Adaptations in human muscle sarcoplasmic reticulum to prolonged submaximal training.

In this study, we employed single-leg submaximal cycle training, conducted over a 10-wk period, to investigate adaptations in sarcoplasmic reticulum (SR) Ca(2+)-regulatory proteins and processes of the vastus lateralis. During the final weeks, the untrained volunteers (age 21.4 +/- 0.3 yr; means +/- SE, n = 10) were exercising 5 times/wk and for 60 min/session. Analyses were performed on tissue extracted by needle biopsy approximately 4 days after the last training session. Compared with the control leg, the trained leg displayed a 19% reduction (P < 0.05) in homogenate maximal Ca(2+)-ATPase activity (192 +/- 11 vs. 156 +/- 18 micromol. g protein(-1). min(-1)), a 4.3% increase (P < 0.05) in pCa(50), defined as the Ca(2+) concentration at half-maximal activity (6.01 +/- 0.05 vs. 6.26 +/- 0.07), and no change in the Hill coefficient (1.75 +/- 0.15 vs. 1.76 +/- 0.21). Western blot analysis using monoclonal antibodies (7E6 and A52) revealed a 13% lower (P < 0.05) sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) 1 in trained vs. control in the absence of differences in SERCA2a. Training also resulted in an 18% lower (P < 0.05) SR Ca(2+) uptake and a 26% lower (P < 0.05) Ca(2+) release. It is concluded that a downregulation in SR Ca(2+) cycling in vastus lateralis occurs with aerobic-based training, which at least in the case of Ca(2+) uptake can be explained by reduction in Ca(2+)-ATPase activity and SERCA1 protein levels.

Post exercise hypotension is not mediated by the serotonergic system in borderline hypertensive individuals.

Recent evidence from our laboratory and others have suggested that the mechanism for a decrease in resting blood pressure after an acute bout of exercise is a centrally mediated decrease in total peripheral resistance. This study examined the effect of the central serotonergic system on post exercise hypotension (PEH) in 11 borderline hypertensive individuals (nine male, two female) aged 24.5 +/- 5.1 years. Each subject completed two, 30-min cycling bouts at 70% of VO2peak while under placebo or a selective serotonin re-uptake inhibitor (SSRI) treatment. Blood pressure was recorded directly from the radial artery, and treatments were randomised, double blinded and separated by at least 14 days. Baseline blood pressure was 145/72 mm Hg for systolic (SBP) and diastolic (DBP) respectively. Peripheral measures of serotonin (5-HT) were lower under SSRI treatment, whereas the major 5-HT metabolite, 5-hydroxyindoleacetic acid, was not significantly changed, indicating elevated central 5-HT levels. There was no difference in any of the haemodynamic variables between trials. Despite an increased heart rate for the initial 75 min post exercise, SBP was decreased as much as 23 mm Hg during the initial 60 min post exercise, after which it had returned to normal. DBP was unchanged after exercise. Circulating adrenaline (0.60 +/- 0.14 ng/mL to 1.3 +/- 1.6 ng/ml) and noradrenaline (0.27 +/- 0.31 ng/ml to 4.5 +/- 2.1 ng/ml) were significantly elevated during exercise. Both returned to pre-exercise levels within 15 min post exercise. Unexpectedly, oxygen uptake was slightly (5%), but significantly increased over the entire duration of the SSRI trial. We conclude that the central serotonergic system is not responsible for PEH in our borderline hypertensive population.

Creatine-dextrose and protein-dextrose induce similar strength gains during training.

BACKGROUND: Creatine supplementation during resistance exercise training has been reported to induce greater increases in fat-free mass (FFM), muscle fiber area, and strength when compared with a placebo. We have recently shown that timing of nutrient delivery in the postexercise period can have positive effects on whole body protein turnover (B. D. Roy et al., Med Sci Sports Exerc. 32(8):1412-1418, 2000). PURPOSE: We tested the hypothesis that a postexercise protein-carbohydrate supplement would result in similar increases in FFM, muscle fiber area, and strength as compared with creatine monohydrate (CM), during a supervised 2-month resistance exercise training program in untrained men. METHODS: Young healthy male subjects were randomized to receive either CM and glucose (N = 11; CM 10 g + glucose 75 g [CR-CHO] (CELL-Tech)) or protein and glucose (N = 8; casein 10 g + glucose 75 g [PRO+CHO]), using double-blinded allocation. Participants performed 8 wk of whole body split-routine straight set weight training, 1 h.d(-1), 6 d.wk(-1). Measurements, pre- and post-training were made of fat-free mass (FFM; DEXA), total body mass, muscle fiber area, isokinetic knee extension strength (45 and 240 degrees.s(-1)), and 1 repetition maximal (1RM) strength for 16 weight training exercises. RESULTS: Total body mass increased more for CR-CHO (+4.3 kg, 5.4%) as compared with PRO-CHO (+1.9 kg, 2.4%) (P < 0.05 for interaction) and FFM increased after training (P < 0.01) but was not significantly different between the groups (CR-CHO = +4.0 kg, 6.4%; PRO-CHO = +2.6 kg, 4.1%) (P = 0.11 for interaction). Muscle fiber area increased similarly after training for both groups (approximately 20%; P < 0.05). Training resulted in an increase in 1RM for each of the 16 activities (range = 14.2-39.9%) (P < 0.001), isokinetic knee extension torque (P < 0.01), with no treatment effects upon any of the variables. CONCLUSIONS: We concluded that postexercise supplementation with PRO-CHO resulted in similar increases in strength after a resistance exercise training program as compared with CR-CHO. However, the greater gains in total mass for the CR-CHO group may have implications for sport-specific performance.

The acute effects of androstenedione supplementation in healthy young males.

We examined the effects of androstenedione supplementation on the hormonal profile of 10 males and its interaction with resistance exercise. Baseline testosterone, luteinizing hormone, estradiol, and androstenedione concentrations were established by venous sampling at 3 hr intervals over 24 hr. Subjects ingested 200 mg of androstenedione daily for 2 days, with second and third day blood samples. Two weeks later, they ingested androstenedione or a placebo for 2 days, in a double-blind, cross-over design. On day 2, they performed heavy resistance exercise with blood sampled before, after, and 90 min post. The supplement elevated plasma androstenedione 2--3-fold and luteinizing hormone approximately 70% but did not alter testosterone concentration. Exercise elevated testosterone, with no difference between conditions. Exercise in the supplemented condition significantly elevated plasma estradiol by approximately 83% for 90 min. Androstenedione supplementation, thus, is unlikely to provide male athletes with any anabolic benefit and, with heavy resistance exercise, elevates estrogen.