Influence of age and moderate-intensity exercise training on heart rate variability in young and mature adults.

The purpose of this study was to examine the influence of age and moderate-intensity exercise training on heart rate variability (HRV), and to elucidate further the mechanism of training-induced bradycardia and cardioprotection. Electrocardiograms were recorded from 12 young (18-24 yrs) and 12 mature (29-43 yrs) individuals during supine rest and submaximal moderate exercise. Recordings were obtained prior to, midway, and following 16 weeks of aerobic exercise training designed to improve cardiorespiratory fitness and health. Training resulted in augmented estimated VO2max and bradycardia during rest and submaximal exercise. Total and low frequency components of HRV during exercise were significantly increased for the mature subjects following training whereas other measures of HRV were not significantly changed for either group. It was concluded that training of moderate intensity was insufficient to induce changes in the autonomic control of heart rate for young to mature subjects. The lack of significant HRV changes may suggest the existence of a vagal critical point, below which training-induced increases in vagal modulation may be forthcoming, and above which changes in vagal modulation may be negligible. Training-induced bradycardia and the cardioprotective effect of regular aerobic exercise may result from factors other than an increased vagal modulation.

Heart rate variability and endogenous sex hormones during the menstrual cycle in young women.

To our knowledge, the relationship between all four endogenous female sex hormones and resting cardiac autonomic function has not been studied. The aim of the current study was to examine the association between the normal endogenous levels of oestrogen (17beta-oestradiol), progesterone, luteinising hormone and follicle-stimulating hormone and heart rate variability (HRV) during the menstrual cycle in young eumenorrheic women. Ten healthy, young, female subjects volunteered for this study. HRV and endogenous hormone levels were recorded at three phases of the menstrual cycle: menses (day 3.8 +/- 0.5), ovulation (day 15.8 +/- 0.7) and luteal (day 22.1 +/- 0.4) to ensure HRV recordings at times of low (menses) and high (ovulation and luteal) hormonal influence. Heart rate recordings were obtained from supine resting subjects and analysed on a Holter analysis system. Total power (TP, 0-1.0 Hz), low frequency (LF, 0.041-0.15 Hz), high frequency (HF, 0.15-0.80 Hz) and LF/HF components of HRV were examined. Despite a significantly greater HR at ovulation and normal cyclic variations in all endogenous sex hormone levels, no measure of HRV was significantly different between menstrual cycle phases. Significant correlations between oestrogen levels and absolute measures of HRV at ovulation were identified. The results of the current study demonstrated that the normal cyclic variations in endogenous sex hormone levels during the menstrual cycle were not significantly associated with changes in cardiac autonomic control as measured by HRV. Significant correlation between peak oestrogen levels and HRV measures at ovulation provided further support for the reported cardioprotective effects of oestrogen in healthy females.

Influence of intensive cycling training on heart rate variability during rest and exercise.

The current study examined whether changes in heart rate variability (HRV) following intensive cycling training contribute to the mechanism of training-induced bradycardia. Thirteen healthy untrained subjects, ages 18-27 years, underwent recordings of heart rate (HR) and VO2max before and after 8 weeks of cycling, 25-60 min/day, 5 days/week at > 80% maximum HR (HRmax). Heart rate recordings were obtained during supine rest and submaximal exercise and were analysed for the following components of HRV: low frequency (LF, 0.041-0.15 Hz); high frequency (HF, 0.15-0.40 Hz); LF/HF ratio and total power (TP, 0-0.40 Hz). At posttraining, VO2max was significantly increased while HR was significantly reduced at rest and all absolute exercise work rates. Training-induced lower HR was accompanied by significantly greater HF and TP during rest as well as LF, HF, and TP during all absolute exercise work rates. Posttraining HR and the majority of HRV measures were similar to pretraining values at the same relative exercise intensity (% HRmax). These results indicated that 8 weeks of intensive cycling training increased HRV and cardiac vagal modulation during rest and absolute exercise work rates but had little effect during relative exercise work rates. Increased vagal modulation resulting from intensive exercise training may contribute to the mechanism of training-induced bradycardia.