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Am J Physiol Heart Circ Physiol (December 22, 2006). doi:10.1152/ajpheart.01240.2006
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Submitted on November 10, 2006
Accepted on December 16, 2006

Heart Failure Attenuates Muscle Metaboreflex Control of Ventricular Contractility During Dynamic Exercise

Javier A. Sala-Mercado1, Robert L Hammond2, Jong-Kyung kim3, Phillip J. McDonald4, Larry W. Stephenson4, and Donal S O'Leary1*

1 Department of Physiology, Wayne State University, Detroit, Michigan, United States
2 Department of Physiology, Wayne State University, Detroit, Michigan, United States; Department of Surgery, Wayne State University, Detroit, Michigan, United States
3 Department of Physiology, Wayne State University, Michigan, United States
4 Department of Surgery, Wayne State University, Detroit, Michigan, United States

* To whom correspondence should be addressed. E-mail: doleary{at}med.wayne.edu.

Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP), however in heart failure (HF) although MAP increases, the rise in CO is virtually abolished which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals is abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance (Emax) and preload-recruitable stroke work (PRSW)] at rest, during mild and moderate exercise under free flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing induced HF. In control experiments MMR activation at both workloads [mild exercise (3.2 km/hr) and moderate exercise (6.4 km/hr @ 10% grade)] significantly increased CO, Emax and PRSW. In contrast, after induction of HF, CO, Emax and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, Emax and PRSW did not change. In addition MMR activation caused no significant change in either CO, Emax or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but this ability is abolished in HF.




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