Heart failure alters the strength and mechanisms of the muscle metaboreflex

We hypothesized that excessive sympathoactivation observed during strenuous exercise in subjects with heart failure (HF) may result from tonic activat ion of the muscle metaboreflex (MMR) via hypoperfusion of active skeletal m uscle. We studied MMR responses in dogs during treadmill exercise by graded reduction of terminal aortic blood flow (TAQ) before and after induction o f HF by rapid ventricular pacing. At a low workload, in both control and HF experiments, large decreases in TAQ were required to elicit the MMR presse r response. During control experiments, this presser response resulted from increased cardiac output (CO), whereas in HF CO did not increase; thus the presser response was solely due to peripheral vasoconstriction. In HF, MMR activation also induced higher plasma levels of vasopressin, norepinephrin e (NE), and renin. At a higher workload, in control experiments any reducti on of TAQ elicited MMR presser responses. In HF, before any vascular occlus ion, TAQ was already below MMR control threshold levels and reductions in T AQ again did not result in higher CO; thus SAP increased via peripheral vas oconstriction. NE rose markedly, indicating intense sympathetic activation. We conclude that in HF, the MMR is likely tonically active at moderate wor kloads and contributes to the tonic sympathoactivation.