Key result
Caffeine ingestion (400 mg) prior to maximal exercise increased maximal heart rate (192 vs 190 bpm, p<0.05) and disrupted post-exercise autonomic recovery compared to placebo.
Why the study?
Does caffeine ingestion alter autonomic function and ventricular repolarization after acute exercise in healthy individuals?
RCT (n=18)
Crossover
Does caffeine ingestion alter autonomic function and ventricular repolarization after acute exercise in healthy individuals?
p-value: p=<0.05
Caffeine ingestion before maximal exercise delays autonomic recovery and prolongs QTc, potentially increasing arrhythmogenic risk during recovery.
Caution against caffeine before maximal exercise; extends RCT evidence on autonomic disruption.
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.
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Bunsawat et al. (2014) conducted an RCT in Healthy individuals (n=18). Caffeine vs. Placebo was evaluated on Autonomic function (HRV) and ventricular depolarization/repolarization (QTc) post-exercise (p=<0.05). Caffeine ingestion (400 mg) prior to maximal exercise increased maximal heart rate (192 vs 190 bpm, p<0.05) and disrupted post-exercise autonomic recovery compared to placebo.
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