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Cardiovascular Research 2007 75(2):369-380; doi:10.1016/j.cardiores.2007.04.015
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Copyright © 2007, European Society of Cardiology

Swim training sensitizes myocardial response to insulin: Role of Akt-dependent eNOS activation

Quan-Jiang Zhanga,1, Qiu-Xia Lia,1, Hai-Feng Zhanga, Kun-Ru Zhanga, Wen-Yi Guoa, Hai-Chang Wanga, Zhuan Zhoub, He-Ping Chengb, Jun Renc and Feng Gaoa,b,*

aDepartment of Physiology and Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi' an 710032, China
bInstitute of Molecular Medicine, Peking University, Beijing 100871, China
cCenter for Cardiovascular Research and Alternative Medicine and Division of Pharmaceutical Sciences, University of Wyoming, Laramie, WY 82071, USA

* Corresponding author. Department of Physiology and Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi' an 710032, China. Tel./fax: +86 29 84776423. fgao{at}fmmu.edu.cn

Objectives Physical activity has been well known to benefit heart function. The improved autonomic nervous activity is considered to be mainly responsible for this beneficial effect. However, the precise mechanism behind the intrinsic myocardial responsiveness to exercise is still unclear. This study was designed to examine the effect of swim training on myocardial response to insulin with a special focus on the endogenous endothelial nitric oxide synthase (eNOS)–nitric oxide (NO) cascade.

Methods Adult male Sprague–Dawley (SD) rats were subjected to a 10-week free-loading swim training (3 h/day, 5 days/week). Contractile response to insulin at the levels of cardiomyocytes and isolated perfused heart, myocardial glucose uptake and post-insulin receptor signaling cascades were evaluated.

Results Swim training enhanced cardiac contractile response to insulin in cardiomyocytes and isolated perfused heart, respectively. The improved cardiac response was accompanied by facilitated insulin-stimulated glucose uptake, GLUT4 translocation and upregulation of Akt and eNOS expression (p<0.01). Treatment with insulin resulted in a 3.6- and 2.2-fold increase of eNOS phosphorylation (p<0.01), as well as a 3.0- and 1.9-fold increase of Akt phosphorylation in exercise and sedentary groups, respectively (p<0.01). In addition, exercise significantly facilitated insulin-induced myocardial NO production (p<0.01 vs. sedentary). Moreover, pretreatment with either LY294002, a phosphatidylinositol-3 kinase (PI-3K) inhibitor or L-NAME, a NOS inhibitor, abolished the exercise-induced sensitization of myocardial contractile response to insulin, insulin-induced NO production and phosphorylation of Akt and eNOS.

Conclusion These results demonstrate that swim training is capable of sensitizing myocardial contractile response to insulin via upregulation of Akt- and eNOS signaling cascades.

KEYWORDS Swim training; Myocardial contraction; Insulin; Nitric oxide

1 These two authors contributed equally to this work.


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