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

Physiological Reports

Cheryl D. Waring²  Beverley J. Henning²  Andrew J. Smith³  Bernardo Nadal-Ginard³  Daniele Torella¹ 

[1] Laboratory of Molecular and Cellular Cardiology, Department of Medical and Surgical Sciences, Magna Graecia University, Catanzaro, Italy;Stem Cell and Regenerative Biology Unit (BioStem), Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK;Centre of Human & Aerospace Physiological Sciences and Centre for Stem Cells & Regenerative Medicine, Faculty of Medicine & Life Sciences, King's College London, London, UK

关键词: Cardiac stem/progenitor cells;    detraining;    physiological remodeling;   

DOI  :  10.14814/phy2.12302

来源: Wiley

【 摘 要 】

Abstract

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 (eCSCs) 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 μm vs. 14.9 ± 0.6 μm), 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 × 10⁶ vs. 42.5 ± 0.4 × 10⁶), c-kit^pos eCSC number (884 ± 112 per 10⁶ cardiomyocytes vs. 482 ± 132 per 10⁶ cardiomyocytes), and capillary density (4123 ± 227 per mm² vs. 2117 ± 118 per mm²) 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 10⁶ cardiomyocytes) and resultant cardiomyocyte hyperplasia (0.4 ± 0.3% BrdU^pos/0.2 ± 0.2% Ki67^pos cardiomyocytes). Capillary density (3673 ± 374 per mm²) and total myocyte number (44.7 ± 0.5 × 10⁶) remained elevated following detraining, but cardiomyocyte hypertrophy (15.0 ± 0.4 μm) 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.

【 授权许可】

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© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

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