1000 resultados para exercise


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The effectiveness of Cognitive Behavioral Therapy (CBT) for eating disorders has established a link between cognitive processes and unhealthy eating behaviors. However, the relationship between individual differences in unhealthy eating behaviors that are not related to clinical eating disorders, such as overeating and restrained eating, and the processing of food related verbal stimuli remains undetermined. Furthermore, the cognitive processes that promote unhealthy and healthy exercise patterns remain virtually unexplored by previous research. The present study compared individual differences in attitudes and behaviors around eating and exercise to responses to food and exercise-related words using a Lexical Decision Task (LDT). Participants were recruited from Colby (n = 61) and the greater Waterville community (n = 16). The results indicate the following trends in the data: Individuals who scored high in “thin ideal” responded faster to food-related words than individuals with low “thin Ideal” scores did. Regarding the exercise-related data, individuals who engage in more “low intensity exercise” responded faster to exercise-related words than individuals who engage in less “low intensity exercise” did. These findings suggest that cognitive schemata about food and exercise might mediate individual’s eating and exercise patterns.

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Human and rodent uncoupling protein (UCP)3 mRNA is upregulated after acute exercise. Moreover, exercise increases plasma levels of free fatty acid (FFA), which are also known to upregulate UCP3. We investigated whether the upregulation of UCP3 after exercise is an effect of exercise per se or an effect of FFA levels or substrate oxidation. Seven healthy untrained men [age: 22.7 ± 0.6 yr; body mass index: 23.8 ± 1.0 kg/m2; maximal O2 uptake (VO2 max): 3,852 ± 211 ml/min] exercised at 50% VO2 max for 2 h and then rested for 4 h. Muscle biopsies and blood samples were taken before and immediately after 2 h of exercise and 1 and 4 h in the postexercise period. To modulate plasma FFA levels and fat/glucose oxidation, the experiment was performed two times, one time with glucose ingestion and one time while fasting. UCP3 mRNA and UCP3 protein were determined by RT-competitive PCR and Western blot. In the fasted state, plasma FFA levels significantly increased (P < 0.0001) during exercise (293 ± 25 vs. 1,050 ± 127 μmol/l), whereas they were unchanged after glucose ingestion (335 ± 54 vs. 392 ± 74 µmol/l). Also, fat oxidation was higher after fasting (P < 0.05), whereas glucose oxidation was higher after glucose ingestion (P < 0.05). In the fasted state, UCP3L mRNA expression was increased significantly (P < 0.05) 4 h after exercise (4.6 ± 1.2 vs. 9.6 ± 3.3 amol/µg RNA). This increase in UCP3L mRNA expression was prevented by glucose ingestion. Acute exercise had no effect on UCP3 protein levels. In conclusion, we found that acute exercise had no direct effect on UCP3 mRNA expression. Abolishing the commonly observed increase in plasma FFA levels and/or fatty acid oxidation during and after exercise prevents the upregulation of UCP3 after acute exercise. Therefore, the previously observed increase in UCP3 expression appears to be an effect of prolonged elevation of plasma FFA levels and/or increased fatty acid oxidation.

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Contrary to previous research, training may improve exercise performance in a lizard, the brown anole. A brief, two-week training period resulted in increased performance speed and distance before exhaustion in trained lizards. Trained lizards were also able to more effectively use leg glycogen stores, however each of these improvements were not found in lizards treated with alcohol. Liver glycogen concentrations were also lower in alcohol-treated lizards, and patterns of liver glycogen concentrations during recovery indicate some hepatic lactate gluconeogenesis.

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The effects were compared of exercise in the fasted state and exercise with a high rate of carbohydrate intake on intramyocellular triglyceride (IMTG) and glycogen content of human muscle. Using a randomized crossover study design, nine young healthy volunteers participated in two experimental sessions with an interval of 3 weeks. In each session subjects performed 2 h of constant-load bicycle exercise (∼75% VO2max ), followed by 4 h of controlled recovery. On one occasion they exercised after an overnight fast (F), and on the other (CHO) they received carbohydrates before (∼150 g) and during (1 g (kg bw)−1 h−1) exercise. In both conditions, subjects ingested 5 g carbohydrates per kg body weight during recovery. Fibre type-specific relative IMTG content was determined by Oil red O staining in needle biopsies from m. vastus lateralis before, immediately after and 4 h after exercise. During F but not during CHO, the exercise bout decreased IMTG content in type I fibres from 18 ± 2% to 6 ± 2% (P= 0.007) area lipid staining. Conversely, during recovery, IMTG in type I fibres decreased from 15 ± 2% to 10 ± 2% in CHO, but did not change in F. Neither exercise nor recovery changed IMTG in type IIa fibres in any experimental condition. Exercise-induced net glycogen breakdown was similar in F and CHO. However, compared with CHO (11.0 ± 7.8 mmol kg−1 h−1), mean rate of postexercise muscle glycogen resynthesis was 3-fold greater in F (32.9 ± 2.7 mmol kg−1 h−1, P= 0.01). Furthermore, oral glucose loading during recovery increased plasma insulin markedly more in F (+46.80 μU ml−1) than in CHO (+14.63 μU ml−1, P= 0.02). We conclude that IMTG breakdown during prolonged submaximal exercise in the fasted state takes place predominantly in type I fibres and that this breakdown is prevented in the CHO-fed state. Furthermore, facilitated glucose-induced insulin secretion may contribute to enhanced muscle glycogen resynthesis following exercise in the fasted state.

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Mitochondrial impairment is hypothesized to contribute to the pathogenesis of insulin resistance. Mitofusin (Mfn) proteins regulate the biogenesis and maintenance of the mitochondrial network, and when inactivated, cause a failure in the mitochondrial architecture and decreases in oxidative capacity and glucose oxidation. Exercise increases muscle mitochondrial content, size, oxidative capacity and aerobic glucose oxidation. To address if Mfn proteins are implicated in these exercise-induced responses, we measured Mfn1 and Mfn2 mRNA levels, pre-, post-, 2 and 24 h post-exercise. Additionally, we measured the expression levels of transcriptional regulators that control mitochondrial biogenesis and functions, including PGC-1α, NRF-1, NRF-2 and the recently implicated ERRα. We show that Mfn1, Mfn2, NRF-2 and COX IV mRNA were increased 24 h post-exercise, while PGC-1α and ERRα mRNA increased 2 h post-exercise. Finally, using in vitro cellular assays, we demonstrate that Mfn2 gene expression is driven by a PGC-1α programme dependent on ERRα. The PGC-1α/ERRα-mediated induction of Mfn2 suggests a role of these two factors in mitochondrial fusion. Our results provide evidence that PGC-1α not only mediates the increased expression of oxidative phosphorylation genes but also mediates alterations in mitochondrial architecture in response to aerobic exercise in humans.

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There is limited research to support the notion that heavy resistive exercise immediately before a power movement may acutely enhance performance. Upper-body acute power enhancement during a stretch-shorten cycle (SSC) movement has not been previously investigated. The aim of this project was to determine whether a set of 5 repetitions of 5 repetition maximum (RM) bench press preceding explosive pushups would significantly influence indicators of power: impulse and maximum rate of force development. Subjects randomly performed either explosive push-ups only over a force platform or a set of 5RM bench press before the explosive push-ups. There were no significant differences for any of the force platform data when the explosive push-ups were preceded by a set of 5RM bench press. It appears that heavy dynamic resistive upper-body exercise on its own before an upper-body power activity is inadequate in augmenting short-term power.

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Sedentary and trained men respond differently to the same intensity of exercise, this is probably related to their platelet reactivity and antioxidant capacity. There is growing interest in the utilization of antioxidant-rich plant extracts as dietary food supplements. The aim of this study was to investigate the effect of an acute bout of sub maximal exercise on platelet count and differential response of platelet activation in trained and sedentary subjects and to observe if cocoa polyphenols reverse the effect of exercise on platelet function. The practical significance of this study was that many sedentary people engage in occasional strenuous exercise that may predispose them to risk of heart disease. Fasting blood samples were collected from 16 male subjects, pre and post 1-h cycling exercise at 70% of maximal aerobic power (VO2max) before and after consumption of cocoa or placebo. Agonist stimulated citrated whole blood was utilized for measuring platelet aggregation, adenosine triphosphate (ATP) release and platelet activation. Baseline platelet count (221 ± 33 times 109/L) and ATP release (1.4 ± 0.6 nmol) increased significantly (P < 0.05) after exercise in all subjects. Baseline platelet numbers in the trained were higher (P < 0.05) than in the sedentary (235 ± 37 vs. 208 ± 34 times 109/L), where as platelet activation in trained was lower (P < 0.05) than sedentary (51 ± 6 vs. 59 ± 5%). Seven days of cocoa polyphenol supplementation had little effect on any of the parameters measured. We conclude that trained subjects show decreased activation of stimulated platelets when compared to the sedentary subjects and short-term cocoa polyphenol supplementation did not decrease platelet activity in response to exercise independent of prior training status.

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Regular physical activity in older populations reduces the risks of cardiovascular diseases, diabetes, osteoporosis and falls and also improves mental health. Some programs of written exercise prescriptions by general practitioners have been shown to significantly increase physical activity levels over the medium-term (six to 12 months). Increasing the confidence and skills of general practitioners to prescribe and monitor exercise programs is important. However, the more challenging barriers to the widespread uptake of exercise prescription programs are the structural and economic constraints within general practice, as well as the competing promotion of prescribing pharmaceutical products. Implementation research on overcoming these barriers is urgently needed.

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