Omega-3 supplementation alters mitochondrial membrane composition and respiration kinetics in human skeletal muscle.
Level 4 - case-series / case-control
Single-arm pre-post intervention study without a parallel control group.
PubMed 24396061 · doi:10.1113/jphysiol.2013.267336
What was done
Eighteen young, healthy male participants received daily fish oil supplementation (2 g eicosapentaenoic acid [EPA] and 1 g docosahexaenoic acid [DHA]) for 12 weeks. Skeletal muscle biopsies were taken before and after the 12-week intervention to assess mitochondrial membrane phospholipid composition, mitochondrial respiratory kinetics in permeabilized muscle fibres, protein expression (ANT1, ANT2, and electron transport chain subunits), and reactive oxygen species (ROS) emission capacity.
What was found
Mitochondrial membrane total EPA and DHA content increased by ~450% and ~320%, respectively (P < 0.05), displacing omega-6 species across several phospholipid classes. Maximal substrate-supported respiration and pyruvate-supported respiration sensitivity (apparent Km) and maximal capacity showed no change. In contrast, ADP titrations demonstrated enhanced ADP sensitivity (decreased apparent Km) independent of the creatine kinase shuttle. Protein content of ANT1, ANT2, and electron transport chain subunits remained unaltered. Mitochondrial ROS emission capacity increased without altering the content of oxidative products.
Why it matters
This study provides direct evidence in humans that dietary omega-3 fatty acids remodel skeletal muscle mitochondrial membrane phospholipids and enhance mitochondrial ADP sensitivity without altering mitochondrial protein expression.
Limits
The study lacked a randomized, placebo-controlled comparison group (single-arm pre-post design). The sample size was small (n = 18) and limited exclusively to young, healthy males. Whole-body physiological and functional performance outcomes were not evaluated.
Cited by
- supports Graham Holloway showed that feeding omega-3s to younger people alters ADP sensitivity and ADP-stimulated respiration in human skeletal muscle mitochondria.