Effects of acute hypoxemia on force and surface EMG during sustained handgrip

Data on the consequences of acute hypoxemia on the strength of contraction are often contradictory. In healthy subjects, we tested the effects of hypo xemia (PaO2 = 56 mmHg), maintained for a 30-min period, on static handgrip elicited by voluntary effort or direct electrical muscle stimulation, in or der to separate the consequences of hypoxemia on central or peripheral fact ors, respectively. Force was measured during maximal voluntary contractions (MVCs), 60% MVCs sustained until exhaustion, and 1-min periods of electric al muscle stimulation at 60 Hz. The evoked compound muscle action potential (M wave) was recorded in resting muscle and after each period of 60-Hz sti mulation or sustained 60% MVC. Power spectrum analysis of surface electromy ogram (EMG) was performed during sustained 60% MVC. Compared to normoxemia, acute hypoxemia lowered MVC (-12%, P < 0.01) but enhanced (+38%, P < 0.01) the peak force elicited by electrical muscle stimulation. In resting muscl e, hypoxemia had no influence on the M-wave amplitude but lengthened the ne uromuscular transmission time(+740 us, P < 0.05). Hypoxemia did not alter t he M wave measured after 60 Hz stimulation and 60% MVC, During sustained 60 % MVC, hypoxemia markedly depressed the EMG changes, abolishing the leftwar d shift of power spectra. These data show that acute hypoxemia reduces MVC through depression of the central drive, whereas it improves the peripheral muscle response to electrical stimulation. In addition, hypoxemia reduces the recruitment of slow firing motor unit, which are highly oxygen-dependen t. This could constitute an adaptative muscle response to a reduced oxygen supply. (C) 2001 John Wiley & Sons, Inc.