Post exercise hypotension is not mediated by the serotonergic system in borderline hypertensive individuals

MacDonald, Jay R.; Rosenfeld, Jack; Tarnopolsky, M A; Hogben, CD; Ballantyne, C; MacDougall, J. D.

doi:10.1038/sj.jhh.1001290

Cited by 16 publications

(23 citation statements)

References 23 publications

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“…Levels have been reported to be increased in normotensives, 60 increased 19 and unchanged 39 in borderline hypertensives, and decreased in hypertensive individuals. 43 Brownley et al 41 reported no change in urinary catecholamines after exercise in both normo and hypertensive individuals, with PEH only occurring in those with high blood pressure.…”

Section: Journal Of Human Hypertensionmentioning

confidence: 99%

“…In those studies that have observed a decline in blood pressure following exercise, the average decrement in pressure was approximately 8/9 (SBP/DBP) mm Hg in the normotensive population, 16,[20][21][22][23]25,[31][32][33][34][35] 14/9 mm Hg in the borderline hypertensive population [10][11][12]34,[36][37][38][39] and 10/7 mm Hg in the hypertensive population. 13 37 We recently examined the effects of the exercising muscle mass by comparing the PEH response to both leg and arm ergometry at the same relative intensity.…”

Section: Magnitude Of the Blood Pressure Declinementioning

confidence: 99%

“…9,10,15,16,19,24,32,[34][35][36][37][38][39][41][42][43]45,47,[57][58][59][60]63,[75][76][77] Inter-experimental comparisons are difficult across studies, since a variety of exer-Journal of Human Hypertension cise intensities and blood pressure measurement techniques have been used.…”

Section: Duration Of the Exercisementioning

confidence: 99%

“…9,16,31,44,49,57,61 Most studies have measured blood pressure for only 1-2 h following exercise 12,13,16,20,22,23,25,34,[36][37][38][39]55,58,75 and the majority of these have found a nadir in blood pressure during that time with a return or trend towards baseline pressure at the cessation of measurement.…”

Section: Duration Of the Responsementioning

confidence: 99%

“…Measures of circulating adrenaline indicate that levels are elevated 60 or unchanged 14,39 during the hypotensive period. Our finding that PEH is largely independent of exercise intensity combined with the fact that it also persists during adrenaline infusion 60 and ␤-receptor blockade 14 suggests that any role of adrenaline in PEH is minimal.…”

Section: Noradrenaline and Adrenalinementioning

confidence: 99%

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Potential causes, mechanisms, and implications of post exercise hypotension

2002

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Post exercise hypotension (PEH) is a phenomenon of a prolonged decrease in resting blood pressure in the minutes and hours following acute exercise. Knowledge of PEH is potentially useful in designing first line strategies against hypertension as well as allowing a further understanding of blood pressure regulation in both Keywords: blood pressure; vascular; cardiac; opioids; exercise Blood pressure responses during exerciseDuring dynamic exercise, cardiac output increases dramatically to ensure adequate perfusion to the working musculature. This increase is achieved by a withdrawal of parasympathetic tone (causing an increased heart rate and contractility), an increase in sympathetic activity (directly and indirectly increasing heart rate and contractility) and pronounced vasoconstriction of the venous vasculature (causing a greater venous return and therefore stroke volume). In parallel, the need for increased blood flow and oxygen delivery to the exercising muscle is achieved through regional vasodilation of those arterioles supplying blood to the exercising tissue in combination with a vasoconstriction of arterioles, which perfuse non-essential tissues. Although the mechanism of vasodilation at the onset of exercise is not fully understood, many compounds (eg, potassium, adenosine, nitric oxide, etc) have been implicated in the exercise induced changes. Contraction of the active muscle mass also assists in returning blood towards the heart. This 'muscle pump' effect further increases venous return and stroke volume.Increased cardiac output and vasoconstriction in non-exercising vascular beds increases systolic blood pressure (SBP), but the significant vasodilation at the exercising muscle beds helps to buffer this increase and results in a minimal rise in diastolic blood pressure (DBP). As exercise continues Correspondence: JR MacDonald, McMaster University Medical Centre, Room 4U18, 1200 Main Street West, Hamilton, Ontario L8N 3Z5, Canada. E-mail: jaymacȰmcmaster.ca health and disease. Following a brief review of blood pressure responses to exercise, this paper will provide a current and comprehensive summary of PEH and integrate the current state of knowledge surrounding it.

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Section: Journal Of Human Hypertensionmentioning

confidence: 99%

Section: Magnitude Of the Blood Pressure Declinementioning

confidence: 99%

Section: Duration Of the Exercisementioning

confidence: 99%

Section: Duration Of the Responsementioning

confidence: 99%

Section: Noradrenaline and Adrenalinementioning

confidence: 99%

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Potential causes, mechanisms, and implications of post exercise hypotension

2002

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Post-exercise effects on aortic wave reflection derived from wave separation analysis in young- to middle-aged pre-hypertensives and hypertensives

2016

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Central and peripheral mechanisms underlying postexercise hypotension: a scoping review

Brasil,

Silva,

Pescatello

et al. 2024

Journal of Hypertension

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Blood pressure (BP) reduction occurs after a single bout of exercise, referred to as postexercise hypotension (PEH). The clinical importance of PEH has been advocated owing to its potential contribution to chronic BP lowering, and as a predictor of responders to exercise training as an antihypertensive therapy. However, the mechanisms underlying PEH have not been well defined. This study undertook a scoping review of research on PEH mechanisms, as disclosed in literature reviews. We searched the PubMed, Web of Science, Scopus, Cumulated Index to Nursing and Allied Health Literature (CINAHL), Cochrane Library, and Sport Discus databases until January 2023 to locate 21 reviews – 13 narrative, four systematic with 102 primary trials, and four meta-analyses with 75 primary trials involving 1566 participants. We classified PEH mechanisms according to major physiological systems, as central (autonomic nervous system, baroreflex, cardiac) or peripheral (vascular, hemodynamic, humoral, and renal). In general, PEH has been related to changes in autonomic control leading to reduced cardiac output and/or sustained vasodilation. However, the role of autonomic control in eliciting PEH has been challenged in favor of local vasodilator factors. The contribution of secondary physiological outcomes to changes in cardiac output and/or vascular resistance during PEH remains unclear, especially by exercise modality and population (normal vs. elevated BP, young vs. older adults). Further research adopting integrated approaches to investigate the potential mechanisms of PEH is warranted, particularly when the magnitude and duration of BP reductions are clinically relevant. (PROSPERO CRD42021256569).

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Post exercise hypotension is not mediated by the serotonergic system in borderline hypertensive individuals

Cited by 16 publications

References 23 publications

Potential causes, mechanisms, and implications of post exercise hypotension

Potential causes, mechanisms, and implications of post exercise hypotension

Post-exercise effects on aortic wave reflection derived from wave separation analysis in young- to middle-aged pre-hypertensives and hypertensives

Central and peripheral mechanisms underlying postexercise hypotension: a scoping review

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