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Intense exercise training induces adaptation in expression and responsiveness of cardiac β-adrenoceptors in diabetic rats.

Lahaye Sle D, Gratas-Delamarche A, Malardé L, Vincent S, Zguira MS, Morel SL, Delamarche P, Zouhal H, Carré F, Bekono FR - Cardiovasc Diabetol (2010)

Bottom Line: It did not blunt the diabetes-induced decrease of β1-adrenoceptors protein expression, displayed a significant decrease in the β2-adrenoceptors protein expression and normalized the β3-adrenoceptors protein expression.This defect stems principally from the β2-adrenoceptors protein expression reduction.Thus, these results demonstrate that intense exercise training induces specific effects on the β-adrenergic system in diabetes.

View Article: PubMed Central - HTML - PubMed

Affiliation: Laboratory Movement Sport and health Sciences, UFR APS, University of Rennes 2, Rennes, France. soleneledouairon@gmail.com

ABSTRACT

Background: Informations about the effects of intense exercise training on diabetes-induced myocardial dysfunctions are lacking. We have examined the effects of intense exercise training on the cardiac function of diabetic rats, especially focusing on the Langendorff β-adrenergic responsiveness and on the β-adrenoceptors protein expression.

Methods: Control or Streptozotocin induced-diabetic male Wistar rats were randomly assigned to sedentary or trained groups. The training program consisted of 8 weeks running on a treadmill (10° incline, up to 25 m/min, 60 min/day) and was considered to be intense for diabetic rats.

Results: This intense exercise training amplified the in vivo diabetes-induced bradycardia. It had no effect on Langendorff basal cardiac contraction and relaxation performances in control and diabetic rats. In diabetic rats, it accentuated the Langendorff reduced responsiveness to β-adrenergic stimulation. It did not blunt the diabetes-induced decrease of β1-adrenoceptors protein expression, displayed a significant decrease in the β2-adrenoceptors protein expression and normalized the β3-adrenoceptors protein expression.

Conclusions: Intense exercise training accentuated the decrease in the myocardial responsiveness to β-adrenergic stimulation induced by diabetes. This defect stems principally from the β2-adrenoceptors protein expression reduction. Thus, these results demonstrate that intense exercise training induces specific effects on the β-adrenergic system in diabetes.

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Effect of intense exercise training on myocardial basal function and responsiveness to isoproterenol stimulation. Isoproterenol was infused to isolated hearts of sedentary control (n = 13), trained control (n = 7), sedentary diabetic (n = 11) and trained diabetic (n = 7) rats in ascending concentrations ranging from 1.10-8 to 1.10-5 M. In trained control rats, 1.10-6 and 1.10-5 M isoproterenol doses were not tested for technical reason. Data are presented as mean ± SEM. *= significantly different from sedentary controls (p <0.05), † = significantly different from trained controls (p <0.05), ‡ = significantly different from sedentary diabetics (p <0.05).
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Figure 1: Effect of intense exercise training on myocardial basal function and responsiveness to isoproterenol stimulation. Isoproterenol was infused to isolated hearts of sedentary control (n = 13), trained control (n = 7), sedentary diabetic (n = 11) and trained diabetic (n = 7) rats in ascending concentrations ranging from 1.10-8 to 1.10-5 M. In trained control rats, 1.10-6 and 1.10-5 M isoproterenol doses were not tested for technical reason. Data are presented as mean ± SEM. *= significantly different from sedentary controls (p <0.05), † = significantly different from trained controls (p <0.05), ‡ = significantly different from sedentary diabetics (p <0.05).

Mentions: Intrinsic heart rate - Diabetes also induced an intrinsic bradycardia. Intrinsic HR was ≈ 50 bpm lower in sedentary diabetic rats than in sedentary control rats (p <0.05) (Figure 1A). Exercise training had no significant effect on the intrinsic diabetic bradycardia. Similarly, no significant effect of exercise training was observed in intrinsic HR of control rats.


Intense exercise training induces adaptation in expression and responsiveness of cardiac β-adrenoceptors in diabetic rats.

Lahaye Sle D, Gratas-Delamarche A, Malardé L, Vincent S, Zguira MS, Morel SL, Delamarche P, Zouhal H, Carré F, Bekono FR - Cardiovasc Diabetol (2010)

Effect of intense exercise training on myocardial basal function and responsiveness to isoproterenol stimulation. Isoproterenol was infused to isolated hearts of sedentary control (n = 13), trained control (n = 7), sedentary diabetic (n = 11) and trained diabetic (n = 7) rats in ascending concentrations ranging from 1.10-8 to 1.10-5 M. In trained control rats, 1.10-6 and 1.10-5 M isoproterenol doses were not tested for technical reason. Data are presented as mean ± SEM. *= significantly different from sedentary controls (p <0.05), † = significantly different from trained controls (p <0.05), ‡ = significantly different from sedentary diabetics (p <0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2992048&req=5

Figure 1: Effect of intense exercise training on myocardial basal function and responsiveness to isoproterenol stimulation. Isoproterenol was infused to isolated hearts of sedentary control (n = 13), trained control (n = 7), sedentary diabetic (n = 11) and trained diabetic (n = 7) rats in ascending concentrations ranging from 1.10-8 to 1.10-5 M. In trained control rats, 1.10-6 and 1.10-5 M isoproterenol doses were not tested for technical reason. Data are presented as mean ± SEM. *= significantly different from sedentary controls (p <0.05), † = significantly different from trained controls (p <0.05), ‡ = significantly different from sedentary diabetics (p <0.05).
Mentions: Intrinsic heart rate - Diabetes also induced an intrinsic bradycardia. Intrinsic HR was ≈ 50 bpm lower in sedentary diabetic rats than in sedentary control rats (p <0.05) (Figure 1A). Exercise training had no significant effect on the intrinsic diabetic bradycardia. Similarly, no significant effect of exercise training was observed in intrinsic HR of control rats.

Bottom Line: It did not blunt the diabetes-induced decrease of β1-adrenoceptors protein expression, displayed a significant decrease in the β2-adrenoceptors protein expression and normalized the β3-adrenoceptors protein expression.This defect stems principally from the β2-adrenoceptors protein expression reduction.Thus, these results demonstrate that intense exercise training induces specific effects on the β-adrenergic system in diabetes.

View Article: PubMed Central - HTML - PubMed

Affiliation: Laboratory Movement Sport and health Sciences, UFR APS, University of Rennes 2, Rennes, France. soleneledouairon@gmail.com

ABSTRACT

Background: Informations about the effects of intense exercise training on diabetes-induced myocardial dysfunctions are lacking. We have examined the effects of intense exercise training on the cardiac function of diabetic rats, especially focusing on the Langendorff β-adrenergic responsiveness and on the β-adrenoceptors protein expression.

Methods: Control or Streptozotocin induced-diabetic male Wistar rats were randomly assigned to sedentary or trained groups. The training program consisted of 8 weeks running on a treadmill (10° incline, up to 25 m/min, 60 min/day) and was considered to be intense for diabetic rats.

Results: This intense exercise training amplified the in vivo diabetes-induced bradycardia. It had no effect on Langendorff basal cardiac contraction and relaxation performances in control and diabetic rats. In diabetic rats, it accentuated the Langendorff reduced responsiveness to β-adrenergic stimulation. It did not blunt the diabetes-induced decrease of β1-adrenoceptors protein expression, displayed a significant decrease in the β2-adrenoceptors protein expression and normalized the β3-adrenoceptors protein expression.

Conclusions: Intense exercise training accentuated the decrease in the myocardial responsiveness to β-adrenergic stimulation induced by diabetes. This defect stems principally from the β2-adrenoceptors protein expression reduction. Thus, these results demonstrate that intense exercise training induces specific effects on the β-adrenergic system in diabetes.

Show MeSH
Related in: MedlinePlus