Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, C105

Oral Communications

The effects of prolonged hypobaric hypoxia on voluntary control of muscle in humans

E. Ross1, R. Comer1, S. Lucas2, J. Cotter3, K. Burgess4, P. Ainslie5

1. Chelsea School, University of Brighton, Eastbourne, Sussex, United Kingdom. 2. Department of Physiology, University of Otago, Dunedin, New Zealand. 3. School of Physical Education, University of Otago, Dunedin, New Zealand. 4. Department of Medicine, University of Sydney, Sydney, New South Wales, Australia. 5. Department of Health and Human Kinetics, University of British Columbia, Kelowna, British Columbia, Canada.

Single limb exercise in normoxia is predominantly limited by peripheral fatigue, whereas in acute severe hypoxia a supraspinal impairment of motor drive plays a greater role in exercise tolerance (1). However, the effects of prolonged exposure to severe hypoxia on supraspinal contributions to fatigue have not been investigated. Twelve healthy volunteers (male = 7) performed a 2-min maximal voluntary contraction (MVC) of the knee extensors at sea-level (SL) and following 2, 8 and 15 days living at 5050m (high altitude, HA). During the 2-min MVC electrical stimulation of the femoral nerve and transcranial magnetic stimulation (TMS) of the motor cortex were delivered intermittently. Immediately before and after the 2-min MVC, femoral nerve stimulation and TMS were delivered at rest and during submaximal and maximal voluntary contractions. Repeated measures ANOVA and Post hoc t-tests were used to compare changes between SL and HA. Partial pressure of arterial O2 and arterial O2 saturation were significantly decreased from SL on arrival at HA (to 44 ±2 mmHg and 79 ±3%, respectively) and remained significantly decreased at HA (P <0.01). In the non-fatigued muscle, force during brief MVCs, cortical voluntary activation (VA) and muscle contractility were unchanged at HA, but a significant decrease in M-wave amplitude (-12 ±33%; P = 0.02) and an increase in motor evoked potential amplitude (54 ± 49%; P = 0.003) were observed on day 8. Following 2, 8 and 15 days at HA, force during the 2-min MVC was similar to SL values at contraction onset, but significantly lower thereafter. Fatigue index during the 2-min MVC was significantly higher in all HA trials, compared to SL (~58% vs. 45%, respectively; P = 0.02). The superimposed twitches evoked by TMS during the 2-min MVC were significantly larger at HA compared to SL (45 ±10 vs. 22 ±4% of pre-stimulus force, respectively; P = 0.02). The size of the twitches elicited by femoral nerve stimulation were similar between trials. Greater levels of supraspinal fatigue (measured by cortical VA) following the 2-min MVC were observed at HA compared to SL; the greatest difference being observed on day 2 at HA (20 ±22% decrease pre-post 2-min MVC vs 6 ±9% decrease at SL; P =0.02). Reductions in potentiated twitch amplitude, a marker of peripheral fatigue, tended to be less following the 2-min MVC at HA (P = 0.12). These findings indicate that: 1) prolonged exposure to hypobaric hypoxia does not influence voluntary activation of muscle or force generating capabilities in resting conditions, although sarcolemmal and corticospinal excitability are affected; 2) fatigability during sustained voluntary contraction is exacerbated during prolonged exposure to hypobaric hypoxia, and 3) this additional fatigue is the result of an oxygen-sensitive source of inhibition of descending voluntary drive, possibly mediated by prolonged arterial hypoxemia.

Where applicable, experiments conform with Society ethical requirements