Purpose: The objective of this study is to investigate the time course of autonomic tone changes after a first-time endurance running race participation and associations with postexertional high-sensitivity troponin (hsTnT) levels in middle-aged males.
Methods: Male (n = 42) first-time long-distance running race (Lidingöloppet 30 km) participants ≥45 yr (50.5 ± 5) were examined. HR and HR variability (HRV) in the time domain (SDANN) was measured continuously from 2 d before to 4 d after the race using a wireless cardiovascular monitor that also recorded arrhythmia episodes. In addition, subjects were assessed pre- and postrace by medical history and physical examination, 12-lead ECG, blood tests including hsTnT, and echocardiography.
Results: Compared with corresponding prerace values, nighttime (2:00–4:00 a.m.) HR was significantly elevated (63.6 ± 9.4 vs 53.9 ± 8.3 bpm, P < 0.001) on the first night postrace, whereas HRV remained reduced for a median of 64 h (interquartile range, 51–102 h). A prolonged HR recovery period (r = 0.48, P = 0.005) and a larger reduction in postrace HRV (r = −0.49, P = 0.003) correlated with higher postrace hsTnT levels. The association between reduced HRV and higher hsTnT remained significant after multivariate analysis (β = −0.48, P = 0.01). No sustained ventricular arrhythmias were recorded, but atrial fibrillation occurred in two subjects.
Conclusion: Endurance running race participation caused a prolonged alteration of autonomic tone. More marked and prolonged changes were associated with higher levels of hsTnT, suggesting that the magnitude of troponin increase after strenuous exercise may reflect the magnitude of exercise-induced cardiovascular stress.
1Department of Cardiology, Karolinska Institutet, Karolinska University Hospital, Stockholm, SWEDEN; 2Department of Medicine, Montefiore Medical Center, The University Hospital of Albert Einstein School of Medicine, Bronx, NY; and 3Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, SWEDEN
Address for correspondence: Philip Aagaard, MD, PhD, Department of Medicine Cardiology N3:05, Karolinska University Hospital, 171 76 Stockholm; Sweden; E-mail: firstname.lastname@example.org.
Submitted for publication August 2013.
Accepted for publication December 2013.