A 10- to 12-week exercise training program in dogs reduced baseline heart rate and increased heart rate variability through enhanced cardiac parasympathetic regulation, without altering intrinsic sinoatrial node function.
RCT (n=25)
Randomly assigned
No
Does exercise training reduce baseline heart rate through enhanced parasympathetic regulation or changes in intrinsic sinoatrial node function in a large-animal model?
In a large-animal model, training bradycardia results from enhanced cardiac parasympathetic regulation rather than changes in intrinsic properties of the sinoatrial node.
Absolute Event Rate: 104.3% vs 116.6%
p-value: p=<0.05
The mechanisms responsible for exercise-induced reductions in baseline heart rate (HR), known as training bradycardia, remain controversial. Therefore, changes in cardiac autonomic regulation and intrinsic sinoatrial nodal (SAN) rate were evaluated using dogs randomly assigned to either a 10- to 12-wk exercise training (Ex, n = 15) or an equivalent sedentary period (Sed, n = 10). Intrinsic HR was revealed by combined autonomic nervous system (ANS) blockade (propranolol + atropine, iv) before and after completion of the study. At the end of the study, SAN function was further evaluated by examining the SAN recovery time (SNRT) following rapid atrial pacing and the response to adenosine in anesthetized animals. As expected, both the response to submaximal exercise and baseline HR significantly (P < 0.01) decreased, and heart rate variability (HRV; e.g., high-frequency R-R interval variability) significantly (P < 0.01) increased in the Ex group but did not change in the Sed group. Atropine also induced significantly (P < 0.01) greater reductions in HRV in the Ex group compared with the Sed group; propranolol elicited similar HR and HRV changes in both groups. In contrast, neither intrinsic HR (Ex before, 141.2 ± 6.7; Ex after, 146.0 ± 8.0 vs. Sed before, 143.3 ± 11.1; Sed after, 141.0 ± 11.3 beats per minute), the response to adenosine, corrected SNRT, nor atrial fibrosis and atrial fibrillation inducibility differed in the Ex group vs. the Sed group. These data suggest that in a large-animal model, training bradycardia results from an enhanced cardiac parasympathetic regulation and not from changes in intrinsic properties of the SAN.
Billman et al. (Fri,) conducted a rct in Healthy (Exercise training-induced bradycardia model) (n=25). Exercise training (treadmill running) vs. Sedentary (placed in a transport cage for equivalent time periods) was evaluated on Baseline heart rate (beats/min) (p=<0.05). A 10- to 12-week exercise training program in dogs reduced baseline heart rate and increased heart rate variability through enhanced cardiac parasympathetic regulation, without altering intrinsic sinoatrial node function.