Abstract

Exercise training (ET) leads to marked resting bradycardia in elite athletes. However, some factors could influence the magnitude of resting bradycardia and its mechanisms of control. PURPOSE: evaluate the influence of sport modality and annual ET period (begging of annual ET - BET and competitive period - CP) on the level of resting heart rate (HR), HR response to head-up tilt test and their mechanisms of control in elite athletes. METHODS: 13 cyclists, 13 runners and 11 rowers (males; 26±3; 29±4 and 24±5years old, respectively, p=0.01 runners vs. rowers) were evaluated. HR was recorded on beat-to-beat basis (ECG) at rest and during head-up tilt test. Intrinsic HR was measured by atropine (0.04µg/kg) and esmolol (500µg/kg) infusions and vagal effect after atropine infusion. The responses to tilt test were expressed as percentage in relation to rest. HR variability was evaluated by time and frequency domains. Non parametric tests were performed (data are shown as median and interquartile range). RESULTS: At rest, runners showed lower HR compared with cyclists at CP [cyclists=50(45/55), runners=44(43/47), rowers=44(43/53)bpm, p<0.03]. Runners and rowers, showed higher vagal effect [cyclists=41(36/46), runners=55(48/59), rowers=50(42/66)bpm, p=0.03] and higher intrinsic HR [cyclists=84(82/87), runners=92(87/94), rowers=96(85/101)bpm, p=0.03] compared with cyclists at CP. Rowers showed higher intrinsic HR than cyclists at BET [cyclists=88(86/92), runners=91(82/99), rowers=95(90/101)bpm, p=0.03]. CP compared with BET decreased vagal effect [41(36/46) vs. 48(43/51)bpm, p<0.05] and intrinsic HR [84(82/87) vs. 88(86/92)bpm, p<0.05] of cyclists. At head-up tilt test, runners showed a lower increase on HR compared with cyclists at BET [cyclists=64(49/73), runners=46(43/55), rowers=53(42/77)%, p<0.05]. Neither sport modality nor ET period influenced HR variability indices (SDNN, rMSSD, pNN50, variance, LF, HF and LF/HF) at rest or tilt test. CONCLUSIONS: Run provokes higher resting bradycardia, mainly mediated by high vagal activity and leads to lower sympathetic activation at head-up tilt test. The bradycardia caused by rowing seems also to be mediated by vagal activity. However, cycling leads to resting bradycardia mainly by decreased intrinsic HR that is exacerbated at CP. Supported by Fapesp

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