Non‐alpha‐adrenergic effects on systemic vascular conductance during lower‐body negative pressure, static exercise and muscle metaboreflex activation

Abstract

Non-α-adrenergic vasoconstriction was present during LBNP. The systemic vasoconstriction during static exercise and isolated muscle metaboreflex activation, in the absence of leg vasoconstriction, was explained by an α-adrenergic mechanism. Therefore, non-α-adrenergic vasoconstriction is more emphasized during baroreflex, but not metaboreflex-mediated sympathetic activation.

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

“…grip exercise in healthy humans, the pressor response occurs via an increase in CO (16, 32, 34 -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.…”

“…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.…”

“…It has been postulated, for example, that cardiovascular responses to muscle metaboreflex activation can be influenced by the types of muscle fibers comprising the working muscles and by their training status (19). Additionally, differences in other factors, including the sensitivity and/or density of group III and IV muscle afferent endings, integration of afferent neural input, regulation of autonomic nervous activity within the central nervous system, and end-organ responsiveness, including ␣-and ␤-adrenergic receptor function (16,31,37), may also contribute to individual differences in cardiovascular responses to muscle metaboreflex activation.…”

“…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).…”

Neural Control of Vascular Function in Skeletal Muscle

“…Orthostatic stress can be induced nonpharmacologically by upright posture, or simulated using lower body negative pressure (LBNP). Many studies illustrate an increase in the groupaveraged forearm and leg vascular resistance during these tests (29,164,253,283) that are sensitive to norepinephrine (NE) release (253). In humans, head-up tilt elicits predictable increases in sympathetic outflow and total vascular resistance, the magnitude of which expresses interindividual variability (105).…”