Resistance exercise training increases mixed muscle protein synthesis rate in frail women and men >/=76 yr old. (9/356)

Muscle atrophy (sarcopenia) in the elderly is associated with a reduced rate of muscle protein synthesis. The purpose of this study was to determine if weight-lifting exercise increases the rate of muscle protein synthesis in physically frail 76- to 92-yr-old women and men. Eight women and 4 men with mild to moderate physical frailty were enrolled in a 3-mo physical therapy program that was followed by 3 mo of supervised weight-lifting exercise. Supervised weight-lifting exercise was performed 3 days/wk at 65-100% of initial 1-repetition maximum on five upper and three lower body exercises. Compared with before resistance training, the in vivo incorporation rate of [(13)C]leucine into vastus lateralis muscle protein was increased after resistance training in women and men (P < 0.01), although it was unchanged in five 82 +/- 2-yr-old control subjects studied two times in 3 mo. Maximum voluntary knee extensor muscle torque production increased in the supervised resistance exercise group. These findings suggest that muscle contractile protein synthetic pathways in physically frail 76- to 92-yr-old women and men respond and adapt to the increased contractile activity associated with progressive resistance exercise training.  (+info)

Insulin-like growth factor I in skeletal muscle after weight-lifting exercise in frail elders. (10/356)

To assess muscle remodeling and functional adaptation to exercise and diet interventions, 26 men and women aged 72-98 yr underwent a vastus lateralis biopsy before and after placebo control condition, and progressive resistance training, multinutrient supplementation, or both. Type II atrophy, Z band, and myofibril damage were present at baseline. Combined weight lifting and nutritional supplementation increased strength by 257 +/- 62% (P = 0.0001) and type II fiber area by 10.1 +/- 9.0% (P = 0.033), with a similar trend for type I fiber area (+12.8 +/- 22.2%). Exercise was associated with a 2. 5-fold increase in neonatal myosin staining (P = 0.0009) and an increase of 491 +/- 137% (P < 0.0001) in IGF-I staining. Ultrastructural damage increased by 141 +/- 59% after exercise training (P = 0.034). Strength increases were largest in those with the greatest increases in myosin, IGF-I, damage, and caloric intake during the trial. Age-related sarcopenia appears largely confined to type II muscle fibers. Frail elders respond robustly to resistance training with musculoskeletal remodeling, and significant increases in muscle area are possible with resistance training in combination with adequate energy intakes.  (+info)

Effects of heavy-resistance training on hormonal response patterns in younger vs. older men. (11/356)

To examine the adaptations of the endocrine system to heavy-resistance training in younger vs. older men, two groups of men (30 and 62 yr old) participated in a 10-wk periodized strength-power training program. Blood was obtained before, immediately after, and 5, 15, and 30 min after exercise at rest before and after training and at rest at -3, 0, 6, and 10 wk for analysis of total testosterone, free testosterone, cortisol, growth hormone, lactate, and ACTH analysis. Resting values for insulin-like growth factor (IGF)-I and IGF-binding protein-3 were determined before and after training. A heavy-resistance exercise test was used to evaluate the exercise-induced responses (4 sets of 10-repetition maximum squats with 90 s of rest between sets). Squat strength and thigh muscle cross-sectional area increased for both groups. The younger group demonstrated higher total and free testosterone and IGF-I than the older men, training-induced increases in free testosterone at rest and with exercise, and increases in resting IGF-binding protein-3. With training the older group demonstrated a significant increase in total testosterone in response to exercise stress along with significant decreases in resting cortisol. These data indicate that older men do respond with an enhanced hormonal profile in the early phase of a resistance training program, but the response is different from that of younger men.  (+info)

Increase in blood bradykinin concentration after eccentric weight-training exercise in men. (12/356)

The purpose of this study was to verify the possible appearance in the blood of bradykinin (BK) and des-Arg(9)-bradykinin (des-Arg(9)-BK) after eccentric exercise in 13 male subjects. Eccentric exercise (5 x 10 leg presses at 120% maximal voluntary concentric contraction) resulted in muscle damage and inflammation, as suggested by the significant increase in serum creatine kinase activity (from 204 +/- 41 to 322 +/- 63 U/l 12 h postexercise) and by severe lasting pain, which also peaked at 12 h postexercise. Blood BK and des-Arg(9)-BK concentrations were measured by competitive enzyme immunoassays using highly specific polyclonal rabbit IgG. Des-Arg(9)-BK concentration was not modified (preexercise: 44 +/- 14 pmol/l; pooled postexercise: 47 +/- 4 pmol/l). In contrast, BK concentration significantly increased immediately after the exercise session (68 +/- 9 vs. 42 +/- 3 pmol/l preexercise) and returned to basal values at 12, 24, and 48 h (pooled value: 40 +/- 4 pmol/l). This observation suggests that the inflammatory process due to eccentric exercise-induced muscle damage could be mediated in part by BK.  (+info)

Dissociation of peak vascular conductance and V(O2) max among highly trained athletes. (13/356)

Previously, a strong relationship has been found between whole body maximal aerobic power (VO(2 max)) and peak vascular conductance in the calf muscle (J. L. Reading, J. M. Goodman, M. J. Plyley, J. S. Floras, P. P. Liu, P. R. McLaughlin, and R. J. Shephard. J. Appl. Physiol. 74: 567-573, 1993; P. G. Snell, W. H. Martin, J. C. Buckley, and C. G. Blomqvist. J. Appl. Physiol. 62: 606-610, 1987), suggesting a matching between maximal exercise capacity and peripheral vasodilatory reserve across a broad range of aerobic power. In contrast, long-term training could alter this relationship because of the unique demands for muscle blood flow and cardiac output imposed by different types of training. In particular, the high local blood flows but relatively low cardiac output demand imposed by the type of resistance training used by bodybuilders may cause a relatively greater development in peripheral vascular reserve than in aerobic power. To examine this possibility, we studied the relationship between treadmill VO(2 max) and vascular conductance in the calf by using strain-gauge plethysmography after maximal ischemic plantar flexion exercise in 8 healthy sedentary subjects (HS) and 28 athletes. The athletes were further divided into three groups: 10 elite middle-distance runners (ER), 11 power athletes (PA), and 7 bodybuilders (BB). We found that both BB and ER deviate from the previously demonstrated relationship between VO(2 max) and vascular conductance. Specifically, for a given vascular conductance, BB had a lower VO(2 max), whereas ER had a higher VO(2 max) than did HS and PA. We conclude that the relationship between peak vascular conductance and aerobic power is altered in BB and ER because of training-specific effects on central vs. peripheral cardiovascular adaptation to local skeletal muscle metabolic demand.  (+info)

Pixel T2 distribution in functional magnetic resonance images of muscle. (14/356)

Increases in skeletal muscle (1)H-NMR transverse relaxation time (T2) observed by magnetic resonance imaging have been used to map whole muscle activity during exercise. Some studies further suggest that intramuscular variations in T2 after exercise can be used to map activity on a pixel-by-pixel basis by defining an active T2 threshold and counting pixels that exceed the threshold as "active muscle." This implies that motor units are nonrandomly distributed across the muscle and, therefore, that the distribution of pixel T2 values ought to be substantially broader after moderate exercise than at rest or after more intense exercise, since moderate-intensity exercise should recruit some motor units, and hence some pixels, but not others. This study examined the distribution of pixel T2 values in three muscles (quadriceps, anterior tibialis, and biceps/brachialis) of healthy subjects (5 men and 2 women, 18-46 yr old) at rest, after exercise to fatigue (50% 1 repetition maximum at 20/min to failure = Max), and at 1/2Max (25% 1 repetition maximum, same number of repetitions as Max). Although for each muscle there was a linear relationship between exercise intensity and mean pixel T2, there was no significant difference in the variance of pixel T2 between 1/2Max and Max exercise. There was a modest (10-43%) increase in variance of pixel T2 after both exercises compared with rest, but this was consistent with a Monte Carlo simulation of muscle activity that assumed a random distribution of motor unit territories across the muscle and a random distribution of muscle cells within each motor unit's territory. In addition, 40% of the pixel-to-pixel muscle T2 variations were shown to be due to imaging noise. The results indicate that magnetic resonance imaging T2 cannot reliably map active muscle on a pixel-by-pixel basis in normal subjects.  (+info)

Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men. (15/356)

This study examined the effects of acute dehydroepiandrosterone (DHEA) ingestion on serum steroid hormones and the effect of chronic DHEA intake on the adaptations to resistance training. In 10 young men (23 +/- 4 yr old), ingestion of 50 mg of DHEA increased serum androstenedione concentrations 150% within 60 min (P < 0.05) but did not affect serum testosterone and estrogen concentrations. An additional 19 men (23 +/- 1 yr old) participated in an 8-wk whole body resistance-training program and ingested DHEA (150 mg/day, n = 9) or placebo (n = 10) during weeks 1, 2, 4, 5, 7, and 8. Serum androstenedione concentrations were significantly (P < 0.05) increased in the DHEA-treated group after 2 and 5 wk. Serum concentrations of free and total testosterone, estrone, estradiol, estriol, lipids, and liver transaminases were unaffected by supplementation and training, while strength and lean body mass increased significantly and similarly (P < 0.05) in the men treated with placebo and DHEA. These results suggest that DHEA ingestion does not enhance serum testosterone concentrations or adaptations associated with resistance training in young men.  (+info)

Skeletal muscle strength and endurance in patients with mild COPD and the effects of weight training. (16/356)

This study poses two questions: 1) is there an abnormality in isokinetic skeletal muscle strength and endurance in mild chronic obstructive pulmonary disease (COPD)? and 2) what is the effect of a randomized, controlled, 12 week hospital outpatient weight training programme in terms of skeletal muscle function and exercise tolerance? Upper and lower limb isokinetic maximum and sustained muscle function were compared in 43 COPD patients (age 49+/-11 yrs), mean forced expiratory volume in one second (FEV1) 77+/-23% pred and 52 healthy, sedentary subjects (age 51 (10) yrs), mean FEV1 109+/-16% pred. The 43 COPD patients were randomly allocated into training (n=26) and control (n=17) groups. Isokinetic and isotonic muscle function, whole body endurance, maximal exercise capacity and lung function were measured. The COPD patients had reduced isokinetic muscle function (with the exception of sustained upper limb strength) as compared with healthy sedentary subjects. Muscle function improved after weight training in the COPD patients. Whole body endurance during treadmill walking also improved with no change in maximal oxygen consumption. A deficit in skeletal muscle function can be identified in patients with mild chronic obstructive pulmonary disease which cannot be explained by factors such as hypoxaemia and malnutrition. Intervention with weight training is effective in countering this deficit which the authors conclude is probably due to muscle deconditioning.  (+info)