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1 Physiology, Wayne State University, school of medicine, Detroit, MI, USA
2 Physiology, Wayne State University, school of medicine, Detroit, MI, USA; Surgery, Wayne state University, school of medicine, Detroit, MI, USA
3 Surgery, Wayne state University, school of medicine, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: doleary{at}med.wayne.edu.
When oxygen delivery to active skeletal muscle is insufficient for the metabolic demands, afferent nerves within muscles are activated, which elicits reflex increases in heart rate (HR), cardiac output (CO), and arterial pressure (AP) termed the muscle metaboreflex (MMR). To what extent the increases in CO are the result of increased ventricular contractility is unclear. A widely accepted index of contractility is maximal left ventricular elastance (Emax), the slope of the end-systolic pressure-volume relationship such as during rapidly imposed reductions in preload. The objective of the present study was to determine whether MMR activation elicits increases in Emax. Experiments were performed using conscious dogs chronically instrumented to measure left ventricular pressure and volume at rest and during mild or moderate treadmill exercise with and without partial hindlimb ischemia to elicit MMR responses. At both workloads, MMR activation significantly increased CO, HR, AP, and maximum rate of change of left ventricular pressure (LV dP/dtmax). During both mild and moderate exercise, MMR activation increased Emax to 159.6 ± 8.83% and 155.8 ± 6.32% of the exercise value under free-flow conditions, respectively. We conclude that the increase of ventricular elastance associated with MMR activation indicates that a substantial increase in ventricular contractility contributes to the rise in CO during dynamic exercise.
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