Muscle metaboreflex is blunted with reduced vascular resistance response of nonexercised limb in patients with chronic heart failure.

Background: Exercise-mediated muscle metaboreflex (MMR) activates the sympathetic nervous system afferently and may play an important role in the reduction in blood flow in nonexercised limb, thus enhancing exercised skeletal muscle blood flow (ie, normal regional blood flow redistribution during exercise). However, few data are available to describe the relationship between MMR and peripheral vascular control during exercise in congestive heart failure (CHF). The aim of this study was to determine whether MMR is impaired in CHF, and, if so, whether MMR is related to clinical severity of CHF and to changes in nonexercised limb vascular resistance in CHF.

Methods And Results: Eleven CHF patients and 9 healthy age- and gender-matched controls were examined. All subjects performed a rhythmic handgrip exercise test at 50% of maximal voluntary contraction for 3 minutes on 2 occasions with and without postexercise upper arm regional circulatory occlusion (RCO/non-RCO). Changes in systolic blood pressure were measured and plotted against protocol time for both RCO and non-RCO. The area under each curve was estimated, and the calculating difference in the area between RCO and non-RCO was regarded as MMR. In addition, changes in calf vascular resistance were measured continuously by plethysmography after the handgrip test and the area differences between the RCO and non-RCO data was taken to represent MMR-provoked resistance changes in the nonexercised limb. During the handgrip exercise, systolic blood pressure increased similarly on the 2 occasions for both groups. MMR was significantly lower in CHF patients than in controls (68.2 +/- 23.1 versus 160.4 +/- 29.6 arbitrary units; P < .05). Decrease in MMR activity was related to clinical severity of CHF (controls, 160.4 +/- 29.6; New York Heart Association class II, 87.6 +/- 29.8; New York Heart Association class III, 34.3 +/- 34.8 arbitrary units; P < .05). The increase in calf vascular resistance between RCO and non-RCO protocols in the control group was significant (+146.5 +/- 38.0 arbitrary units; P < .05), whereas the difference in the CHF group was not significant (-72.9 +/- 126.9 arbitrary units; not significant).

Conclusions: Exercise-induced MMR control in mild to moderate CHF is impaired in association with a blunted increase in nonexercised limb vascular resistance. This suggests that blunted MMR activity impairs regional blood flow redistribution and may contribute in part to exercise intolerance in this disorder.