Aerobic training requires regular periods of stress and recovery
The body improves its capacity to perform work by responding to physical exertion. However, one must meet four conditions to achieve a training effect, or adaptation to exercise. First, the intensity of the activity must be higher than a critical threshold. For aerobic training (e.g., running, cycling, and swimming), the level of stress increases with the intensity of the activity. N60-3 Second, each period of activity must be of sufficient duration. Third, one must repeat the activity over time on a regular basis (e.g., several times per week). Finally, sufficient rest must occur between each training session, because it is during the recovery period that the adaptations to exercise actually occur.
A great deal of research has focused on optimizing the foregoing four factors, as well as task specificity, for individual athletes competing in specific events. Increasing levels of exertion progressively recruit (see pp. 1204–1205) and thereby adapt type I muscle fibers, followed by type IIa fibers, and then type IIx fibers. In strength training, repetitive powerful bursts of activity favor hypertrophy of type IIx fibers. Regardless of how long or intensely an individual trains, prolonged inactivity reverses these adaptations with an associated decrement in aerobic performance (type I and IIa fibers) or loss or muscle mass (primarily type IIx fibers). Aerobic conditioning increases (see pp. 1213–1214) as well as the body's ability to eliminate excess heat that is produced during exercise (see Fig. 59-5).
Aerobic training increases maximal O2 delivery by increasing plasma volume and maximal cardiac output
could increase as the result of either optimizing O2 delivery to active muscle or optimizing O2 extraction by active muscle, as demonstrated in the following modification of Equation 60-7:
In fact, aerobic training improves both O2 delivery and O2 extraction; the problem for physiologists has been to determine to what extent each system contributes to the whole-body response. For example, an increase in the circulatory system's capacity to deliver O2 could reflect an increase in either the maximal arterial O2 content or the maximal cardiac output, or both.
Maximizing Arterial O2 Content
Several factors could theoretically contribute to maximizing :
1. Increasing the maximal alveolar ventilation enhances the driving force for O2 uptake by the lungs (see Fig. 31-4).
2. Increasing the pulmonary diffusing capacity (see p. 668) could enhance O2 uptake at very high cardiac output, particularly at high altitude (see Fig. 30-10).
3. Improving the matching of pulmonary ventilation to perfusion should increase arterial and the saturation of hemoglobin (see pp. 689–690).
4. Increasing the concentration of hemoglobin enables a given volume of arterial blood to carry a greater amount of O2 (see pp. 651–652).
Under nearly all conditions of exercise, the pulmonary system maintains alveolar at levels that are sufficiently high to ensure nearly complete (i.e., ~97%) saturation of hemoglobin with O2, even at maximal power output. Thus, it is unlikely that an increase in the maximal alveolar ventilation or pulmonary diffusing capacity could explain the large increase in that occurs with training.
would be increased by elevating the blood's hemoglobin concentration. However, no evidence exists to indicate that physical training induces such an increase. On the contrary, [hemoglobin] tends to be slightly lower in endurance athletes, a phenomenon called sports anemia, which reflects an expansion of the plasma compartment (discussed below). Whereas increasing [hemoglobin] provides a greater O2-carrying capacity in blood, maximal O2 transport does not necessarily increase accordingly because blood viscosity, and therefore total vascular resistance, also increase. The heart would be required to develop a higher arterial pressure to generate an equivalent cardiac output. The resultant increased cardiac work would thus be counterproductive to the overall adaptive response. Blood doping—transfusion of blood before competition—is thus not only illegal but also hazardous to athletes, particularly when water loss through sweating leads to further hemoconcentration.
Maximizing Cardiac Output
Factors that contribute to increasing maximal cardiac output include optimizing the increases in heart rate and cardiac stroke volume so that their product (i.e., cardiac output) is maximal (see Equation 60-9 and pp. 580–583). Because aerobic training does not increase maximal heart rate and has a relatively small effect on O2 extraction, nearly all the increase in that occurs with training must be the result of an increase in maximal cardiac output, the product of optimal heart rate and optimal stroke volume (see Equation 60-9). The athlete achieves this increased cardiac output by increasing maximal cardiac stroke volume. Maximal cardiac output can increase by ~40% during physical conditioning that also increases maximal aerobic power by 50%. The difference between 40% and 50% is accounted for by increased extraction: . Enhanced extraction in endurance training is a consequence of capillary proliferation and increased mitochondrial content of muscle fibers, which creates a greater O2 sink under maximal aerobic conditions.
Maximal cardiac stroke volume increases during aerobic training because expansion of the plasma—and thus blood volume—increases the heart's preload (see p. 526), with a concomitant hypertrophy of the heart. An increase in preload increases ventricular filling and proportionally increases stroke volume (Starling's law of the heart; see pp. 524–526), thereby elevating maximal cardiac output accordingly. An additional benefit is that a trained athlete achieves a given cardiac output at a lower heart rate, both at rest and during moderate exercise. Because it is more efficient to increase stroke volume than heart rate, increasing stroke volume reduces the myocardial metabolic load for any particular level of activity.
The expansion of plasma volume probably reflects an increase in albumin content (1 g albumin is dissolved in 18 g of plasma H2O). This increase appears to be caused both by translocation from the interstitial compartment and by increased synthesis by the liver. The result of more colloid in the capillaries is a shift of fluid from the interstitium to the blood. Although the total volume of red blood cells also increases with aerobic training, the plasma volume expansion is greater than the red blood cell expansion, so that the hemoglobin concentration falls. This sports anemia occurs in highly trained endurance athletes, particularly those acclimatized to hot environments.
The increased blood volume has another beneficial effect. It enhances the ability to maintain high skin blood flow in potentially compromising conditions (e.g., heavy exercise in the heat), thus providing greater heat transport from core to skin and relatively lower storage of heat (see pp. 1195–1196).
Aerobic training enhances O2 diffusion into muscle
Whereas an increase in maximal cardiac output accounts for a major fraction of the increased O2 delivery to muscle with training, a lesser fraction reflects increased O2 extraction from blood. Fick's law describes the diffusion of O2 between the alveolar air and pulmonary capillary blood (see Equation 30-4). A similar relationship describes the diffusion of O2 from the systemic capillary blood to the mitochondria.
The factors that contribute to O2 diffusing capacity () are analogous to those that affect the diffusing capacity in the lung (see pp. 663–664). Trained muscle can accommodate a greater maximal blood flow because of the growth of new microvessels, particularly capillaries. Indeed, well-conditioned individuals have a 60% greater number of capillaries per cross-sectional area of muscle than do sedentary people. This increased capillary density increases because it provides a greater surface area for diffusion. Increase in capillary density also reduces the diffusion distance for O2 between the capillary and muscle fibers (see Fig. 20-4). In addition, training increases total capillary length and volume, prolonging the transit time of red blood cells along capillaries and thereby promoting the extraction of O2 and nutrients from the blood as well as the removal of metabolic byproducts. Finally, the increase in cardiac output enhances muscle blood flow, which helps to preserve a relatively high capillary throughout the muscle and thereby maintain the driving force for O2 diffusion from capillaries to mitochondria.
Aerobic training increases mitochondrial content
In untrained (but otherwise healthy) individuals, the maximum ability of mitochondria to consume O2 is considerably greater than that of the cardiovascular system to supply O2. Thus, mitochondrial content does not limit . We have already seen that endurance training markedly increases O2 delivery. In parallel, endurance training can also increase the mitochondrial content of skeletal muscle fibers nearly 2-fold by stimulating the synthesis of mitochondrial enzymes and other proteins (Fig. 60-11). The stimulus for mitochondrial biogenesis is the repeated activation of the muscle fiber during training, leading to increases in the time-averaged [Ca2+]i, which may act in two ways (Fig. 60-12). One is by directly modulating the transcription of nuclear genes. The other is by increasing cross-bridge cycling and raising [AMP]i, thereby stimulating the fuel sensor AMP kinase (AMPK), which, in turn, can modulate transcription. Some of the newly synthesized proteins are themselves transcription factors that modulate the transcription of nuclear genes. At least one protein—transcription factor A, mitochondrial (TFAM)—enters the mitochondrion and stimulates the transcription and translation of mitochondrial genes (see p. 22) for key elements of the electron-transport chain (see p. 118). Finally, some newly synthesized proteins encoded by genomic DNA, guided by cytoplasmic chaperones, target to the mitochondrial import machinery and become part of multisubunit complexes—together with proteins of mitochondrial origin.
FIGURE 60-11 Enzyme adaptation during aerobic training. Endurance training causes a slow increase in the level of several enzymes, as well as in the number of capillaries, maximal O2 uptake, and size of muscle fibers. These changes reverse rapidly on the cessation of training. (Data from Saltin B, Henriksson J, Nygaard E, Andersen P: Fiber types and metabolic potentials of skeletal muscles in sedentary man and endurance runners. Ann N Y Acad Sci 301:3–29, 1977.)
FIGURE 60-12 Exercise-induced mitochondrial biogenesis. mRNA, messenger RNA; mtDNA, mitochondrial DNA. (Adapted from Chabi B, Adhihetty PJ, Ljubicic V, Hood DA: How is mitochondrial biogenesis affected in mitochondrial disease? Med Sci Sports Exerc 37:2102–2110, 2005.)
Because mitochondria create the sink for O2 consumption during the oxidative phosphorylation of ADP to ATP, increased mitochondrial content promotes O2 extraction from the blood. However, the primary benefit from mitochondrial adaptation in aerobic conditioning is the capacity to oxidize substrates, particularly fat, an ability that enhances endurance of muscle. Recall that mitochondria are responsible not only for the citric acid cycle (see p. 1185) and oxidative phosphorylation (see p. 1185) but also for β-oxidation of fatty acids (see p. 1185). As exemplified by marathon and ultramarathon athletes, the greater reliance on fat at a given level of is the metabolic basis of glycogen sparing, and thus reduced production of lactate and H+ (see p. 1176).