Brandt · Physiological reports 2018 · non-randomized controlled trial · n=12

Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle.

Cited 121 times in the scientific literature.

Level 3 - non-randomized controlled study

Small non-randomized or unstated randomization controlled interventional trial in humans

PubMed 29626392 · doi:10.14814/phy2.13651 · record verified 2026-08-30

What was done

Twelve moderately trained men (mean age 25 years, range 19–33) completed an 8-week cycling intervention (3 days per week) comparing continuous moderate cycling at 157 ± 20 W for 60 min (MOD, n = 6) with work-matched moderate cycling interspersed with 30-second sprints at 473 ± 79 W every 10 min (SPRINT, n = 6). Muscle biopsies were taken before, immediately after, and 2 hours after the first training bout, as well as at rest following the 8-week intervention to assess autophagy and mitophagy signaling markers.

What was found

Immediately after the first session, AMPK Thr172 and ULK Ser317 phosphorylation increased in both groups, with no change in mTOR Ser2448 or ULK Ser757 phosphorylation. At 2 hours post-exercise, LC3I, LC3II, and BNIP3 protein content were increased across groups without changes in p62; Beclin1 increased immediately and at 2 hours only in MOD. Following 8 weeks of training, Oxphos complex I, LC3I, BNIP3, and Parkin protein levels increased in both groups, while LC3II and p62 were unchanged; Beclin1 increased only in MOD. No quantitative effect sizes, variances, or p-values were reported in the abstract.

Why it matters

The study shows that both single exercise bouts and chronic training upregulate markers associated with autophagy and mitophagy pathways in human skeletal muscle, indicating that continuous endurance and interval-based cycling elicit broadly similar cellular clearance responses.

Limits

The sample size is very small (n = 6 per group), and the cohort was restricted to young, moderately trained men. Randomization is not stated in the abstract, no quantitative data or precision metrics are reported, and static protein marker measurements cannot establish actual autophagic flux.

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