Granata · FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2016 · Randomized parallel-group trial · n=29

Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle.

Cited 218 times in the scientific literature.

Level 2 - randomized trial

Individual randomized controlled trial

PubMed 26572168 · doi:10.1096/fj.15-276907 · record verified 2026-08-30

What was done

Twenty-nine healthy men were randomized to 4 weeks (12 cycling sessions) of one of three training protocols: sprint interval training (SIT; 4–10 × 30-s all-out bouts at ~200% peak power output [WPeak]), high-intensity interval training (HIIT; 4–7 × 4-min intervals at ~90% WPeak), or sublactate threshold continuous training (STCT; 20–36 min at ~65% WPeak). HIIT and STCT were matched for total work. Resting vastus lateralis muscle biopsies were obtained before and after the 4-week training period to evaluate maximal mitochondrial respiration in permeabilized fibers alongside markers of mitochondrial content and biogenesis.

What was found

Maximal mitochondrial respiration in permeabilized muscle fibers increased significantly only following SIT (25% increase). Protein levels of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, p53, and plant homeodomain finger-containing protein 20 (PHF20) also increased exclusively in the SIT group (60–90% increases). Conversely, citrate synthase activity, mitochondrial transcription factor A (TFAM) protein content, and subunits of the electron transport system complexes remained unchanged across all groups.

Why it matters

This study demonstrates that training intensity directly modulates short-term improvements in mitochondrial respiratory capacity and upstream signaling proteins, showing these functional adaptations can occur independently of changes in mitochondrial content.

Limits

The study had a small sample size (n = 29 across three arms) and was restricted entirely to healthy men, limiting generalizability to females, older individuals, or clinical populations. The 4-week duration was relatively short, leaving unclear whether mitochondrial content markers would dissociate from respiratory capacity over longer training periods.

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