HUMAN CAROTID BAROREFLEX DURING ISOMETRIC LOWER ARM CONTRACTION AND ISCHEMIA

Our aim was to determine the roles of somatomotor activation and muscl e ischemia for the tachycardia and hypertension of isometric arm contr action. Carotid-cardiac and carotid-mean arterial pressure (MAP) baror eflex response curves were determined in 10 men during rest, during is ometric arm contraction at 30% of maximum, and during postcontraction ischemia. Carotid distending pressure (CDP) was changed by applying pr essure and suction in a neck chamber. Pressures ranged from +40 to -80 mmHg and were applied repeatedly for 15 s during the three conditions . Maximum slopes and ranges of the response curves did not differ amon g conditions. The heart rate (HR) curve was shifted to a 14 +/- 1.8 (m ean +/- SE) beats/min higher HR and a 9 +/- 5.7 mmHg higher CDP during contraction and to a 14 +/- 5.9 mmHg higher CDP during postcontractio n ischemia with no change of HR compared with rest. The MAP curve was shifted to a 20 +/- 2.8 mmHg higher MAP and to a 18 +/- 5.4 mmHg highe r CDP during contraction, and the same shifts were recorded during pos tcontraction ischemia. We conclude that neither somatomotor activation nor muscle ischemia changes the sensitivity of arterial baroreflexes. The upward shift of the MAP response curve, with no shift of the HR r esponse curve during postexercise ischemia, supports the notion of par allel pathways for MAP and HR regulation in which HR responses are ent irely caused by somatomotor activation and the presser response is mai nly caused by muscle ischemia.