Comparison of exercise training effects on mitochondrial substrate oxidation of skeletal muscle and adipose tissue of humans

Introduction:

Adaptations in skeletal muscle mitochondria are considered to play an important role in the beneficial effect of exercise on metabolic control, while the contribution of adipose tissue is less clear.

Methods:

26 obese, sedentary participants (17f/9 m, 30 ± 8years) performed an 8-week supervised exercise intervention at 80% VO2peak. Mitochondrial respiration was analyzed in muscle fibers and subcutaneous adipose tissue by high resolution respirometry. Body composition was assessed by whole body MR imaging, hepatic lipids by MR spectroscopy.

Results:

Training increased the individual anaerobic threshold (IAT 1.1 ± 0.3 vs. 1.3 ± 0.3W/kg; p < 0.001) and cardiorespiratory fitness (VO2peak 25 ± 4 vs. 27 ± 5 ml/min/kg; p = 0.005). BMI was slightly reduced (31.5 ± 4.2 vs. 31.2 ± 4.3 kg/m2; p = 0.03). Specifically, subcutaneous adipose tissue (-3%; p = 0.01), femoral adipose tissue (-4%; p = 0.02), and liver fat content decreased (-22%; p = 0.0086). Ex-vivo respirometry revealed that oxygen flux in muscle fibers was higher than in adipose tissue. Relative to total phosphorylating respiration, muscle mitochondria had higher complex I-linked respiration, while adipose tissue exhibited higher fatty acid and complex II-linked respiration. In muscle fibers, training increased complex I-linked and maximal coupled and uncoupled respiration (all p < 0.01), while in adipose tissue only uncoupled respiration was increased (p = 0.007). The effects of training on IAT, VO2peak as well as BMI, subcutaneous and ectopic did not correlate with changes in skeletal muscle and adipose tissue respiration.

Conclusions:

The data provide evidence for differences in substrate oxidation and training response of muscle and adipose tissue mitochondria. They suggest that improved in-tissue respiration is an independent contributor to the beneficial effects of exercise.