SIRT3 gene expression but not subcellular localization is altered in response to fasting and exercise in human skeletal muscle

The present study examined SIRT3 expression and mitochondrial localization in response to acute exercise and short-term fasting in human skeletal muscle. Experiment 1 involved 8 healthy men (age, 21.4 ± 2.8 years; VO₂peak, 47.1 ± 11.8 ml min⁻¹ kg⁻¹) who performed a single bout of exercise at ∼55% of peak aerobic work rate for 1 h. Muscle biopsies were obtained at rest (Rest), immediately after exercise (EX-0), and 3 h post-exercise (EX-3). Experiment 2 involved 10 healthy men (age, 22.0 ± 1.5 years; VO₂peak, 47.2 ± 6.7 ml min⁻¹ kg⁻¹) who underwent a 48-hour fast, with muscle biopsies collected 1 h postprandial (Fed) and following 48 h of fasting (Fast). Mitochondrial respiration was measured using high-resolution respirometry in permeabilized muscle fibre bundles to assess substrate oxidation. Whole body fat oxidation increased after both exercise (Rest: 0.96 ± 0.32, Exercise: 5.66 ± 1.97, P < 0.001) and fasting (Fed: 0.87 ± 0.51, Fast: 1.30 ± 0.37 kcal min⁻¹, P < 0.05). SIRT3 gene expression decreased (P < 0.05) following both exercise (−8%) and fasting (−19%); however SIRT3 whole muscle protein content was unaltered following fasting. No changes were observed in SIRT3 mitochondrial localization following either exercise or fasting. Fasting also decreased the V_max of glutamate (80 ± 43 vs. 50 ± 21 pmol sec⁻¹ mg⁻¹ dry wt, P < 0.05). These findings suggest that SIRT3 does not appear to be regulated by changes in mitochondrial localization at the time points measured in the current study in response to cellular energy stress in human skeletal muscle.

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