Experimental Physiology (2007)DOI: 10.1113/expphysiol.2007.038851
Olivier Rouyer 1, Joffrey Zoll 1, Frederic Daussin 1, Christiane Damge 2, Pauline Helms 1, Samy Talha 1, Laurence Rasseneur 3, Francois Piquard 2, Bernard Geny 1*1 Physiologie et Explorations Fonctionnelles2 Institut de Physiologie3 STAPS
Since exercise capacity relates to the mitochondrial respiration rate in skeletal muscle and both parameters are potentially modulated by the onset of diabetes and by inhibition of the angiotensin-converting enzyme (ACE), we investigated whether skeletal muscle oxidative functions and exercise capacities are impaired in chronic streptozotocin-induced diabetic (STZ) rats and whether ACE inhibition could reverse such abnormalities. The ACE inhibitor perindopril (2mg/kg/day) was given for a period of 5 weeks to seven month old STZ rats (DIA-PE, n=8) whose hemodynamic, skeletal muscle mitochondrial function and exercise capacity were compared to that of untreated diabetic (DIA, n=8) and control (CONT, n=8) rats. Increased arterial blood pressureand reduced exercise capacitywere observed in DIA compared to CONT.The oxidative capacity of the gastrocnemius muscle was significantly reduced in DIA compared to CONT ratsMoreover, the coupling between oxidation and phosphorylation was significantly impaired in DIA . ACE inhibition (ACEi) normalized blood pressure without improving mitochondrial function but actually reduced exercise capacity to even lower levels.Exercise capacity correlated positively with blood pressure in DIA-PE
In experimental type 1 diabetic rats, both skeletal muscle mitochondrial respiration and exercise capacity are impaired. ACEi failed to restore the muscular function and worsened exercise capacity. Further studies will be useful to determine whether an inadequate muscular blood flow secondary to the mean systemic blood pressure reduction can explain these results.
(N.B/Reference of the picture: Essentials of Human Physiology by Thomas M. Nosek, Ph.D)
Olivier Rouyer 1, Joffrey Zoll 1, Frederic Daussin 1, Christiane Damge 2, Pauline Helms 1, Samy Talha 1, Laurence Rasseneur 3, Francois Piquard 2, Bernard Geny 1*1 Physiologie et Explorations Fonctionnelles2 Institut de Physiologie3 STAPS
Since exercise capacity relates to the mitochondrial respiration rate in skeletal muscle and both parameters are potentially modulated by the onset of diabetes and by inhibition of the angiotensin-converting enzyme (ACE), we investigated whether skeletal muscle oxidative functions and exercise capacities are impaired in chronic streptozotocin-induced diabetic (STZ) rats and whether ACE inhibition could reverse such abnormalities. The ACE inhibitor perindopril (2mg/kg/day) was given for a period of 5 weeks to seven month old STZ rats (DIA-PE, n=8) whose hemodynamic, skeletal muscle mitochondrial function and exercise capacity were compared to that of untreated diabetic (DIA, n=8) and control (CONT, n=8) rats. Increased arterial blood pressureand reduced exercise capacitywere observed in DIA compared to CONT.The oxidative capacity of the gastrocnemius muscle was significantly reduced in DIA compared to CONT ratsMoreover, the coupling between oxidation and phosphorylation was significantly impaired in DIA . ACE inhibition (ACEi) normalized blood pressure without improving mitochondrial function but actually reduced exercise capacity to even lower levels.Exercise capacity correlated positively with blood pressure in DIA-PE
In experimental type 1 diabetic rats, both skeletal muscle mitochondrial respiration and exercise capacity are impaired. ACEi failed to restore the muscular function and worsened exercise capacity. Further studies will be useful to determine whether an inadequate muscular blood flow secondary to the mean systemic blood pressure reduction can explain these results.
(N.B/Reference of the picture: Essentials of Human Physiology by Thomas M. Nosek, Ph.D)
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