The Calcineurin Antagonist, RCAN1-4 is Induced by Exhaustive Exercise in Rat Skeletal Muscle

International audienceThe aim of this work was to study the regulation of the calcineurin antagonist regulator of calcineurin 1 (RCAN1) in rat skeletal muscles after exhaustive physical exercise, which is a physiological modulator of oxidative stress. Three skeletal muscles, namely extensor digitorum longus (EDL), gastrocnemius, and soleus, were investigated. Exhaustive exercise increased RCAN1-4 protein levels in EDL and gastrocnemius, but not in soleus. Protein oxidation as an index of oxidative stress was increased in EDL and gastrocnemius, but remained unchanged in soleus. However, lipid peroxidation was increased in all three muscles. CuZnSOD and catalase protein levels were increased at 3 h postexercise in soleus, whereas they remained unchanged in EDL and gastrocnemius. Calcineurin enzymatic activity declined in EDL and gastrocnemius but not in soleus, and its protein expression was decreased in all three muscles. The level of PGC1-α protein remained unchanged, whereas the protein expression of the transcription factor NFATc4 was decreased in all three muscles. Adiponectin expression was increased in all three muscles. RCAN1-4 expression in EDL and gastrocnemius muscles was augmented by the oxidative stress generated from exhaustive exercise. We propose that increased RCAN1-4 expression and the signal transduction pathways it regulates represent important components of the physiological adaptation to exercise-induced oxidative stress

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

<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>This intense exercise training amplified the <it>in vivo </it>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.</p> <p>Conclusions</p> <p>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.</p

La sédentarité au coeur des maladies sociétales.

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Inactivité physique et risque cardiovasculaire du diabète.

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Femmes et sports d'ultra-endurance : impact sur la fonction de reproduction et la fonction endothéliale.

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Antioxidant supplementation: more harm than good for exercise performance? Nutritional implications.

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Physiologie du sport et de l'exercice. Version française de l'ouvrage américain "Physiology of sport and exercice"

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Physical inactivity and insulin resistance- Role of oxidative stress

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Implication du stress oxydant dans la physiopathologie des maladies chroniques : intérêts de l'entrainement.

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