Resistance exercise can acutely increase the concentrations of circulating neuroendocrine factors, but the effect of mode on this response is not established. The purpose of this study was to examine the effect of resistance exercise selection on the acute hormonal response using similar lower-body multijoint movement free weight and machine weight exercises. Ten resistance trained men (25 ± 3 years, 179 ± 7 cm, 84.2 ± 10.5 kg) completed 6 sets of 10 repetitions of squat or leg press at the same relative intensity separated by 1 week. Blood samples were collected before (PRE), immediately after (IP), and 15 (P15) and 30 minutes (P30) after exercise, and analyzed for testosterone (T), growth hormone (GH), and cortisol (C) concentrations. Exercise increased (p ≤ 0.05) T and GH at IP, but the concentrations at IP were greater for the squat (T: 31.4 ± 10.3 nmol·L(-1); GH: 9.5 ± 7.3 μg·L(-1)) than for the leg press (T: 26.9 ± 7.8 nmol·L(-1); GH: 2.8 ± 3.2 μg·L(-1)). At P15 and P30, GH was greater for the squat (P15: 12.3 ± 8.9 μg·L(-1); P30: 12.0 ± 8.9 μg·L(-1)) than for the leg press (P15: 4.8 ± 3.4 μg·L(-1); P30: 5.4 ± 4.1 μg·L(-1)). C was increased after exercise and was greater for the squat than for the leg press. Although total work (external load and body mass moved) was greater for the squat than for the leg press, rating of perceived exertion did not differ between the modes. Free weight exercises seem to induce greater hormonal responses to resistance exercise than machine weight exercises using similar lower-body multijoint movements and primary movers.

Duplanty, AA, Budnar, RG, Luk, HY, Levitt, DE, Hill, DW, McFarlin, BK, Huggett, DB, and Vingren, JL. Effect of acute alcohol ingestion on resistance exercise–induced mTORC1 signaling in human muscle. J Strength Cond Res 31(1): 54–61, 2017—The purpose of this project was to further elucidate the effects postexercise alcohol ingestion. This project had many novel aspects including using a resistance exercise (RE) only exercise design and the inclusion of women. Ten resistance-trained males and 9 resistance-trained females completed 2 identical acute heavy RE trials (6 sets of Smith machine squats) followed by ingestion of either alcohol or placebo. All participants completed both conditions. Before exercise (PRE) and 3 (+3 hours) and 5 (+5 hours) hours postexercise, muscle tissue samples were obtained from the vastus lateralis by biopsies. Muscle samples were analyzed for phosphorylated mTOR, S6K1, and 4E-BP1. For men, there was a significant interaction effect for mTOR and S6K1 phosphorylation. At +3 hours, mTOR and S6K1 phosphorylation was higher for placebo than for alcohol. For women, there was a significant main effect for time. mTOR phosphorylation was higher at +3 hours than at PRE and at +5 hours. There were no significant effects found for 4E-BP1 phosphorylation in men or women. The major findings of this study was that although RE elicited similar mTORC1 signaling both in men and in women, alcohol ingestion seemed to only attenuate RE-induced phosphorylation of the mTORC1 signaling pathway in men. This study provides evidence that alcohol should not be ingested after RE as this ingestion could potentially hamper the desired muscular adaptations to RE by reducing anabolic signaling, at least in men.

Fter a bout of heavy resistance exercise. Methods Eight resistance-trained men (mean ± SD: 25.3 ± 3.2 yr, 87.7 ± 15.1 kg, 177 ± 7 cm) completed two identical acute heavy resistance exercise tests (AHRET: six sets of 10 repetitions of Smith machine squats) separated by 1 wk. Post-AHRET, participants consumed either 1.09 g of grain ethanol per kilogram lean mass (EtOH condition) or no ethanol (placebo condition). Blood samples were collected immediately before exercise (PRE), immediately after exercise (IP), and every 20 min postexercise for 300 min. Samples after IP were pooled into phases (20–40 min, 60–120 min, and 140–300 min after exercise) and analyzed for total testosterone (TT) and free testosterone (FT), sex hormone-binding globulin (SHBG), cortisol, and estradiol. Results Peak blood ethanol concentration (0.088 ± 0.015 g·dL−1) was achieved 60–90 min postexercise. TT and FT were elevated significantly (P ≤ 0.05) at IP for both conditions. At 140–300 min postexercise, TT, FT, and free androgen index were significantly higher for EtOH (TT: 22.5 ± 12.5 nmol·L−1; FT: 40.5 ± 7.6 pmol·L−1) than for placebo (TT: 13.9 ± 6.8 nmol·L−1; FT: 22.7 ± 10.0 pmol·L−1). No differences between conditions were noted for SHBG, cortisol, or estradiol. Conclusion Postexercise ethanol ingestion affects the hormonal milieu including testosterone concentration and bioavailability during recovery from resistance exercise....

The purpose of this investigation was to examine the acute hormonal response to the kettlebell swing exercise. Ten recreationally resistance trained men (age, 24 ± 4 years; height, 175 ± 6 cm; body mass, 78.7 ± 9.9 kg) performed 12 rounds of 30 seconds of 16 kg kettlebell swings alternated with 30 seconds of rest. Blood samples were collected before (PRE), immediately after (IP), and 15 (P15) and 30 minutes after exercise (P30) and analyzed for testosterone (T), immunoreactive growth hormone, cortisol (C), and lactate concentrations. Heart rate and rating of perceived exertion were measured at the end of each round. Testosterone was significantly higher (p ≤ 0.05) at IP than at PRE, P15, or P30 (PRE: 28 ± 3; IP: 32 ± 4; P15: 29 ± 3; P30: 27 ± 3 nmol·L). Growth hormone was higher at IP, P15, and P30 than at PRE (PRE: 0.1 ± 0.1; IP: 1.8 ± 1.2; P15: 2.1 ± 1.1; P30: 1.6 ± 1.3 μg·L). Cortisol was higher at IP and P15 than at PRE and P30 (PRE: 617 ± 266; IP: 894 ± 354; P15: 875 ± 243; P30: 645 ± 285 nmol·L). Lactate was higher at IP, P15, and P30 than at PRE (PRE: 1.1 ± 0.5; IP: 7.0 ± 3.0; P15: 4.0 ± 2.7; P30: 2.5 ± 1.8 mmol·L). Heart rate increased progressively from 57 ± 12 at PRE to 170 ± 10 at IP. The exercise protocol produced an acute increase in hormones involved in muscle adaptations. Thus, the kettlebell swing exercise might provide a good supplement to resistance training programs.

Alcohol use disorders are more prevalent in HIV patients than the general population. Both chronic alcohol consumption and HIV infection have been linked to mitochondrial dysregulation; and this is considered an important mechanism in the pathogenesis of muscle myopathy. This study investigated if chronic binge alcohol (CBA) administration impairs the expression of genes involved in mitochondrial homeostasis in SIV-infected macaques. Male rhesus macaques were administered daily CBA (to achieve peak blood alcohol concentrations of 50–60 mM within 2 h after start of infusion) or sucrose (SUC) intragastrically 3 months prior to intravenous SIV_mac251 inoculation and continued until macaques met criteria for end-stage disease. Skeletal muscle (SKM) samples were obtained at necropsy. Muscle samples were obtained from a cohort of healthy uninfected macaque controls and used for comparison of analyzed variables. Total RNA was extracted and gene expression was analyzed by quantitative polymerase chain reaction. The relative expression of peroxisome proliferator-activated receptor gamma coactivator-1 beta (PGC-1β) was significantly decreased in the SKM of CBA/simian immunodeficiency virus (SIV) macaques compared to uninfected controls (P < 0.05). SIV infection resulted in a significant upregulation (P < 0.05) of mitophagy-related gene expression, which was prevented by CBA. CBA suppressed expression of anti-apoptotic genes and increased expression of pro-apoptotic genes (P < 0.05). These findings suggest that SIV infection disrupts mitochondrial homeostasis and when combined with CBA, results in differential expression of genes involved in apoptotic signaling. We speculate that impaired mitochondrial homeostasis may contribute to the underlying pathophysiology of alcoholic and HIV/AIDS associated myopathy. This study investigated if CBA administration dysregulates gene expression associated with mitochondrial homeostasis in the SKM of SIV-infected macaques. The results suggest that SIV infection disrupts mitochondrial homeostasis and when combined with CBA, results in differential expression of genes involved in apoptotic signaling.

Supplementation with cannabidiol (CBD) may expedite recovery when consumed after exercise. The purpose of this study was to determine if supplementation with CBD reduces inflammation and enhances performance following strenuous eccentric exercise in collegiate athletes. Twenty-four well-trained females (age = 21.2 ± 1.8 years, height = 166.4 ± 8 cm, weight = 64.9 ± 9.1 kg) completed 100 repetitions of unilateral eccentric leg extension to induce muscle damage. In this crossover design, participants were randomized to receive 5 mg/kg of CBD in pill form or a placebo 2 h prior to, immediately following, and 10 h following muscle damage. Blood was collected, and performance and fatigue were measured prior to, and 4 h, 24 h, and 48 h following the muscle damage. Approximately 28 days separated treatment administration to control for the menstrual cycle. No significant differences were observed between the treatments for inflammation, muscle damage, or subjective fatigue. Peak torque at 60°/s (p = 0.001) and peak isometric torque (p = 0.02) were significantly lower 24 h following muscle damage, but no difference in performance was observed between treatments at any timepoint. Cannabidiol supplementation was unable to reduce fatigue, limit inflammation, or restore performance in well-trained female athletes.