Premium
Exercise training induced bradycardia: evidence for enhanced parasympathetic regulation without changes in “intrinsic” sino‐atrial node function (881.5)
Author(s) -
Billman George,
Cagnoli Kristen,
Fedorov Vadim
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.881.5
Subject(s) - bradycardia , atropine , heart rate , medicine , heart rate variability , cardiology , propranolol , autonomic nervous system , parasympathetic nervous system , anesthesia , blood pressure
Although bradycardia is a well‐established consequence of endurance exercise training, the mechanisms responsible for this reduction in baseline heart rate (HR) remain controversial. Therefore, changes in cardiac autonomic regulation and intrinsic sino‐atrial nodal (SAN) rate were evaluated using mixed‐breed dogs randomly assigned to either a 10‐wk exercise training (ET, n = 15) or an equivalent sedentary period (SP, n = 10). Intrinsic HR was revealed by combined autonomic neural blockade (propranolol HCl, 1.0 mg/kg + atropine sulfate, 50 ug/kg, i.v.) before and after completion of the 10‐wk study. At the end of the study, SAN function was further evaluated by examining the SAN recovery time (SNRT) following rapid atrial pacing (1 min at 3.3 ‐ 10Hz). As expected, baseline HR decreased and heart rate variability [HRV, indices of cardiac vagal tone ‐ as measured by the high frequency component of R‐R variability (HF) and R‐R interval standard deviation (SD)] increased in the ET (HR pre 113.4 ± 3.9, post 105.2 ± 3.9 beats/min; HF pre 7.0 ± 0.2, post 8.2 ± 0.2 ln ms 2 ; SD pre 57.8 ± 100.5 ± 9.2 ms) but not in the SP group (HR pre 113.0 ± 10.3, post 122.4 ± 5.4 beats/min; HF pre 7.4 ± 0.5, post 7.0 ± 0.6 ln ms 2 ; SD pre 62.2 ± 9.9, post 63.6 ± 7.3 ms). Atropine induced significantly (ANOVA, P <0.01) greater reductions in HRV in the ET (HF pre ‐6.9 ± 0.3. post ‐7.6 ln ms 2 ; SD, pre ‐50.0 ± 3.7, post ‐90.6 ± 9.7 ms) as compared to the SP (HF ‐7.1 ± 0.5, post ‐6.6 ± 0.5 ln ms2; SD pre ‐66.0 ± 11.3, post ‐59.2 ± 6.8 ms) group. In contrast, neither intrinsic HR (e.g., ET pre 141.2 ± 6.7, post 146.0 ± 8.0; SP pre 149.8 ± 8.9, Post 150.0 ± 12.6 beats/min) nor SNRT (HR corrected) differed in the ET and SP groups. These data suggest that endurance exercise training induced changes in baseline HR result from an enhanced cardiac parasympathetic regulation and not from changes in the intrinsic function of the sino‐atrial node.