Carter 2018 J Physiol

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
Carter HN, Kim Y, Erlich AT, Zarrin-Khat D, Hood DA (2018) Autophagy and mitophagy flux in young and aged skeletal muscle following chronic contractile activity. J Physiol 596:3567-84.

» PMID: 29781176

Carter HN, Kim Y, Erlich AT, Zarrin-Khat D, Hood DA (2018) J Physiol

Abstract: Skeletal muscle exhibits deficits in mitochondrial quality with age. Central to the maintenance of a healthy mitochondrial pool is the removal of dysfunctional organelles via mitophagy. Little is known on how mitophagy is altered with ageing and chronic exercise. We assessed mitophagy flux using colchicine treatment in vivo following chronic contractile activity (CCA) of muscle in young and aged rats. CCA evoked mitochondrial biogenesis in young muscle, with an attenuated response in aged muscle. Mitophagy flux was higher in aged muscle and was correlated with the enhanced expression of mitophagy receptors and upstream transcriptional regulators. CCA decreased mitophagy flux in both age groups, suggesting an improvement in organelle quality. CCA also reduced the exaggerated expression of TFEB evident in aged muscle, which may be promoting the age-induced increase in lysosomal markers. Thus, aged muscle possesses an elevated drive for autophagy and mitophagy which may contribute to the decline in organelle content observed with age, but which may serve to maintain mitochondrial quality. CCA improves organelle integrity and reduces mitophagy, illustrating that chronic exercise is a modality to improve muscle quality in aged populations.

© 2018 The Authors. The Journal of Physiology © 2018 The Physiological Society.

Keywords: Aging, Exercise, Mitochondria Bioblast editor: Kandolf G


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Aging;senescence 

Organism: Rat  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 


Coupling state: LEAK, OXPHOS  Pathway: N, NS  HRR: Oxygraph-2k 

Labels, 2018-07