Altitude Training and Competition

Altitude Environment

• 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.

  

• Temperature decreases at a rate of approximately 6.5°C per 1000 m.

• Other features include dry air (increasing the risk of dehydration), decrease in air density and therefore air resistance (marked effects in high-velocity sports such as cycling or speed skating and flight characteristics of objects; i.e., golf, baseball, archery, or soccer; or people; i.e., ski jumping, or even ice skating), and increase in the amount of ultraviolet light (4% per 300 m), which increases the risk of sunburn.

  • Therefore, athletes must cope with hypoxia, cold, and dehydration and yet maintain maximal performance.

  • Timing of altitude exposure and degree of acclimatization are critical to successful outcomes.

  • 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.

• In a laboratory or home-based setting at or near sea level, hypoxia can be simulated by reducing the fraction of inspired O ₂ by adding exogenous N ₂ (termed normobaric hypoxia [NH]). This exposure is in contrast to terrestrial altitude, or hypobaric hypoxia (HH), where the ambient pressure is reduced.

• The method of hypoxia utilized (NH or HH) is relevant to consider, as some physiologic responses that affect performance or adaptive function may differ between methods, despite the partial pressure of O ₂ being the same (e.g., oxygen saturation is lower and oxidative stress is higher in HH; acute mountain sickness [AMS] is more severe in HH; plasma volume decline and diuresis are greater in NH). It must be emphasized, though, that most of these differences between HH and NH are small and of questionable physiologic significance; the most prominent and physiologic important stressor at altitude is the reduction in partial pressure of oxygen. Athletes who choose to use home-based methods of NH versus travel to terrestrial altitude will need to carefully consider exposure time and level of hypoxia if the goal is to achieve equivalent erythropoietic and performance improvements (see “Altitude Dose Recommendation” section later).

Effect of Altitude on Exercise

• 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 adenosine triphosphate (ATP) production.

• Altitude-induced hypoxia reduces the amount of oxygen available to perform physical activity.

  • Maximal aerobic power (V.O ₂ max) is reduced by approximately 1% for every 100 m above 1500 m in nonathletic but healthy individuals.

  • For endurance-trained athletes, this effect is even greater—reductions in V.O 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.

    • 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).

    • This magnitude of V.O 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.

  • 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.

    • As a result of this increased rate of perceived exertion and dyspnea, training velocity (runners), training power output (e.g., cyclists), and V.O ₂ max are lower during training at altitude.

    • 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.

  • 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.

• 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.

  • 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.

  • 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 October 2020, 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 V.O ₂ max at these altitudes.

Acclimatization Process

• 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 are dependent on the altitude of residence (i.e., the hypoxic dose). For example, at high and extreme altitudes (≥4000 m), V.O 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.

  • Increases in alveolar ventilation and reductions in mixed venous oxygen content minimize the decline in exercise capacity at altitude— this begins immediately on ascent.

  • Hyperventilation causes respiratory alkalosis, which stimulates renal excretion of bicarbonate and loss of plasma volume over the first week to normalize acid–base balance.

  • 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.

  • 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).

  • 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.

  • 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.

  • The buffering capacity of skeletal muscles may be increased as well.

Failure of Acclimatization: High-Altitude Illness and Overtraining