Physical exercise increases autophagic signaling through ULK1 in human skeletal muscle.
Level 3 - non-randomized controlled study
Within-subject crossover physiological study in healthy humans without stated randomization
PubMed 25678702 · doi:10.1152/japplphysiol.01116.2014
What was done
Healthy humans completed 1 hour of cycling exercise at 50% maximal oxygen uptake on two separate occasions: during a 36-hour fast and during continuous glucose infusion (0.2 kg/h). Skeletal muscle biopsies were obtained to measure autophagic signaling markers, including ULK1 phosphorylation at Ser555 and Ser757, AMPK-alpha Thr172 phosphorylation, LC3B lipidation, and p62 protein expression.
What was found
The abstract reports directional findings without numerical values or effect sizes. Physical exercise increased ULK1 phosphorylation at Ser555 and decreased LC3B lipidation. ULK1 Ser555 phosphorylation correlated positively with AMPK-alpha Thr172 phosphorylation and negatively with LC3B lipidation. Exercise did not alter ULK1 Ser757 phosphorylation. Fasting increased ULK1 and p62 protein expression but did not alter the exercise-induced increase in ULK1 Ser555 phosphorylation.
Why it matters
This study provides human in vivo evidence that acute aerobic exercise stimulates skeletal muscle autophagic signaling through ULK1. It shows that this signaling pathway is activated independently of acute nutritional status.
Limits
The abstract does not state the sample size, participant sex, or age. No quantitative values, p-values, or effect sizes are provided. The findings are limited to acute moderate-intensity cycling and cannot be generalized to other exercise modalities, chronic training adaptations, or clinical populations.
Cited by
- supports High-intensity exercise stimulates skeletal muscle autophagy more potently than an overnight fast.