AEROBIC TRAINING

Training Increases the Resistance to Fatigue

Aerobic conditioning increases the resistance to fatigue at all exercise intensities. As already noted, training
increases VO
2max
(p. 1248) as well as the body's ability to eliminate excess heat that is produced during
exercise (see Fig. 58-5).
The increased VO
2max
that occurs with training has obvious practical benefits. As the requirement for
energy release in active muscle approaches VO
2max
, anaerobic processes become increasingly important
in maintaining ATP production. Increasing one's VO
2max
allows a given rate of ATP production to occur
relatively more aerobically, all other factors being equal. When VO
2
is less than 50% of the maximum,
essentially all of the net energy release in active muscle is aerobic. In this condition, the O
2
transport via
the pulmonary and circulatory systems matches the O
2
demand in the muscle, avoiding disturbances in
acid-base balance.
When O
2
uptake exceeds 60% of VO
2max
, muscle anaerobiosis increases roughly in proportion to the
increase in relative power output. In addition, the muscle produces excess lactic acid and protons, and
these byproducts diffuse into the bloodstream. The body partially compensates for the resulting decrease in
blood pH by hyperventilation (p. 723). Increasing the VO
2max
thus raises the threshold of exercise intensity
at which lactic acid appears, suggesting that physical training alters both the O
2
-transport and
O
2
-acceptance systems.
Aerobic Training Increases Maximal O
2
Delivery By Increasing Plasma Volume, Thereby Increasing
Maximal Cardiac Output
Maximal O
2
uptake could increase as the result of either optimizing O
2
delivery to active muscle or
optimizing O
2
extraction by active muscle, as demonstrated in the following modification of Equation 59-6:
In fact, aerobic training improves both O
2
delivery and 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 O
2
could reflect an increase in either the maximal arterial O
2
content or the maximal cardiac output, or both.
MAXIMIZING ARTERIAL O
2
CONTENT.
Several factors could theoretically contribute to maximizing Ca
O
2
:
Increasing the maximal alveolar ventilation enhances the driving force for O
2
uptake by the lungs
(see Fig. 30-4).
1.
Increasing the capacity for gases to diffuse across the alveolarcapillary barrier in the lungs could
enhance O
2
uptake at very high cardiac output, particularly at high altitude (see Fig. 26-8).
2.
Improving the matching of pulmonary ventilation to perfusion increases arterial PO
2
and increases
the saturation of hemoglobin (p. 705).
3.
Increasing the concentration of hemoglobin enables a given volume of arterial blood to carry a
greater amount of O
2
(p. 656).
4.
In nearly all conditions of exercise, the pulmonary system maintains alveolar PO
2
at levels that are
sufficiently high to ensure nearly complete (i.e., 97%) O
2
saturation of hemoglobin, 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 VO
2max
that occurs with training.
Ca
O
2
would be increased by elevating the blood's hemoglobin concentration. However, there is no evidence
that physical training induces such an increase. To the contrary, [hemoglobin] tends to be slightly lower in
endurance athletes, a phenomenon called "sports anemia," which reflects an expansion of the plasma
compartment (see later). Whereas increasing [hemoglobin] provides a greater O
2
-carrying capacity in
blood, the maximal O
2
transport does not necessarily increase accordingly because blood viscosity, and
therefore total vascular resistance, would 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.
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 59-7).
Figure 59-8 illustrates how conditioning affects cardiac output and the arteriovenous difference for O
2
content. Compared with a control situation (blue curves), prolonged bed rest (red curves) has little effect on
maximal heart rate, diminishes maximal stroke volume, and greatly reduces maximal cardiac output.
However, training (green curves) increases maximal stroke volume, slightly decreases maximal heart rate,
but greatly increases maximal cardiac output. Neither training nor bed rest has a substantial effect on (Ca
O
2
- Cv
O
2
)
max
(i.e., maximal O
2
extraction).
page 1252
page 1253
Figure 59-8 Effect of training on various cardiovascular parameters. The four graphs show changes in four cardiovascular parameters at
different levels of O
2
uptake (i.e., different intensities of exercise). The four blue curves represent mean values for five untrained subjects. The
purple curves summarize similar data for the same five subjects after 20 days of bed rest. The green curves summarize data after 50 days of
physical training. (Data from Saltin B, Blomqvist G, Mitchell JH, et al: Response to submaximal and maximal exercise after bed rest and
training. Circulation 38(Suppl. 7):1968.)
Because training produces no dramatic increase in either maximal heart rate or maximal O
2
extraction,
nearly all of the increase in VO
2max
that occurs with training must be due to an increase in maximal cardiac
output, the product of optimal heart rate and optimal stroke volume in Equation 59-7. The athlete achieves
this increased cardiac output by increasing maximal cardiac stroke volume. Maximal cardiac output can
increase by approximately 40% during physical conditioning that also increases maximal aerobic power by
50%. The difference between 40% and 50% is accounted for by an increased extraction, (Ca
O
2
- Cv
O
2
)
max
.
The latter is the consequence of capillary proliferation and of elevating key oxidative enzymes in the
mitochondria of type I muscle fibers, creating a greater O
2
sink under maximal conditions (see the next
section).
Maximal cardiac stroke volume increases during aerobic training because expansion of the plasma
compartment increases the heart's preload (p. 528). An increase in preload increases ventricular filling and
proportionally increases stroke volume (Starling's law of the heart), elevating maximal cardiac output
accordingly. An additional benefit is that a trained athlete achieves a given cardiac output at a lower cardiac
frequency, 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 H
2
O). This increase appears to be due both to translocation (by an unknown mechanism)
from the interstitial compartment and to increased synthesis by the liver. The result is increased colloid
osmotic pressure in the capillaries, promoting a shift of fluid from the interstitium to the blood. Although the
total volume of red blood cells increases with aerobic training, the plasma-volume expansion is greater than
the red-cell expansion, thus reducing the hemoglobin concentration; hence, the sports anemia.
The increased blood volume has another beneficial effect: it enhances the ability to maintain a high skin
blood flow in potentially compromising conditions (e.g., heavy exercise in the heat), thus providing a greater
heat transport from core to skin and thus a relatively lower storage of heat (p. 1233).
Training Enhances Diffusion of O
2
into Muscle
Whereas an increase in maximal cardiac output accounts for most of the increased delivery of O
2
to
muscle with training, a lesser fraction reflects increased O
2
extraction from blood. Fick's law describes the
diffusion of O
2
between the alveolar air and pulmonary capillary blood (see Equation 29-7). A similar
relationship, shown in Equation 58-8, describes the diffusion of O
2
from the systemic capillary blood to the
mitochondria.
The factors that contribute to DO
2
are analogous to those that affect the diffusing capacity in the lung.
Trained muscle can accommodate a greater maximal blood flow (and therefore an increased blood volume)
because of the growth of new capillaries. Indeed, well-conditioned people have a 60% greater number of
capillaries for a given cross-sectional area of muscle fiber than sedentary people do. This increased
capillary density increases DO
2
, thus providing a greater surface area for diffusion. Increased capillary
density also reduces the diffusion distance for O
2
between the capillary and muscle fibers (see Fig. 19-4).
page 1253
page 1254
Another consequence of increased capillary density (and perhaps increased capillary length as well) is that
at a given blood flow the mean transit time of blood in muscle increases. Because the blood lingers for a
longer time in the muscle capillaries, O
2
extraction increases. However, training also increases maximal
skeletal-muscle blood flow, reflecting an increase in maximal cardiac output and the greater number of
parallel vessels in muscle. The increase in blood flow through active skeletal muscle minimizes the decay in
capillary PO
2
that tends to occur along the vessel as the result of increased DO
2
and capillary density. This
preservation of capillary PO
2
maintains the blood-to-mitochondrion PO
2
gradient, enhancing O
2
diffusion.
Aerobic Training Also Increases the Expression of Key Mitochondrial Enzymes
Another factor that accounts for the increased uptake of O
2
by muscle in trained people is elevated
oxidative enzyme activity in the muscle mitochondria (Fig. 59-9). Levels of mRNA increase for specific
enzymes, implying increased transcription owing to signals associated with the exercise stimulus (e.g.,
elevated hormones, altered plasma osmolality). Prolonged aerobic conditioning increases levels of succinic
dehydrogenase, NADH dehydrogenase, and cytochrome oxidase.
Increased oxidative enzyme activity increases the muscle PO
2
sink (i.e., decreases PO
2 mito
as illustrated in
Equation 59-8), enhancing O
2
diffusion from capillary to mitochondrion. This increased diffusion is also the
reason why (Ca
O
2
- Cv
O
2
)
max
in Equation 59-7 remained approximately constant with training, even though
blood flow increased markedly. If O
2
diffusion had not increased, [O
2
]
V
would have risen, and (Ca
O
2
-
Cv
O
2
)
max
would have decreased.
Figure 59-9 Enzyme adaptation during training. Training causes a slow increase in the level of several enzymes, as well as in the number of
capillaries, maximal O
2
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. The
Marathon: Physiological, Medical, Epidemiological, and Psychological Studies. Ann NY Acad Sci 301:3-29, 1977.)
Trained athletes mobilize free fatty acids more rapidly during exercise. Increasing mitochondrial oxidative
enzyme activity provides an increased ability to oxidize these free fatty acids during a demand for fuel
delivery. This change is accompanied by an adaptive decrease in the activity of glycolytic rate-limiting
enzymes. These adaptations conserve muscle glycogen and thus delay glycogen depletion during a given
demand for fuel.
Aerobically trained people have a decreased tissue sensitivity to insulin during exercise, in contrast to the
increase that occurs during exercise in the general (untrained) population. A decreased insulin sensitivity
slows glucose transport into muscle, increasing the reliance on the oxidation of free fatty acids, and further
sparing muscle glycogen.
References
REFERENCES
Books and Reviews
Booth FW, Thomason DB: Molecular and cellular adaptation of muscle in response to exercise: Perspectives of various models. Physiol
Rev 71:541-585, 1991.
Fitts RH: Cellular mechanisms of muscle fatigue. Physiol Rev 74:49-94, 1994.
Jones JH, Lindstedt SL: Limits to maximal performance. Annu Rev Physiol 55:547-569, 1993.
Lehmann MJ, Lormes W, Opitz-Gress A, et al: Training and overtraining: An overview and experimental results in endurance sports. J
Sports Med Phys Fitness 37:7-17, 1997.
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Nadel ER: Physiological adaptations to aerobic training. Am Scientist 73: 334-343, 1985.
Saltin B, Strange S: Maximal oxygen uptake: Old and new arguments for a cardiovascular limitation. Med Sci Sports Ex 24:30-37, 1992.
Wagner PD: Determinants of maximal oxygen transport and utilization. Annu Rev Physiol 58:21-50, 1996.
Journal Articles
Gollnick PD, Armstrong RB, Saubert CW IV, et al: Enzyme activity and fiber composition in skeletal muscle of untrained and trained men.
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Nadel ER, Bussolari SR: The Daedalus Project: Physiological problems and solutions. Am Scientist 76:351-360, 1988.
Saltin B, Blomqvist G, Mitchell JH, et al: Response to submaximal and maximal exercise after bed rest and training. Circulation 38(Suppl
7): 1-78, 1968.
Printed from STUDENT CONSULT: Medical Physiology (on 28 August 2006)
2006 Elsevier