WISE 2005: stroke volume changes contribute to the pressor response during ischemic handgrip exercise in women

Abstract

The mechanism of the pressor response to small muscle mass (e.g., forearm) exercise and during metaboreflex activation may include elevations in cardiac output (Q) or total peripheral resistance (TPR). Increases in Q must be supported by reductions in visceral venous volume to sustain venous return as heart rate (HR) increases. Therefore, this study tested the hypothesis that increases in Q, supported by reductions in splanchnic volume (portal vein constriction), explain the pressor response during handgrip exercise and metaboreflex activation. Seventeen healthy women performed 2 min of static ischemic handgrip exercise and 2 min of postexercise circulatory occlusion (PECO) while HR, stroke volume and superficial femoral artery flow (Doppler), blood pressure (Finometer), portal vein diameter (ultrasound imaging), and muscle sympathetic nerve activity (MSNA; microneurography) were measured followed by the calculation of Q, TPR, and leg vascular resistance (LVR). Compared with baseline, mean arterial blood pressure (MAP) (P < 0.001) and Q (P < 0.001) both increased in each minute of exercise accompanied by a approximately 5% reduction in portal vein diameter (P < 0.05). MAP remained elevated during PECO, whereas Q decreased below exercise levels. MSNA was elevated above baseline during the second minute of exercise and through the PECO period (P < 0.05). Neither TPR nor LVR was changed from baseline during exercise and PECO. The data indicate that the majority of the blood pressure response to isometric handgrip exercise in women was due to mobilization of central blood volume and elevated stroke volume and Q rather than elevations in TVR or LVR resistance.

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

“…For correlations between ⌬LVR and ⌬MAP, ⌬CO, or ⌬TPR from the rest period to the exercise period, n ϭ 31 subjects; for all other correlations, n ϭ 35 subjects. *P Ͻ 0.05; †P Ͻ 0.01. ric exercise, as was suggested by measurements of renal and splanchnic vascular resistance and blood flow in both animals (8,12,63) and humans (39,42,(57)(58)(59)64). This might explain our observation that individual differences in LVR and CO responses were dissociated during exercise, despite a strong relationship between TPR and CO responses.…”

“…While the increase in arterial pressure during isometric exercise is a well-established response, the responses of the components mediating the pressor response, cardiac output (CO) and total peripheral vascular resistance (TPR), remain controversial. In fact, previous studies have shown that, during isometric handgrip exercise in healthy humans, the pressor response occurs via an increase in CO (16,32,[34][35][36]57), an increase in TPR (6, 17), or both of those (3,31,58,59,61,62). The variability of those findings leads one to speculate that there are considerable individual differences in the components of the pressor response to exercise, which is in stark contrast to the nearly invariant arterial pressure response.…”

“…This reflex is a feedback system operating via chemosensitive afferents (group III and IV fibers) that can elicit a reflex pressor response (7,29,38). 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).…”

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

“…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).…”

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).…”