Normal mitochondrial function and increased fat oxidation capacity in leg and arm muscles in obese humans

Abstract

Aim/hypothesis: The aim of this study was to investigate mitochondrial function, fibre-type distribution and substrate oxidation during exercise in arm and leg muscles in male postobese (PO), obese (O) and age-and body mass index (BMI)-matched control (C) subjects. The hypothesis of the study was that fat oxidation during exercise might be differentially preserved in leg and arm muscles after weight loss. Methods: Indirect calorimetry was used to calculate fat and carbohydrate oxidation during both progressive arm-cranking and leg-cycling exercises. Muscle biopsy samples were obtained from musculus deltoideus (m. deltoideus) and m. vastus lateralis muscles. Fibre-type composition, enzyme activity and O 2 flux capacity of saponin-permeabilized muscle fibres were measured, the latter by high-resolution respirometry. Results: During the graded exercise tests, peak fat oxidation during leg cycling and the relative workload at which it occurred (FatMax) were higher in PO and O than in C. During arm cranking, peak fat oxidation was higher in O than in C, and FatMax was higher in O than in PO and C. Similar fibre-type composition was found between groups. Plasma adiponectin was higher in PO than in C and O, and plasma leptin was higher in O than in PO and C. Conclusions: In O subjects, maximal fat oxidation during exercise and the eliciting relative exercise intensity are increased. This is associated with higher intramuscular triglyceride levels and higher resting non esterified fatty acid (NEFA) concentrations, but not with differences in fibre-type composition, mitochondrial function or muscle enzyme levels compared with Cs. In PO subjects, the changes in fat oxidation are preserved during leg, but not during arm, exercise.

Comparison of Substrate Oxidation during Walking and Running in Normal-Weight and Overweight/Obese Men

“…Bogdanis et al [25] have observed that the Fat max in overweight and sedentary men and women have a low exercise intensity (about 50% and 40% VO 2max , respectively). Ara et al [43] have reported that young male obese individuals have higher exercise intensity than normal-weight individuals for the Fat max . In contrast, the present study results show that Fat max and the corresponding exercise intensity are similar in the groups for absolute and relative lean body mass.…”

Effect of regional muscle location but not adiposity on mitochondrial biogenesis-regulating proteins

“…Greater capacity to oxidize fat during exercise in the muscle has been reported in obese compared to lean subjects well matched for physical fitness, showing an association between fat oxidation capacity and body fat mass (Schutz et al 1992;Goodpaster et al 2002;Horowitz and Klein 2000;Ara et al 2011). The higher fat oxidation in obese compared to lean was due to higher oxidation of intramuscular triglycerides since plasma fatty acid oxidation was similar (Goodpaster et al 2002;Horowitz and Klein 2000).…”

“…The inclusion criteria for the PO group were: (1) BMI levels lower than 30 kg m −2 like C subjects; (2) weight loss through non-pharmacological or surgical therapies of at least 10 % of their body weight [on average the weight loss was 26 % (range 15-37 %)] and, (3) weight stability at the time of the study (±2 kg for at least 1 month prior to the beginning of the experiments) for all groups. The weight loss of the PO subjects had on average occurred 6 ± 1 years earlier (range 1-10 years) (Ara et al 2011) and the weight loss was achieved by means of a combination of hypo-caloric dieting and increased physical activity and none had undergone bariatric surgery.…”

“…Skeletal muscle leptin receptors and leptin signaling are reduced in obese, particularly in the leg muscles, showing lower levels of Thr 172 -AMPKα and Ser 221 -ACCβ basal phosphorylation levels compared to lean men ). Yet, in a prior publication, muscle mitochondrial respiratory capacity was similar in obese compared to lean subjects (Ara et al 2011). Overall, the regulatory mechanism leading to higher fat oxidation in obese compared to lean subjects remains unknown.…”

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

“…However, other observations report discrepant results, showing that high-fat feeding in rats was associated with no variation (Atgié et al 1993, De Feyter et al 2008a or even a higher mitochondrial capacity (Hancock et al 2008), and IR could be related to incomplete intramitochondrial β-oxidation (Koves et al 2008). Several studies show that insulin resistance arises when mitochondrial function is unaffected or even improved , Ara et al 2011, Boudina et al 2012, or conversely that impaired mitochondrial functioning alone does not cause insulin resistance (Wredenberg et al 2006). These latter findings data seem to indicate that, at least in rodents, consumption of high-fat diet is not always accompanied by mitochondrial dysfunction, but rather leads to improved mitochondrial oxidative capacity and/or biogenesis (Gómez-Pérez et al 2012, Wessels et al 2015, even in the presence of IR.…”