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1 Physiology, Wayne State University School of Medicine, Detroit, MI, USA; Internal Medicine, Wayne State University School of Medicine, Detroit, MI, USA
2 Physiology, Wayne State University School of Medicine, Detroit, MI, USA
3 Physiology, Wayne State University School of Medicine, Detroit, MI, USA; Surgery, Wayne State University School of Medicine, Detroit, MI, USA
4 Physiology, Wayne State University School of Medicine, Detroit, MI, USA; Internal Medicine, Wayne State University School of Medicine, Detroit, MI, USA; Medicine, John D. Dingell Veterans Administration Medical Center, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: raugustyniak{at}med.wayne.edu.
Rapid recovery of resting hemodynamics from tachycardia- or arrhythmia-induced heart failure (HF) has been demonstrated in both humans and animals. However, little is known about cardiovascular responses to exercise in animals, or reflex control of the cardiovascular system during exercise while recovering from HF. Inasmuch as the reduced cardiac output (CO) during exercise in HF has been shown to lead to underperfusion of active skeletal muscle and tonic activation of the muscle metaboreflex, an improved CO during exercise in subjects recovering from HF may lead to higher skeletal muscle blood flows, and relief of this metabolic stimulus. We investigated cardiovascular responses to graded treadmill exercise and metaboreflex activation (evoked by imposed graded reductions in hindlimb blood flow (HLBF) during mild and moderate exercise) in chronically instrumented dogs during control, mild to moderate HF (induced by rapid ventricular pacing), and recovery from HF. Most hemodynamic responses to graded exercise returned to control within twenty-four hours of disconnecting the pacemaker. After two weeks of recovery, CO and HLBF at each workload were significantly higher than control. In addition, whereas the increase in CO that normally occurs with metaboreflex activation was markedly attenuated in HF, it completely returned in the recovery experiments. We conclude that cardiovascular responses to graded exercise during the recovery from pacing induced HF return rapidly to near or above control, and that the increased CO and HLBF in recovery likely relieved the metabolic stimulus and tonic metaboreflex activation that may have occurred during moderate exercise in HF.
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