“Human physiology is affected in different ways at high altitude. In general, the various systems of the human body—pulmonary, cardiovascular, endocrine, skeletal muscles—respond and adjust in an effort to provide enough oxygen to survive in the hypoxic environment of high altitude. Some of these life-supporting physiological responses may also enhance athletic performance, particularly in endurance sports.
The scientific rationale for using altitude training for the enhancement of aerobic performance is based on the body’s response to changes in the partial pressure of inspired oxygen (PIO2) and the partial pressure of oxygen in the arterial blood (PaO2). PIO2 at sea level is equal to 149 mmHg. At Mexico City (2300 m, 7544 ft), PIO2 drops to approximately 123 mmHg. At the summit of Mt. Everest (8852 m, 29,035 ft), PIO2 is approximately 50 mmHg or only about 30% of sea level PIO2.
Because of the altitude-induced decrease in PIO2, there is a decrease in PaO2, which leads to a drop in renal PaO2 and renal tissue oxygenation (Ou et al. 1998; Richalet et al. 1994). It is hypothesized that this reduction in renal tissue oxygenation stimulates the synthesis and release of erythropoietin (EPO) (Porter and Goldberg 1994; Richalet et al. 1994), the principal hormone that regulates erythrocyte (RBC) and hemoglobin production. In turn, an increase in serum EPO concentration stimulates the synthesis of new RBCs in the red bone marrow by promoting the cellular growth of immature erythrocytes, specifically the colony-forming unit-erythroid (CFU-E). Erythropoietin receptors are present on the surface of CFU-E. Binding of EPO to CFU-E receptors initiates the production of cellular transcription factors, synthesis of membrane and cytoskeletal proteins, synthesis of heme and hemoglobin, and the terminal differentiation of cells (Bell 1996). The RBC maturation process takes five to seven days from the initial altitude-induced increase in serum EPO (Bell 1996; Flaharty et al. 1990).
These hematological changes may significantly improve an athlete’s V·O2max by enhancing the blood’s ability to deliver oxygen to exercising muscles. It has been shown that improvements in RBC mass, hemoglobin concentration, and V·O2max enhance aerobic performance (Berglund and Ekblom 1991; Birkeland et al. 2000; Ekblom and Berglund 1991). Essentially, many athletes and coaches view altitude training as a natural or legal method of blood doping.
Research by Chapman, Stray-Gundersen, and Levine (1998) suggests that some athletes experience a better hematological response at altitude than others do. Female and male collegiate runners who completed either LHTL or traditional “live high, train high” altitude training were classified as responders or nonresponders based on their performance in a postaltitude 5-km run. On average, responders demonstrated a significant 4% improvement (37 s) in the postaltitude 5-km run versus their prealtitude performance; nonresponders were approximately 1% slower (14 s). Hematological data showed that responders had a significantly larger increase in serum EPO (52%) compared with nonresponders, who demonstrated a 34% increase in serum EPO. Similarly, postaltitude RBC mass for responders was 8% higher (p < 0.05), but nonresponders’ RBC mass was only 1% higher (not statistically significant) compared with prealtitude values. A breakdown of responders indicated that 82% came from the LHTL group, and 18% came from the “live high, train high” group. The authors concluded that each athlete may need to follow an altitude training program that places the athlete at an individualized, optimal altitude for living and another altitude for training, thereby producing the best possible hematological response.
As described, the primary reason endurance athletes train at altitude is to increase RBC mass and hemoglobin concentration. In addition, they may gain secondary physiological benefits as a result of altitude exposure. For example, altitude training has been shown to increase skeletal muscle capillarity (Desplanches et al. 1993; Mizuno et al. 1990). In theory, this physiological adaptation enhances the exercising muscles’ ability to extract oxygen from the blood.
Other favorable skeletal muscle microstructure changes that occur as a result of training at altitude include increased concentrations of myoglobin (Terrados et al. 1990), increased mitochondrial oxidative enzyme activity (Terrados et al. 1990), and a greater number of mitochondria (Desplanches et al. 1993), all of which serve to enhance the rate of oxygen utilization and aerobic energy production.
Nevertheless, scientific data in support of altitude-induced skeletal muscle adaptations are minimal, particularly among well-trained athletes. Only Mizuno and colleagues (1990) examined elite athletes; Desplanches and colleagues (1993) and Terrados and colleagues (1990) examined the effect of altitude training on the skeletal muscle characteristics of untrained individuals. Additional studies conducted on elite athletes failed to demonstrate significant changes in skeletal muscle microstructure caused by altitude training (Saltin et al. 1995; Terrados et al. 1988). Furthermore, Desplanches and colleagues (1993) conducted their study at impractical simulated elevations (4100 to 5700 m, 13,450 to 18,700 ft), an altitude too high for athletes to train at. Thus, based on the current scientific literature, it is unclear whether altitude training, as practiced by most elite athletes at moderate elevations of 1800 to 3050 m (6000 to 10,000 ft) improves oxygen extraction and utilization via favorable changes in skeletal muscle capillarity, myoglobin, mitochondrial oxidative enzyme activity, and mitochondrial density. Additional research is warranted.
Another important physiological adaptation that may occur as a result of exposure to moderate altitude is an improvement in the capacity of the skeletal muscle and blood to buffer the concentration of hydrogen ions (H+). High concentrations of H+ are known to contribute to skeletal muscle fatigue by impairing actin-myosin crossbridge cycling, reducing the sensitivity of troponin for calcium (Ca2+) and inhibiting the enzyme phosphofructokinase (PFK) (McComas 1996). Thus, an enhanced H+ buffering capacity may have a beneficial effect on aerobic and anaerobic performance.
In support of this, Mizuno and colleagues (1990) reported a significant 6% increase in the buffering capacity of the gastrocnemius muscle of elite male cross-country skiers who lived at 2100 m (6890 ft) and trained at 2700 m (8860 ft) for 14 days. Significant improvements in maximal O2 deficit (29%) and treadmill run time to exhaustion (17%) were observed after the athletes returned to sea level. In addition, a positive correlation (r = 0.91, p < 0.05) was demonstrated between the relative increase in buffering capacity of the gastrocnemius muscle and treadmill run time to exhaustion.
Gore and colleagues (2001) reported that skeletal muscle buffer capacity increased 18% (p < 0.05) in male triathletes, cyclists, and cross-country skiers following 23 days of living at 3000 m (9840 ft) and training at 600 m (1970 ft). Furthermore, they found that mechanical efficiency significantly improved during a 4 3 4-min submaximal cycling test following the 23-day LHTL period.
The precise mechanisms responsible for enhanced skeletal muscle buffering capacity following high altitude training are unclear but may be related to changes in creatine phosphate and/or muscle protein concentrations (Mizuno et al. 1990). Improvements in blood buffering capacity may be due to increases in bicarbonate (Nummela and Rusko 2000) or hemoglobin concentration.