Latency of muscle chemoreflex to vascular occlusion of active muscle during dynamic exercise

Abstract

When oxygen delivery to active muscle is too low for the ongoing rate of metabolism, metabolites accumulate and activate a muscle chemoreflex that raises arterial pressure. During static muscular contractions, the latency of the onset of increments in sympathetic activity attributed to the muscle chemoreflex is long (1-2 min). This long latency might be caused by slow accumulation of metabolites attributable to low rates of metabolism. Because shortening contractions at a given force per unit time have a much higher energy cost than do static contractions, the muscle chemoreflex should have a much shorter latency during dynamic exercise than during static contractions, and the latency should shorten further with rising exercise intensity. To test these ideas, the latency to the onset of the rise in arterial pressure induced by the muscle chemoreflex following vascular occlusion of active muscle was measured in four dogs exercising on a treadmill. During steady-state exercise of mild to moderate intensity, pressor responses to muscle ischemia were elicited by rapid, complete occlusion of the terminal aorta; this procedure mimics the blockage of muscle blood flow that occurs normally during static contractions. There was a statistically significant effect of exercise intensity on latency (P < 0.001). The latency was 23.5 +/- 4.5, 16.4 +/- 5.6, and 10.1 +/- 2.3 s (means +/- SE) at 3.2 km/h 0% grade, 6.5 km/h 0% grade, and 6.5 km/h 10% grade, respectively. Also, the rate of rise of arterial pressure during chemoreflex activation increased progressively with rising exercise intensity from 0.8 +/- 0.2 mmHg/s during exercise at 3.2 km/h 0% grade to 2.0 +/- 0.5 mmHg/s during exercise at 6.5 km/h 10% grade. Thus the latency of the muscle chemoreflex in response to vascular occlusion during mild dynamic exercise is shorter than has been reported during static contractions of moderate intensity.