Time course of haemodynamic changes after maximal exercise

Isea, Jesús; Piepoli, Massimo F; Adamopoulos, Stamatis; Pannarale, Giuseppe; Sleight, Peter; Coats, A.J.S.

doi:10.1111/j.1365-2362.1994.tb02026.x

Cited by 28 publications

(24 citation statements)

References 26 publications

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“…A number of studies have found decreased peripheral resistance at sites other than those of the exercising muscle, suggesting that the reduction is a whole body phenomenon. 22,35,43 However, Hagberg et al 13 found increases in total peripheral resistance in older…”

Section: Peripheral Resistancementioning

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%

“…10,11,19,22,24,[31][32][33]35,41,[43][44][45][59][60][61]63,71,72 Treadmill exercise at similar intensities has also been documented to elicit PEH. 14,15,20,25,34,40,[55][56][57][58] Direct comparisons of the effect of exercise intensity have, for the most part, found that PEH occurs independent of exercise intensity.…”

Section: Intensity Of the Exercisementioning

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%

“…13,15,57 In all such instances the decrements were found to be due to reductions in stroke volume. In humans, it is common to observe an increased heart rate during some or all of the hypotensive period, 20,22,33,35,58,63,77 whereas rodents often display decreased or unchanged heart rates. 30,[48][49][50]54 Of interest is that, with the exception of one study, 43 changes in human cardiac output post exercise appear dependent on the initial state of hypertension.…”

Section: Cardiac Output (Q · C)mentioning

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: Peripheral Resistancementioning

confidence: 99%

Section: Magnitude Of the Blood Pressure Declinementioning

confidence: 99%

Section: Intensity Of the Exercisementioning

confidence: 99%

Section: Duration Of the Exercisementioning

confidence: 99%

Section: Cardiac Output (Q · C)mentioning

confidence: 99%

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Potential causes, mechanisms, and implications of post exercise hypotension

2002

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Pathophysiology of Noncardiac Syncope in Athletes

Christou

Kiortsis

2018

Sports Med

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The most frequent cause of syncope in young athletes is noncardiac etiology. The mechanism of noncardiac syncope (NCS) in young athletes is neurally-mediated (reflex). NCS in athletes usually occurs either as orthostasis-induced, due to a gravity-mediated reduced venous return to the heart, or in the context of exercise. Exercise-related NCS typically occurs after the cessation of an exercise bout, while syncope occurring during exercise is highly indicative of the existence of a cardiac disorder. Postexercise NCS appears to result from hypotension due to impaired postexercise vasoconstriction, as well as from hypocapnia. The mechanisms of postexercise hypotension can be divided into obligatory (which are always present and include sympathoinhibition, histaminergic vasodilation, and downregulation of cardiovagal baroreflex) and situational (which include dehydration, hyperthermia and gravitational stress). Regarding postexercise hypocapnia, both hyperventilation during recovery from exercise and orthostasis-induced hypocapnia when recovery occurs in an upright posture can produce postexercise cerebral vasoconstriction. Athletes have been shown to exhibit differential orthostatic responses compared with nonathletes, involving augmented stroke volume and increased peripheral vasodilation in the former, with possibly lower propensity to orthostatic intolerance.

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The effects of exercise and training on human cardiovascular reflex control

O’Sullivan

Bell

2000

Journal of the Autonomic Nervous System

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Time course of haemodynamic changes after maximal exercise

Cited by 28 publications

References 26 publications

Potential causes, mechanisms, and implications of post exercise hypotension

Potential causes, mechanisms, and implications of post exercise hypotension

Pathophysiology of Noncardiac Syncope in Athletes

The effects of exercise and training on human cardiovascular reflex control

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