Balancing Cardiac Activation and Peripheral Vasodilation: Determinants of Cardiovascular Circuit Flow During Leg Exercise
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Abstract
The extent to which central mechanisms can independently increase cardiovascular circuit blood flow (CBF) during exercise is not well defined. Studies using atrial pacing during exercise to evoke a proportionally greater cardiac activation response observe no increases in CBF but fail to replicate exercise-induced cardiac activation. Therefore, we investigated whether excess exercise-induced cardiac activation was able to independently drive CBF at exercise onset. To isolate the contribution of exercise-induced cardiac activation of CBF, 30 participants performed knee extension/flexion exercise at 50% WRPEAK during two conditions. 1) CON: right leg exercise, with left leg blood flow occlusion (pneumatic cuff; 280 mmHg); 2) ECA: dual leg exercise, with left leg blood flow occlusion to increase cardiac activation above single leg exercise, without additional vasculature participating in CBF. Central and peripheral hemodynamics were measured continuously. Heart rate and cardiac output were higher in ECA compared to CON during the first 30 seconds of exercise, while stroke volume remained unchanged between conditions. Mean arterial pressure was also higher in ECA, primarily due to the increased cardiac output as there were greater increases in total vascular conductance during ECA. Leg blood flow was greater in ECA compared to CON, but this increase was not due to a greater leg vascular conductance. Instead, leg blood flow appears to be driven by a pressor- mediated response caused by the higher cardiac output in ECA. These results demonstrate that excess exercise-induced cardiac activation can increase the CO and exercising leg perfusion response within the first 30 seconds of sub-maximal knee extension/flexion exercise onset.

