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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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In dogs running on a treadmill at 2 or 4 mph or 4 mph plus 10% incline, graded reductions in hindlimb perfusion reflexly elicited pressor responses. To test the idea that systemic arterial pressure (SAP) is raised by accumulation in muscle of a nerve-activating "pressor substance" release when O2 delivery becomes inadequate, arterial O2 content (CaO2) was reduced 29.1% by carbon monoxide (CO) inhalation before repeating exercise at 2 mph. We reasoned that the pressor substance, or related substances, should appear in femoral venous blood and be correlated to SAP. [K+] behaved inappropriately as a signal to raise SAP, i.e., when flow was reduced, SAP rose markedly with little or no change in [K+]. SAP was well correlated to pH and [lactate] over the three work loads. Compared with the same work load with normal CaO2, CO shifted the relation between SAP and terminal aortic flow rightward 0.30 l/min (34.5%) and the relation between SAP and PO2 leftward 7.7 mmHg. CO did not affect the relation of SAP to terminal aortic O2 delivery, hindlimb O2 uptake index, pH, or [lactate]. Thus pressor responses are apparently generated when O2 delivery falls below some critical level causing accumulation of a pressor substance the release of which is linked to a metabolic event that precipitates lactate accumulation.