Effects of acute vasodilation on the hemodynamic response to muscle metaboreflex

Abstract

The aim of the present study was to test the contribution of stroke volume (SV) in hemodynamic response to muscle metaboreflex activation in healthy individuals. We hypothesized that an acute decrease in cardiac afterload and preload due to the administration of a vasodilating agent could reduce postexercise muscle ischemia (PEMI)-induced SV response. Ten healthy males (age 33.6 ± 1.3 yr) were enrolled and randomly assigned to the following study protocol: 1) PEMI session, 2) control exercise recovery (CER) session, 3) PEMI after sublingual administration of 5 mg of isosorbide dinitrate (ISDN), and 4) CER after ISDN. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were a blunted SV response during metaboreflex following acute arterial and venous vasodilation, associated with a reduction in cardiac diastolic time and filling, and a decrement of systemic vascular resistance. These hemodynamic changes restrain blood pressure response during metaboreflex activation. Our results indicate that hemodynamic response to metaboreflex activation is a highly integrated phenomenon encompassing complex interplay between heart rate, cardiac performance, preload, and afterload and that impairment of one or more of these parameters leads to altered hemodynamic response to metaboreflex.

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

“…The response in this parameter was higher in the CTL than in the OMS group, whereas no difference was present between the two groups with obesity, with the MHO group showing a behavior in the medium between those of the CTL and of the OMS group. The increase in VFR occurring in the CTL and in the MHO group is similar to what has been reported in previous human research with similar experimental settings (13,14,29) and confirms that an increase in diastolic flow takes place during the metaboreflex in normal individuals, probably because of a sympathetic-mediated venous and splanchnic constriction (32,53,54). The lack of VFR response in the OMS group appears to suggest that, in subjects with complicated obesity, certain phenomena likely prevented the normal increase in venous return and cardiac preload.…”

“…The possibility to modulate SV has been defined crucial in the metaboreflex activation by means of PEMI, since in this setting HR does not normally have an evident response because of the elevated vagal tone, which counteracts the sympathetic activation (25,38). Thus, to increase/or to maintain stable CO values, cardiovascular regulatory mechanisms can only rely on the SV reserve, which can be recruited by enhancing cardiac performance and/or cardiac preload (11,13,29,33). In the present study, the OMS group showed a tendency to decrease SV response during the metaboreflex, whereas normal subjects increased this parameter.…”

“…MEAN BLOOD PRESSURE RESPONSE (MBP) to metaboreflex activation in healthy individuals is normally the consequence of increases in both systemic vascular resistance (SVR) and cardiac output (CO) (3,9,10,12,14,24,29,31,54,56). This response is achieved as the result of an elevation in sympathetic tone, which produces arteriolar constriction and enhancement in myocardial performance and in cardiac preload (18,35,39).…”

“…Three minutes of recovery were further allowed after the cuff was deflated, for a total of 6 min of recovery. This protocol has been shown to trap the muscle metabolites in the exercising limb and to maintain stimulation of the metaboreceptors (9,15,29,49).…”

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

“…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). To avoid this obstacle, we chose to use a 1-min 50% MVC handgrip model, which is known to evoke the muscle metaboreflex without increasing HR, SV, or CO.…”