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The purpose of this study was to determine the influence of transiently elevated endogenous hormone concentrations during exercise on strength training adaptations. Nine subjects performed four unilateral strength training session per week on the elbow flexors for 11 weeks. During two of the weekly sessions, leg exercises were performed to acutely increase the systemic anabolic hormone concentration immediately before the exercises for one of the elbow flexors (L + A). On the two other weekly training sessions, the contralateral elbow flexors were trained without prior leg exercises (A). By randomizing one arm of the subjects to serve as a control and the other as experimental, both conditions have the same nutritional and genetic environment. Serum testosterone and growth hormone was significantly increased during the L - A training session, while no hormonal changes occurred in the A session. Both A and L + A increased 1RM in biceps curl, peak power in elbow flexors at 30 and 60% of 1RM, and muscle volume of the elbow flexors (p < 0.05). However, only L + A achieved increase in CSA at the part of the arm flexors with largest cross sectional area (p < 0.001), while no changes occurred in A. L + A had superior relative improvement in 1RM biceps curl and favorable muscle adaptations in elbow flexors compared to A (p < 0.05). In conclusion, performing leg exercises prior to arm exercises, and thereby increasing the levels of serum testosterone and growth hormone, induced superior strength training adaptations compared to arm training without acute elevation of hormones. [ABSTRACT FROM AUTHOR]

The response of calf muscle strength, resting (R (bf)) and post-occlusive (PO(bf)) blood flow were investigated following 4 weeks resistance training with and without blood flow restriction in a matched leg design. Sixteen untrained females performed unilateral plantar-flexion low-load resistance training (LLRT) at either 25% (n = 8) or 50% (n = 8) one-repetition maximum (1 RM). One limb was trained with unrestricted blood flow whilst in the other limb blood flow was restricted with the use of a pressure applied cuff above the knee (110 mmHg). Regardless of the training load, peak PO(bf), measured using venous occlusion plethysmography increased when LLRT was performed with blood flow restriction compared to no change following LLRT with unrestricted blood flow. A significant increase (P < 0.05) in the area under the blood time-flow curve was also observed following LLRT with blood flow restriction when compared LLRT with unrestricted blood flow. No changes were observed in R (bf) between groups following training. Maximal dynamic strength (1 RM), maximal voluntary contraction and isokinetic strength at 0.52 and 1.05 rad s(-1) also increased (P < 0.05) by a greater extent following resistance training with blood flow restriction. Moreover, 1 RM increased to a greater extent following training at 50% 1 RM compared to 25% 1 RM. These results suggest that 4 weeks LLRT with blood flow restriction provides a greater stimulus to increase peak PO(bf) as well as strength parameters than LLRT with unrestricted blood flow. [ABSTRACT FROM AUTHOR]

Investigations of training effects on exercise energy cost have yielded conflicting results. The purpose of the present study was to compare quadriceps energy cost and oxidative capacity between endurance-trained and sedentary subjects during a heavy dynamic knee extension exercise. We quantified the rates of ATP turnover from oxidative and anaerobic pathways with (31)P-MRS, and we measured simultaneously pulmonary oxygen uptake in order to assess both total ATP production [i.e., energy cost (EC)] and O(2) consumption (O(2) cost) scaled to power output. Seven sedentary (SED) and seven endurance-trained (TRA) subjects performed a dynamic standardized rest-exercise-recovery protocol at an exercise intensity corresponding to 35% of maximal voluntary contraction. We showed that during a dynamic heavy exercise, the O(2) cost and EC were similar in the SED and endurance-trained groups. For a given EC, endurance-trained subjects exhibited a higher relative mitochondrial contribution to ATP production at the muscle level (84 +/- 12% in TRA and 57 +/- 12% in SED; P < 0.01) whereas the anaerobic contribution was reduced (18 +/- 12% in TRA and 44 +/- 11% in SED; P < 0.01). Our results obtained in vivo illustrate that on the one hand the beneficial effects of endurance training are not related to any reduction in EC or O(2) cost and on the other hand that this similar EC was linked to a change regarding the contribution of anaerobic and oxidative processes to energy production, i.e., a greater aerobic energy contribution associated with a concomitant reduction of the anaerobic energy supply. [ABSTRACT FROM AUTHOR]

In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and VO(2peak). Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO(2)) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO(2), heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at VO(2peak) (IHE group, SaO(2) at VO(2peak) baseline 91.23 +/- 1.10%, post 94.10 +/- 2.19%; P < 0.01, mean +/- SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO(2) (P < 0.01), and lowered cerebral TOI during heavy exercise (90% VO(2peak): -6.1 +/- 6.0 Delta%, P = 0.04). Conversely, muscle tHb at maximal exercise, was increased (2.4 +/- 1.8 DeltamicroM, P = 0.01, mean +/- 95 CL) following IHE, whilst de-oxygenated Hb at 90% of VO(2peak) was reduced (-0.9 +/- 0.8 DeltamicroM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged VO(2peak) following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations. [ABSTRACT FROM AUTHOR]

Evidence indicates that repeated-bouts of eccentric exercise (EE) do not exacerbate the extent of muscle damage indices, as compared to a single-bout. We hypothesized that molecular adaptations, under repeated-bouts of EE, would include suppression of muscle repair inhibitory factors such as myostatin and up-regulation of muscle repair positive regulatory factors such as myogenic regulatory factors (MRFs). Fifteen males were recruited for this study. The exercise group (n=9) successfully completed six sets of 15 reps of maximum voluntary eccentric contractions, for six consecutive days, using a dynamometer (Multicont-II). Blood and muscle biopsy samples were obtained from each subject 1 week prior to exercise, 2 days post the first training session, and 24 h after the last training session. Gene expression levels were determined using real-time RT-PCR. Blood samples were analyzed for creatine kinase (CK) and lactate-dehydrogenase (LDH) activity. Repeated-bouts of EE induced a large down-regulation of myostatin mRNA (-73%) which persisted throughout the study. The responses of MRFs were mild. At day 3 only myogenin increased significantly (1.9 fold) while MyoD decreased by 45%. Surprisingly, at day 7, despite the presence of muscle damage indices, all MRFs returned to the pre-exercise levels. The results of the present study showed that repeated-bouts of EE, for six consecutive days, dramatically decreased Myostatin mRNA expression but impaired the expression patterns of MRFs such that, with the exception of myogenin that showed a moderate non-sustained increase, MyoD and MYf5 response was minimal. [ABSTRACT FROM AUTHOR]