Point:Counterpoint.

[Extract] TO THE EDITOR: In the recent Point:Counterpoint debate (2, 3), both research groups argued that training-induced bradycardia was a result of changes in intrinsic, sinoatrial node firing (i.e., intrinsic rate) or cardiac autonomic/parasympathetic regulation. While Billman (2) stated the possibility of a combination of these mechanisms, no further discussion of this was provided by either research group. Rather, the discussion focused on either mechanism and we would urge researchers to consider a more complex scenario – contribution of either mechanism that is moderated by other factors, or both mechanisms, potentially in combination with other elements (e.g., cardiac tructural changes). For example, training-induced bradycardia was reported in young adults with no changes in heart rate variability (HRV)(4), supporting an intrinsic rate mechanism. However, bradycardia was induced similarly with enhanced HRV in young adults following high-intensity exercise, supporting a cardiac autonomic mechanism (5).