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In six dogs trained to run at 2, 4, and 6 mph, we caused graded reductions in hindlimb perfusion by compressing the terminal aorta. Our goal was to examine the relationship between hindlimb perfusion [terminal aortic flow (TAQ) and femoral arterial pressure (FP)] and cardiovascular responses [aortic pressure (AP), heart rate, and ascending aortic flow (CO)]. Small reductions in TAQ and FP produced bradycardia, small decreases in CO, and small increases in AP. Further reductions in TAQ and FP produced tachycardia, increased CO, and large increases in AP. AP rose by about 1 mmHg for each 1-mmHg fall in FP. The response was similar at all speeds, but as work load increased it required smaller reductions in FP and TAQ to cause a pressor response (e.g., at 6 mph we could not demonstrate a nonlinear relationship between TAQ and AP). At low work loads the cardiovascular responses to exercise were most likely set by signals other than feedback from exercising muscle because substantial reductions in hindlimb perfusion caused no significant cardiovascular responses. At moderate-to-high work loads or where muscle perfusion is restricted, metabolic feedback from muscle may play a role in cardiovascular responses to exercise.

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