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Resistance Exercise (resistance + exercise)
Selected AbstractsEFFECTS OF ANTIOXIDANT SUPPLEMENTS COMBINED WITH RESISTANCE EXERCISE ON GAINS IN FAT-FREE MASS IN HEALTHY ELDERLY SUBJECTS: A PILOT STUDYJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 9 2008Mélissa Labonté Dtp No abstract is available for this article. [source] The role of phosphoinositide 3-kinase and phosphatidic acid in the regulation of mammalian target of rapamycin following eccentric contractionsTHE JOURNAL OF PHYSIOLOGY, Issue 14 2009T. K. O'Neil Resistance exercise induces a hypertrophic response in skeletal muscle and recent studies have begun to shed light on the molecular mechanisms involved in this process. For example, several studies indicate that signalling by the mammalian target of rapamycin (mTOR) is necessary for a hypertrophic response. Furthermore, resistance exercise has been proposed to activate mTOR signalling through an upstream pathway involving the phosphoinositide 3-kinase (PI3K) and protein kinase B (PKB); however, this hypothesis has not been thoroughly tested. To test this hypothesis, we first evaluated the temporal pattern of signalling through PI3K,PKB and mTOR following a bout of resistance exercise with eccentric contractions (EC). Our results indicated that the activation of signalling through PI3K,PKB is a transient event (<15 min), while the activation of mTOR is sustained for a long duration (>12 h). Furthermore, inhibition of PI3K,PKB activity did not prevent the activation of mTOR signalling by ECs, indicating that PI3K,PKB is not part of the upstream regulatory pathway. These observations led us to investigate an alternative pathway for the activation of mTOR signalling involving the synthesis of phosphatidic acid (PA) by phospholipase D (PLD). Our results demonstrate that ECs induce a sustained elevation in [PA] and inhibiting the synthesis of PA by PLD prevented the activation of mTOR. Furthermore, we determined that similar to ECs, PA activates mTOR signalling through a PI3K,PKB-independent mechanism. Combined, the results of this study indicate that the activation of mTOR following eccentric contractions occurs through a PI3K,PKB-independent mechanism that requires PLD and PA. [source] Resistance exercise increases leg muscle protein synthesis and mTOR signalling independent of sexACTA PHYSIOLOGICA, Issue 1 2010H. C. Dreyer Abstract Aim:, Sex differences are evident in human skeletal muscle as the cross-sectional area of individual muscle fibres is greater in men than in women. We have recently shown that resistance exercise stimulates mammalian target of rapamycin (mTOR) signalling and muscle protein synthesis in humans during early post-exercise recovery. Therefore, the aim of this study was to determine if sex influences the muscle protein synthesis response during recovery from resistance exercise. Methods:, Seventeen subjects, nine male and eight female, were studied in the fasted state before, during and for 2 h following a bout of high-intensity leg resistance exercise. Mixed muscle protein fractional synthetic rate was measured using stable isotope techniques and mTOR signalling was assessed by immunoblotting from repeated vastus lateralis muscle biopsy samples. Results:, Post-exercise muscle protein synthesis increased by 52% in the men and by 47% in the women (P < 0.05) and was not different between groups (P > 0.05). Akt phosphorylation increased in both groups at 1 h post-exercise (P < 0.05) and returned to baseline during 2 h post-exercise with no differences between groups (P > 0.05). Phosphorylation of mTOR and its downstream effector S6K1 increased significantly and similarly between groups during post-exercise recovery (P < 0.05). eEF2 phosphorylation decreased at 1- and 2 h post-exercise (P < 0.05) to a similar extent in both groups. Conclusion:, The contraction-induced increase in early post-exercise mTOR signalling and muscle protein synthesis is independent of sex and appears to not play a role in the sexual dimorphism of leg skeletal muscle in young men and women. [source] Cardiac autonomic function and baroreflex changes following 4 weeks of resistance versus aerobic training in individuals with pre-hypertensionACTA PHYSIOLOGICA, Issue 3 2009S. R. Collier Abstract Aim:, Cardiac autonomic modulation and baroreflex sensitivity (BRS) are altered in individuals with hypertension. Aerobic exercise (AE) training has been shown to improve both measures, yet little is known about the effects of resistance exercise (RE). The purpose of this study was to examine the heart rate variability (HRV) and BRS following 4 weeks of resistance or aerobic training in a population with borderline high blood pressure (BP). Methods:, Twenty-nine mild hypertensives were recruited and randomly assigned to 4 weeks of RE or AE training. Before and after training, resting measures of HRV frequencies and BRS were obtained. Results:, There was a significant decrease in resting systolic BP for both exercise training modes (RE 136 ± 3.0 pre- to 132 ± 3.4 post-training vs. AE 142 ± 4.0 pre- to 137 ± 3.6 mmHg post-training, P = 0.019). Diastolic BP decreased significantly following both exercise training modes (RE 78 ± 1.31 pre to 74 ± 1.1 post vs. AE 80 ± 1.7 pre to 77 ± 1.6 mmHg post, P = 0.002). A significant time by training mode interaction for low frequency : high frequency (HF) ratio (P = 0.017) with AE decreasing the ratio (275.21 ± 67.28 to 161.26 ± 61.49) and RE increasing this ratio (143.73 ± 65.00 to 227.83 ± 59.41). Natural log-transformed (ln) HRV values showed a time-by-training mode interaction for ln HF (P = 0.05) as ln HF increased (4.7 ± 0.38 to 5.4 ± 0.35 ms2) following AE and decreased (5.98 ± 0.37 to 5.76 ± 0.42 ms2) following RE. BRS increased following aerobic training and decreased after resistance training (6.74 ± 1.2 to 7.94 ± 1.3 and 10.44 ± 1.2 to 9.1 ± 1.2 ms mmHg,1 respectively, P = 0.021). Conclusions:, Aerobic exercise improved the autonomic nervous system (increasing vagal tone, reducing sympathovagal balance while increasing BRS) while RE showed no improvements in cardiac autonomic tone and decreased BRS. [source] Human soleus muscle protein synthesis following resistance exerciseACTA PHYSIOLOGICA, Issue 2 2004T. A. Trappe Abstract Aim:, It is generally believed the calf muscles in humans are relatively unresponsive to resistance training when compared with other muscles of the body. The purpose of this investigation was to determine the muscle protein synthesis response of the soleus muscle following a standard high intensity bout of resistance exercise. Methods:, Eight recreationally active males (27 ± 4 years) completed three unilateral calf muscle exercises: standing calf press/heel raise, bent-knee calf press/heel raise, and seated calf press/heel raise. Each exercise consisted of four sets of 15 repetitions (,15 repetition maximum, RM, or ,70% 1RM). Fractional rate of muscle protein synthesis (FSR) was determined with a primed constant infusion of [2H5]phenylalanine coupled with muscle biopsies immediately and 3 h following the exercise in both the exercise and non-exercise (resting control) leg. Results:, FSR was elevated (P < 0.05) in the exercise (0.069 ± 0.010) vs. the control (0.051 ± 0.012) leg. Muscle glycogen concentration was lower (P < 0.05) in the exercise compared with the control leg (Decrease from control; immediate post-exercise: 54 ± 5; 3 h post-exercise: 36 ±4 mmol kg,1 wet wt.). This relatively high amount of glycogen use is comparable with previous studies of resistance exercise of the thigh (i.e. vastus lateralis; ,41,49 mmol kg,1 wet wt.). However, the exercise-induced increase in FSR that has been consistently reported for the vastus lateralis (,0.045,0.060% h,1) is on average ,200% higher than reported here for the soleus (0.019 ± 0.003% h,1). Conclusions:, These results suggest the relatively poor response of soleus muscle protein synthesis to an acute bout of resistance exercise may be the basis for the relative inability of the calf muscles to respond to resistance training programs. [source] Myotendinous plasticity to ageing and resistance exercise in humansEXPERIMENTAL PHYSIOLOGY, Issue 3 2006N. D. Reeves The age-related loss of muscle mass known as senile sarcopenia is one of the main determinants of frailty in old age. Molecular, cellular, nutritional and hormonal mechanisms are at the basis of sarcopenia and are responsible for a progressive deterioration in skeletal muscle size and function. Both at single-fibre and at whole-muscle level, the loss of force exceeds that predicted by the decrease in muscle size. For single fibres, the loss of intrinsic force is mostly due to a loss in myofibrillar protein content. For whole muscle, in addition to changes in neural drive, alterations in muscle architecture and in tendon mechanical properties, exemplified by a reduction in tendon stiffness, have recently been shown to contribute to this phenomenon. Resistance training can, however, cause substantial gains in muscle mass and strength and provides a protective effect against several of the cellular and molecular changes associated with muscle wasting and weakness. In old age, not only muscles but also tendons are highly responsive to training, since an increase in tendon stiffness has been observed after a period of increased loading. Many of the myotendinous factors characterizing ageing can be at least partly reversed by resistance training. [source] Growth Hormone Administration and Exercise Effects on Muscle Fiber Type and Diameter in Moderately Frail Older PeopleJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 7 2001James V. Hennessey MD OBJECTIVE: Reduced muscle mass and strength are characteristic findings of growth hormone deficiency (GHD) and aging. We evaluated measures of muscle strength, muscle fiber type, and cross sectional area in response to treatment with recombinant human growth hormone (rhGH) with or without a structured resistance exercise program in frail older subjects. DESIGN: Placebo-controlled, randomized, double blind trial. SETTING: Outpatient clinical research center at an urban university-affiliated teaching hospital. PARTICIPANTS: Thirty-one consenting older subjects (mean age 71.3 ± 4.5 years) recruited as a subset of a larger project evaluating rhGH and exercise in older people, who underwent 62 quadricep-muscle biopsies. INTERVENTION: Random assignment to a 6-month course of one of four protocols: rhGH administered subcutaneously daily at bedtime, rhGH and a structured resistance exercise program, structured resistance exercise with placebo injections, or placebo injections only. MEASUREMENTS: Muscle biopsy specimens were obtained from the vastus lateralis muscle. Isokinetic dynamometry strength tests were used to monitor individual progress and to adjust the weights used in the exercise program. Serum insulin-like growth factor-I (IGF-I) was measured and body composition was measured using a Hologic QDR 1000W dual X-ray densitometer. RESULTS: The administration of rhGH resulted in significant increase in circulating IGF-I levels in the individuals receiving rhGH treatment. Muscle strength increased significantly in both the rhGH/exercise (+55.6%, P = .0004) as well as the exercise alone (+47.8%, P = .0005) groups. There was a significant increase in the proportion of type 2 fibers between baseline and six months in the combined rhGH treated subjects versus those not receiving rhGH (P = .027). CONCLUSIONS: Our results are encouraging in that they suggest an effect of growth hormone on a specific aging-correlated deficit. IGF-I was increased by administrating rhGH and muscle strength was increased by exercise. The administration of rhGH to frail older individuals in this study resulted in significant changes in the proportions of fiber types. Whether changes in fiber cross-sectional area or absolute number occur with long-term growth hormone administration requires further study. [source] Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young menTHE JOURNAL OF PHYSIOLOGY, Issue 21 2009Daniel W. D. West We aimed to determine whether exercise-induced elevations in systemic concentration of testosterone, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) enhanced post-exercise myofibrillar protein synthesis (MPS) and phosphorylation of signalling proteins important in regulating mRNA translation. Eight young men (20 ± 1.1 years, BMI = 26 ± 3.5 kg m,2) completed two exercise protocols designed to maintain basal hormone concentrations (low hormone, LH) or elicit increases in endogenous hormones (high hormone, HH). In the LH protocol, participants performed a bout of unilateral resistance exercise with the elbow flexors. The HH protocol consisted of the same elbow flexor exercise with the contralateral arm followed immediately by high-volume leg resistance exercise. Participants consumed 25 g of protein after arm exercise to maximize MPS. Muscle biopsies and blood samples were taken as appropriate. There were no changes in serum testosterone, GH or IGF-1 after the LH protocol, whereas there were marked elevations after HH (testosterone, P < 0.001; GH, P < 0.001; IGF-1, P < 0.05). Exercise stimulated a rise in MPS in the biceps brachii (rest = 0.040 ± 0.007, LH = 0.071 ± 0.008, HH = 0.064 ± 0.014% h,1; P < 0.05) with no effect of elevated hormones (P= 0.72). Phosphorylation of the 70 kDa S6 protein kinase (p70S6K) also increased post-exercise (P < 0.05) with no differences between conditions. We conclude that the transient increases in endogenous purportedly anabolic hormones do not enhance fed-state anabolic signalling or MPS following resistance exercise. Local mechanisms are likely to be of predominant importance for the post-exercise increase in MPS. [source] The role of phosphoinositide 3-kinase and phosphatidic acid in the regulation of mammalian target of rapamycin following eccentric contractionsTHE JOURNAL OF PHYSIOLOGY, Issue 14 2009T. K. O'Neil Resistance exercise induces a hypertrophic response in skeletal muscle and recent studies have begun to shed light on the molecular mechanisms involved in this process. For example, several studies indicate that signalling by the mammalian target of rapamycin (mTOR) is necessary for a hypertrophic response. Furthermore, resistance exercise has been proposed to activate mTOR signalling through an upstream pathway involving the phosphoinositide 3-kinase (PI3K) and protein kinase B (PKB); however, this hypothesis has not been thoroughly tested. To test this hypothesis, we first evaluated the temporal pattern of signalling through PI3K,PKB and mTOR following a bout of resistance exercise with eccentric contractions (EC). Our results indicated that the activation of signalling through PI3K,PKB is a transient event (<15 min), while the activation of mTOR is sustained for a long duration (>12 h). Furthermore, inhibition of PI3K,PKB activity did not prevent the activation of mTOR signalling by ECs, indicating that PI3K,PKB is not part of the upstream regulatory pathway. These observations led us to investigate an alternative pathway for the activation of mTOR signalling involving the synthesis of phosphatidic acid (PA) by phospholipase D (PLD). Our results demonstrate that ECs induce a sustained elevation in [PA] and inhibiting the synthesis of PA by PLD prevented the activation of mTOR. Furthermore, we determined that similar to ECs, PA activates mTOR signalling through a PI3K,PKB-independent mechanism. Combined, the results of this study indicate that the activation of mTOR following eccentric contractions occurs through a PI3K,PKB-independent mechanism that requires PLD and PA. [source] Acidosis and Catecholamine Evaluation Following Simulated Law Enforcement "Use of Force" EncountersACADEMIC EMERGENCY MEDICINE, Issue 7 2010Jeffrey D. Ho MD ACADEMIC EMERGENCY MEDICINE 2010; 17:E60,E68 © 2010 by the Society for Academic Emergency Medicine Abstract Objectives:, Law enforcement authorities are often charged with controlling resisting suspects. These encounters sometimes result in the sudden and unexpected death of the suspect. Drug intoxication, excited delirium syndrome, or excessive uses of force are factors that are often blamed, but sometimes the mechanism of these deaths is not fully understood. It is possible that worsening acidosis or excessive catecholamine release play a part. The objective of this study was to determine the effect on markers of acidosis and catecholamines of various tasks intended to simulate common arrest-related situations. Methods:, Subjects were assigned to one of five task groups: 1) a 150-meter sprint and wall hurdle (simulated flight from arrest); 2) 45 seconds of striking a heavy bag (simulated physical resistance); 3) a 10-second TASER X26 electronic control device exposure; 4) a fleeing and resistance exercise involving a law enforcement dog (K-9); or 5) an oleoresin capsicum (OC) exposure to the face and neck. Baseline serum pH, lactate, potassium, troponin I, catecholamines, and creatine kinase (CK) were evaluated. Serum catecholamines, pH, lactate, and potassium were sampled immediately after the task and every 2 minutes for 10 minutes posttask. Vital signs were repeated immediately after the task. Serum CK and troponin I were evaluated again at 24 hours posttask. Results:, Sixty-six subjects were enrolled; four did not complete their assigned task. One subject lost the intravenous (IV) access after completing the task and did not have data collected, and one subject only received a 5-second TASER device exposure and was excluded from the study, leaving 12 subjects in each task group. The greatest changes in acidosis markers occurred in the sprint and heavy bag groups. Catecholamines increased the most in the heavy bag group and the sprint group and increased to a lesser degree in the TASER, OC, and K-9 groups. Only the sprint group showed an increase in CK at 24 hours. There were no elevations in troponin I in any group, nor any clinically important changes in potassium. Conclusions:, The simulations of physical resistance and fleeing on foot led to the greatest changes in markers of acidosis and catecholamines. These changes may be contributing or causal mechanisms in sudden custodial arrest-related deaths (ARDs). This initial work may have implications in guiding applications of force for law enforcement authorities (LEAs) when apprehending resisting subjects. [source] Comparative effects of resistance training on peak isometric torque, muscle hypertrophy, voluntary activation and surface EMG between young and elderly womenCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 2 2007Jack Cannon Summary We compared the effect of a 10-week resistance training program on peak isometric torque, muscle hypertrophy, voluntary activation and electromyogram signal amplitude (EMG) of the knee extensors between young and elderly women. Nine young women (YW; range 20,30 years) and eight elderly women (EW; 64,78 years) performed three sets of ten repetitions at 75% 1 repetition maximum for the bilateral leg extension and bilateral leg curl 3 days per week for 10 weeks. Peak isometric torque, EMG and voluntary activation were assessed before, during, and after the training period, while knee extensor lean muscle cross-sectional area (LCSA) and lean muscle volume (LMV) were assessed before and after the training period only. Similar increases in peak isometric torque (16% and 18%), LCSA (13% and 12%), LMV (10% and 9%) and EMG (19% and 21%) were observed between YW and EW, respectively, at the completion of training (P<0·05), while the increase in voluntary activation in YW (1·9%) and EW (2·1%) was not significant (P>0·05). These findings provide evidence to indicate that participation in regular resistance exercise can have significant neuromuscular benefits in women independent of age. The lack of change in voluntary activation following resistance training in both age groups despite the increase in EMG may be related to differences between measurements in their ability to detect resistance training-induced changes in motor unit activity. However, it is possible that neural adaptation did not occur and that the increase in EMG was due to peripheral adaptations. [source] |