TACHYCARDIA AFTER POST-EXERCISE MUSCLE ISCHEMIA IS NOT CAUSED BY CENTRAL VOLUME DEPLETION

Abstract

1062 We evaluated if tachycardia after muscle ischemia is caused by a reduced central blood volume as indicated by thoracic electrical impedance (TI). Fourteen supine subjects performed 90 s of ischemic one-legged knee extensions followed by post-exercise muscle ischemia for 120 s. For comparison, resting leg ischemia for 9 min was also evaluated. Ischemic exercise at 10 and 30 W increased heart rate (HR) by 22±4 and 35±4 bpm and mean arterial pressure (MAP) by 21±4 and 32±4 mmHg, respectively (mean±S.E.). During post-exercise muscle ischemia HR returned to the pre-exercise level, while MAP remained elevated. 15 s after release of the occluding cuff MAP had dropped 21±4 and 24±4 mmHg, respectively. The increase in HR was delayed 45 s and was by 12±2 and 14±2 bpm after 10 and 30 W, respectively. HR was unaffected by resting leg ischemia, while blood pressure was elevated 5±2 mmHg. Release of the cuff decreased MAP by 19±2 mmHg, and increased HR 15±2 bpm after 45 s. TI increased during both exercise trials, but it remained unchanged from deflation of the pressure cuff until the peak HR was established after reperfusion of the ischemic leg. Resting leg ischemia caused no change in TI nor did the release of the occluding cuff. After release of the cuff the rapid decrease in MAP suggests that the arterial baroreceptors are of importance for the increase in HR. Further the response may be supported by a blood-borne substance released to the circulation from the muscles. The data indicate that tachycardia after muscle ischemia is unrelated to central volume depletion.