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Autonomic dysfunction decreases within-subject correlation between R-R interval length (RRi) and vagally mediated RRi variability in cardiac disease. We tested the hypothesis that overtraining syndrome (OTS) may also weaken this relationship. Nine OTS and 10 control endurance athletes underwent 24-h electrocardiogram monitoring, which was repeated in eight OTS and nine control athletes after 6 months, when two OTS athletes still had symptoms of OTS. The power of high-frequency (HF) oscillations of RRi was analyzed in 5-min epochs over the whole recording. Quadratic regression was performed between 5-min values of RRi and log-transformed (ln) HF to obtain R(2) for each recording. The relationship between RRi and HFln was higher in the OTS athletes than controls [R(2): 0.87 (90% confidence interval, CI: 0.84-0.89) vs 0.78 (90% CI: 0.72-0.84); P = 0.034; effect size = 1.22]. Large decrease in R(2) was observed in six recovered OTS athletes after 6 months follow-up [ΔR(2): -0.12 (90% CI: -0.25-0.01); P = 0.11; effect size = 1.44] with no changes in the controls. Mean values of RRi and its variability did not differ between the groups. The within-subject correlation between RRi and vagally mediated RRi variability was stronger in endurance athletes with OTS compared with controls. The present findings may improve the detection of OTS and recovery from OTS in endurance athletes., (© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Our aim was to estimate causal relationships of genetic factors and different specific environmental factors in determination of the level of cardiac autonomic modulation, i.e., heart rate variability (HRV), in healthy male twins and male twins with chronic diseases. The subjects were 208 monozygotic (MZ, 104 healthy) and 296 dizygotic (DZ, 173 healthy) male twins. A structured interview was used to obtain data on lifetime exposures of occupational loading, regularly performed leisure-time sport activities, coffee consumption, smoking history, and chronic diseases from 12 yr of age through the present. A 5-min ECG at supine rest was recorded for the HRV analyses. In univariate statistical analyses based on genetic models with additive genetic, dominance genetic, and unique environmental effects, genetic effects accounted for 31-57% of HRV variance. In multivariate statistical analysis, body mass index, percent body fat, coffee consumption, smoking, medication, and chronic diseases were associated with different HRV variables, accounting for 1-11% of their variance. Occupational physical loading and leisure-time sport activities did not account for variation in any HRV variable. However, in the subgroup analysis of healthy and diseased twins, occupational loading explained 4% of the variability in heart periods. Otherwise, the interaction between health status and genetic effects was significant for only two HRV variables. In conclusion, genetic factors accounted for a major portion of the interindividual differences in HRV, with no remarkable effect of health status. No single behavioral determinant appeared to have a major influence on HRV. The effects of medication and diseases may mask the minimal effect of occupational loading on HRV.

We studied the effect of regular physical activity on cardiac and vascular autonomic modulation during a 5-yr controlled randomized training intervention in a representative sample of older Finnish men. Heart rate variability (HRV) and blood pressure variability (BPV) are markers of cardiac and vascular health, reflecting cardiac and vascular autonomic modulation. One hundred and forty randomly selected 53- to 63-yr-old men were randomized into two identical groups: an intervention (EX) group and a reference (CO) group, of which 89 men remained until the final analysis (EX: n = 47; CO: n = 42). The EX group trained for 30-60 min three to five times a week with an intensity of 40-60% of maximal oxygen consumption. The mean weekly energy expenditure of the training program for the 5-yr training period was 3.80 MJ, and 71% of the EX group exceeded the mean. The EX group had a significantly (P < 0.01) higher oxygen consumption at ventilatory aerobic threshold (VO2VT) than the CO group at the 5-yr time point. VO2VT had a tendency to increase in the EX group and decrease in the CO group (interaction P < 0.001) from the baseline to the 5-yr time point. Peak performance did not change. Low-frequency power of R-R interval variability decreased in the EX group (P < 0.01, by 6%) from the baseline to the 5-yr time point. BPV did not change. In conclusion, low-intensity regular exercise training did not prevent HRV from decreasing or change BPV in 5 yr in older Finnish men.

Purpose: To study the influences of a 1-year controlled, randomized endurance exercise training period on heart rate (HR) and blood pressure variability in a representative sample of Finnish men in their late middle age., Methods and Results: Subjects were 140 sedentary men aged 53-63 years. The men were randomized into two identical groups: an intervention (EX) and a reference (CO) group. One hundred and twelve of them remained in the final analysis (EX: n=59, CO: n=53). EX trained for 30-60 min three to five times a week with the intensity of 40-60% of maximal oxygen consumption. In EX, 1 year of regular exercise training increased oxygen consumption at respiratory compensation threshold by 11% (P < or = 0.001) in a maximal cardiorespiratory test. Total power and very low frequency power of R-R interval variability (ms2) tended to increase in the EX group by 26 and 42% and to decrease in the CO group by 13 and 10% (interaction P<0.05 and P<0.01), respectively. There were no significant changes in blood pressure variability., Conclusion: Regular low- to moderate-intensity exercise training could retard the declining tendency in cardiac autonomic nervous function in older men during 1 year.

We investigated heavy training- and overtraining-induced changes in heart rate and blood pressure variability during supine rest and in response to head-up tilt in female endurance athletes. Nine young female experimental athletes (ETG) increased their training volume at the intensity of 70-90% of maximal oxygen uptake (VO2max) by 125% and training volume at the intensity of < 70% of VO2max by 100% during 6-9 weeks. The corresponding increases in 6 female control athletes were 5% and 10%. The VO2max of the ETG and the control athletes did not change, but it decreased from 53.0 +/- 2.2 ml x kg(-1) x min(-1) to 50.2 +/- 2.3 ml x kg(-1) x min(-1) (mean+/-SEM, p < 0.01) in five overtrained experimental athletes. In the ETG, low-frequency power of R-R interval (RRI) variability during supine rest increased from 6 +/- 1 ms2 x 10(2) to 9 +/- 2 ms2 x 10(2) (p < 0.05). The 30/15 index (= RRI(max 30)/RRI(min 15), where RRI(max 30) denotes the longest RRI close to the 30th RRI and RRI(min 15) denotes the shortest RRI close to the 15th RRI after assuming upright position in the head-up tilt test), decreased as a result of training (analysis of variance, p = 0.05). In the ETG, changes in VO2max were related to the changes in total power of RRI variability during standing (r = 0.74, p < 0.05). Heart rate response to prolonged standing after head-up tilt was either accentuated or attenuated in the overtrained athletes as compared to the normal training state. We conclude that heavy training could increase cardiac sympathetic modulation during supine rest and attenuated biphasic baroreflex-mediated response appearing just after shifting to an upright position. Heavy-training-/overtraining-induced decrease in maximal aerobic power was related to decreased heart rate variability during standing. Physiological responses to overtraining were individual.

We investigated the effects of progressively increased training load and overtraining on resting and intrinsic heart rate (IHR) and cardiac autonomic modulation (CAM), and their relationships to performance variables. Nine athletes (ETG) increased training volume at 70-90% of maximal oxygen uptake (VO2max) by 130% (p<0.01) and training volume at <70% VO2max by 100% (p < 0.01) during 6-9 weeks. The corresponding increases in six female control athletes (CG) were 5 and 10%. Pharmacological blocking through atropine and propranolol and the Rosenblueth and Simeone model were used to calculate the sympathovagal balance index (Abal) and to measure IHR. The results were analysed using two-way analysis of variance. VO2max, IHR and Abal did not change. Resting heart rate had a tendency to decrease in the ETG and increase in the CG during the training period (interaction p < 0.01). Five ETG athletes demonstrated overtraining state (OA subgroup). Their VO2max (mean+/-SEM) decreased from 53.0+/-2.2 ml x kg(-1) x min(-1) to 50.2+/-2.3 ml x kg(-1) x min(-1) (p < 0.01), but no changes in resting HR, IHR and Abal were found. A significant correlation between the baseline values of VO2max and the parasympathetic activity index was found (r=-0.59, p < 0.05). In conclusion, progressively increased training load and overtraining did not induce significant changes in intrinsic heart rate or cardiac autonomic modulation in female endurance athletes. Resting heart rate rather decreased with heavy endurance training and overtraining. High maximal oxygen uptake was correlated with high cardiac parasympathetic modulation.

We examined how the time and frequency domain measures of heart rate and blood pressure variability at supine rest reflect the sympathovagal balance of 23 female and male endurance athletes. Pharmacological blocking by atropine and propranolol was used as a standard for defining autonomic control of the heart. The Rosenblueth and Simeone model for neural control of heart rate was used to calculate the sympathovagal balance index (Abal). Atropinization significantly decreased all time and frequency domain measures of heart rate and blood pressure variability. beta-Blockade significantly decreased further the low- (< 0.07 Hz) and medium-frequency power (0.07-0.15 Hz) variability of R-R intervals (RRI) and SD of RRI. Abal was 0.629 +/- 0.019, indicating that parasympathetic activity predominated in the athletes. Basal heart rate (r = 0.519, P < 0.01), SD of RRI (r = -0.533, P < 0.01), root-mean-square of successive RRIs (RRI RMSSD) (r = -0.579, P < 0.05), RRI total (r = -0.557, P < 0.01) and RRI high-frequency (HF) power (r = -0.582, P < 0.01) correlated significantly with Abal and parasympathetic activity index. We concluded that the best non-invasive method of evaluating the sympathovagal balance of athletes at supine rest is to measure SD of RRI, RRI RMSSD, HF and total power of RRI variability. All heart rate variability measures were mainly parasympathetically modulated. The nature of blood pressure variability measures remained unclear and they could not be used to evaluate the sympathovagal balance among athletes.