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Key points OPA1 is a mitochondrial protein well known to play a fundamental role in the fusion of the inner membrane, in the organization of mitochondrial cristae and in apoptosis., Although the function of mitochondrial dynamics is becoming well understood, its impact on mitochondrial biogenesis is poorly studied, especially in differentiated adult tissues., Here we report a novel finding that in fast skeletal muscles OPA1 deletion impairs training-induced mitochondrial biogenesis., However, our data reveal that Opa1+/− skeletal muscles after training possess better exercise endurance capacity, obviously due to a modification of mitochondrial fatty acid utilization., Thus OPA1 deficiency induces a unique pattern of adaptation to endurance training in fast skeletal muscles., Abstract The role of OPA1, a GTPase dynamin protein mainly involved in the fusion of inner mitochondrial membranes, has been studied in many cell types, but only a few studies have been conducted on adult differentiated tissues such as cardiac or skeletal muscle cells. Yet OPA1 is highly expressed in these cells, and could play different roles, especially in response to an environmental stress like exercise. Endurance exercise increases energy demand in skeletal muscle and repeated activity induces mitochondrial biogenesis and activation of fusion-fission cycles for the synthesis of new mitochondria. But currently no study has clearly shown a link between mitochondrial dynamics and biogenesis. Using a mouse model of haploinsufficiency for the Opa1 gene ( Opa1+/−), we therefore studied the impact of OPA1 deficiency on the adaptation ability of fast skeletal muscles to endurance exercise training. Our results show that, surprisingly, Opa1+/− mice were able to perform the same physical activity as control mice. However, the adaptation strategies of both strains after training differed: while in control mice mitochondrial biogenesis was increased as expected, in Opa1+/− mice this process was blunted. Instead, training in Opa1+/− mice led to an increase in endurance capacity, and a specific adaptive response involving a metabolic remodelling towards enhanced fatty acid utilization. In conclusion, OPA1 appears necessary for the normal adaptive response and mitochondrial biogenesis of skeletal muscle to training. This work opens new perspectives on the role of mitochondrial dynamics in skeletal muscle cells and during adaptation to stress. [ABSTRACT FROM AUTHOR]

The author comments on a study published in a recent issue of the journal which examined whether resveratrol can improve physiological adaptations to physical training. Information on the beneficial effects of resveratrol is provided. According to the author, pharmacokinetic data showed that there is poor bioavailability of resveratrol. She points out the safety of resveratrol doses in humans. She questions the mechanism by which resveratrol mimics the effects of exercise.

An abstract of the article "Voluntary Physical Activity Alterations in Endothelial Nitric Oxide Synthase Knock-Out Mice," by I. Momken and colleagues, is presented.

An abstract of the article "Generalized Metabolic Myopathy in Pressure Overload-Induced Heart Failure: Is Circulating Angiotensin II Involved," by I. Momken and colleagues, is presented.

An abstract of the article "Role of Calcineurin in Chronic Hypoxia-Induced Hypertrophic Response of Right Ventricle" by N. Koulmann and colleagues is presented.

An abstract of the study "PGC-1alpha correlates with cardiac and skeletal muscle oxidative capacity in heart failure," by A. Garnier et al, is presented.

An abstract of the article "The Intrinsic Mitochondrial Oxidative Capacity of Human Failing Hearts Is Depressed and Relates to Disease Severity But Keeps Normal Regulatory Properties," by B. Mettauer and colleagues, is presented.

An abstract of the article "Effects of ACE Inhibition on Mitochondrial Substrates Utilization Pathways of Cardiac and Skeletal Muscles in Rats Postmyocardial Infarction," by J. Zoll and colleagues, is presented.

An abstract of the article "Quantitative and Qualitative Mitochondrial Adaptations of Substrates Utilization in Cardiac and Skeletal Muscles," by E. Ponsot and colleagues, is presented.

The developmental changes in the myosin heavy chain (MHC) profile, creatine kinase (CK) and lactate dehydrogenase (LDH) activities and isozyme expression occurring in heart were examined in rats born and living at altitude (La Paz, Bolivia, 3700 m, HLP) for 16 generations. We hypothesized that HLP rats respond differently to hypoxia than rats born and living at sea level, and secondarily exposed to altitude during 3 weeks (H3W).The cardiac expression of MHC, CK and LDH was studied in left (LV) and right ventricle (RV) of HLP animals 1, 2, 3, 4 and 18 weeks after birth, and compared with control normoxic (C groups) and H3W animals.Rats secondarily exposed to hypoxia showed a lowerα-MHC content than C or HLP rats in both LV and RV, 3 weeks after birth (P < 0.05), consistent with a delay in the maturation of the heart contractile phenotype. A global increase in the total CK activity was observed in the LV of H3W animals in comparison with C rats (P < 0.05), while no change was reported in HLP animals. In both ventricles, M-LDH activity was higher in H3W than in HLP and C rats (P < 0.05). The relative amount ofα-MHC decreased by 20% in RV of 18-week-old HLP and H3W rats in comparison with C animals, consistent with the hypoxia-induced ventricular enlargement (P < 0.01). An increased activity of the foetal B-CK subunit was observed in both LV and RV of H3W rats in comparison with HLP and C animals (P < 0.05).This study demonstrates that rats native and living at altitude for several generations present some features relevant to genetic selection to altitude. [ABSTRACT FROM AUTHOR]