Besides reduced air density and decreased oxygen content in ambient air, a number of environmental factors affect athletes’ responses at altitude, namely:
increased sun and ultra-violet radiation, reduced temperature and humidity, delightful landscapes and mountainous beauty. Traditionally, consideration of altitude exposure and training is focused on the hypoxia factor; but in fact, many environmental factors operate collectively and this determines the athletes’ response. As it is known, the considerable effects of altitude exposure start from an elevation of 1600m; altitudes higher than 2600m are usually not utilized for training camps.
Let us consider the responses that occur during initial exposure: acute
responses lasting from a few hours to a few days; and longer-term responses lasting two-five weeks or even more (Table 9.1).
Table 9.1
Acute and longer-term responses of athletes to altitude exposure and training (based on McArdle et al., 1991; Brooks et al., 1996; Wilber, 2004)
Physiological
functions Acute responses Longer-term responses Pulmonary
ventilation
Increased pulmonary ventilation due to reduced oxygen content
Pulmonary ventilation remains increased
Heart rate Increased heart rate at rest and during exercises; decreased maximal heart rate values
Return of exercise and rest heart rates to pre-altitude level; maximal heart rate remains decreased
Stroke volume Reduced stroke volume at rest and during any intensive exercise
Return of exercise and rest stroke volume to pre-altitude levels
Cardiac output Reduced cardiac output at rest and during any intensive
Return of exercise and rest cardiac output to pre-altitude
exercise levels Blood lactate Increased lactate accumulation
after intensive and maximal exercise
Decreased lactate values after intensive and maximal exercise as compared with pre-altitude levels
Aerobic energy
supply Reduction of maximal oxygen uptake by 1% for each 100m of altitude elevation
Increase of aerobic enzymes; return of maximal oxygen uptake to near pre-altitude levels Anaerobic
capacity
Hypoxia accelerates glycolitic reactions and glycogenolysis
Increased muscle buffering enlarges anaerobic capacity Hormones
regulation Increased catecholamine level; release of erythropoietin that stimulates production of
erythrocytes and hemoglobin
Increased cortisol that indicates stress reaction and affects muscle catabolism
Hematological responses
Plasma volume and total blood volume decrease immediately after arrival
Increased total blood volume, number of erythrocytes and mass of hemoglobin
Skeletal muscles Increased capillary density; possible muscle mass decrease due to cortisol catabolic action Fluid balance Tendency to dehydration due
to increased respiratory and urinary water loss
Increased fluid intake can be as much as four-five liters per day Immune system Increased risk of upper
respiratory infections Increased level of stress hormones (catecholamines, cortisol) suppress immune function
Let us consider the scenario of physiological changes induced by exposure to and training at medium level altitude. Arrival at altitude and breathing air with lower oxygen content causes an excitation of chemoreceptors and a reflexive increase in pulmonary ventilation. This increase is a compensatory mechanism to bring the same amount of oxygen into the lung as at sea level. Such hyperventilation occurs both at rest and during exercise. The blood plasma volume declines immediately after arrival at altitude; after a week or more it returns to pre-altitude levels and even increases above sea-level values (Saltin, 1996). Heart rate at rest and during moderate
workloads elevates proportionally to the decrease of partial pressure of oxygen. An additional reason for the heart rate increase could be also catecholamine excretion (mostly adrenalin) that occurs in particular at initial exposure. Stroke volume at rest and during moderately and highly intensive workloads decreases substantially within the initial two days. After a number of days stroke volume returns to pre-attitude levels. Nevertheless, heart rate increases markedly, and cardiac output remains decreased at rest and during various workloads for several days (Wilber, 2004). One of the important outcomes of hypoxia is reduction of kidney oxygenation that stimulates synthesis of erythropoietin (EPO), a hormone that regulates production of erythrocytes and hemoglobin. The increased concentration of EPO elicits synthesis of additional erythrocytes and hemoglobin, a process that takes approximately five-seven days. After that, oxygen carrying capacity of the blood increases markedly as does athletes’ aerobic ability. These perturbations explain the dramatic reduction of maximal oxygen uptake during acute exposure and its gradual increase during
acclimatization. In the initial days, the hypoxic environment accelerates glycolitic reactions and glycogen breakdown. At this time anaerobic threshold dramatically decreases and the corresponding velocity regimes decrease as well. Correspondingly, the metabolic response to habitual exercise changes as well; as athletes approach their previously comfortable velocity regime there is a sharp increase in blood lactate. Further acclimatization follows to increase muscle buffering capacity that prevents excessive acidosis (pH reduction) during severe workloads.
Serious altitude training over a week or a little more leads to increased secretion of cortisol that stimulates catabolic reactions and possible reduction of muscle mass. Indeed, remarkable decreases of muscle mass and body weight have been noted among top-level athletes (Issurin, Kaverin, 1990). One more consequence of increased cortisol is suppression of the immune function with increased risk of upper respiratory infections a concern of sport physicians. Immediately after arrival at altitude increased respiratory and urinary loss of water may cause dehydration.
Therefore, during the entire altitude exposure, fluid intake should be increased by four-five liters per day.
For a long time the potential benefits of the altitude training were associated with hematological changes, i.e., increased oxygen delivery to muscles. In fact these changes are transient and very soon after returning at sea level (a few days to one week) erythrocytes and hemoglobin return to pre-altitude levels. Another potential contributor to the post-altitude ergogenic effect is enhancement of anaerobic abilities due to increased buffering capacity of muscles and blood. An additional potential contributor may be enhanced cellular adaptation of muscles. This factor has been studied less and is rarely considered. Nevertheless, it is known that training at altitude (or altitude-simulated conditions) leads to increased muscle capillarity, which
facilitates oxygen extraction from the blood (Mizuno et al., 1990). Other favorable changes can also occur in the muscular microstructure (Terrados et al., 1990).
Study and example. Ten male subjects trained for four weeks on a cycle-
ergometer with one leg. The training protocol consisted of exercising one leg under normobaric (sea-level) conditions, and another leg under hypoxic conditions corresponded to an altitude of 2300 m. Tests battery included endurance trials and needle biopsy with subsequent evaluation of muscle enzymes and myoglobin in the extracted sample. Comparison of altitude- trained leg with the other one allowed researchers to assess the effect of altitude-simulated training. It resulted in significantly superior endurance, markedly increased activity of oxidative enzymes and a higher concentration of myoglobin (Terrados et al., 1990).
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In summary, even a simplified consideration of acute and longer-term responses to altitude exposure indicates many difficulties related to athletes’
preparation planning while the potential benefits still look complicated and dubious.