Effets de la supplémentation en créatine sur la cinétique de régénérescence du muscle squelettique après lésion étendue

Résumé Objectif. – Il s'agit ici d'étudier, sur modèle animal, les effets d'une supplémentation prolongée avec de la créatine sur la cinétique de récupération d'un muscle lent et oxydatif, le soléaire, après induction d'une dégénérescence étendue (par infiltration de notexine). Résultats et Discussion. – Que les animaux aient été ou non supplémentés en créatine, les résultats suivants ont été obtenus : 1) La masse du muscle soléaire est récupérée 35 jours après la lésion. 2) Le profil d'expression des isoformes de MHC est similaire à celui d'un muscle soléaire intact 28 jours après la lésion. 3) L'activité de la CS est récupérée 14 jours après la lésion, tandis que l'activité spécifique H-LDH reste légèrement inférieure à celle du muscle intact. 4) La myogénine a un pic d'expression à trois jours. Conclusion. – Contrairement à l'hypothèse initiale, proposée après des études in vitro, la supplémentation en créatine n'a pas d'effet bénéfique sur la cinétique de récupération du muscle squelettique évaluée in vivo après lésion par un myotoxique. Abstract Objective. – The aim of the experiment was to study, in rats, the effects of Cr supplementation on the time course of recovery of the soleus, a slow-twitch oxidative muscle, after a notexin-induced injury. Results and Discussion. – Whether or not animals have been supplemented with oral creatine, we observed: 1) soleus muscle mass was recovered at day 35 following injury. 2) MHC profile of regenerated muscles was similar to that of intact muscles at day 28. 3) A full recovery of the CS activity was observed from day 14, while the specific H-LDH activity remained slightly lower than in intact muscles. 4) Myogenin expression peaked at day 3. Conclusion. – In contrast with our hypothesis resulting from in vitro experiments, creatine supplementation failed to show any beneficial effect on the time course of recovery of skeletal muscle assessed in vivo after a myotoxic-induced injury

Hypoxic stimulus alters hypothalamic AMP-activated protein kinase phosphorylation concomitant to hypophagia.

International audienceAcute exposure to hypobaric hypoxia is known to decrease food intake, but the molecular mechanisms of such alteration in feeding behavior remain unknown. We tested the hypothesis that hypothalamic AMP-activated protein kinase (AMPK) phosphorylation is affected by acute exposure to hypobaric hypoxia and thus would be involved in initial anorexia. To address this issue, male rats weighing 255-270 g were either submitted to hypobaric hypoxia (H, equivalent altitude of 5,500 m), maintained under local barometric pressure conditions (N), or pair-fed an equivalent quantity of food to that consumed by H rats (PF), for 6, 24, or 48 h. Daily food intake dropped by 73% during the first day of hypoxia (P<0.01) and remained by 46% lower than in N rats thereafter (P<0.01). Hypoxia per se, as estimated by comparing experimental data between the H and PF groups, increased ob gene transcription and plasma leptin concentration. A transient increase in glucose availability occurred in the H group compared with PF animals (P<0.05). The hypoxic stimulus led to an early and transient decrease in hypothalamic AMPK and acetyl-CoA carboxylase (ACC) phosphorylation, concomitant with hypophagia and associated alterations in nutrients and hormones. An increase in NPY mRNA levels occurred from day 1, similarly in H and PF rats, and thus mainly related to food restriction alone (P<0.05). In conclusion, the present study demonstrates that hypoxia per se inhibited AMPK and ACC phosphorylation in the hypothalamus, concomitant with profound anorexia. A powerful counterregulation occurs rapidly, mediated by NPY and devoted to avoid prolonged anorexia

Larger strength losses and muscle activation deficits in plantar flexors induced by backward downhill in reference to distance-matched forward uphill treadmill walk

We tested the hypothesis that backward downhill walking (eccentric component) impairs both voluntary activation and muscle contractile properties in the plantar flexors and delays recovery as compared to a gradient and distance-matched uphill walk. Fourteen males performed two 30-min walking exercises (velocity: 1 m/ s; grade: 25%; load: 12% of body weight), one downhill (DW) and one uphill (UP), in a counterbalanced order, separated by 6 weeks. Neuromuscular test sessions were performed before, after, 24-, 48- and 72-h post-exercise, including motor nerve stimulations during brief (5 s) and sustained (1 min) maximal isometric voluntary contractions of the plantar flexors. DW (−18.1 ± 11.1%, P  .05). Using a direct comparison, the capacity to drive the plantar flexors during sustained contractions remains sub-optimal during the three-day recovery period in response to non-exhaustive, downhill backward walking in reference to an uphill exercise matched for distance covered

Changes in circulating microRNAs levels with exercise modality

Here, we studied muscle-specific and muscle-related miRNAs in plasma of exercising humans. Our aim was to determine whether they are affected by eccentric and/or concentric exercise modes and could be biomarkers of muscle injuries or possible signaling molecules. On two separate days, nine healthy subjects randomly performed two 30-min walking exercises, one downhill (high eccentric component) and one uphill (high concentric component). Perceived exertion and heart rate were higher during the uphill exercise, while subjective pain and ankle plantar flexor strength losses within the first 48-h were higher following the downhill exercise. Both exercises increased serum creatine kinase and myoglobin with no significant differences between conditions. Plasma levels of circulating miRNAs assessed before, immediately after, and at 2-, 6-, 24-, 48-, and 72-h recovery showed that 1) hsa-mir-1, 133a, 133b, and 208b were not affected by concentric exercise but significantly increased during early recovery of eccentric exercise (2 to 6 h); 2) hsa-mir-181b and 214 significantly and transiently increased immediately after the uphill, but not downhill, exercise. The muscle-specific hsa-mir-206 was not reliably quantified and cardiac-specific hsa-mir-208a remained undetectable. In conclusion, changes in circulating miRNAs were dependent on the exercise mode. Circulating muscle-specific miRNAs primarily responded to a downhill exercise (high eccentric component) and could potentially be alternative biomarkers of muscle damage. Two muscle-related miRNAs primarily responded to an uphill exercise (high exercise intensity), suggesting they could be markers or mediators of physiological adaptations