Journal
JOURNAL OF APPLIED PHYSIOLOGY
Volume 118, Issue 8, Pages 971-979Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.01116.2014
Keywords
autophagy signaling; exercise training; skeletal muscle; nutritional status; ULK1; human
Categories
Funding
- Danish Council for Strategic Research (Keto-group) [0603-00479B]
- Beckett Foundation
- Danish PhD Schools of Metabolism and Endocrinology (SUND, SDU) [94-101-12676]
- A. P. Moller Foundation for the Advancement of Medical Science
- Novo Nordisk Fonden [NNF13OC0007869] Funding Source: researchfish
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Data from transgenic animal models suggest that exercise-induced autophagy is critical for adaptation to physical training, and that Unc-51 like kinase-1 (ULK1) serves as an important regulator of autophagy. Phosphorylation of ULK1 at Ser(555) stimulates autophagy, whereas phosphorylation at Ser(757) is inhibitory. To determine whether exercise regulates ULK1 phosphorylation in humans in vivo in a nutrient-dependent manner, we examined skeletal muscle biopsies from healthy humans after 1-h cycling exercise at 50% maximal O-2 uptake on two occasions: 1) during a 36-h fast, and 2) during continuous glucose infusion at 0.2 kg/h. Physical exercise increased ULK1 phosphorylation at Ser(555) and decreased lipidation of light chain 3B. ULK1 phosphorylation at Ser(555) correlated positively with AMP-activated protein kinase-alpha Thr(172) phosphorylation and negatively with light chain 3B lipidation. ULK1 phosphorylation at Ser(757) was not affected by exercise. Fasting increased ULK1 and p62 protein expression, but did not affect exercise-induced ULK1 phosphorylation. These data demonstrate that autophagy signaling is activated in human skeletal muscle after 60 min of exercise, independently of nutritional status, and suggest that initiation of autophagy constitutes an important physiological response to exercise in humans.
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