Alcohol (ethanol) and resistance exercise can independently affect circulating bioavailable testosterone concentration. PURPOSE: The purpose of this study was to examine the testosterone bioavailability and the anabolic endocrine milieu in response to acute ethanol ingestion following a bout of heavy resistance exercise. METHODS: Eight resistance trained men (mean +/- SD: 25.3 +/- 3.2 yrs, 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 week. Post-AHRET participants consumed either 1.086 g of grain ethanol per kg 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 following IP were pooled into phases (20-40 min, 60-120 min, and 140-300 min after exercise) and analyzed for total (TT) and free testosterone (FT), sex hormone binding globulin (SHBG), cortisol, and estradiol. RESULTS: Peak blood ethanol concentration (0.088 +/- 0.015 g[middle dot]dl-1) was achieved 60-90 min post-exercise. TT and FT was elevated significantly (p<=0.05) at IP for both conditions. At 140-300 min post-exercise TT, FT, and free androgen index were significantly higher for EtOH (TT: 22.5 +/- 12.5 nmol[middle dot]l-1 ; FT: 40.5 +/- 7.6 pmol[middle dot]l-1) than for Placebo (TT: 13.9 +/- 6.8 nmol[middle dot]l-1; FT: 22.7 +/- 10.0 pmol[middle dot]l-1). No differences between conditions were noted for SHBG, Cortisol, or Estradiol. CONCLUSION: Post-exercise ethanol ingestion affects the hormonal milieu including testosterone concentration and bioavailability during recovery from resistance exercise.
Mittwoch, 3. Juli 2013
Science: Resistance to aerobic exercise training causes metabolicdysfunction and reveals novel exercise-regulated signaling networks.
Low aerobic exercise capacity is a risk factor for diabetes and strong predictor of mortality; yet some individuals are "exercise resistant", and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease-risk, we used selective breeding for 15 generation to develop rat models of low- and high-aerobic response to training. Before exercise training, rats selected as low- and high-responders had similar exercise capacities. However, after 8-wks of treadmill training low-responders failed to improve their exercise capacity, while high-responders improved by 54%. Remarkably, low-responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the "exercise resistant" phenotype segregates with disease risk. Low-responders had impaired exercise-induced angiogenes0is in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low-responders. Low-responders had increased stress/inflammatory signaling and altered TGFβ signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease.
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