This review proposes a theoretical framework where limb congestion in heart failure increases muscle mechanoreceptor activity, maintaining sympathoexcitatory responses to exercise despite metaboreceptor desensitization.
Limb congestion may sustain exercise sympathoexcitation in HF via mechanoreceptors; hypothesis-generating and requires prospective validation before clinical consideration.
During static handgrip exercise, muscle metaboreceptors are stimulated, evoking the 'exercise pressor reflex.' As part of this reflex, sympathetic discharge to skeletal muscle is increased. The muscle 'metaboreceptors' are thought to be free nerve endings of unmyelinated group IV nerve fibres. These receptors are stimulated by a number of metabolites, including lactic acid, H+, diprotonated phosphate, adenosine and the biproducts of prostaglandin synthesis. 2. During chronic, repetitive activity, muscle metabolite-sensitive afferents may be desensitized. We speculate that metaboreceptor desensitization also occurs in congestive heart failure (HF). Despite this desensitization, sympathoexcitatory responses to forearm exercise are preserved. This suggest that some other neural system aside from muscle metaboreceptors must be activated to a greater degree in HF. We speculate that in HF the activity of muscle mechanoreceptors is increased. Furthermore, we believe that limb congestion can increase the discharge of muscle mechanoreceptors, thereby evoking non-metaboreceptor-mediated increases in sympathetic discharge. Future studies in our laboratory will examine the role limb congestion and decongestion play in evoking muscle mechano-receptor-mediated sympathoexcitatory responses.
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Lawrence I. Sinoway (1996) studied this question.
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