Physical training, UCP1 expression, mitochondrial density, and coupling in adipose tissue from women with obesity

Abstract

Background: Exercise training may improve energy expenditure, thermogenesis, and oxidative capacities. Therefore, we hypothesized that physical training enhances white adipose tissue mitochondrial oxidative capacity from obese women. Objective: To evaluate mitochondrial respiratory capacity, mitochondrial content, and UCP1 gene expression in white adipose tissue from women with obesity before and after the physical training program. Methods: Women (n = 14, BMI 33 ± 3 kg/m 2 , 35 ± 6 years, mean ± SD) were submitted to strength and aerobic exercises (75%-90% maximum heart rate and multiple repetitions), 3 times/week during 8 weeks. All evaluated subjects were paired, before and after training for resting metabolic rate (RMR), substrate oxidation (lipid and carbohydrate) by indirect calorimeter, deuterium oxide body composition, and aerobic maximum velocity (V max ) test. At the beginning and at the ending of the protocol, abdominal subcutaneous adipose tissue was collected to measure the mitochondrial respiration by high-resolution respirometry, mitochondrial content by citrate synthase (CS) activity, and UCP1 gene expression by RT-qPCR. Results: Combined physical training increased RMR, lipid oxidation, and V max but did not change body weight/composition. In WAT, exercise increased CS activity, decreased mitochondrial uncoupled respiration and mRNA of UCP1. RMR was positively correlated with fat-free mass. Conclusion: Physical training promotes an increase in mitochondrial content without changing tissue respiratory capacity, a reduction in mitochondrial uncoupling degree and UCP1 mRNA expression in WAT. Finally, it improved the resting metabolic rate, lipid oxidation and physical performance, independent of the body changing free, or fat mass in obese women. K E Y W O R D Scitrate synthase, human energy metabolism, mitochondria, obesity, physical training, uncoupling protein 1, white adipose tissue

Mitochondrial respiration variability and simulations in human skeletal muscle: The Gene SMART study

“…Mitochondrial respiration capacity in human exercise intervention studies is not exclusive to skeletal muscle samples. Although such investigations are less common, different studies have measured respiration capacity in adipose tissue, 21,22 and blood cells (including lymphocytes and platelet). [23][24][25][26] Tests run in duplicates (or more) enable researchers to capture technical variability, and/or biological day-to-day variability within participants.…”

“…Mitochondrial respiration capacity in human exercise intervention studies is not exclusive to skeletal muscle samples. Although such investigations are less common, different studies have measured respiration capacity in adipose tissue, and blood cells (including lymphocytes and platelet) …”

Human white-fat thermogenesis: Experimental and meta-analytic findings

“…The search process identified eight eligible studies conducted in humans and 19 eligible studies conducted in animals (see supplement) [19]. Four of the studies in humans [16][17][18]39] together with data from study 5 provided data for a meta-analysis showing no effect of chronic exercise on UCP1 mRNA (p > 0.05; no data were available to test this hypothesis for UCP1 protein expression). Seven of the studies in animals identified in the systematic review that used a normal diet [11][12][13][14][15]40,41] provided data for a meta-analysis showing no effect of chronic exercise on UCP1 mRNA (p > 0.05).…”

Is Exercise a Match for Cold Exposure? Common Molecular Framework for Adipose Tissue Browning

“…Treadmill training for a longer duration (8-9 weeks), however, yields much more inconclusive results, with increases [21], no changes [94,184], and decreases all observed [22,95]. Both swimming and running protocols up to 8 weeks consistently increased [8, 21, 22, 56, 81, 95, 98-101, 111-113, 185] or yielded insignificant changes [8,22,99,111,180,185] in UCP1, although longer durations (10 weeks) did not change UCP1 concentrations [114,115,137].…”

“…Though FGF21 is mainly released by hepatocytes into circulation [119], its expression can be induced in skeletal muscle in response to acute exercise [120,121]. A co-receptor of FGF21, ßKlotho, is a singletransmembrane protein essential for FGF21 activity, which is abun- R [180] ↑mRNA in sWAT swim training (30d) R [100] ↑mRNA, protein in iWAT treadmill training (5 wk) R [56], [98] ↑mRNA in sWAT resistance training (8 wk) R [199] ↑mRNA in sWAT aerobic training (8 wk) R [200] ↑mRNA in sWAT treadmill (8 wk) R [22], [95], [185] mRNA in vWAT treadmill (8 wk) R [22], [185] ↑mRNA in eWAT treadmill training (8 wk) R [21] ↑protein in eWAT treadmill training (8 wk) R [112] ↑mRNA in iWAT treadmill training (8 wk) R [113] ↑protein in iWAT voluntary wheel running (10 wk) R [114] protein in eWAT voluntary wheel running (10 wk) R [114] mRNA in eWAT resistance, endurance training (10 wk) R [115] mRNA in sWAT endurance, interval training (10 wk) dantly found in adipose tissue, but not skeletal muscle [122,123]. This enables FGF21 to have unique actions on adipose tissue and skeletal muscle upon release [124].…”