Modulation of cardiac contractility by muscle metaboreflex following efforts of different intensities in humans

Abstract

Accumulation of metabolic end products within skeletal muscle stimulates sensory nerves, thus evoking a pressor response termed "metaboreflex." The aim of this study was to evaluate changes in hemodynamics occurring during metaboreflex activation obtained by postexercise muscle ischemia (PEMI) after two different exercise intensities. In twelve healthy subjects, the metaboreflex was studied with the PEMI method at the start of recovery from one leg-dynamic knee extension performed at intensities of 30% (PEMI 30%) and 70% (PEMI 70%) of the maximum workload achieved in a preliminary test. Control exercise recovery tests at the same intensities were also conducted. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were that 1) during metaboreflex, exercise conducted against the higher workload caused a more pronounced blood pressure increase than the strain conducted against the lower workload; and 2) during PEMI 70%, this blood pressure response was mainly achieved through enhancement of myocardial contractility that increased stroke volume and, in turn, cardiac output, whereas during PEMI 30%, the blood pressure response was reached predominantly by means of vasoconstriction. Thus a substantial enhancement of myocardial contractility was reached only in the PEMI 70% test. These results suggest that hemodynamic regulation during metaboreflex engagement caused by PEMI in humans is dependent on the intensity of the previous effort. Moreover, the cardiovascular response during metaboreflex is not merely achieved by vasoconstriction alone, but it appears that there is a complex interplay between peripheral vasoconstriction and heart contractility recruitment.

Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

“…The primary function of this reflex-induced blood pressure response is to restore blood flow and arterial oxygen delivery to hypoperfused muscles (29). This pressure effect is thought to be mediated by several mechanisms: 1) a vasoconstriction in the nonischemic vascular beds (8,38), 2) an enhancement in cardiac filling (14,42), and 3) an improvement in myocardial contractility (11,12,30,39). Furthermore, there is general consensus that HR does not participate in this response since the metaboreflex-induced increase in sympathetic tone occurring during PEMI is counterbalanced by the concomitant baroreflex-induced rise in parasympa- thetic activity along with the withdrawal of central command due to the cessation of exercise (8,12,16,18,26,39).…”

“…This additional test aimed at verifying whether or not this condition "per se" could affect hemodynamics in heart failure patients, even though we as well as others (5,11,12) have demonstrated that, in normal individuals, RCO that was not preceded by exercise was incapable of eliciting any substantial hemodynamic modifications. On a day following the PEMI and CER tests, a RCO session consisting of 12 min (i.e., the same duration as the PEMI and CER tests) was applied: after 6 min of resting, 3 min of regional circulatory occlusion of the arm was applied followed by 3 more min of rest.…”

“…The data acquisition method is described in detail in our previous works (9,11,12). Briefly, by using a digital chart recorder (ADInstruments, PowerLab 8sp, Castle Hill, Australia), we stored NCCOM 3-derived analog traces of electrocardiogram, thorax impedance (Z0), and Z0 first derivative.…”

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

“…When the reflex is selectively activated in humans by postexercise muscle ischemia (PEMI) after isometric handgrip exercise, the pressor response occurs mainly via peripheral vasoconstriction; CO remains at the resting level (16,27,31,44,57). However, humans can also reportedly show an increase in CO during PEMI after leg cycling (5), dynamic knee extension (10), and dynamic handgrip exercise (9,11). Although differences in the type of exercise and muscle mass used in the exercise could potentially affect the results, an alternative explanation for this inconsistency is that the components of the muscle metaboreflex-mediated pressor response vary widely among human subjects.…”

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

“…Third, with respect to the limitations of the model used to evoke the metaboreflex, both static and dynamic contractions followed by local circulatory occlusion increase HR, SV, and CO in humans (3,24,32) and in dogs (29), but the effects on the heart appear to be intensity-dependent (7,8,40). However, the local circulatory occlusion used to trap metabolites that activate metaboreflex prevents venous dilation, which is a major component of metaboreflex activation (10,25).…”