Effect of chronic intermittent hypoxia (CIH) on neuromuscular junctions and mitochondria in slow- and fast-twitch skeletal muscles of mice-the role of iNOS

Autor: L I, Bannow, G A, Bonaterra, M, Bertoune, S, Maus, R, Schulz, N, Weissmann, S, Kraut, R, Kinscherf, W, Hildebrandt
Rok vydání: 2020
Předmět:
Zdroj: Skeletal muscle. 12(1)
ISSN: 2044-5040
Popis: Obstructive sleep apnea (OSA) imposes vascular and metabolic risks through chronic intermittent hypoxia (CIH) and impairs skeletal muscle performance. As studies addressing limb muscles are rare, the reasons for the lower exercise capacity are unknown. We hypothesize that CIH-related morphological alterations in neuromuscular junctions (NMJ) and mitochondrial integrity might be the cause of functional disorders in skeletal muscles.Mice were kept under 6 weeks of CIH (alternating 7% and 21% OIn WT soleus muscle, CIH vs. NOX reduced NMJ size (- 37.0%, p0.001) and length (- 25.0%, p0.05) together with fiber CSA of type IIa fibers (- 14%, p0.05) and increased centronucleated fiber fraction (p0.001). Moreover, CIH vs. NOX increased the fraction of damaged mitochondria (1.8-fold, p0.001). Compared to WT, iNOSCIH leads to NMJ and mitochondrial damage associated with fiber atrophy/centronucleation selectively in slow-twitch muscle of WT. This effect is largely mimicked by iNOS
Databáze: OpenAIRE