J Physiol 594.3 (2016) pp 745–761
Regulation of autophagy in human skeletal muscle: effects of exercise, exercise training and insulin stimulation Andreas M. Fritzen1 , Agnete B. Madsen1 , Maximilian Kleinert1 , Jonas T. Treebak1,2 , Anne-Marie Lundsgaard1 , Thomas E. Jensen1 , Erik A. Richter1 , Jørgen Wojtaszewski1 , Bente Kiens1 and Christian Frøsig1 1
Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, the August Krogh Centre, Faculty of Science, University of Copenhagen, Copenhagen, Denmark 2 The Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Integrative Physiology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
The Journal of Physiology
r Regulation of autophagy in human muscle in many aspects differs from the majority of previous reports based on studies in cell systems and rodent muscle.
r An acute bout of exercise and insulin stimulation reduce human muscle autophagosome content.
r An acute bout of exercise regulates autophagy by a local contraction-induced mechanism. r Exercise training increases the capacity for formation of autophagosomes in human muscle. r AMPK activation during exercise seems insufficient to regulate autophagosome content in muscle, while mTORC1 signalling via ULK1 probably mediates the autophagy-inhibiting effect of insulin.
Abstract Studies in rodent muscle suggest that autophagy is regulated by acute exercise, exercise training and insulin stimulation. However, little is known about the regulation of autophagy in human skeletal muscle. Here we investigate the autophagic response to acute one-legged exercise, one-legged exercise training and subsequent insulin stimulation in exercised and non-exercised human muscle. Acute one-legged exercise decreased (P