribution 4. Increased blood volume Resting blood pressure generally is reduced by endurance training in those with borderline or moderate hypertension but not in healthy, normotensive subjects. Endurance training results in a reduction in blood pressure during submaximal exercise at a given exercise intensity, but at maximal exercise intensity the systolic blood pressure is increased and diastolic blood pressure is decreased compared to pretraining values. Blood volume increases as a result of endurance training. Plasma volume is expanded through increased protein content (returned from lymph and upregulated protein synthesis). This effect is maintained and supported by fluidconserving hormones. Red blood cell volume also increases, but the increase in plasma volume is typically higher. Increased plasma volume decreases blood viscosity, which can improve tissue perfusion and oxygen availability. Respiratory Adaptations to Training No matter how proficient the cardiovascular system is at supplying blood to exercising muscle, endurance would be hindered if the respiratory system were not able to bring in enough oxygen to fully oxygenate red blood cells. Respiratory system function does not usually limit performance because ventilation can be increased to a much greater extent than cardiovascular function. But, as with the cardiovascular system, the respiratory system undergoes specific adaptations to endurance training to maximize its efficiency. Pulmonary Ventilation After training, pulmonary ventilation is essentially unchanged at rest. Although endurance training does not change the structure or basic physiology of the lung, it does decrease ventilation during submaximal exercise by as much as 20% to 30% at a given 688 submaximal intensity. Maximal pulmonary ventilation is substantially increased from a rate of about 100 to 120 L/min in untrained sedentary individuals to about 130 to 150 L/min or more following endurance training. Pulmonary ventilation rates typically increase to about 180 L/min in highly trained athletes and can exceed 200 L/min in very large, highly trained endurance athletes. Two factors can account for the increase in maximal pulmonary ventilation following training: increased tidal volume and increased respiratory frequency at maximal exercise. Ventilation is not usually a limiting factor for endurance exercise performance. However, some evidence suggests that at some point in a highly trained person’s adaptation, the pulmonary system’s capacity for oxygen transport may not be able to meet the demands of the limbs and the cardiovascular system. This results in what has been termed exercise-induced arterial hypoxemia, in which arterial oxygen saturation decreases below 96%. This desaturation in highly trained elite athletes likely results from the large right heart cardiac output directed to the lung during exercise and consequently a decrease in the time the blood spends in the lung. Pulmonary Diffusion Pulmonary diffusion, or gas exchange occurring in the alveoli, is unaltered at rest and during submaximal exercise following training. However, it increases at maximal exercise intensity. Pulmonary blood flow (blood coming from the right side of the heart to the lungs) increases following training, particularly flow to the upper regions of the lungs when a person is sitting or standing. This increases lung perfusion. More blood is brought into the lungs for gas exchange, and at the same time ventilation increases so that more air is brought into the lungs. This means that more alveoli will be involved in pulmonary diffusion. The net result is that pulmonary diffusion increases. Arterial–Venous Oxygen Difference The oxygen content of arterial blood changes very little with endurance training. Even though total hemoglobin is increased, the amount of hemoglobin per unit of blood is the same or even slightly reduced. The (a- )O2 difference, however, does increase with training, particularly at maximal exercise intensity. This increase results from a lower mixed venous oxygen content, which means that the blood returning to the heart (which is a mixture of venous blood from all body parts, not just the active tissues) contains less oxygen than it would in an untrained person. This reflects both greater oxygen extraction by active tissues and a more effective distribution of blood flow to active tissues. The increased extraction results in part from an increase in oxidative capacity of active muscle fibers, as described later in this chapter. In summary, the respiratory system is quite adept at bringing adequate oxygen into the body. For this reason, the respiratory system seldom limits endurance performance. Not 689 surprisingly, the major training adaptations noted in the respiratory system are apparent mainly during maximal exercise, when all systems are being maximally stressed. In Review Unlike what happens with the cardiovascular system, endurance training has little effect on lung structure and function. To support increases in O2max, there is an increase in pulmonary ventilation during maximal effort following training as both tidal volume and respiratory rate increase. Pulmonary diffusion at maximal intensity increases, especially to upper regions of the lung that are not normally perfused. Although the largest part of the increase in O2max results from the increases in cardiac output and muscle blood flow, an increase in (a- )O2 difference also plays a key role. This increase in (a- )O2 difference is attributable to a more effective distribution of arterial blood away from inactive tissue to the active tissue and an increased ability of active muscle to extract oxygen. Adaptations in Muscle Repeated excitation and contraction of muscle fibers during endurance training stimulate changes in their structure and function. Our main interest here is in aerobic training and the changes it produces in muscle fiber type, mitochondrial function, and oxidative enzymes. Muscle Fiber Type As noted in chapter 1, low- to moderate-intensity aerobic activities rely extensively on type I (slow-twitch) fibers. In response to aerobic training, type I fibers become larger. More specifically, they develop a larger cross-sectional area, although the magnitude of change depends on the intensity and duration of each training bout and the length of the training program. Increases in cross-sectional area of up to 25% have been reported. Fasttwitch (type II) fibers, because they are not being recruited to the same extent during endurance exercise, generally do not increase cross-sectional area. Most early studies showed no change in the percentage of type I versus type II fibers following aerobic training, but subtle changes were noted among the different type II fiber subtypes. Type IIx fibers have a low oxidative capacity and are recruited less often than type IIa fibers during aerobic exercise. However, during long-duration exercise, these fibers may eventually be recruited to perform in a manner resembling type IIa fibers. This can cause 690 some type IIx fibers to take on the characteristics of the more oxidative type IIa fibers. Recent evidence suggests that not only is there a transition of type IIx to IIa fibers; there can also be a transition of type II to type I fibers. The magnitude of change is generally small, not more than a few percent. As an example, in the HERITAGE Family Study,26 a 20-week program of aerobic training increased type I fibers from 43% pretraining to almost 47% posttraining and decreased type IIx fibers from 20% to 15%, with type IIa remaining essentially unchanged. These more recent studies have included larger numbers of subjects and have taken advantage of improved measurement technology; both might explain why fiber type composition changes within a muscle are now recognized. Capillary Supply One of the most important adaptations to aerobic training is an increase in the number of capillaries surrounding each muscle fiber. Table 11.2 illustrates that endurance-trained men have considerably more capillaries in their leg muscles than sedentary individuals.14 With long periods of aerobic training, the number of capillaries may increase by more than 15%.26 Having more capillaries allows for greater exchange of gases, heat, nutrients, and metabolic by-products between the blood and contracting muscle fibers. In fact, the increase in capillary density (i.e., increase in capillaries per muscle fiber) is potentially one of the most important alterations in response to training that causes the increase in O2max. It is now clear that the diffusion of oxygen from the capillary to the mitochondria is a major factor limiting the maximal rate of oxygen consumption by the muscle. Increasing capillary density facilitates this diffusion, thus maintaining an environment well suited to energy production and repeated muscle contractions. Myoglobin Content When oxygen enters the muscle fiber, it binds to myoglobin, a molecule similar to hemoglobin. This iron-containing molecule shuttles the oxygen molecules from the cell membrane to the mitochondria. Type I fibers contain large quantities of myoglobin, which gives these fibers their red appearance (myoglobin is a pigment that turns red when bound to oxygen). Type II fibers, on the other hand, are highly glycolytic, so they contain (and require) little myoglobin—hence their whiter appearance. More important, their limited myoglobin supply limits their oxidative capacity, resulting in poor endurance for these fibers. Myoglobin transports oxygen and releases it to the mitochondria when oxygen becomes limited during muscle action. This oxygen reserve is used during the transition from rest to exercise, providing oxygen to the mitochondria during the lag between the beginning of exercise and the increased cardiovascular delivery of oxygen. Endurance training has been shown to increase muscle myoglobin content by 75% to 80%. This adaptation clearly supports a muscle’s increased capacity for oxidative metabolism after training. 691 Mitochondrial Function As noted in chapter 2, oxidative energy production takes place in the mitochondria. Not surprisingly, aerobic training also induces changes in mitochondrial function that improve the muscle fibers’ capacity to produce ATP. The ability to use oxygen and produce ATP via oxidation depends on the number and size of the muscle mitochondria. Both increase with aerobic training. During one study that involved endurance training in rats, the number of mitochondria increased approximately 15% during 27 weeks of exercise.15 Average mitochondrial size also increased by about 35% over that training period. As with other training-induced adaptations, the magnitude of change depends on training volume. Research Perspective 11.2 Endurance Training Improves Mitochondrial Quality Not all mitochondria within a muscle fiber are equally efficient, as new mitochondria are constantly being formed (biogenesis) and old, weakened mitochondria are being cleared (mitophagy) (see figure). Regulation of this mitochondrial turnover cycle determines not only the number of mitochondria in a fiber, but also the overall quantity and function of those mitochondria,31 which in turn determine overall metabolic function and performance of skeletal muscles. There has been an explosion of new research aimed at understanding the underlying molecular mechanisms that regulate mitochondrial biogenesis, the process by which new mitochondria are formed. These efforts resulted in the discovery of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), a key regulator protein that is integrally involved in mitochondrial biogenesis in skeletal muscle. It is also now well established that both acute exercise and exercise training—both endurance and resistance exercise—enhance PGC-1α expression. Increased expression of PGC-1α protein can be measured in skeletal muscle even after a single bout of exercise; and after two or three repeated bouts, markers for mitochondrial biogenesis can be observed. Increased PGC-1α not only increases mitochondrial biogenesis but also controls the replacement of old weakened mitochondria with new healthy mitochondria. Mitochondrial damage induced by such insults as hypoxia, inflammation, or increased oxidant stress can lead to the accumulation of metabolic by-products that impair mitochondrial function. Although addition of new mitochondria is of extreme importance, the maintenance of a healthy population of mitochondria is equally critical for optimal metabolic capacity. Continuous removal of damaged mitochondria is likewise important for optimal function of skeletal muscle. Endurance exercise training causes a wide variety of phenotypic adaptations in skeletal muscle, including angiogenesis (creation of new capillaries), transformation of fiber types from glycolytic to oxidative, increased ability to mobilize and use fats as a substrate, and increased glucose uptake by muscle fibers. We now can add its role in both (1) increasing 692 the number of mitochondria and (2) improving the overall quality of the existing mitochondrial pool. The first effect results from both increased rates of mitochondrial biogenesis and efficient removal of weak or damaged mitochondria. The second role slows the processes through which mitochondria become impaired. Because of its multiple important roles in enhancing metabolic function, PGC-1α is often called the master regulator or master switch. As shown in the accompanying figure, exercise training promotes biogenesis of new mitochondria, slows the decline in mitochondrial function by remodeling mitochondria through processes of fusion and fission, and helps maintain mitophagy in skeletal muscle. Thus, mitochondrial “quality control” is an important exercise-induced adaptation.31 693 Exercise training affects the quality of muscle mitochondria by increasing the production of new, healthy mitochondria (biogenesis), decreasing the degradation of mitochondria, and clearing away damaged mitochondria (mitophagy). The first two processes are regulated by the regulator protein PGC-1α. Solid arrows indicate a positive effect while dotted arrows indicate a negative effect. Oxidative Enzymes Regular endurance exercise has been shown to induce major adaptations in skeletal muscle, including an increase in the number and size of the muscle fiber mitochondria as just discussed. These changes are further enhanced by an increase in mitochondrial capacity. The oxidative breakdown of fuels and the ultimate production of ATP depend on the action of mitochondrial oxidative enzymes, the specialized proteins that catalyze (i.e., speed up) the breakdown of nutrients to form ATP. Aerobic training increases the activity of these important enzymes. Figure 11.8 illustrates the changes in the activity of succinate dehydrogenase (SDH), a key muscle oxidative enzyme, over 7 months of progressive swim training. While the rate of increases in O2max slowed after the first 2 months of training, activity of this key oxidative enzyme continued to increase throughout the entire training period. This suggests that training-induced increases in O2max might be limited more by the circulatory system’s ability to transport oxygen than by the muscles’ oxidative potential. 694 Figure 11.8 The percentage change in maximal oxygen uptake ( O2max) and the activity of succinate dehydrogenase (SDH), one of the muscles’ key oxidative enzymes, during 7 months of swim training. Interestingly, although this enzyme activity continues to increase with increasing levels of training, the swimmers’ maximal oxygen uptake appears to level off after the first 8 to 10 weeks of training. This implies that mitochondrial enzyme activity is not a direct indication of whole-body endurance capacity. 695 The activities of muscle enzymes such as SDH and citrate synthase are dramatically influenced by aerobic training. This is seen in figure 11.9, which compares the activities of 696 these enzymes in untrained people, moderately trained joggers, and highly trained runners.8 Even moderate daily exercise increases the activity of these enzymes and thus the oxidative capacity of the muscle. For example, jogging or cycling for as little as 20 min per day has been shown to increase SDH activity in leg muscles by more than 25%. Training more vigorously—for example, for 60 to 90 min per day—produces a two- to threefold increase in this enzyme’s activity. 697 Figure 11.9 Leg muscle (gastrocnemius) enzyme activities of untrained (UT) subjects, moderately trained (MT) joggers, and highly trained (HT) marathon runners. Enzyme levels are shown for two of many key enzymes that participate in the oxidative production of adenosine triphosphate. 698 Adapted, by permission, from D.L. Costill et al., 1979, “Lipid metabolism in skeletal muscle of endurance-trained males and females,” Journal of Applied Physiology 47: 787-791; and D.L. Costill et al., 1979, “Adaptations in skeletal muscle following strength training,” Journal of Applied Physiology 46: 96-99. One metabolic consequence of mitochondrial changes induced by aerobic training is glycogen sparing, a slower rate of utilization of muscle glycogen and enhanced reliance on fat as a fuel source at a given exercise intensity. Enhanced glycogen sparing with endurance training most likely improves the ability to sustain a higher exercise intensity, such as maintaining a faster race pace in a 10 km run. In Review Aerobic training selectively recruits type I muscle fibers and fewer type II fibers. Consequently, the type I fibers increase their cross-sectional area with aerobic training. After training, there appears to be a small increase in the percentage of type I fibers, as well as a transition of some type IIx to type IIa fibers. 699 Aerobic training increases both the number of capillaries per muscle fiber and the number of capillaries for a given cross-sectional area of muscle. These changes improve blood perfusion through the muscles, enhancing the diffusion of oxygen, carbon dioxide, nutrients, and by-products of metabolism between the blood and muscle fibers. Aerobic training increases muscle myoglobin content by as much as 75% to 80%. Myoglobin transports oxygen from cell membranes to the mitochondria. Aerobic training increases both the number and the size of muscle fiber mitochondria, providing the muscle with an increased capacity for oxidative metabolism. Activities of many oxidative enzymes are increased with aerobic training. These changes occurring in the muscles, combined with adaptations in the oxygen transport system, enhance the capacity of oxidative metabolism and improve endurance performance. Metabolic Adaptations to Training Now that we have discussed training changes in both the cardiovascular and respiratory systems, as well as skeletal muscle adaptations, we are ready to examine how these integrated adaptations are reflected by changes in three important physiological variables related to metabolism: Lactate threshold Respiratory exchange ratio Oxygen consumption Lactate Threshold Lactate threshold, discussed in chapter 5, is a physiological marker that is closely associated with endurance performance—the higher the lactate threshold, the better the performance capacity. Figure 11.10a illustrates the difference in lactate threshold between an endurance-trained individual and an untrained individual. This figure also accurately represents the changes in lactate threshold that would occur following a 6- to 12-month program of endurance training. In either case, in the trained state, one can exercise at a higher percentage of one’s O2max before lactate begins to accumulate in the blood. In this example, the trained runner could sustain a race pace of 70% to 75% of O2max, an intensity that would result in continued lactate accumulation in the blood of the untrained runner. This translates into a much faster race pace (see figure 11.10b). Above the lactate threshold, the lower lactate at a given rate of work is likely attributable to a combination of reduced lactate production and increased lactate clearance. As athletes become better 700 trained, their postexercise blood lactate concentrations are lower for a given rate of work. 701 Figure 11.10 Changes in lactate threshold (LT) with training expressed as (a) a percentage of maximal oxygen uptake (% O2max) and (b) an increase in speed on the treadmill. Lactate threshold occurs at a speed of 8.4 km/h (5.2 mph) in the untrained state and at 11.6 km/h (7.2 mph) in the trained state. 702 Respiratory Exchange Ratio Recall from chapter 5 that the respiratory exchange ratio (RER) is the ratio of carbon dioxide released to oxygen consumed during metabolism. The RER reflects the composition of the mixture of substrates being used as an energy source, with a lower RER reflecting an increased reliance on fats for energy production and a higher RER reflecting a higher contribution of carbohydrates. After training, the RER decreases at both absolute and relative submaximal exercise intensities. These changes are attributable to a greater utilization of free fatty acids instead of carbohydrate at these work rates following training. Resting and Submaximal Oxygen Consumption Oxygen consumption ( O2) at rest is unchanged following endurance training. While a few cross-sectional comparisons have suggested that training elevates resting O2, the HERITAGE Family Study—with a large number of subjects and with duplicate measures 703 of resting metabolic rate both before and after 20 weeks of training—showed no evidence of an increased resting metabolic rate after training.30 During submaximal exercise at a given intensity, O2 is either unchanged or slightly reduced following training. In the HERITAGE Family Study, training reduced submaximal O2 by 3.5% at a work rate of 50 W. There was a corresponding reduction in cardiac output at 50 W, reinforcing the strong interrelationship between O2 and cardiac output.29 This small decrease in O2 during submaximal exercise, not seen in many studies, could have resulted from an increase in exercise economy (performing the same exercise intensity with less extraneous movement). Maximal Oxygen Consumption O2max is the best indicator of cardiorespiratory endurance capacity and increases substantially in response to endurance training. While small and very large increases have been reported, an increase of 15% to 20% is typical for a previously sedentary person who trains at 50% to 85% of his or her O2max three to five times per week, 20 to 60 min per day, for 6 months. For example, the O2max of a sedentary individual could reasonably increase from 35 ml · kg−1 · min−1 to 42 ml · kg−1 · min−1 as a result of such a program. This is far below the values we see in world-class endurance athletes, whose values generally range from 70 to 94 ml · kg−1 · min−1. The more sedentary an individual is when starting an exercise program, the larger the increase in O2max. Integrated Adaptations to Chronic Endurance Exercise It should now be clear that the adaptations that accompany endurance training are many and that they affect multiple physiological systems. Physiologists commonly establish models to help explain how various physiological factors or variables work together to affect a specific outcome or component of performance. Dr. Donna H. Korzick, an exercise physiologist at Pennsylvania State University, has created a unifying figure to model the factors that contribute to the cardiovascular adaptation to chronic endurance training (see figure 11.11). 704 Figure 11.11 Modeling cardiovascular adaptations to chronic endurance exercise. 705 Adapted, by permission, from Donna H. Korzick, Pennsylvania State University, 2006. Research Perspective 11.3 Intensity–Duration Trade-Offs and O2peak: The HUNT Study The health-promoting benefits of a physically active lifestyle are well known. However, improvement in O2peak only partially accounts for reductions in metabolic and cardiovascular risk. Furthermore, within large populations, habitual physical activity level and O2peak are only modestly correlated. The American College of Sports Medicine (ACSM) and American Heart Association (AHA) recommend that adults of all ages exercise at a moderate intensity most days of the week for at least 150 total minutes or at a vigorous intensity for at least 75 min per week. That leaves open the question whether “long duration–moderate intensity” or “shorter duration–vigorous intensity” exercise patterns lead to greater improvements in O2peak. In a large Norwegian cohort study (HUNT Study), 4,631 healthy adults aged 19 to 89 years self-reported their exercise patterns, then underwent a treadmill test to determine O2peak.23 O2peak did not differ much between people who reported ≥150 min of moderate-intensity exercise per week (men: 45, women: 37 ml · kg−1 · min−1) and those who reported 75 to 149 min of vigorous activity (men: 48, women: 37 ml · kg−1 · min−1). However, both groups had higher O2peak values than individuals who did little exercise or did low-intensity exercise (men: 40, women: 32 ml · kg−1 · min−1). Thus, long duration– 706 moderate intensity and shorter duration–vigorous intensity exercise patterns that fall within current ACSM/AHA guidelines similarly improve O2peak. Interestingly, an additional group that reported “very vigorous” exercise for