Strength training combined with plyometric jumps in adults: sex differences in fat-bone axis adaptations

[EN] Leptin and osteocalcin play a role in the regulation of the fat-bone axis and may be altered by exercise. To determine whether osteocalcin reduces fat mass in humans fed ad libitum and if there is a sex dimorphism in the serum osteocalcin and leptin responses to strength training, we studied 43 male (age 23.9 2.4 yr, mean +/- SD) and 23 female physical education students (age 23.2 +/- 2.7 yr). Subjects were randomly assigned to two groups: training (TG) and control (CG). TG followed a strength combined with plyometric jumps training program during 9 wk, whereas the CG did not train. Physical fitness, body composition (dual-energy X-ray absorptiometry), and serum concentrations of hormones were determined pre- and posttraining. In the whole group of subjects (pretraining), the serum concentration of osteocalcin was positively correlated (r = 0.29-0.42, P < 0.05) with whole body and regional bone mineral content, lean mass, dynamic strength, and serum-free testosterone concentration (r = 0.32). However, osteocalcin was negatively correlated with leptin concentration (r = -0.37), fat mass (r = -0.31), and the percent body fat (r = -0.44). Both sexes experienced similar relative improvements in performance, lean mass (+4-5%), and whole body (+0.78%) and lumbar spine bone mineral content (+1.2-2%) with training. Serum osteocalcin concentration was increased after training by 45 and 27% in men and women, respectively (P < 0.05). Fat mass was not altered by training. Vastus lateralis type II MHC composition at the start of the training program predicted 25% of the osteocalcin increase after training. Serum leptin concentration was reduced with training in women. In summary, while the relative effects of strength training plus plyometric jumps in performance, muscle hypertrophy, and osteogenesis are similar in men and women, serum leptin concentration is reduced only in women. The osteocalcin response to strength training is, in part, modulated by the muscle phenotype (MHC isoform composition). Despite the increase in osteocalcin, fat mass was not reduced.

Leptin receptor 170 kDa (OB-R170) protein expression is reduced in obese human skeletal muscle: a potential mechanism of leptin resistance

[EN] To examine whether obesity-associated leptin resistance could be due to down-regulation of leptin receptors (OB-Rs) and/or up-regulation of suppressor of cytokine signalling 3 (SOCS3) and protein tyrosine phosphatase 1B (PTP1B) in skeletal muscle, which blunt janus kinase 2-dependent leptin signalling and signal transducer and activator of transcription 3 (STAT3) phosphorylation and reduce AMP-activated protein kinase (AMPK) and acetyl-coenzyme A carboxylase (ACC) phosphorylation. Deltoid and vastus lateralis muscle biopsies were obtained from 20 men: 10 non-obese control subjects (mean +/- s.d. age, 31 +/- 5 years; height, 184 +/- 9 cm; weight, 91 +/- 13 kg; and percentage body fat, 24.8 +/- 5.8%) and 10 obese (age, 30 +/- 7 years; height, 184 +/- 8 cm; weight, 115 +/- 8 kg; and percentage body fat, 34.9 +/- 5.1%). Skeletal muscle OB-R170 (OB-R long isoform) protein expression was 28 and 25% lower (both P < 0.05) in arm and leg muscles, respectively, of obese men compared with control subjects. In normal-weight subjects, SOCS3 protein expression, and STAT3, AMPKalpha and ACCbeta phosphorylation, were similar in the deltoid and vastus lateralis muscles. In obese subjects, the deltoid muscle had a greater amount of leptin receptors than the vastus lateralis, whilst SOCS3 protein expression was increased and basal STAT3, AMPKalpha and ACCbeta phosphorylation levels were reduced in the vastus lateralis compared with the deltoid muscle (all P < 0.05). In summary, skeletal muscle leptin receptors and leptin signalling are reduced in obesity, particularly in the leg muscles.