Effects of prolonged hypobaric hypoxia on human skeletal muscle function and electromyographic events.

This study tested the hypothesis that a prolonged decrease in arterial oxygen pressure in resting or contracting skeletal muscles alters their ability to develop force through an impairment of energy-dependent metabolic processes and also through an alteration of electrophysiological events. The experiment was conducted during a 32-day simulated ascent of Mt. Everest (8848 m altitude) (Everest III Comex '97), which also allowed testing of the effects of re-oxygenation on muscle function. Maximal voluntary contractions (MVCs) of the flexor digitorum, and static handgrips sustained at 60% of MVC, were performed by eight subjects before the ascent (control), then during the stays at simulated altitudes of 5000 m, 6000 m and 7000 m, and finally 1 day after the return to 0 m. The evoked muscle compound action potential (M-wave) was recorded at rest and during the manoeuvres at 60% of MVC. The changes in median frequency of electromyographic (EMG) power spectra were also studied during the contraction at 60% of MVC. In four individuals, transient re-oxygenation during the ascent allowed us to test the reversibility of hypoxia-induced MVC and M-wave changes. At rest, a significant decrease in M-wave amplitude was noted at 5000 m. This effect was associated with a prolonged M-wave conduction time at 6000 m and an increased M-wave duration at 7000 m, and persisted after the return to 0 m. Re-oxygenation did not modify the changes in M-wave characteristics. A significant decrease in MVC was measured only during the ascent (-10 to -24%) in the non-dominant forearm of subjects who underwent re-oxygenation; this intervention slightly improved muscle strength at 6000 m and 7000 m. During the ascent and after the return to 0 m, there was a significant reduction of the median frequency decrease throughout contraction at 60% of MVC compared with the EMG changes measured before the ascent. It is concluded that prolonged exposure to hypoxia slows the propagation of myopotentials and alters sensorimotor control during sustained effort. Re-oxygenation did not affect the hypoxia-induced EMG changes and had a modest influence on muscle strength.

Correlation between surface electromyogram, oxygen uptake and blood lactate concentration during dynamic leg exercises.

Very few data are found in the literature on the adjustment of the motor drive to contracting muscles to their oxygen uptake (V(O2)). The present study examines in seven untrained and trained individuals, who performed a progressive 8 min and two 5 min constant-load cycling exercises, the changes in the ratio between total EMG energy (root mean square or RMS), recorded in a leg extensor (vastus lateralis), to the corresponding V(O2) value and their correlations with the anaerobic threshold (V(O2)AT) and the peak blood lactate concentration. In all circumstances, the RMS/V(O2) ratio began to increase, then it decreased progressively despite V(O2) continued to rise (progressive exercise) or plateaued (constant-load exercises preseted at a sub- or suprathreshold level). The decrease in RMS/V(O2) ratio persisted and it was often accentuated during the first 2 min of the recovery period. In all exercise protocols, the rate of RMS/V(O2) decrease was positively correlated with the initial peak increase in this ratio. During progressive exercise, the peak increase in RMS/V(O2) ratio as well as its rate of decrease were negatively correlated with V(O2)AT. Thus, training and/or the reduction of anaerobic muscle metabolism attenuate the changes in RMS/V(O2) ratio. During constant-load exercise trials, the rate of decrease in RMS/V(O2) ratio was positively correlated with the plateau V(O2) value and also the peak blood lactate concentration. This suggests that information on the magnitude of the anaerobic muscle metabolism play a key role in the mechanisms which adjust RMS to V(O2).