Mechanisms mediating muscle metaboreflex control of cardiac output during exercise: Impaired regulation in heart failure

Figures

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  FIGURE 1. Average metaboreflex responses during mild exercise (3.2 km/h 0% grade) from 36 animals. Data points are during free flow exercise (no occlusion; Free Flow), the metaboreflex threshold (Threshold) determined as the intersection between the initial response line and the pressor response line, and the maximal value observed with the lowest level of occlusion performed during that experiment (Max MMA).

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  FIGURE 2. (a) The relationship between coronary vascular conductance (CVC) and cardiac power at rest, during mild exercise (Ex) and during muscle metaboreflex activation (MMA) before and after i.v. infusion of the α1‐adrenergic antagonist prazosin. In control experiments, coronary vasodilatation occurred in response to exercise and an increase in cardiac power. In response to MMA, cardiac power increased with little change in CVC. Prazosin had little effect at rest or during exercise, but with MMA marked increases in CVC occurred in response to much greater increases in cardiac power. The slope of this relationship was significantly increased after prazosin. (b) This same experiment after induction of HF. See text for explanations. Adapted from Coutsos et al. 2010, 2013).

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  FIGURE 3. The relationship between an index of cardiac contractility (preload recruitable stroke work) versus coronary blood flow at rest, during mild exercise and during muscle metaboreflex activation before and after prazosin and in the same animals before and after the induction of heart failure (abbreviations as in Figure 2). In normal animals prazosin extends the linear relationship to higher levels of coronary blood flow and higher cardiac contractility (dashed blue arrow). After induction of HF, the slope of the relationship is significantly lower. Prazosin had a progressively greater effect as baseline coronary blood flow increased. With MMA, prazosin had a marked effect on flow and contractility increased significantly. Adapted from Coutsos et al. (2010, 2013).

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  FIGURE 4. The relationship between the changes in central venous pressure (CVP) in response to MMA as a function of the observed change in cardiac output before and after the induction of HF. As the rise in cardiac output is attenuated, larger increases in CVP occur during MMA. Adapted from O'Leary et al. (2019).