Why the study?
Does 6 weeks of high-intensity training (HIT) alter mitochondrial ADP sensitivity and respiratory capacity in skeletal muscle and subcutaneous adipose tissue?
Does 6 weeks of high-intensity training (HIT) alter mitochondrial ADP sensitivity and respiratory capacity in skeletal muscle and subcutaneous adipose tissue?
High-intensity interval training induces divergent mitochondrial adaptations, increasing respiratory capacity in skeletal muscle while decreasing it in subcutaneous adipose tissue.
HIT-induced mitochondrial shifts in muscle and SAT remain hypothesis-generating; randomized trials needed before clinical consideration.
The effect of high-intensity training (HIT) on mitochondrial ADP sensitivity and respiratory capacity was investigated in human skeletal muscle and subcutaneous adipose tissue (SAT). Twelve men and women underwent 6 weeks of HIT (7 × 1 min at app. 100% of maximal oxygen uptake (VO2max )). Mitochondrial respiration was measured in permeabilized muscle fibers and in abdominal SAT. Mitochondrial ADP sensitivity was determined using Michaelis Menten enzyme kinetics. VO2max , body composition and citrate synthase (CS) activity (skeletal muscle) and mtDNA (SAT) were measured before and after training. VO2max increased from 2.6 ± 0.2 to 2.8 ± 0.2 L O₂ /min (P = 0.011) accompanied by a decreased mitochondrial ADP sensitivity in skeletal muscle (Km : 0.14 ± 0.02 to 0.29 ± 0.03 mmol/L ADP (P = 0.002)), with no changes in SAT (Km : 0.12 ± 0.02 to 0.16 ± 0.05 mmol/L ADP; P = 0.186), following training. Mitochondrial respiratory capacity increased in skeletal muscle from 57 ± 4 to 67 ± 4 pmol O₂ ·mg⁻¹ ·sec⁻¹ (P < 0.001), but decreased with training in SAT from 1.3 ± 0.1 to 1.0 ± 0.1 pmol O₂ ·mg⁻¹ ·sec⁻¹ (P < 0.001). CS activity increased (P = 0.027) and mtDNA was unchanged following training. Intrinsic mitochondrial respiratory capacity was unchanged in skeletal muscle, but increased in SAT after HIT. In summary, our results demonstrate that mitochondrial adaptations to HIT in skeletal muscle are comparable to adaptations to endurance training, with an increased mitochondrial respiratory capacity and CS activity. However, mitochondria in SAT adapts differently compared to skeletal muscle mitochondria, where mitochondrial respiratory capacity decreased and mtDNA remained unchanged after HIT.
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Dohlmann et al. (2018) studied this question.
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