Also, the variability of heart rate has been shown to be dependent on the diastolic depolarization rate ( Wilders and Jongsma, 1993 Rocchetti et al., 2000). While a change in CANA will elicit changes in both heart rate and HRV, heart rate is also affected by other factors, namely intrinsic heart rate. Nevertheless, many studies have reported an increase in HRV parameters quantifying beat-to-beat variability and therefore suggested a causative role of CANA ( al-Ani et al., 1996 Levy et al., 1998 Iwasaki et al., 2003 Madden et al., 2006).Īn often neglected, but possibly important, role may be held by heart rate ( Sacha and Pluta, 2008 Monfredi et al., 2014 Kazmi et al., 2016). However, it should not be assumed that underlying mechanisms for chronic change in HRV are identical to those of acute change ( Mourot et al., 2004 Valenzano et al., 2016). These findings come from acute experiments conducted to assess how heart rate is controlled by the CANA using pharmacological blockades ( Pagani et al., 1986), direct neural stimulation ( Chess et al., 1975), or selective denervation in animal studies ( Chiou and Zipes, 1998). Especially, beat-to-beat variability of heart rate seems to be modulated by vagal activity ( Akselrod et al., 1985 Pomeranz et al., 1985 Pagani et al., 1986). Heart rate variability (HRV) is widely used as a marker of the cardiac autonomic nervous system activity (CANA). Based on current evidence, we discourage the use of HRV as a marker of CANA when measuring the effect of chronic exercise. Due to the intrinsic association between heart rate and HRV, conclusions based on HRV parameters do not necessarily reflect differences in CANA. These associations disappeared when controlling for heart rate and LVEDVI. HRV markers of vagal activity were moderately associated with exercise variables (standardized β = 0.28–0.40, all p < 0.01). Exercise was quantified by VO 2peak, training volume, and race performance.

Left ventricular end diastolic volume indexed to body surface area (LVEDVI) was assessed by transthoracic echocardiography and peak oxygen consumption (VO 2peak) by cardiopulmonary exercise testing.

R-R intervals were recorded by electrocardiography over 24 h. One-hundred-and-seventy-two runners (52 females and 120 males) ranging from novice runners with a first participation to an endurance event to highly trained runners, with up to 15 h of training per week, were included in the analysis. In a cross-sectional study in participants of a 10 mile race, we investigated the influence of endurance exercise on HRV parameters independently of heart size and heart rate. There is strong evidence from basic studies that lower heart rate in response to exercise training is caused by morphological and electrical remodeling of the heart. HRV is strongly associated with heart rate, which in turn, is associated with heart size. Changes in HRV with exercise training have often been interpreted as increases in vagal activity. Heart rate variability (HRV) is a widely used marker of cardiac autonomic nervous activity (CANA). University Clinic for Cardiology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.David Herzig * Babken Asatryan Nicolas Brugger Prisca Eser Matthias Wilhelm

Endurance training