Muscle Metaboreflex (MMR) Responses During Recovery From Pacing‐Induced Heart Failure

We studied MMR responses in eight chronically instrumented dogs before and after modest pacing‐induced heart failure (HF; 225 bpm for ~30 days; ~Class II HF) and during recovery from HF. The MMR was activated during mild and moderate exercise via imposed graded reductions in hindlimb blood flow (HLBF). In control experiments, decreases in HLBF were necessary to evoke the MMR suggesting that it is not tonically active. MMR activation led to a rise mean arterial pressure (MAP) that was mediated almost solely via a large increase in cardiac output (CO). During HF, the levels of HLBF at both workloads were at or near the threshold for the MMR determined during control experiments, which suggests that the MMR may already have been tonically active. Even small reductions in HLBF induced a pressor response; however, CO remained largely unchanged and the rise in MAP was mediated via peripheral vasoconstriction. With recovery from HF ( 18 days after disconnecting the pacemaker), during free‐flow dynamic exercise at both workloads, CO and HLBF tended to be higher than during control experiments. Reductions in HLBF were necessary to evoke the MMR (i.e., there was again a clear threshold) and the mechanisms of the pressor response reverted back to CO, as observed in control experiments. In conclusion, dynamic exercise during recovery from pacing induced HF was accompanied by increased CO and HLBF which likely relieved the metabolic stimulus that led to tonic MMR activation during HF. Supported by NIH HL55473 and VA‐DoD Grant.