1000 resultados para Exercise


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Several studies have demonstrated that oral glucose tolerance is impaired in the immediate postexercise period. A double-tracer technique was used to examine glucose kinetics during a 2-h oral glucose (75 g) tolerance test (OGTT) 30 min after exercise (Ex, 55 min at 71 ± 2% of peak O2 uptake) and 24 h after exercise (Rest) in endurance-trained men. The area under the plasma glucose curve was 71% greater in Ex than in Rest (P = 0.01). The higher glucose response occurred even though whole body rate of glucose disappearance was 24% higher after exercise (P = 0.04, main effect). Whole body rate of glucose appearance was 25% higher after exercise (P = 0.03, main effect). There were no differences in total (2 h) endogenous glucose appearance (RaE) or the magnitude of suppression of RaE, although RaE was higher from 15 to 30 min during the OGTT in Ex. However, the cumulative appearance of oral glucose was 30% higher in Ex (P = 0.03, main effect). There were no differences in glucose clearance rate or plasma insulin responses between the two conditions. These results suggest that adaptations in splanchnic tissues by prior exercise facilitate greater glucose output from the splanchnic region after glucose ingestion, resulting in a greater glycemic response and, consequently, a greater rate of whole body glucose uptake.

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# 1.
To evaluate the role of adrenaline in regulating carbohydrate metabolism during moderate exercise, 10 moderately trained men completed two 20 min exercise bouts at 58 ± 2 % peak pulmonary oxygen uptake (̇Vo2,peak). On one occasion saline was infused (CON), and on the other adrenaline was infused intravenously for 5 min prior to and throughout exercise (ADR). Glucose kinetics were measured by a primed, continuous infusion of 6,6-[2H]glucose and muscle samples were obtained prior to and at 1 and 20 min of exercise.

# 2.
The infusion of adrenaline elevated (P < 0.01) plasma adrenaline concentrations at rest (pre-infusion, 0.28 ± 0.09; post-infusion, 1.70 ± 0.45 nmol l−1; means ±s.e.m.) and this effect was maintained throughout exercise. Total carbohydrate oxidation increased by 18 % and this effect was due to greater skeletal muscle glycogenolysis (P < 0.05) and pyruvate dehydrogenase (PDH) activation (P < 0.05, treatment effect). Glucose rate of appearance was not different between trials, but the infusion of adrenaline decreased (P < 0.05, treatment effect) skeletal muscle glucose uptake in ADR.

# 3.
During exercise muscle glucose 6-phosphate (G-6-P) (P = 0.055, treatment effect) and lactate (P < 0.05) were elevated in ADR compared with CON and no changes were observed for pyruvate, creatine, phosphocreatine, ATP and the calculated free concentrations of ADP and AMP.

# 4.
The data demonstrate that elevated plasma adrenaline levels during moderate exercise in untrained men increase skeletal muscle glycogen breakdown and PDH activation, which results in greater carbohydrate oxidation. The greater muscle glycogenolysis appears to be due to increased glycogen phosphorylase transformation whilst the increased PDH activity cannot be readily explained. Finally, the decreased glucose uptake observed during exercise in ADR is likely to be due to the increased intracellular G-6-P and a subsequent decrease in glucose phosphorylation.

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This study examined the effect of reduced plasma free fatty acid (FFA) availability on carbohydrate metabolism during exercise. Six untrained women cycled for 60 minutes at approximately 58% of maximum oxygen uptake after ingestion of a placebo (CON) or nicotinic acid (NA), 30 minutes before exercise (7.4 ± 0.5 mg·kg−1 body weight), and at 0 minutes (3.7 ± 0.3 mg·kg−1) and 30 minutes (3.7 ± 0.3 mg·kg−1) of exercise. Glucose kinetics were measured using a primed, continuous infusion of [6,6-2H] glucose. Plasma FFA (CON, 0.86 ± 0.12; NA, 0.21 ± 0.11 mmol·L−1 at 60 minutes, P < .05) and glycerol (CON, 0.34 ± 0.05; NA, 0.10 ± 0.04 mmol·L−1 at 60 minutes, P < .05) were suppressed throughout exercise. Mean respiratory exchange ratio (RER) during exercise was higher (P < .05) in NA (0.89 ± 0.02) than CON (0.83 ± 0.02). Plasma glucose and glucose production were similar between trials. Total glucose uptake during exercise was greater (P < .05) in NA (1,876 ± 161 μmol·kg−1) than in CON (1,525 ± 107 μmol·kg−1). Total fat oxidation was reduced (P < .05) by approximately 32% during exercise in NA. Total carbohydrate oxidized was approximately 42% greater (P < .05) in NA (412 ± 40 mmol) than CON (290 ± 37 mmol), of which, approximately 16% (20 ± 10 mmol) could be attributed to glucose. Plasma insulin and glucagon were similar between trials. Catecholamines were higher (P < .05) during exercise in NA. In summary, during prolonged moderate exercise in untrained women, reduced FFA availability results in a compensatory increase in carbohydrate oxidation, which appears to be due predominantly to an increase in glycogen utilization, although there was a small, but significant, increase in whole body glucose uptake.

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Skeletal muscle insulin sensitivity is enhanced after acute exercise and short-term endurance training. We investigated the impact of exercise on the gene expression of key insulin-signaling proteins in humans. Seven untrained subjects (4 women and 3 men) completed 9 days of cycling at 63 ± 2% of peak O2 uptake for 60 min/day. Muscle biopsies were taken before, immediately after, and 3 h after the exercise bouts (on days 1 and 9). The gene expression of insulin receptor substrate-2 and the p85α subunit of phosphatidylinositol 3-kinase was significantly higher 3 h after a single exercise bout, although short-term training ameliorated this effect. Gene expression of insulin receptor and insulin receptor substrate-1 was not significantly altered at any time point. These results suggest that exercise may have a transitory impact on the expression of insulin receptor substrate-2 and phosphatidylinositol 3-kinase; however, the predominant actions of exercise on insulin sensitivity appear not to reside in the transcriptional activation of the genes encoding major insulin-signaling proteins.

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Osteoporosis is a major public health problem because of the morbidity and mortality associated with fracture. Minimizing the risk of fracture is the primary objective of osteoporosis management. The role of exercise in osteoporosis management is to increase and maintain peak bone density and reduce the rate of bone loss and the risk of falling. This article provides recommendations focusing on a life-span approach to minimizing the risk of fracture associated with osteoporosis. Osteoporosis prevention begins in childhood, when exercise can increase peak bone strength. In young adults, it can maintain peak bone mineral density. In elderly individuals, physical activity can slow bone loss and improve fitness and muscle strength, helping prevent falls and lower the risk of fracture. Exercise goals for individuals with osteoporosis should include reducing pain, increasing mobility, and improving muscle endurance, balance, and stability in order to improve the quality of life and reduce the risk of falling. Thus, exercise plays a significant part in reducing fractures in later life.

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Background: This study aimed to investigate relationships between environmental aesthetics, convenience, and walking companions and walking for exercise or recreation and to investigate differences in these relationships by sex and by reported physical and mental health.

Methods: Analyses of cross-sectional self-report data from a statewide population survey of 3,392 Australian adults were used.

Results: Men and women reporting a less aesthetically pleasing or less convenient environment were less likely to report walking for exercise or recreation in the past 2 weeks. Those respondents, particularly women, reporting no company or pet to walk with were also less likely to walk for exercise or recreation. Associations with environmental and social influences were observed for men and women reporting both good and poor physical and mental health.

Conclusions: Perceived environmental aesthetics and convenience and walking companions are important correlates of walking for exercise among urban Australians. Acknowledging the cross-sectional nature of these data, findings support a case for evaluation of environmental policies to promote physical activity.


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The article explores the lived experiences of older women with a high commitment to exercise. The methods of investigation were in-depth interviews with 17 women fitness instructors for the over-50s and the author's observations as a participant in a variety of exercise programs. The subjective experience of embodiment of older women, the ways in which the body is constructed discursively, and the objective processes of aging are explored. The women's narratives are placed in the wider context of consumption, lifestyle, and identity construction. The study analyzes whether older women's commitment to exercise is a reflection of a climate of constraint, in which individuals seek to shape and manage the body to combat the effects of aging, or is one of empowerment and enablement. More important, the article explores the ways in which the women used fitness programs as a means of constructing intimacy, a sense of community, and satisfaction in interpersonal relations.

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Skeletal muscle, as a consequence of its mass and great capacity for altered metabolism, has a major impact on whole-body metabolic homeostasis and is capable of remarkable adaptation in response to various physiological stimuli, including exercise and dietary intervention. Exercise-induced increases in skeletal muscle mRNA levels of a number of genes have been reported, due to transcriptional activation and/or increased mRNA stability. The cellular adaptations to exercise training appear to be due to the cumulative effects of transient increases in gene transcription after repeated exercise bouts. The relative importance of transcriptional (mRNA synthesis) and translational (mRNA stability or translational efficiency) mechanisms for the training-induced increases in skeletal muscle protein abundance remains to be fully elucidated. Dietary manipulation, and the associated alterations in nutrient availability and hormone levels, can also modify skeletal muscle gene expression, although fewer studies have been reported. A major challenge is to understand how exercise and diet exert their effects on gene and protein expression in skeletal muscle. In relation to exercise, potential stimuli include stretch and muscle tension, the pattern of motor nerve activity and the resultant calcium transients, the energy charge of the cell and substrate availability, oxygen tension and circulating hormones. These are detected by various cellular signaling mechanisms, acting on a range of downstream targets and a wide range of putative transcription factors. A key goal in the years ahead is to identify how alterations at the level of gene expression are coupled to the changes in skeletal muscle phenotype. It is clear that gene expression, although representing a specific site of regulation, is only one step in a complex cascade from the initial stimulus to the final phenotypic adaptation and integrated physiological response.

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This study examined the effect of epinephrine on glucose disposal during moderate exercise when glycogenolytic flux was limited by low preexercise skeletal muscle glycogen availability. Six male subjects cycled for 40 min at 59 ± 1% peak pulmonary O2 uptake on two occasions, either without (CON) or with (EPI) epinephrine infusion starting after 20 min of exercise. On the day before each experimental trial, subjects completed fatiguing exercise and then maintained a low carbohydrate diet to lower muscle glycogen. Muscle samples were obtained after 20 and 40 min of exercise, and glucose kinetics were measured using [6,6-2H]glucose. Exercise increased plasma epinephrine above resting concentrations in both trials, and plasma epinephrine was higher (P < 0.05) during the final 20 min in EPI compared with CON. Muscle glycogen levels were low after 20 min of exercise (CON, 117 ± 25; EPI, 122 ± 20 mmol/kg dry matter), and net muscle glycogen breakdown and muscle glucose 6-phosphate levels during the subsequent 20 min of exercise were unaffected by epinephrine infusion. Plasma glucose increased with epinephrine infusion (i.e., 20-40 min), and this was due to a decrease in glucose disposal (Rd) (40 min: CON, 33.8 ± 3; EPI, 20.9 ± 4.9 µmol · kg-1 · min-1, P < 0.05), because the exercise-induced rise in glucose rate of appearance was similar in the trials. These results show that glucose Rd during exercise is reduced by elevated plasma epinephrine, even when muscle glycogen availability and utilization are low. This suggests that the effect of epinephrine does not appear to be mediated by increased glucose 6-phosphate, secondary to enhanced muscle glycogenolysis, but may be linked to a direct effect of epinephrine on sarcolemmal glucose transport.

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The effects of a single bout of exercise and exercise training on the expression of genes necessary for the transport and beta -oxidation of fatty acids (FA), together with the gene expression of transcription factors implicated in the regulation of FA homeostasis were investigated. Seven human subjects (3 male, 4 female, 28.9 ± 3.1 yr of age, range 20-42 yr, body mass index 22.6 kg/m2, range 17-26 kg/m2) underwent a 9-day exercise training program of 60 min cycling per day at 63% peak oxygen uptake (VO2 peak; 104 ± 14 W). On days 1 and 9 of the program, muscle biopsies were sampled from the vastus lateralis muscle at rest, at the completion of exercise, and again 3 h postexercise. Gene expression of key components of FA transport [FA translocase (FAT/CD36), plasma membrane-associated FA-binding protein], beta -oxidation [carntine palmitoyltransferase(CPT) I, beta -hydroxyacyl-CoA dehydrogenase] and transcriptional control [peroxisome proliferator-activated receptor (PPAR)alpha , PPARgamma , PPARgamma coactivator 1, sterol regulatory element-binding protein-1c] were unaltered by exercise when measured at the completion and at 3 h postexercise. Training increased total lipid oxidation by 24% (P < 0.05) for the 1-h cycling bout. This increased capacity for lipid oxidation was accompanied by an increased expression of FAT/CD36 and CPT I mRNA. Similarly, FAT/CD36 protein abundance was also upregulated by exercise training. We conclude that enhanced fat oxidation after exercise training is most closely associated with the genes involved in regulating FA uptake across the plasma membrane (FAT/CD36) and across the mitochondrial membrane (CPT I).

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The present study was designed to develop a Body Modification Scale (BMS) to measure body change among adolescents and to modify an Excessive Exercise Scale (EES) into a shorter form for adolescents. Two hundred and twenty-one girls and 192 boys from Grades 7 to 10 completed the BMS and the EES. Factor analysis revealed three identical factors for the BMS for girls and boys: weight loss, weight gain, and muscle mass. Two identical factors for girls and boys were also revealed for the EES. Both factor structures were further validated on a separate sample of 286 adolescents (140 girls, 146 boys). The BMS and EES demon-strated excellent reliability (alpha > .86) and high test-retest reliability (alpha > .82) over 1 month. Good concurrent validity was also found for the weight loss factor of the BMS. These findings demonstrate the utility of these two scales for use with adolescents.

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1. Skeletal muscle is a complex and heterogenous tissue capable of remarkable adaptation in response to exercise training. The role of gene transcription, as an initial target to control protein synthesis, is poorly understood.
2. Mature myofibres contain several hundred nuclei, all of which maintain transcriptional competency, although the localized responsiveness of nuclei is not well known. Myofibres are capable of hypertrophy. These processes require the activation and myogenic differentiation of mononuclear satellite cells that fuse with the enlarging or repairing myofibre.
3. A single bout of exercise in human subjects is capable of activating the expression of many diverse groups of genes.
4. The impact of repeated exercise bouts, typical of exercise training, on gene expression has yet to receive systematic investigation.
5. The molecular programme elicited by resistance exercise and endurance exercise differs markedly. Muscular hypertrophy following resistance exercise is dependent on the activation of satellite cells and their subsequent myogenic maturation. Endurance exercise requires the simultaneous activation of mitochondrial and nuclear genes to enable mitochondrial biogenesis.
6. Future analysis of the regulation of genes by exercise may combine high-throughput technologies, such as gene-chips, enabling the rapid detection and analysis of changes in the expression of many thousands of genes.

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The following article refers to a performed paper, Did the Paradigm Shift for You, Darling? given as a collaboration between John Cumming, Yoni Prior, David Ritchie and me at the Double Dialogues Conference, Lines of Flight, at Theatreworks in Melbourne, November, 1997. The performance involved the staging of a mock analysis of a section of my choreographic work, Kim’s Style Guide for the Kinaesthetic Boffin, by three fictitious ‘critics’. The performance functioned as an implicit critique of three different approaches to interpreting dance. This article explores a theoretical position which supports that critique.

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An acute bout of exercise increases skeletal muscle glucose uptake, improves glucose homeostasis and insulin sensitivity, and enhances muscle oxidative capacity. Recent studies have shown an association between these adaptations and the energy-sensing 5' AMP-activated protein kinase (AMPK), the activity of which is increased in response to exercise. Activation of AMPK has been associated with enhanced expression of key metabolic proteins such as GLUT-4, hexokinase II (HKII), and mitochondrial enzymes, similar to exercise. It has been hypothesized that AMPK might regulate gene and protein expression through direct interaction with the nucleus. The purpose of this study was to determine if nuclear AMPK α2 content in human skeletal muscle was increased by exercise. Following 60 min of cycling at 72 +/- 1% of VO2peak in six male volunteers (20.6 +/- 2.1 years; 72.9 +/- 2.1 kg; VO2peak = 3.62 +/- 0.18 l/min), nuclear AMPK α2 content was increased 1.9 +/- 0.4-fold (P = 0.024). There was no change in whole-cell AMPK α2 content or AMPK α2 mRNA abundance. These results suggest that nuclear translocation of AMPK might mediate the effects of exercise on skeletal muscle gene and protein expression.