DI-UMONS : Dépôt institutionnel de l’université de Mons

Recherche transversale
(titres de publication, de périodique et noms de colloque inclus)
2016-06-29 - Colloque/Article dans les actes avec comité de lecture - Anglais - 1 page(s)

Conotte Stéphanie, Tassin Alexandra , Nuyens Vincent, Zouaoui Boudjeltia Karim , Legrand Alexandre , "effect of chronic intermittent hypoxia on muscle function in a mouse model of obstructive sleep apnea" in Federation of European Physiological Societies, Paris, France, 2016

  • Codes CREF : Physiologie générale [animale] (DI3228)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)

Abstract(s) :

(Anglais) Effect of the chronic intermittent hypoxia on muscle function in a mouse model of obstructive sleep apnea S. Conotte1, A. Tassin1, K. Zouaoui Boudjeltia2 and A. Legrand1 1Lab. Respiratory Physiology and Rehabilitation, Health Institute, University of Mons (UMONS) and 2 Experimental Medicine Laboratory, Université libre de Bruxelles (ULB)and CHU Charleroi, Belgium. Obstructive sleep apnea (OSA) is characterized by recurrent episodes of upper airway (UA) collapse leading to chronic intermittent hypoxia (ChIH), a dominant feature of OSA known to be associated to an increased reactive oxygen species production. There is evidence of structural and functional abnormalities in UA muscles but the exact origin of this dysfunction is hardly known and probably multifactorial. To better understand the contribution of ChIH and associated oxidative stress (OS) to OSA pathophysiology, C57BL/6J mice were exposed to ChIH (FIO2 6%-21%, 30sec/30sec) 8 h/day using a standardized and well-controlled device (Chodzynsky et al., 2013, PLoS One). After 35 days, ChIH mice recapitulate key features of OSA (polycythemia, cardiac and metabolic alterations). The analysis of muscle contractile properties has shown a significant increase in sternohyoïd muscle fatigability while diaphragm exhibited an improvement of fatigue resistance. An improved recovery was seen in the sternohyoïd at 35 days as compared to other time-points. No change was observed in EDL (fast) and soleus (slow) muscles as regards to mechanical properties. However, in all investigated muscles, the evaluation of myofiber size has revealed a surface distribution shift towards a greater cellular cross section indicative of a hypertrophy, without change in fibre-type distribution. In conclusion, ChIH per se is sufficient to induce a UA muscle dysfunction and structural alterations of respiratory and limb muscles in a mouse model of OSA. Moreover, current analyses of protein carbonylation and lipid peroxidation indicate an OS in limb muscles.