Skeletal muscle metaboreceptor exercise responses are attenuated in heart failure.

Abstract

Skeletal muscle metaboreceptor responses are impaired in heart failure. Because MSNA responses during static exercise are similar in the two groups, mechanisms aside from metaboreceptor stimulation must be important in increasing sympathetic nervous system activity.

Role of the Exercise Pressor Reflex in Rats With Dilated Cardiomyopathy

“…As discussed, the mechanisms by which the mechanoreflex becomes exaggerated are presently unclear. Furthermore, a great deal of controversy exists regarding the contribution of the metabolic component of the EPR, because its activity has been reported to be both enhanced 14,15,21,34 and reduced 10,22 in response to exercise in CHF patients. As stated, it is plausible that initial reductions in peripheral blood flow result in an abnormal accumulation of exercise-induced metabolites in the muscle interstitium.…”

“…5,9 As a result, mechanically sensitive neurons may become sensitized to physical distortion, 33 whereas metaboreceptors undergo a period of hyperexcitability. Prolonged exposure to these metabolites may eventually serve to desensitize 22,35 or downregulate metabolically sensitive neurons, culminating in a decrease in their activity. In response to a blunting of the metaboreflex, molecular adaptations may begin within mechanically sensitive afferents to compensate for the functional loss of these fibers.…”

“…23 If this scenario proves valid, there may be periods of hyperexcitability for both metabolically and mechanically sensitive afferents during the course of heart failure that explain some of the discrepancies reported in previous human studies. 10,14,21,22 In addition, other factors, including modifications in muscle metabolism and fiber type composition (eg, reductions in the percentage of oxidative fibers and increases in the percentage of glycolytic fibers), 2,3,25 may facilitate these disease-induced alterations in reflex function. For example, because the EPR-mediated circulatory response to activation of glycolytic muscle has been shown to be greater than the response elicited from oxidative muscle, 36 fiber-type transformations could profoundly effect the physiological expression of the pressor reflex.…”

“…18 -20 Because of the peripheral skeletal myopathy that develops in heart failure, 4 the EPR has been implicated as a possible mechanism by which circulatory control is dysregulated in cardiomyopathic individuals, thereby contributing to exercise intolerance. 21 Because the metabolic component of the reflex may be blunted in CHF, 10,22 it has been hypothesized that the mechanical component of the reflex preferentially drives the EPR hyperactivity that develops. 11,23 The contribution of neurally mediated peripheral mechanisms to the evolution of reduced exercise capacity in heart failure is poorly understood.…”

Changes of Compound Muscle Action Potential after Low-Intensity Exercise with Transient Restriction of Blood Flow: a Randomized, Placebo-Controlled Trial

“…The skeletal muscle metaboreflex system consists of Group III and Group VI fibers 25) . The endings of these fibers are located in the skeletal muscle interstitium, and react to the changes in metabolic concentration, through increases in lactate acid and decreases in intramuscular pH 26,27) . These responses of the metaboreflex system increase sympathetic nerve activity to the skeletal muscles, which affects motor unit activation 9) .…”