Hypoxia is known to change neuronal activity in vitro and to impair performance in vivo. The present study was designed to study neuromuscular fatigue in acute hypoxia, and we hypothesized that hypoxia results in additional fatigue during sustained contractions, presumably because of increased central fatigue.
Twelve healthy subjects participated in a normoxic (NX) and hypoxic (HX) experiment performed on separate days. Hypoxia was induced by breathing an HX air mixture containing 12% oxygen. Before, during, and after a 90-s sustained voluntary maximal contraction (MVC) of the first dorsal interosseus muscle, we measured force, voluntary activation (VA), and parameters of motor cortical excitability (motor-evoked potentials (MEP) and silent periods (SP)). Measures of peripheral nerve and muscle function, compound motor action potential (M-wave), and muscle twitch forces were also taken.
During the MVC, force declined similarly during both HX and NX. VA decreased throughout the contraction in HX, but, surprisingly, this decrease in VA in HX did not exceed that observed in NX. Also, motor cortical excitability changed to a similar degree in HX and NX; that is, MEP amplitude and SP duration increased. M-wave amplitude decreased significantly during the sustained MVC in NX and HX. The only difference observed between NX and HX was the quicker recovery of the muscle twitch in HX, which was even potentiated after 5 min of recovery.
The present results show that peripheral and central neuromuscular adaptations during a sustained fatiguing contraction are similar in NX and HX. The quicker recovery and potentiation of twitch forces in HX suggest alterations in myosin phosphorylation, which may enhance contractile force.
1Department of Sports Science, University of Innsbruck, Innsbruck, AUSTRIA; and 2Department of Neurology, Innsbruck Medical University, Innsbruck, AUSTRIA
Address for correspondence: Dr. Wolfgang N. Löscher, Department of Neurology, Innsbruck Medical University, Anichstrasse, 35 A - 6020 Innsbruck, Austria; E-mail: email@example.com.
Submitted for publication November 2006.
Accepted for publication February 2007.