Relationship between intracellular oxygenation and neuromuscular conduction during hypoxic hypoxia

Previous studies have shown that high-altitude hypoxic hypoxia is associated with reduced ventilatory capacity that may be related to skeletal muscle weakness. In the present investigation, ascent to high altitude (4, 000 m) was simulated experimentally by exposure of male rats (Sprague-Dawley, 250–350 g), anesthetized with thiopental sodium (25 mg/kg, i.p.), to a breathing gas mixture of 12% oxygen diluted in 88% nitrogen (F iO 2 = 0.12). Determinations of oxygen saturation on micro- samples (250 ul) of arterial and central venous blood were made spectrophotometrically. Neuromuscular conduction latency was measured following electrostimulation of the sciatic nerve (1–5 V, 0.5 msec duration, 1–40 Hz) and recording of the electromyogram from the gastrocnemius muscle. Experimental hypoxia (F iO 2 = 0.12) produced a highly significant increase in conduction latency from a control value (mean ± SEM) of 3.06 ± 0.16 msec to 4.02 ± 0.31 msec (n = 10, P < 0.001). Conduction latency increased with decreasing arterial oxygen saturation from a control value of 92.9% ± 0.18% to 83.2% ± 0.76% (P