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Increased maximum muscle strength and reduced muscle damage in elite weightlifters following low-load, high-repetition resistance training

This study investigated the effects of different resistance training (RT) interventions on body composition, muscle dam­ age, intramuscular anabolic signaling, and maximum muscle strength (MMS). Eighteen male weightlifters (age: 20.22±0.24 years; body weight: 86.39±3.99 kg; Height: 172.27±8.09; experience: 9.5±0.27 years) were randomly assigned to three groups that completed 8 weeks of RT (3–4 h/day, 3 days/week, 8 exercises): (a) high-load, low-repetition (HL) (60–90% of 1-repetition maximum [1-RM], 2–3 sets, 1–3 repetitions, n=6), (b) low-load, high-repetition (LH) (30–60% of 1-RM, 4–5 sets, 5–8 repetitions, n=6), and (c) combination thereof (COMBI, n=6). All RT interventions significantly (p<0.05) increased skeletal muscle mass and growth hormone levels, which ultimately contributed to improvement in MMS as indicated by the 1-RM of back squat and back muscle strength (BMS) (p<0.05, respectively). Interestingly, phosphorylation of p70 ribosomal protein S6 kinase 1 (p70S6K1) was higher, whereas phosphorylation of eukaryotic initiation factor 4E-binding protein 1 (4E­ BP1) was lower following LH- compared with HL- and COMBI-RT. Phosphorylation of eukaryotic elongation factor 2 (eEF2) significantly decreased after RT in the LH-RT and HL-RT groups. Furthermore, creatine kinase and lactate dehydrogenase levels were significantly lower in the LH- compared with the HL- and COMBI-RT groups. Thus, our results demonstrated that LH-RT increases skeletal muscle mass and MMS, similarly to HL-RT, while reducing RT-induced muscle damage mark­ ers in elite weightlifters. These results may help elite weightlifters and coaches in the development of RT programs to im­ prove exercise performance. Sex steroid hormones (androgens and estrogens) are involved in a variety of physiological and pathological processes. Sex steroid hormone levels also decrease with aging and are thought to be a factor in muscle atrophy such as sarcopenia. Thus, sex steroid hormones play an important role in skeletal muscular homeostasis. The plasticity of skeletal muscle facilitates adaptation to various stimuli. Recently, skeletal muscle is recognized as a secre­ tory organ because a numbers of studies have demonstrated that bioactive factors such as irisin, IL-6, are secreted from skel­ etal muscle. Sex steroid hormones are synthesized from cholesterol by steroidogenic enzymes. Testosterone is also converted into its bioactive metabolite dihydrotestosterone (DHT) by 5α-reductase. Previous study reported that sex steroid hormones are produced by various peripheral target tissues including the kidney, liver, and brain in addition to endocrine organs such as the testis or ovary. We and others demonstrated that these steroidogenic enzymes were expressed in skeletal muscle, and skeletal muscle locally converted testosterone and estradiol from dehydroepiandrosterone (DHEA). It is likely that skeletal muscles are capable of locally synthesizing sex hormones. Exercise is known to stimulate the secretion of circulating sex steroid hormones, resulting in skeletal muscular adaptation. We evaluated whether the muscular steroidogenetic system is changed by exercise stimulation. Interestingly, physical exercise activates local steroidogenic enzymes expression and steroidogenesis in skeletal muscle of rats and humans. Previous reported that endurance exercise training enhances the muscular DHT concentration through 5α-reductase in the skeletal muscle of rats, suggesting that local bioactive androgen metabolism may participate in exercise training-induced skeletal muscular adap­ tation. Therefore, local steroidogenesis in skeletal muscle may play an important role in the plasticity of skeletal muscle and have the physiological significance of the sex steroid hormone network of circulation and skeletal muscle.