Response of Mitochondrial Respiration in Adipose Tissue and Muscle to 8 Weeks of Endurance Exercise in Obese Subjects

Abstract

Context Exercise training improves glycemic control and increases mitochondrial content and respiration capacity in skeletal muscle. Rodent studies suggest that training increases mitochondrial respiration in adipose tissue. Objective To assess the effects of endurance training on respiratory capacities of human skeletal muscle and abdominal subcutaneous adipose tissue and to study the correlation with improvement in insulin sensitivity. Design Using high resolution respirometry, we analyzed biopsies from 25 sedentary (VO2 peak 25.1 ± 4.0 VO2 ml/(kg*min)) subjects (16 females, 9 males; 29.8 ± 8.4 yrs) with obesity (BMI 31.5 ± 4.3 kg/m 2 ), who did not have diabetes. They performed a supervised endurance training over 8 weeks (3 x 1 hour/week at 80% VO 2 peak). Results Based on change in insulin sensitivity after intervention, subjects were grouped in responders (>15% increase in ISIMatsuda) and low responders. The response in ISIMatsuda was correlated to a reduction of subcutaneous and visceral adipose tissue volume. Both groups exhibited similar increases in fitness, respiratory capacity, and in abundance of mitochondrial enzymes in skeletal muscle fibers. Respiratory capacities in subcutaneous adipose tissue were not altered by the intervention. Compared to muscle fibers, adipose tissue respiration showed a preference for β-oxidation and complex II substrates. Respiratory capacities were higher in adipose tissue from females. Conclusion Our data show that the improvement of peripheral insulin sensitivity after endurance training is not directly related to an increase in mitochondrial respiratory capacities in skeletal muscle and occurs without an increase in the respiratory capacity of subcutaneous adipose tissue.

Assessing mitochondrial respiration in permeabilized fibres and biomarkers for mitochondrial content in human skeletal muscle

“…Consequently, the use of permeabilized muscle fibres with high-resolution respirometry has become the most common method to measure mitochondrial respiration in human skeletal muscle. 6,17,18 However, despite its widespread use in human exercise training studies, 5,[19][20][21][22][23][24][25][26][27][28][29][30][31] and the several studies conducted to assess factors that might contribute to technical and/or biological variation, [32][33][34] uncertainty remains regarding the reliability of this method. As such, additional research is needed to establish the reliability of mitochondrial respiration measures using permeabilized muscle fibres with high-resolution respirometry.…”

Methodological considerations when assessing mitochondrial respiration and biomarkers for mitochondrial content in human skeletal muscle

“…Consequently, the use of permeabilized muscle fibres with highresolution respirometry has become the most common method to measure mitochondrial respiration in human skeletal muscle [6,17,18]. However, despite its widespread use in human exercise training studies ( [5,[19][20][21][22][23][24][25][26][27][28][29][30][31], and several studies have been conducted to assess factors that might cause technical and/or biological variation [32][33][34], uncertainty remains regarding the reliability of this method. As such, additional research is needed to establish the reliability of mitochondrial respiration measures using permeabilized muscle fibres with high-resolution respirometry.…”

TGF-β Induction of miR-143/145 Is Associated to Exercise Response by Influencing Differentiation and Insulin Signaling Molecules in Human Skeletal Muscle

“…Next, we analyzed transcripts related to TGF-β signaling and TGF-β-regulated miRNAs in skeletal muscle of responders (RE) and low responders (LRE) based on insulin sensitivity after an 8-week exercise intervention [ 12 , 36 ]. The cohort consisting of n = 40 individuals was stratified according to their training response, defined as an improvement in insulin sensitivity (ISIMats) with a cutoff at 1.1 ( Figure 3 A).…”

“…The analyses performed in this manuscript were based on two recently published exercise intervention studies. Participants and design of the two studies were described recently [ 12 , 36 ] (NCT03151590 at Clinicaltrials.gov). Healthy but overweight individuals with a high risk for T2D: <120 min of physical activity per week and at least one of the following risk factors (BMI > 27 kg/m 2 , family history of T2D, former gestational diabetes) were recruited ( Table 1 ).…”