Severe exercise alters the strength and mechanisms of the muscle metaboreflex

Abstract

Previous studies have shown that in dogs performing mild to moderate treadmill exercise, partial graded reductions in hindlimb blood flow cause active skeletal muscle to become ischemic and metabolites to accumulate thus evoking the muscle metaboreflex. This leads to a substantial reflex increase in mean arterial pressure (MAP) mediated almost solely via a rise in cardiac output (CO). However, during severe exercise CO is likely near maximal and thus metaboreflex-mediated increases in MAP may be attenuated. We therefore evoked the metaboreflex via partial graded reductions in hindlimb blood flow in seven dogs during mild, moderate, and severe treadmill exercise. During mild and moderate exercise there was a large rise in CO (1.5 +/- 0.2 and 2.2 +/- 0.3 l/min, respectively), whereas during severe exercise no significant increase in CO occurred. The rise in CO caused a marked pressor response that was significantly attenuated during severe exercise (26.3 +/- 7.0, 33.2 +/- 5.6, and 12.2 +/- 4.8 mmHg, respectively). We conclude that during severe exercise the metaboreflex pressor response mechanisms are altered such that the ability of this reflex to increase CO is abolished, and reduced pressor response occurs only via peripheral vasoconstriction. This shift in mechanisms likely limits the effectiveness of the metaboreflex to increase blood flow to ischemic active skeletal muscle. Furthermore, because the metaboreflex is a flow-raising reflex and not a pressure-raising reflex, it may be most appropriate to describe the metaboreflex magnitude based on its ability to evoke a rise in CO and not a rise in MAP.

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

“…Our laboratory demonstrated previously (1,2,18) that in normal dogs during mild to moderate exercise, the mechanism mediating the pressor response initiated by muscle metaboreflex activation depends primarily on an increase in CO. In contrast, we previously observed in dogs (3) that the pressor response to bilateral carotid occlusion is mediated via peripheral vasoconstriction at rest and across a broad range of workloads.…”

“…With partial vascular occlusion of the terminal aorta, MAP can rise via the mechanical effects of partial aortic occlusion, e.g., decreasing vascular conductance to the hindlimbs by inflating the occluder will increase arterial pressure independently of any reflexes because of the mechanical reduction in total vascular conductance. This increase in MAP by the passive mechanical effects of the occluder was calculated as described by Augustyniak et al (2) and subtracted from the observed pressor response to yield MAPactive, which reflects the rise in MAP due to the reflex (e.g., via increases in CO and/or peripheral vasoconstriction). All reflex MAP values reported are the active levels.…”

Sample Entropy and Traditional Measures of Heart Rate Dynamics Reveal Different Modes of Cardiovascular Control During Low Intensity Exercise

“…Compared to DYN, ISO was characterized by higher SBP and DBP, larger HRV HF-and LF-power and lower HRV complexity. Metabolite accumulation as well as mechanical stimuli in the isometrically working muscle (muscle metaboreflex) can lead to an enhanced vascular response [45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61]. This metaboreflex likely overrides the baroreflex, leading to a stronger sympathetic efferent activity to the vessels during ISO [46,47,53,[62][63][64][65][66].…”

Muscle metaboreflex control of ventricular contractility during dynamic exercise

“…Thus the authors hypothesized that during mild exercise, the rise in SV at constant HR during MMR activation is not likely to be a result of the Frank-Starling mechanism but indirectly reflects an increase in contractility. In a subsequent study, Augustyniak et al (2) showed that there was no change in CVP from rest to mild exercise. On the other hand, CVP did increase as exercise intensity increased, but there was no further significant rise between free-flow exercise and maximal MMR activation during any of the workloads.…”

“…The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (26,35). In this way the MMR-induced increases in ventricular performance act to sustain or slightly increase stroke volume (SV) despite decreases in ventricular filling time due to the reflex tachycardia (2,26,44). Furthermore, O'Leary an Augustyniak (26) showed that in normal dogs in which HR was fixed at 225 beats/min during mild exercise, MMR activation caused such a rise in SV that the increases in CO were approximately equal to those observed in control experiments.…”