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Limiting factors of performance at moderate altitude : Consequences for training.

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Maximal aerobic performance progressively decreases with increasing levels of hypoxia, because of a reduction in arterial oxygen content (CaO2) due to both hypoxia and exercise (4, 15, 16).
Autor(es): Jean-Paul Richalet, Nicolas Bourdillon, Pascal Mollard
Entidades(es): Université Paris 13
Congreso: International symposium of altitude training
Granada 2008
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Limiting factors of performance at moderate altitude : Consequences for training.

Maximal aerobic performance progressively decreases with increasing levels of hypoxia, because of a reduction in arterial oxygen content (CaO2) due to both hypoxia and exercise (4, 15, 16). Hypoxia limits the oxygen transfer between the lung alveoli and the capillary which results in a drop in CaO2. The successive steps of oxygen transport from the ambient air to the tissues are greatly affected by this drop. Moreover, at and above 4000 m the O2 peak reduction is larger than expected only from the reduction in CaO2 (6). Although this drop has been widely studied in the past (1, 16), far less attention has been paid to tissue oxygenation because of technical difficulties to monitor this variable. Recent studies have used Near Infra Red Spectroscopy (NIRS) to measure changes in oxy (O2Hb) and deoxy (HHb) hemoglobin in the tissues (12, 13).

NIRS data have been well correlated to both oxygen tension in the muscle cell (3, 9, 14) and venous oxygen saturation (5). The use of this technique during exercise has also been validated (2). Most recent studies (12, 13) report a progressive decrease in muscle oxygenation along with increasing work rate and a plateau near maximal exercise (80% O2 peak). However, no previous study compared trained and sedentary subjects. While Subudhi et al (13) focused both on cerebral and muscular oxygenation in athletes, there is no assertion for NIRS values under severe acute hypoxic conditions in the vastus lateralis of trained and untrained men. Endurance trained athletes are known to undergo a more drastic decrease in peak oxygen uptake compared with sedentary subjects in hypoxic conditions (16). Although the facts have been extensively reported (4, 11), it remains paradoxical and no clear explanation is available. Endurance training implies adaptative changes in the skeletal muscle, including an increase in capillary density, and an increase in vascular reactivity which contribute to enhance whole body maximal oxygen uptake. Capillary density and vascular reactivity are likely to influence local blood flow and available exchange surface area for diffusion at exercise and play a crucial role in the improved oxygen extraction in endurance trained men (7).

During exercise in hypoxic conditions, untrained subjects can increase oxygen extraction to compensate for a lower CaO2, while athletes cannot because of an already maximal oxygen extraction in normoxia (8). This lack of compensation may contribute to the observed larger decrease in O2 peak in endurance athletes. A study was conducted to explore the potential differences in muscle oxygenation of trained and untrained men at exercise in hypoxic conditions. Our hypothesis was that hypoxic exposure may shift the relative balance between the limiting factors in endurance trained subjects. Five endurance trained and six sedentary subjects, performed five maximal exercise tests on a cycloergometer in normoxia and at various levels of acute hypoxia (inspired PO2 of 131.4, 107.3, and 87 mmHg). Peak oxygen uptake ( O2 peak), and ventilatory parameters were monitored. Cardiac output was monitored by thransthoracic bio- impedance and regional muscle oxygenation was assessed by NIRS on the right vastus lateralis. Results demonstrated that muscle oxyhemoglobin (O2Hb) decreased as workload increased, and reached a plateau at 75% O2 peak. No effect of altitude was found on muscle oxygenation of sedentary subjects. Athletes were more affected by hypoxia, with a progressive inversion of muscle O2Hb and HHb (deoxyhemoglobin) values, O2Hb being higher than HHb in normoxia and mild hypoxia while HHb was higher than O2Hb in severe hypoxia. These results suggest that athletes loose their advantageous muscular adaptations to training when exposed to severe acute hypoxia when compared to sedentary subjects. This may contribute to explain the observed greater decrease in O2 peak in athletes compared with sedentary subjects.

To evaluate the difference in tissue oxygen transfer between trained and untrained subjects, we studied non invasively the control of vasomotricity within the skeletal muscle during exercise and under hypoxic condition. Our study was based on the analysis of oxygen transport variables measured during incremental exercise in endurance trained men (n=8) and in their sedentary counterparts (n=8). Maximal exercise tests were performed on a cycloergometer in normoxia and at 4 simulated normobaric levels of hypoxia (altitude equivalent to 1000, 2500 and 4500m). We made the assumption that the relationship between the oxygen diffusion coefficient (Kt) and cardiac output ( ) was : Kt = k. Nc. We propose to name Nc the capillary recruitement coefficient during exercise. Our results demonstrate that Nc is greater in trained than in untrained subjects and increases at high altitude (4500m) especially in trained subjects. We conclude that athletes lose their advantageous muscular vasomotricity in acute hypoxia and that it contributes to the greater decrease in O2 peak observed in the latter population. In conclusion, given a great amount of observations about the impact of acute hypoxia on aerobic performance in trained athletes, a great attention should be paid to the conditions of training in athletes exposed to continuous or intermittent hypoxia.


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