Altitude training, which describes the practice of training for several weeks at altitudes above 2,500 metres, prompts the body to adapt to hypoxia by increasing the number of red blood cells.
Proponents claim that higher concentrations of red blood cells give athletes an advantage by increasing the oxygen-carrying capacity of blood. “But we've found no significant effect of altitude training on aerobic performance, a phenomenon we've dubbed 'the altitude training paradox',” says Cyril Reboul, from Avignon, France, who believes that the most likely candidate to explain the paradox is the heart.
There is clear evidence from both human and animal studies, he explains, that altitude training does not provide any advantage over training at sea level on maximal oxygen uptake and aerobic performances. Indeed, prolonged exposure to altitude and hypoxic stress has been associated with specific adaptations, including pulmonary hypertension, decreased blood plasma volume and hyperactivity of sympathetic drive.
Reboul and colleagues have explored the impact of prolonged exercise training at altitude in animal models, where rats were randomly assigned to live continuously under conditions of hypobaric oxygen (PIO2 = 110 mmHg, obtained by using a specific vacuum pump), or at normal oxygen concentrations (PIO 2= 110 mmHg). The rats were further assigned to treadmill exercise or sedentary life styles.
Results of echocardiography studies showed that five weeks of aerobic training at the equivalent of sea level resulted in increased left ventricular internal capacity dimensions and wall thickness, but that animals trained at altitude showed increased LV wall thickness without chamber enlargement. Furthermore, animals trained at sea level showed improved resting and maximal stroke volume, which did not prove to be the case for animals trained at altitude. “This led to the conclusion that altitude training depressed the contractile properties of myocytes,” says Reboul.
Further study investigating the molecular mechanisms, conducted with Olivier Cazorla from INSERM, showed that animals trained at sea level presented with greater stretch-dependent calcium sensitisation of myofilaments than those trained at altitude. When the myosin heavy chain (MHC) isoform expression was measured, it was found that rats trained at sea level showed a shift from beta MHC to alpha MHC, whereas those trained at altitude did not.
“This result could play an important role in explaining the beneficial effects of sea-level exercise training on myofilaments sensitisation following a stretch procedure, since beta MHC is characterised by lower ATPase activity and lower filament sliding velocity which would result in less powerful contractions,” explains Reboul.