Hemodynamics and muscle sympathetic nerve activity after 8 h of sustained hypoxia in healthy humans

Hemodynamics, muscle sympathetic nerve activity (MSNA), and forearm blood flow were evaluated in 12 normal subjects before, during (1 and 7 h), and after ventilatory acclimatization to hypoxia achieved with 8 h of continuous poikilocapnic hypoxia. All results are means [+ or -] SD. Subjects experienced mean oxygen saturation of 84.3 [+ or -] 2.3% during exposure. The exposure resulted in hypoxic acclimatization as suggested by end-tidal C[O.sub.2] [44.7 [+ or -] 2.7 (pre) vs. 39.5 [+ or -] 2.2 mmHg (post), P < 0.001] and by ventilatory response to hypoxia [1.2 [+ or -] 0.8 (pre) vs. 2.3 [+ or -] 1.3 1 x [min.sup.-1] x 1% fall in [saturation.sup.-1] (post), P < 0.05]. Subjects exhibited a significant increase in heart rate across the exposure that remained elevated even upon return to room air breathing compared with preexposure (67.3 [+ or -] 15.9 vs. 59.8 [+ or -] 12.1 beats/min, P < 0.008). Although arterial pressure exhibited a trend toward an increase across the exposure, this did not reach significance. MSNA initially increased from room air to poikilocapnic hypoxia (26.2 [+ or -] 10.3 to 32.0 [+ or -] 10.3 bursts/100 beats, not significant at 1 h of exposure); however, MSNA then decreased below the normoxic baseline despite continued poikilocapnic hypoxia (20.9 [+ or -] 8.0 bursts/100 beats, 7 h Hx vs. 1 h Hx; P < 0.008 at 7 h). MSNA decreased further after subjects returned to room air (16.6 [+ or -] 6.0 bursts/100 beats; P < 0.008 compared with baseline). Forearm conductance increased after exposure from 2.9 [+ or -] 1.5 to 4.3 [+ or -] 1.6 conductance units (P < 0.01). These findings indicate alterations of cardiovascular and respiratory control following 8 h of sustained hypoxia producing not only acclimatization but sympathoinhibition. chemosensitivity; vascular resistance; pathophysiology