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POINT-COUNTERPOINT
Physiologically, considerable overlap exists between these two types of afferents; during exercise both are almost inevitably activated in a seamless transition. Ischemia (being the trigger of the metaboreflex) increased the muscle contraction responses of some group III fibers but not all group IV afferents (1). To get a clear picture, we need to look at both animal and clinical studies. In a canine HF model during moderate exercise the metaboreflex was tonically active, stimulated at a lower threshold, and increased blood pressure primarily by reflex vasoconstriction (3). In HF patients we may quote the outstanding study of our opponents (6), where rhythmic forearm exercise lead to premature fatigue and accumulation of muscle metabolites and metaboreflex overactivation. Resting muscle levels of triggers of the metaboreflex, e.g., H+ and H2PO4 (5), were similar between HF and controls, whereas peak exercise levels were greater in HF, demonstrating not only activation but the mechanism triggering the reflex responses. In an earlier study, the muscle metaboreceptor responses to static exercise were seen to be attenuated (8). Our antagonist himself provides a possible explanation based on the different responses to static versus rhythmic exercise: in the latter, the hemodynamic abnormalities may be more exaggerated because of intermittent blood flow washing out metabolites (7).
The only human study using a similar protocol to ours, but in disagreement, was performed in middle-aged CHF men with relatively preserved exercise tolerance (mean peak VO2 22 ml·kg–1·min–1) exercising at a submaximal load (77% capacity), a situation in which different mechanisms may predominate (i.e., mechanoreflex, blood-borne factors; Ref. 2).
The main argument proposed for our opponents' hypothesis is based on animal experiments where the response to vanilloid type 1 (VR1) receptor stimulation by capsaicin was attenuated. Since this receptor colocalizes with acid-sensing ion channel (ASIC) receptors, our opponents speculate that attenuated VR1 is a marker for impaired metaboreflex (4). However this is only part of the story because different triggers such as H+ stimulate ASIC, but not VR1. Moreover, animal models do not simulate human HF, for the animals are not treated nor live long enough to develop the syndrome.
Our opponents provide no explanation for the origin and etiology of the described mechanoreflex hyperactivation, which remains an interesting acute exercise reflex of debatable clinical importance, in contrast to the major role of metaboreceptors in cachectic human HF.
REFERENCES
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