Cardiovascular response to prescribed detraining among recreational athletes.

Exercise-induced cardiac remodeling (EICR) and the attendant myocardial adaptations characteristic of the athlete's heart may regress during periods of exercise reduction or abstinence. The time course and mechanisms underlying this reverse remodeling, specifically the impact of concomitant plasma volume (PV) contraction on cardiac chamber size, remain incompletely understood. We therefore studied recreational runners (n=21, aged 34 ± 7 years; 48% male) who completed an 18-week training program (~7 h.w^-1) culminating in the 2016 Boston Marathon after which total exercise exposure was confined to <2 h.w^-1 (no single session >1 hour) for 8 weeks. Cardiac structure and function, exercise capacity, and PV were assessed at peak fitness (10-14 days before) and at 4- and 8-weeks post marathon. Mixed linear modeling adjusting for age, sex, VO_2peak and marathon finish time was used to compare data across time points. Physiologic detraining was evidenced by serial reductions in treadmill performance. Two distinct phases of myocardial remodeling and hematologic adaptation were observed. After 4 weeks of detraining, there were significant reductions in PV ( -6.0%, P<0.01), left ventricular (LV) wall thickness ( -8.1%, <0.05), LV mass ( -10.3%, P<0.001), and right atrial area ( -8.2%, P<0.001). After 8 weeks of detraining, there was a significant reduction in right ventricle chamber size (end-diastolic area = -8.0%, P <0.05) without further concomitant reductions in PV or LV wall thickness. Abrupt reductions in exercise training stimulus result in a structure-specific time course of reverse cardiac remodeling that occurs largely independently of PV contraction.

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