Heart failure abolishes muscle metaboreflex induced increases in left ventricular contractility during moderate dynamic exercise.

Underperfusion of active skeletal muscle elicits a reflex pressor response -- termed the muscle metaboreflex (MMR). In normal dogs during moderate dynamic exercise (MOD), MMR activation causes large increases in left ventricular contractility (LVC), cardiac output (CO) and mean arterial pressure (MAP) whereas in heart failure (HF), although MAP increases, the rise in CO is virtually abolished which may be due to an impaired ability to increase LVC. A widely accepted index of contractility is preload recruitable stroke work (PRSW) calculated from the stroke work-end diastolic volume relationship. The objective of the present study was to determine whether MMR increases in PRSW observed in normal dogs during MOD are abolished in HF. Conscious dogs were chronically instrumented to measure left ventricular pressure and volume at rest, during MOD with and without partial hind-limb ischemia to elicit MMR responses. In normal conditions, MMR activation increased PRSW from 107.1 ± 6 to 142.9 ± 10 mmHg (P < 0.05) and CO increased from 8.4 ± 0.5 to 9.8 ± 0.6 l/min. After induction of HF, CO and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, MMR activation caused no significant change in either CO or PRSW. We conclude that the ability of the MMR to induce increases in LVC is abolished in HF and that the reflex increases in MAP occur solely via peripheral vasoconstriction. [ABSTRACT FROM AUTHOR]