Scientific Research on Physiological Effects of High Altitude

Oxygen Diffusion and Athletic Performance

Information adapted from:
Levine, B. D. and J. Stray-Gunderson. 1997. “Living high-training low”: effect of moderate-altitude acclimatization with low-altitude training on performance.  Journal of Applied Physiology 83: 102-112.

Altitude training is often used by competitive athletes to improve their sea-level performance.  Athletes train at altitude to generate increased production of red blood cells and raise their blood concentrations of DPG and myoglobin as a result of the previously detailed physiological acclimatization to altitude.  Research verifies that acclimatization to moderate altitude combined with training at low altitude results in an improvement in sea-level running performance over 5000 m in well-trained competitive runners.
This increased velocity results from two basic mechanisms.  In the first, an altitude-acclimatization effect, ventilatory adaptations improve alveolar oxygenation of blood.  After transport to tissues, oxygen extraction and substrate utilization is improved by structural and biochemical adaptations in skeletal muscle.  Furthermore, the increase in red blood cell mass increases blood oxygen carrying capacity which improves aerobic power.  Finally, the lower cardiac output resulting from altitude acclimatization allows more peripheral diffusion time for oxygen extraction and an additional cardiac flow reserve.  The second mechanism results from training at low altitude where athletes can maintain their training intensity and oxygen flux.

Hypobaric Hypoxia in High Altitude Pulmonary Edema

Information adapted from:
Levine, B., K. Kubo, T. Kaoayashi, M. Fukushima, T. Shibamoto, and G. Ueda. 1988. Role of barometric pressure in pulmonary fluid balance and oxygen transport. Journal of Applied Physiology 64: 419-428.

Studies of the treatment of victims of HAPE show that relief from symptoms occurs more rapidly with descent than with supplemental administration of oxygen.  This response points to a pathogenesis caused more by barometric pressure than hypoxia.  Acclimatization to high altitudes raises pulmonary arterial pressure, cardiac output, and heart rate under hypoxic conditions. Under conditions of combined hypobaric hypoxia.  Pulmonary hypertension caused by hypoxic vasoconstriction leads to an increase in capillary pressure resulting in fluid retention in the lungs.  Additionally, the increased capillary pressure under hypobaric hypoxia may cause a net increase in pulmonary fluid filtration.  This added alveolar pressure is accompanied by a lower rate of filtration and significantly alters the forces that determine transcapillary fluid flux in the lung. Higher alveolar pressure may also affect the alveolar-arterial gradient for oxygen.
 

High Altitude Body Energetics

Information adapted from:
Cibella, F., G. Cuttitta, S. Romero, B. grassi, G. Bonsignore, and J. Milic-Emili.  1999. Respiratory energetics during exercise at high altitude. Journal of Applied Physiology 86(6) 1785-1792.

“Breathing becomes such a strenuous business that we scarcely have strength to go on.”
-Reinhold Messner on the first human ascent of Mt. Everest (8848 m) without bottled oxygen

Information about the work of breathing at high altitude is critical to athletes who’s endurance of hypoxic conditions can be a matter of life and death. The high rate of ventilation during rest and tripled work of breathing at altitude contribute to the limitation of exercise performance under hypobaric conditions.  Research in the field of body energetics shows that maximal external power and total body ventilation of oxygen are lower at high altitude than at sea level.  If the oxygen gained from hyperventilation is less than that required for the increased work of breathing, the energy required to maintain constant hyperventilation does not increase the energetic economy of the body.  Since mountaineers no longer gain energy from increased respiration, they must rely on bottled oxygen for their respiratory needs.

Metabolic Adaptation

Information adapted from:
Westerterp-Plantenga M., K. Westerterp, M. Rubbins, C. Berwegen, J. Richelet, and B. Gardette. 1999. Appetite at “high altitude” [Operation Everest III (Comex-’97)]: a simulated ascent of Mount Everest. Journal of Applied Physiology 87: 391-399.

Acclimatization to high altitude often causes initial loss of body weight (5.0 kg at 8848 m).  This loss of body mass is attributed to loss of appetite leading to decreased food intake.   Since average energy intake decreases with altitude, scientists hypothesize that loss of appetite is correlated with conditions hypobaric hypoxia.  Furthermore, research indicates that Acute Mountain Sickness uncouples hunger and the desire to eat preventing nutritional intake needed to maintain energy balance at demanding levels of physical exertion.  Ultimately, humans have great difficulty maintaining energy balance at high altitude, even at low levels of activity.  This reduced metabolic rate results primarily from decreased energy intake though changes in water balance and digestive ability may also lower metabolic efficiency.
 

The Heart and Lungs at Extreme Altitude

Information adapted from:
Reeves, J. T. 1994. The heart and lungs at high altitude. Thorax 49: 631-633.

Cardiologists and respiratory physicians benefit from knowing how organ systems transport oxygen from ambient air to lung capillary blood and then from the lung to the systemic capillaries.  This information proves valuable not only for high altitude athletes but for a variety of medical cases that involve hypoxaemia at sea level such as upper airway obstruction, sleep apnoea, and hypoventilation.  Hypoxic conditions are known to decrease maximum oxygen uptake, exercise heart rate, and maximal cardiac output limiting exercise.  In addition, the forced vital capacity of the lungs progressively decreases with increasing altitude.  In medical experiments, interstitial edema and pulmonary hypertension at altitude adversely affected ventilation and perfusion.  This interstitial edema probably contributes to the poor ventilation of some alveoli and a lack of oxygen-related pulmonary vasomotor control.  Without this control, circulation results in the overperfusion of poorly oxygenated areas.