Blood pressure regulation X: what happens when the muscle pump is lost? Post-exercise hypotension and syncope

Halliwill, John R.; Sieck, Dylan C.; Romero, Steven A.; Buck, Tahisha M.; Ely, Matthew R.

doi:10.1007/s00421-013-2761-1

Cited by 73 publications

(85 citation statements)

References 134 publications

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“…Regarding the lack of additive effect of the active recovery in the post‐exercise blood pressure responses in comparison with the passive recovery session, it should be noted that even the passive recovery did not promote a great hypotension, as might be expected (Halliwill et al ., ). Accordingly, none of the subjects experienced any discomfort or pre‐syncopal symptoms after this session.…”

Section: Discussionmentioning

confidence: 97%

Effects of active recovery on autonomic and haemodynamic responses after aerobic exercise

Germano-Soares

Peçanha

Cavalcante

et al. 2015

Clin Physio Funct Imaging

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The aim of this study was to examine the effect of active recovery on autonomic and haemodynamic responses after exercise in healthy adults. Nineteen healthy young male individuals underwent two experimental sessions: exercise with active recovery (AR) and exercise with passive recovery (PR). The exercise sessions comprised three phases: warm-up (5 min), exercise phase (cycle ergometer, 30 min, intensity between 60 and 70% of the heart rate reserve) and recovery (5 min). In the AR, the subjects remained cycling in the recovery phase at intensity between 30% and 35% of heart rate reserve, while in the PR, the subjects stopped the exercise after finishing the exercise phase. Blood pressure and heart rate were measured before and over the 30 min after the interventions. There were no differences for systolic and diastolic blood pressures, heart rate and rate pressure product between active and passive recovery sessions. Also, all heart rate variability parameters changed similarly after exercise with passive or active recovery sessions. In summary, exercise with active recovery does not affect the autonomic and haemodynamic responses after moderate-intensity aerobic exercise in healthy young male individuals.

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Section: Discussionmentioning

confidence: 97%

Effects of active recovery on autonomic and haemodynamic responses after aerobic exercise

Germano-Soares

Peçanha

Cavalcante

et al. 2015

Clin Physio Funct Imaging

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“…Blood flow to the previously active skeletal muscle remains elevated for several hours following an acute bout of aerobic exercise (Laughlin et al , 2012; Halliwill et al , 2013, 2014). This sustained post-exercise vasodilatation occurs following both whole-body exercise (i.e.…”

Section: Introductionmentioning

confidence: 99%

Effect of antioxidants on histamine receptor activation and sustained postexercise vasodilatation in humans

Romero

Ely

Sieck

et al. 2015

Experimental Physiology

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An acute bout of aerobic exercise elicits a sustained post-exercise vasodilatation that is mediated by histamine H1 and H2 receptor activation. However, the upstream signaling pathway that leads to post-exercise histamine receptor activation is unknown. We tested the hypothesis that the potent antioxidant ascorbate would inhibit this histaminergic vasodilatation following exercise. Subjects performed 1 hr unilateral dynamic knee extension at 60% of peak power in three conditions: 1) control; 2) intravenous ascorbate infusion; and, 3) ascorbate infusion plus oral H1/H2 histamine receptor blockade. Femoral artery blood flow (Doppler ultrasound) was measured before exercise and for 2 hr post-exercise. Femoral vascular conductance was calculated as flow/pressure. Post-exercise vascular conductance was greater for control condition (3.4 ± 0.1 ml min−1 mmHg−1) compared with ascorbate (2.7 ± 0.1 ml min−1 mmHg−1, P < 0.05) and ascorbate plus H1/H2 blockade (2.8 ± 0.1 ml min−1 mmHg−1, P < 0.05), which did not differ from one another (P = 0.9). Because ascorbate may catalyze the degradation of histamine in vivo, we conducted a follow-up study where subjects performed exercise in two conditions: 1) control and 2) intravenous N-acetylcysteine infusion. Post-exercise vascular conductance was similar for control (4.0 ± 0.1 ml min−1 mmHg−1) and N-acetylcysteine conditions (4.0 ± 0.1 ml min−1 mmHg−1; P = 0.8). Thus, the results in study 1 were due to the degradation of histamine in skeletal muscle by ascorbate, since the histaminergic vasodilatation was unaffected by N-acetylcysteine. Taken together, exercise-induced oxidative stress does not appear to contribute to sustained post-exercise vasodilatation.

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“…Unexpectedly, the postictal BP in our patients returned to baseline levels 5 min after cessation of BCS, whereas HR remained increased. This opposed modulation of BP is possibly caused by an immediate muscular hyperemia that commonly follows exercise of skeletal muscles, and ultimately leads to a decreased systemic vascular resistance and a subsequent drop in systemic BP . The extent of this postexercise hyperemia depends on the type, intensity, and duration of the exercise and can last for up to 20 min, possibly linking the duration and intensity of the tonic–clonic phase to the magnitude of postictal systemic BP .…”

Section: Discussionmentioning

confidence: 99%

Seizure‐related modulation of systemic arterial blood pressure in focal epilepsy

et al. 2016

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Dr. Hampel is neurologist with special interest in autonomic function and epilepsy surgery. SUMMARYObjective: Cardiorespiratory function alterations are commonly observed with epileptic seizures and may lead to syncope and sudden unexpected death in epilepsy (SUDEP). Although most previous research has focused on controlling heart rate (HR) and respiration, little is known about seizure-related regulation of systemic blood pressure (BP). Herein, we have investigated whether the periictal modulation of systemic BP and HR depends on seizure characteristics. Methods: Systemic arterial BP, HR, and peripheral capillary oxygen saturation (SPO 2 ) were continuously and noninvasively monitored using the ccNexfin device in those epilepsy patients undergoing video-electroencephalography (EEG) telemetry. Data are given as mean AE standard deviation (SD). Results: Forty-five seizures in 37 patients were included. In focal seizures (FS, n = 35), the mean arterial BP (MAP) increased by 33 AE 35% and the HR by 53 AE 44%, whereas the SPO 2 remained unaltered. The MAP and HR increases were significantly greater in FS with alterations in consciousness than in those without. For those FS that evolved to bilateral convulsive seizures (BCS, n = 10), all of the ictal recordings were compromised by artifacts. However, 2 min after seizure cessation, the MAP was enhanced by only 16 AE 14% and returned to a baseline slightly below preictal levels after 5 min, whereas the HR was increased by 77 AE 33% and remained elevated throughout the postictal phase. Significance: Periictal regulation of systemic BP and HR displays distinct patterns depending on the type of seizure with focal onset. These changes were unrelated to alterations in SPO 2 . The potential clinical implications of these findings are discussed in the article. KEY WORDS: Systemic blood pressure, Syncope, Sudden unexpected death in epilepsy.Epileptic seizures affect the autonomic nervous system in many ways including modulation of the gastrointestinal (e.g., spitting, vomiting), cardiac (tachycardia, bradycardia), and respiratory (tachypnea, hypopnea and apnea) functions.1,2 Depending on their severity, cardiorespiratory alterations can lead to syncope or sudden unexpected death in epilepsy (SUDEP).3-5 In most of the previous studies addressing seizure-related cardiorespiratory function, the cardiac rhythm and oxygen saturation were assessed either separately or together. [6][7][8][9] The supply of oxygen and metabolites, however, critically depends on the blood perfusion of the different organs which is, in turn, tightly regulated in most organs and connected to systemic blood pressure (BP). In this context, a recent study has shown that during the interictal period, the diastolic BP for those individuals who subsequently died as a result of SUDEP, tended to be higher than for the epilepsy controls.10 This could be due to an epilepsy-related increase in the activity of the sympathetic branch of the autonomic nervous system. 11 To date, however, little is known about seizure-r...

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Blood pressure regulation X: what happens when the muscle pump is lost? Post-exercise hypotension and syncope

Cited by 73 publications

References 134 publications

Effects of active recovery on autonomic and haemodynamic responses after aerobic exercise

Effects of active recovery on autonomic and haemodynamic responses after aerobic exercise

Effect of antioxidants on histamine receptor activation and sustained postexercise vasodilatation in humans

Seizure‐related modulation of systemic arterial blood pressure in focal epilepsy

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