Abstract
BackgroundPost-exercise hypotension (PEH) following prolonged dynamic exercise arises from increased total vascular conductance (TVC) via skeletal muscle vasodilation. However, arterial vasodilation of skeletal musculatures does not entirely account for the rise in TVC. The aim of the present study was to determine the contribution of vascular conductance (VC) of the legs, arms, kidneys and viscera to TVC during PEH.MethodsEight subjects performed a single period of cycling at 60% of heart rate (HR) reserve for 60 minutes. Blood flow in the right renal, superior mesenteric, right brachial and right femoral arteries was measured by Doppler ultrasonography in a supine position before exercise and during recovery. HR and mean arterial pressure (MAP) were measured continuously. MAP decreased significantly from approximately 25 minutes after exercise cessation compared with pre-exercise baseline. TVC significantly increased (approximately 23%; P <0.05) after exercise compared with baseline, which resulted from increased VC in the leg (approximately 33%) and arm (approximately 20%), but not in the abdomen.ConclusionPEH was not induced by decreased cardiac output, but by increased TVC, two-thirds of the rise in which can be attributed to increased VC in active and inactive limbs.
Highlights
Post-exercise hypotension (PEH) following prolonged dynamic exercise arises from increased total vascular conductance (TVC) via skeletal muscle vasodilation
PEH is considered to be caused by an increase in total vascular conductance (TVC) that is incompletely offset by an increase in cardiac output [1,2,3], in older hypertensive patients [4] and in endurance-trained men [5], PEH is largely mediated by decreased cardiac output
Heart rate and blood pressure response during exercise heart rate (HR) significantly increased during exercise from 55 ± 3 to 135 ± 3 bpm
Summary
Post-exercise hypotension (PEH) following prolonged dynamic exercise arises from increased total vascular conductance (TVC) via skeletal muscle vasodilation. An acute period of dynamic exercise is known to elicit a reduction in arterial blood pressure relative to pre-exercise levels for approximately two hours [1,2,3]. This post-exercise hypotension (PEH) produces anti-hypertensive effects relevant to hypertensive patients [2]. The increased TVC that causes PEH is predominantly attributed to increased vascular conductance (VC) resulting from vasodilation physical stress to the subjects compared with the previous invasive method [7], it enables to exclude the effect of such stress on the hemodynamics responses during PEH
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