Altitude Environment
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Barometric pressure is reduced at high altitudes, with a parallel decrease in inspired partial pressure of oxygen (P I O 2 ); thus, hypobaric hypoxia is the most prominent physiologic manifestation at high altitudes. Fig. 23.1 shows the accepted terminology for the range of terrestrial altitudes as well as the magnitude of effects on selected outcome variables.
Figure 23.1
Accepted altitude definitions and ranges, from 2007 FIFA Consensus Conference. The amount of shading in the vertical bars represents the magnitude of variable (as influenced by altitude), with darker shading indicating a high level.
(Data from Scand J Med Sci Sports. 2008:18[S1]:96-99.)
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Temperature decreases at a rate of approximately 6.5°C per 1000 m.
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Other features include dry air (increasing risk of dehydration), decrease in air density and therefore air resistance (marked effects in high-velocity sports such as cycling and onflight characteristics of objects—i.e., golf, baseball, or soccer), and increase in the amount of ultraviolet light (4% per 300 m), which increases the risk of sunburn.
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Therefore, athletes must cope with hypoxia, cold, and dehydration and yet maintain maximal performance.
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Timing of altitude exposure and degree of acclimatization are critical to successful outcomes.
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Physiologic adaptation to high altitude may be beneficial. Altitude training is frequently used by elite athletes in an attempt to improve sea-level performance, but the manner in which it is completed will considerably affect the outcomes.
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Effect of Altitude on Exercise
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Oxygen cascade is the term used to describe the physiologic effects of altitude on exercise: Oxygen moves from the environment (determined by the altitude achieved) to the alveoli (function of ventilation and hypoxic ventilatory response) across the pulmonary capillary bed (limited by diffusion) to be transported by the cardiovascular system (function of cardiac output and hemoglobin concentration) and diffused into skeletal muscles (depends on capillarity and biochemical state of muscles) to be used by muscle mitochondria (influenced by oxidative enzyme activity) for aerobic respiration and ATP production.
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Altitude-induced hypoxia reduces the amount of oxygen available to perform physical activity.
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Maximal aerobic power (V̇O 2 max) is reduced by approximately 1% for every 100 m above 1500 m in nonathletic but healthy individuals.
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For endurance-trained athletes, this effect is even greater—reductions in V̇O 2 max and performance can be identified at altitudes as low as 500 m and are linear (decrease of approximately 0.5%–1.5% for every 100-m increase in altitude) at altitudes ranging from 300 m to 3000 m.
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Occurs because of diffusion limitation in both lung and skeletal muscles exacerbated by high pulmonary and systemic blood flow (cardiac output) in endurance athletes; severe hypoxemia can develop even during submaximal exercise (e.g., oxyhemoglobin saturation [SaO 2 ] < 80% in an elite male runner at a pace of 6 min/mile at 2700 m)
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This magnitude of V̇O 2 max and performance decline at altitude, particularly in endurance-trained athletes, shows substantial interindividual variability. Data from several studies and other reports indicate the ability to maintain SaO 2 as a primary factor.
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During submaximal exercise at altitude, ventilation, lactate, and heart rate are greater for the same absolute work rate, which increases the sensations of dyspnea and fatigue.
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As a result of this increased rate of perceived exertion and dyspnea, training velocity (runners), training power output (e.g., cyclists), and V̇O 2 are lower during training at altitude.
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Heart rate and lactate responses to training at altitude are the same as training at sea level at the same relative effort, which complicates the determination of appropriate training zones/paces at altitude.
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Peak blood lactate concentration is lower in individuals acclimatized to high altitude (termed lactate paradox ), although this outcome is controversial and depends on nuances of workload and training altitude.
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Competitive performance outcomes at altitude, compared with that at sea level, is strongly influenced by the amount of aerodynamic drag on the body and the primary energy system utilized.
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Lower-velocity events (e.g., distance running): in event distances requiring high levels of aerobic power (>2 minutes), performance is impaired at altitude because of a reduction in skeletal muscle oxygen delivery. In event distances requiring higher sustained power outputs (30 seconds to 2 minutes), performance may or may not be impaired at altitude, depending on the interplay of oxidative and glycolytic energy pathways.
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Higher-velocity events (i.e., sprint running, cycling, or speed skating): the reduced air resistance at altitude actually results in an improvement in performance, despite systemic hypoxemia. In sprint events requiring short bursts of high-intensity activity (≤30 seconds), ATP production is not primarily dependent on oxygen transport. In high-velocity events lasting >2 minutes, the decline in aerobic power with reduced skeletal muscle oxygen delivery is effectively smaller than the influence of reduced air resistance. For example, as of January 2016, every world record in speed skating events from 500 m to 10,000 m in length was set at altitudes >1200 m, despite an expected reduction in V̇O 2 max at these altitudes.
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Acclimatization Process
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Chronic exposure to altitude stimulates acclimatization, which includes adaptations that improve submaximal work performance at altitude. Individual physiologic components of acclimatization have unique time frames of response, ranging from minutes to hours, days, months, or even generations. In addition, the rate and completeness of acclimatization is dependent on the altitude of residence—i.e., the hypoxic dose. For example, at high and extreme altitudes (≥4000 m), V̇O 2 max never returns to sea-level values despite prolonged acclimatization. At low altitudes (<2000 m), the maximal oxygen uptake may approach sea-level values after 1–2 weeks in nonathletic individuals.
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Increases in alveolar ventilation and reductions in mixed venous oxygen content minimize the decline in exercise capacity at altitude— this begins immediately on ascent .
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Hyperventilation causes respiratory alkalosis, which stimulates renal excretion of bicarbonate and loss of plasma volume over the first week to normalize acid-base balance.
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Ventilation at rest (and to some extent during exercise) at altitude is influenced by the sensitivity of peripheral chemoreceptors; this hypoxic ventilatory response (HVR) is highly individualistic, with elite endurance athletes commonly showing blunted HVRs in comparison with untrained individuals. At low and moderate altitudes, a high HVR may affect the magnitude of dyspnea; at high and extreme altitudes, a high HVR may be critical for maintenance of even basic levels of physical activity and even survival.
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Sympathetic activation acutely (minutes to hours) increases heart rate and cardiac output so that oxygen delivery to tissues remains close to sea-level values at rest and during submaximal activity. By 2–3 weeks, systemic and regional blood flow return to sea-level values as oxygenation improves. However, sympathetic activity continues to increase and may reach extraordinary levels, particularly at higher altitudes (>4000 m).
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The oxygen-carrying capacity of blood increases as a result of the increase in hemoglobin and hematocrit: early (1–2 days) increases result from plasma volume reduction; later (weeks to months) increases result from increases in red cell mass. This critical adaptation offsets the reduction in atmospheric oxygen availability, thereby restoring oxygen transport to normal sea-level values .
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Peripheral uptake of oxygen by skeletal muscles is facilitated by increased capillary density, mitochondrial number, myoglobin concentration, and 2,3-diphosphoglycerate (2,3-DPG), although these local changes may take weeks or months to manifest and are not universally observed.
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The buffering capacity of skeletal muscles may be increased as well.
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Failure of Acclimatization: High-Altitude Illness and Overtraining
Acute Mountain Sickness
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With moderate or higher altitudes (>2000 m) and rapid ascent rates (>300 m sleeping altitude per day above 3000 m), a maladaptive state called acute mountain sickness (AMS) may develop.
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Symptoms include headache, nausea, anorexia, fatigue, and difficulty in sleeping.
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Symptoms are usually mild and self-limited; rest and analgesics are sufficiently effective treatment.
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There is no evidence that competitive athletes are at any greater risk of developing AMS than nonathletes, although exercise may exacerbate the development of AMS, and physical activity should be appropriately reduced in symptomatic individuals.
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For patients who do not improve with rest, supplemental oxygen or descent to lower altitude virtually always results in prompt symptom relief.
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Other effective treatments include acetazolamide, dexamethasone, and simulated descent with a portable hyperbaric bag.
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AMS is best prevented by limiting the rate of ascent, allowing for rest or acclimatization days, maintaining adequate hydration, avoiding alcohol or sedatives during early acclimatization phase, and limiting training volume and intensity during first few days at altitude.
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Use of drugs to prevent AMS is discouraged in endurance athletes who are going to moderate altitude (<3000 m) unless a clear history of recurrent AMS is reported.
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The most frequently used drug is acetazolamide, which may be effective at low doses (125 mg at night or twice daily). However, diuretics including acetazolamide are on the World Anti-Doping Agency banned list as masking agents. Dexamethasone is probably more potent but is also banned as a steroid.
Severe High-Altitude Illness
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In some individuals, AMS may progress to or be associated with more severe and life-threatening forms, including high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE).
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HAPE is characterized by dyspnea at rest, cyanosis, severe hypoxemia, and noncardiogenic pulmonary edema.
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HACE is characterized by vomiting, ataxia, reduction in level of consciousness, and, in some cases, frank coma.
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Both of these syndromes can quickly result in death. Immediate descent is mandatory. High-flow supplemental oxygen or a portable hyperbaric bag, if available, may be useful adjunctive therapy while descending or if descent is delayed.
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Both HAPE and HACE are rare at moderate altitudes to which most athletes are exposed (<0.1%) although occurrence in athletes at low–moderate-altitude (<2000 m) should initiate search for congenital abnormalities of the pulmonary circulation.
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Medications that lower pulmonary arterial pressure may be used for adjunctive treatment of HAPE (this is less effective than descent and oxygen). Nifedipine has been most extensively studied and is effective both for treatment and prophylaxis. Phosphodiesterase inhibitors (e.g., sildenafil or tadalafil) are being investigated, but they may exacerbate AMS. Very recent studies suggest that dexamethasone is effective at preventing both AMS and HAPE and is the most effective adjunctive therapy for HACE. Drug treatment should be considered in athletes only if oxygen is unavailable or descent/evacuation is delayed. A staged slow ascent is the most effective preventive strategy, and it sidesteps the need to use banned substances for prevention.
Overtraining
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Another potentially serious problem with training at altitude is the increased risk of overtraining.
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A comparison between exercise training and administration of medication, as shown in Fig. 23.2 , is helpful. Every medication has a specific dose–response relationship, accompanied by a toxic/therapeutic range. These parameters define the optimal dose and frequency of administration to maximize benefits but minimize side effects and toxicity. Exercise can be conceived as medication (so-called “exercise is medicine”): training response is proportional to volume and intensity (ED 50), but too much exercise results in clear toxic effects of musculoskeletal injury and systemic effects of overtraining (LD 50).
