Cardiac adaptations from 4 weeks of intensity‐controlled vigorous exercise are lost after a similar period of detraining

Intensity‐controlled (relative to VO 2max ) treadmill exercise training in adult rats results in the activation and ensuing differentiation of endogenous c‐kit pos cardiac stem/progenitor cells ( eCSC s) into newly formed cardiomyocytes and capillaries. Whether these training‐induced adaptations persist following detraining is undetermined. Twelve male Wistar rats (~230 g) were exercised at 80–85% of their VO 2max for 30 min day −1 , 4 days week −1 for 4 weeks ( TR ; n  = 6), followed by 4 weeks of detraining ( DTR ; n  = 6). Twelve untrained rats acted as controls ( CTRL ). Exercise training significantly enhanced VO 2max (11.34 mL kg −1  min −1 ) and wet heart weight (29%) above CTRL ( P  < 0.05). Echocardiography revealed that exercise training increased LV mass (~32%), posterior and septal wall thickness (~15%), ejection fraction and fractional shortening (~10%) compared to CTRL ( P  < 0.05). Cardiomyocyte diameter (17.9 ± 0.1  μ m vs. 14.9 ± 0.6  μ m), newly formed (BrdU pos /Ki67 pos ) cardiomyocytes (7.2 ± 1.3%/1.9 ± 0.7% vs. 0.2 ± 0.1%/0.1 ± 0.1%), total cardiomyocyte number (45.6 ± 0.6 × 10 6 vs. 42.5 ± 0.4 × 10 6 ), c‐kit pos eCSC number (884 ± 112 per 10 6 cardiomyocytes vs. 482 ± 132 per 10 6 cardiomyocytes), and capillary density (4123 ± 227 per mm 2 vs. 2117 ± 118 per mm 2 ) were significantly greater in the LV of trained animals ( P  < 0.05) than CTRL . Detraining removed the stimulus for c‐kit pos eCSC activation (640 ± 98 per 10 6 cardiomyocytes) and resultant cardiomyocyte hyperplasia (0.4 ± 0.3% BrdU pos /0.2 ± 0.2% Ki67 pos cardiomyocytes). Capillary density (3673 ± 374 per mm 2 ) and total myocyte number (44.7 ± 0.5 × 10 6 ) remained elevated following detraining, but cardiomyocyte hypertrophy (15.0 ± 0.4  μ m) was lost, resulting in a reduction of anatomical (wall thickness ~4%; LV mass ~10% and cardiac mass ~8%, above CTRL ) and functional ( EF & FS ~2% above CTRL ) parameters gained through exercise training. These findings demonstrate that cardiac adaptations, produced by 4 weeks of intensity‐controlled exercise training are lost after a similar period of detraining.