Civitarese · PLoS medicine 2007 · randomized controlled trial · n=36

Calorie restriction increases muscle mitochondrial biogenesis in healthy humans.

Cited 791 times in the scientific literature.

Level 2 - randomized trial

Individual randomized controlled trial

PubMed 17341128 · doi:10.1371/journal.pmed.0040076 · record verified 2026-08-31

What was done

Thirty-six young, overweight adults (mean age 36.8 ± 1.0 years, BMI 27.8 ± 0.7 kg/m²) were randomized to one of three 6-month interventions: Control (100% of energy requirements), CR (25% caloric restriction), or CREX (12.5% caloric restriction plus 12.5% increased energy expenditure via exercise). Investigators measured adjusted 24-hour energy expenditure, skeletal muscle mitochondrial gene expression, mitochondrial DNA content, mitochondrial enzyme activities, and DNA damage, alongside an in vitro study in primary human myotubes.

What was found

Adjusted 24-hour energy expenditure decreased in CR (-135 ± 42 kcal/d, p = 0.002) and CREX (-117 ± 52 kcal/d, p = 0.008), with no change in controls. Expression of genes involved in mitochondrial function (PPARGC1A, TFAM, eNOS, SIRT1, and PARL) increased in both CR and CREX (all p < 0.05). Muscle mitochondrial DNA content increased by 35% ± 5% in CR (p = 0.005) and 21% ± 4% in CREX (p < 0.004), while remaining unchanged in controls (2% ± 2%). Mitochondrial enzyme activities (citrate synthase, beta-hydroxyacyl-CoA dehydrogenase, cytochrome C oxidase II) were unchanged. DNA damage fell in CR (-0.56 ± 0.11 arbitrary units, p = 0.003) and CREX (-0.45 ± 0.12 arbitrary units, p = 0.011), but not in controls.

Why it matters

This study provides randomized evidence in humans that caloric restriction induces muscle mitochondrial biogenesis and decreases DNA damage, supporting mechanisms of metabolic adaptation previously seen mainly in animal models.

Limits

The sample size is small (n = 36 across three arms) and limited to young overweight adults over 6 months. Key mitochondrial enzyme activities did not increase despite higher mitochondrial DNA content, and clinical or lifespan endpoints were not evaluated.

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