Kanokwan Bunsawat 1 , Daniel W White 2 , Rebecca M Kappus 2 , Tracy Baynard 2 . Show Affiliations »
Abstract
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BACKGROUND: Impaired autonomic recovery of heart rate (HR ) following exercise is associated with an increased risk of sudden death. Caffeine , a potent stimulator of catecholamine release, has been shown to augment blood pressure (BP) and sympathetic nerve activity ; however, whether caffeine alters autonomic function after a bout of exercise bout remains unclear. METHODS: In a randomized, crossover study, 18 healthy individuals (26 ± 1 years; 23.9 ± 0.8 kg·m(-2)) ingested caffeine (400 mg) or placebo pills, followed by a maximal treadmill test to exhaustion . Autonomic function and ventricular depolarization/repolarization were determined using heart rate variability (HRV) and corrected QT interval (QTc ), respectively, at baseline, 5, 15, and 30 minutes post-exercise. RESULTS: Maximal HR (HRmax ) was greater with caffeine (192 ± 2 vs. 190 ± 2 beat·min(-1), p < 0.05). During recovery, HR, mean arterial pressure (MAP), and diastolic blood pressure (DBP ) remained elevated with caffeine (p < 0.05). Natural log transformation of low-to-high frequency ratio (LnLF/LnHF) of HRV was increased compared with baseline at all time points in both trials (p < 0.05), with less of an increase during 5 and 15 minutes post-exercise in the caffeine trial (p < 0.05). QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05). CONCLUSIONS: Caffeine ingestion disrupts post-exercise autonomic recovery because of increased sympathetic nerve activity. The prolonged sympathetic recovery time could subsequently hinder baroreflex function during recovery and disrupt the stability of autonomic function, potentiating a pro-arrhythmogenic state in young adults . © The European Society of Cardiology 2014.
RCT Entities: Population
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BACKGROUND: Impaired autonomic recovery of heart rate (HR) following exercise is associated with an increased risk of sudden death . Caffeine , a potent stimulator of catecholamine release, has been shown to augment blood pressure (BP) and sympathetic nerve activity; however, whether caffeine alters autonomic function after a bout of exercise bout remains unclear. METHODS: In a randomized, crossover study, 18 healthy individuals (26 ± 1 years; 23.9 ± 0.8 kg·m(-2)) ingested caffeine (400 mg) or placebo pills, followed by a maximal treadmill test to exhaustion. Autonomic function and ventricular depolarization/repolarization were determined using heart rate variability (HRV) and corrected QT interval (QTc ), respectively, at baseline, 5, 15, and 30 minutes post-exercise. RESULTS: Maximal HR (HRmax) was greater with caffeine (192 ± 2 vs. 190 ± 2 beat·min(-1 ), p < 0.05). During recovery, HR, mean arterial pressure (MAP), and diastolic blood pressure (DBP) remained elevated with caffeine (p < 0.05). Natural log transformation of low-to-high frequency ratio (LnLF/LnHF) of HRV was increased compared with baseline at all time points in both trials (p < 0.05), with less of an increase during 5 and 15 minutes post-exercise in the caffeine trial (p < 0.05). QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05). CONCLUSIONS: Caffeine ingestion disrupts post-exercise autonomic recovery because of increased sympathetic nerve activity. The prolonged sympathetic recovery time could subsequently hinder baroreflex function during recovery and disrupt the stability of autonomic function, potentiating a pro-arrhythmogenic state in young adults. © The European Society of Cardiology 2014.
Entities: Chemical
Disease
Gene
Keywords:
Caffeine; autonomic function; exercise recovery
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Year: 2014
PMID: 25297344 DOI: 10.1177/2047487314554867
Source DB: PubMed Journal: Eur J Prev Cardiol ISSN: 2047-4873 Impact factor: 7.804