Title | Caffeine delays autonomic recovery following acute exercise. | ||
Author | Bunsawat, Kanokwan; White, Daniel W; Kappus, Rebecca M; Baynard, Tracy | ||
Journal | Eur J Prev Cardiol | Publication Year/Month | 2015-Nov |
PMID | 25297344 | PMCID | -N/A- |
Affiliation + expend | 1.Department of Kinesiology and Nutrition, The University of Illinois at Chicago, IL, USA bunsawa2@uic.edu. |
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.