Abstract
Sustained postexercise vasodilation, which may be mediated at both a neural and vascular level, is seen in previously active skeletal muscle vascular beds following both large and small muscle-mass exercise. Blunted sympathetic vascular transduction and a downward resetting of the arterial baroreflex contribute to this vasodilation after cycling (large muscle-mass exercise), but it is unknown if these responses also contribute to sustained vasodilation following small muscle-mass exercise. This study aimed to determine if baroreflex sensitivity is altered, the baroreflex is reset, or if sympathetic vascular transduction is blunted following small muscle-mass exercise. Eleven healthy, college-aged subjects (five males, six females) completed one-leg dynamic knee-extension exercise for 1 h at 60% of peak power output. While cardiovagal baroreflex sensitivity was increased ∼23% postexercise relative to preexercise (P < 0.05), vascular and integrated baroreflex sensitivity were not altered following exercise (P = 0.31 and P = 0.48). The baroreflex did not exhibit resetting (P > 0.69), and there was no evidence of changes in vascular transduction following exercise (P = 0.73). In conclusion, and in contrast to large muscle-mass exercise, it appears that small muscle-mass exercise produces a sustained postexercise vasodilation that is largely independent of central changes in the baroreflex.
Highlights
Arterial blood pressure is reduced following large muscle mass exercise such as treadmill running and cycling in humans (Halliwill et al 2013). Associated with this postexercise hypotension, is a sustained postexercise vasodilation, which is due in part to a downward resetting of the arterial baroreflex and a reduction in vascular responsiveness to sympathetic stimulation (Halliwill et al 1996a), but mostly caused by activation of histamine H1 and H2 receptors within the vascular bed of the previously exercised muscle (Lockwood et al 2005; McCord and Halliwill 2006; McCord et al 2006)
Findings from the current study show that cardiovagal baroreflex sensitivity was augmented after exercise, while vascular baroreflex sensitivity was unchanged
Previous work has shown a resetting of the arterial baroreflex toward lower pressures after exercise in humans (Halliwill et al 1996a) and in rats (Kajekar et al 2002; Miki et al 2003), the current findings provided no evidence to support the presence of resetting of the baroreflex after dynamic knee-extension exercise
Summary
Arterial blood pressure is reduced following large muscle mass exercise such as treadmill running and cycling in humans (Halliwill et al 2013) Associated with this postexercise hypotension, is a sustained postexercise vasodilation, which is due in part (perhaps 20%) to a downward resetting of the arterial baroreflex and a reduction in vascular responsiveness to sympathetic stimulation (Halliwill et al 1996a), but mostly caused (perhaps 80%) by activation of histamine H1 and H2 receptors within the vascular bed of the previously exercised muscle (Lockwood et al 2005; McCord and Halliwill 2006; McCord et al 2006). Postexercise hypotension has been reported using a small muscle-mass exercise model of single-leg dynamic knee-extension exercise, albeit less consistently, and this hypotension is thought to be primarily mediated by sustained local vasodilation of the previously exercised quadriceps muscle (Barrett-O’Keefe et al 2013). Changes in transduction may be related to the relative metabolic state of the exercising muscle, and independent of the amount of muscle mass
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