996 resultados para Maximum exercise


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1. The role of adrenaline in regulating hepatic glucose production and muscle glucose uptake during exercise was examined in six adrenaline deficient, bilaterally adrenalectomised humans. Six sex and age matched healthy individuals served as controls (CON).

2. Adrenalectomised subjects cycled for 45 min at 68 ± 1% maximum pulmonary Oμ uptake (VOμ,max), followed by 15 min at 84 ± 2% VOμ,max without (−ADR) or with (+ADR) adrenaline infusion, which elevated plasma adrenaline levels (45 min, 4·49 ± 0·69 nmol l¢; 60 min, 12·41 ± 1·80 nmol l¢; means ± s.e.m.). Glucose kinetics were measured using [3_ÅH]glucose.

3. Euglycaemia was maintained during exercise in CON and −ADR, whilst in +ADR plasma glucose was elevated. The exercise induced increase in hepatic glucose production was similar in +ADR and −ADR; however, adrenaline infusion augmented the rise in hepatic glucose production early in exercise. Glucose uptake increased during exercise in +ADR and −ADR, but was lower and metabolic clearance rate was reduced in +ADR.

4. During exercise noradrenaline and glucagon concentrations increased, and insulin and cortisol concentrations decreased, but plasma levels were similar between trials. Adrenaline infusion suppressed growth hormone and elevated plasma free fatty acids, glycerol and lactate. Alanine and â_hydroxybutyrate levels were similar between trials.

5. The results demonstrate that glucose homeostasis was maintained during exercise in adrenalectomised subjects. Adrenaline does not appear to play a major role in matching hepatic glucose production to the increase in glucose clearance. In contrast, adrenaline infusion results in a mismatch by simultaneously enhancing hepatic glucose production and inhibiting glucose clearance.

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Classical proinflammatory eicosanoids, and more recently discovered lipid mediators with anti-inflammatory and proresolving bioactivity, exert a complex role in the initiation, control, and resolution of inflammation. Using a targeted lipidomics approach, we investigated circulating lipid mediator responses to resistance exercise and treatment with the NSAID ibuprofen. Human subjects undertook a single bout of unaccustomed resistance exercise (80% of one repetition maximum) following oral ingestion of ibuprofen (400 mg) or placebo control. Venous blood was collected during early recovery (0–3 h and 24 h postexercise), and serum lipid mediator composition was analyzed by LC-MS-based targeted lipidomics. Postexercise recovery was characterized by elevated levels of cyclooxygenase (COX)-1 and 2-derived prostanoids (TXB2, PGE2, PGD2, PGF2α, and PGI2), lipooxygenase (5-LOX, 12-LOX, and 15-LOX)-derived hydroxyeicosatetraenoic acids (HETEs), and leukotrienes (e.g., LTB4), and epoxygenase (CYP)-derived epoxy/dihydroxy eicosatrienoic acids (EpETrEs/DiHETrEs). Additionally, we detected elevated levels of bioactive lipid mediators with anti-inflammatory and proresolving properties, including arachidonic acid-derived lipoxins (LXA4 and LXB4), and the EPA (E-series) and DHA (D-series)-derived resolvins (RvD1 and RvE1), and protectins (PD1 isomer 10S, 17S-diHDoHE). Ibuprofen treatment blocked exercise-induced increases in COX-1 and COX-2-derived prostanoids but also resulted in off-target reductions in leukotriene biosynthesis, and a diminished proresolving lipid mediator response. CYP pathway product metabolism was also altered by ibuprofen treatment, as indicated by elevated postexercise serum 5,6-DiHETrE and 8,9-DiHETrE only in those receiving ibuprofen. These findings characterize the blood inflammatory lipid mediator response to unaccustomed resistance exercise in humans and show that acute proinflammatory signals are mechanistically linked to the induction of a biological active inflammatory resolution program, regulated by proresolving lipid mediators during postexercise recovery.

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Hypoxia is an important modulator of endurance exercise-induced oxidative adaptations in skeletal muscle. However, whether hypoxia affects resistance exercise-induced muscle adaptations remains unknown. Here, we determined the effect of resistance exercise training under systemic hypoxia on muscular adaptations known to occur following both resistance and endurance exercise training, including muscle cross-sectional area (CSA), one-repetition maximum (1RM), muscular endurance, and makers of mitochondrial biogenesis and angiogenesis, such as peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), citrate synthase (CS) activity, nitric oxide synthase (NOS), vascular endothelial growth factor (VEGF), hypoxia-inducible factor-1 (HIF-1), and capillary-to-fiber ratio. Sixteen healthy male subjects were randomly assigned to either a normoxic resistance training group (NRT, n = 7) or a hypoxic (14.4% oxygen) resistance training group (HRT, n = 9) and performed 8 weeks of resistance training. Blood and muscle biopsy samples were obtained before and after training. After training muscle CSA of the femoral region, 1RM for bench-press and leg-press, muscular endurance, and skeletal muscle VEGF protein levels significantly increased in both groups. The increase in muscular endurance was significantly higher in the HRT group. Plasma VEGF concentration and skeletal muscle capillary-to-fiber ratio were significantly higher in the HRT group than the NRT group following training. Our results suggest that, in addition to increases in muscle size and strength, HRT may also lead to increased muscular endurance and the promotion of angiogenesis in skeletal muscle.

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Cyclooxygenase-1 and -2 pathway-derived prostaglandins (PGs) have been implicated in adaptive muscle responses to exercise, but the role of PGs in contraction-induced muscle signaling has not been determined. We investigated the effect of inhibition of cyclooxygenase-1 and -2 activities with the nonsteroidal anti-inflammatory drug ibuprofen on human muscle signaling responses to resistance exercise. Subjects orally ingested 1,200 mg ibuprofen (or placebo control) in three 400-mg doses administered ∼30 min before and ∼6 h and ∼12 h following a bout of unaccustomed resistance exercise (80% one repetition maximum). Muscle biopsies were obtained at rest (preexercise), immediately postexercise (0 h), 3 h postexercise, and at 24 h of recovery. In the placebo (PLA) group, phosphorylation of ERK1/2 (Thr202/Tyr204), ribosomal protein S6 kinase (RSK, Ser380), mitogen-activated kinase 1 (Mnk1, Thr197/202), and p70S6 kinase (p70S6K, Thr421/Ser424) increased at both 0 and 3 h postexercise, with delayed elevation of phospho (p)-p70S6K (Thr389) and p-rpS6 (Ser235/S36 and Ser240/244) at 3 h postexercise. Only p-ERK1/2 (Thr202/Tyr204) remained significantly elevated in the 24-h postexercise biopsy. Ibuprofen treatment prevented sustained elevation of MEK-ERK signaling at 3 h (p-ERK1/2, p-RSK, p-Mnk1, p-p70S6K Thr421/Ser424) and 24 h (p-ERK1/2) postexercise, and this was associated with suppressed phosphorylation of ribosomal protein S6 (Ser235/236 and Ser240/244). Early contraction-induced p-Akt (Ser473) and p-p70S6K (Thr389) were not influenced by ibuprofen, but p-p70S6K (Thr389) remained elevated 24 h postexercise only in those receiving ibuprofen treatment. Early muscle signaling responses to resistance exercise are, in part, ibuprofen sensitive, suggesting that PGs are important signaling molecules during early postexercise recovery.

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PURPOSE: The study's purpose was to assess the effectiveness of a short-duration three-times-weekly high-load resistive exercise program on preventing deterioration in neuromuscular function after prolonged bed rest. METHODS: Twenty-four male subjects performed high-load resistive exercise (n = 8), high-load resistive exercise with whole-body vibration (n = 9), or no exercise (control, n = 9) during 60-d head-down tilt bed rest as part of the 2nd Berlin Bed Rest Study. Peak countermovement jump power and height, sit-to-stand performance, sprint time over 15 and 30 m, and leg press one-repetition maximum were measured before and after bed rest. RESULTS: The exercise interventions were capable of ameliorating losses of peak countermovement jump power (P < 0.001) and height (P < 0.001), deterioration of sit-to-stand time from 45-cm (P = 0.034) and 30-cm (P < 0.001) sitting positions, increases of 15-m (P = 0.037) and 30-m (P = 0.005) sprint time, and losses of leg press one-repetition maximum (P < 0.001). CONCLUSIONS: The short-duration (6-min time under tension per training session) exercise countermeasure program performed three times a week was capable of reducing the effect of prolonged bed rest on many neuromuscular function measures.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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We compared the effect of three different exercise programs on patients with chronic obstructive pulmonary disease including strength training at 50_80% of one-repetition maximum (1-RM) (ST; N = 11), low-intensity general training (LGT; N = 13), or combined training groups (CT; N = 11). Body composition, muscle strength, treadmill endurance test (TEnd), 6-min walk test (6MWT), Saint George's Respiratory Questionnaire (SGRQ), and baseline dyspnea (BDI) were assessed prior to and after the training programs (12 weeks). The training modalities showed similar improvements (P > 0.05) in SGRQ-total (ST = 13 ± 14%; CT = 12 ± 14%; LGT = 11 ± 10%), BDI (ST = 1.8 ± 4; CT = 1.8 ± 3; LGT = 1 ± 2), 6MWT (ST = 43 ± 51 m; CT = 48 ± 50 m; LGT = 31 ± 75 m), and TEnd (ST = 11 ± 20 min; CT = 11 ± 11 min; LGT = 7 ± 5 min). In the ST and CT groups, an additional improvement in 1-RM values was shown (P < 0.05) compared to the LGT group (ST = 10 ± 6 to 57 ± 36 kg; CT = 6 ± 2 to 38 ± 16 kg; LGT = 1 ± 2 to 16 ± 12 kg). The addition of strength training to our current training program increased muscle strength; however, it produced no additional improvement in walking endurance, dyspnea or quality of life. A simple combined training program provides benefits without increasing the duration of the training sessions.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Reactive oxygen species (ROS) are constantly produced by cells that promote cellular oxidative damage and are neutralized by an antioxidant system including superoxide dismutase, glutathione, peroxidase and catalase. Male volunteers were exercised for 20 minutes, three days (60, 70 and 80% of maximum heart rate). Catalase activity and plasma malondialdehyde concentration were measured. The mean age of the volunteers was 25 +/- 7 years, with body mass index 2 of 24.03 +/- 4.32 kg/m(2). Acute exercise training produced an increase of malondialdehyde concentration that was exercise intensity-dependent in young volunteers. However, catalase activity shows a great variability at baseline and the percentual of reduction was exercise intensity-independent in this particular population. Therefore, our study shows that acute cycling exercise promotes an increase of oxidative stress that was exercise intensity-dependent in young volunteers. Furthermore, the antioxidant system measured by catalase activity was effective to counterbalance the ROS production showing a saturation behavior at an intensity of 70% of maximum heart rate.

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The aim of this study was to evaluate the EMG activity of lumbar multifidus (MU), longissimus thoracis (LT) and iliocostalis (IC) muscles during an upper limb resistance exercise (biceps curl). Ten healthy males performed maximal voluntary isometric contraction (MVC) of the trunk extensors, after this, the biceps curl exercise was executed at 25%, 30%, 35% and 40% one repetition maximum during 1 min, with 10 min rest between them. EMG root mean square (RMS) and median frequency (MFreq) were calculated for each lifting and lowering of the bar during the exercise bouts, to calculate slopes and intercepts. The results showed increases in the RMS and decreases in the MFreq slopes. RMS slopes were no different between muscles, indicating similar fatigue process along the exercise irrespective of the load level. MU and LT presented higher RMS irrespective of the load level, which can be related to the specific function during the standing position. on the other hand, IC and MU presented higher MFreq intercepts compared to LT, demonstrating possible differences in the muscle fiber conduction velocity of these muscles. These findings suggest that trunk muscles are differently activate during upper limb exercises, and the fatigue process affects the lumbar muscles similarly. (C) 2008 Elsevier Ltd. All rights reserved.

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OBJETIVO: O objetivo deste estudo foi analisar os efeitos da corrida contínua prolongada realizada na intensidade correspondente ao início do acúmulo do lactato no sangue (OBLA) sobre o torque máximo dos extensores do joelho analisado em diferentes tipos de contração e velocidade de movimento em indivíduos ativos. MÉTODO: Oito indivíduos do gênero masculino (23,4 ± 2,1 anos; 75,8 ± 8,7 kg; 171,1 ± 4,5 cm) participaram deste estudo. Primeiramente, os sujeitos realizaram um teste incremental até a exaustão voluntária para determinar a velocidade correspondente ao OBLA. Posteriormente, os sujeitos retornaram ao laboratório em duas ocasiões, separadas por pelo menos sete dias, para realizar 5 contrações isocinéticas máximas para os extensores do joelho em duas velocidades angulares (60 e 180º.s-1) sob as condições excêntrica (PTE) e concêntrica (PTC). Uma sessão foi realizada após um período de aquecimento padronizado (5 min a 50%VO2max). A outra sessão foi realizada após uma corrida contínua no OBLA até a exaustão voluntária. Essas sessões foram executadas em ordem randômica. RESULTADOS: Houve redução significante do PTC somente a 60º.s-1 (259,0 ± 46,4 e 244,0 ± 41,4 N.m). Entretanto, a redução do PTE foi significante a 60º.s-1 (337,3 ± 43,2 e 321,7 ± 60,0 N.m) e 180º.s-1 (346,1 ± 38,0 e 319,7 ± 43,6 N.m). As reduções relativas da força após o exercício de corrida foram significantemente diferentes entre os tipos de contração somente a 180º.s-1. CONCLUSÃO: Podemos concluir que, em indivíduos ativos, a redução no torque máximo após uma corrida contínua prolongada no OBLA pode ser dependente do tipo de contração e da velocidade angular.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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The aim of this study was to determine the effect of exercise mode on the blood lactate removal during recovery of high-intensity exercise. Nine male individuals performed the following tests in order to determine the blood lactate removal: Running - 2x200 m, the subjects ran at their maximum capacity, and rested 2 min between each bout. Swimming - 2x50 m, the subjects swam at their maximum capacity, and rested 2 min between each bout. Each test was realized on different days with three recovery modes: passive (sitting down), swimming, or running. Recovery exercise intensity was corresponding to the aerobic threshold. All recovery activities lasted 30 min. The two forms of active recovery were initiated 2 min after the end of high-intensity exercise and lasted 15 min, and were followed by 13 min of seated rest. After 1,7, 12,17, and 30 min of the end of high-intensity exercise, blood samples (25 mu l) were collected in order to determine the blood lactate concentration. By linear regression, between the logarithm of lactate concentration and its respective time of recovery, the half-time of blood lactate removal (t1/2) was determined. Time of high-intensity exercise and the lactate concentration obtained in the 1(st) min of recovery were not different between running and swimming. Passive recovery (PR) following running (R-PR=25.5+/-4.3 min) showed a t1/2 significantly higher than PR after swimming (S-PR=18.6+/-4.3 min). The t1/2 of the sequences running-running (R-R=13.0 min), running-swimming (R-S=12.9+/-3.8 min), swimming-swimming (S-S=13.2+/-2.8 min), and swimming-running (S-R=12.9+/-3.8 min) were significantly lower than the t1/2 of the R-PR and S-PR. There was no difference between the t1/2 of the sequences R-R R-S, and S-S. on the other hand the sequence S-R showed a t1/2 significantly lower than the sequences S-S and R-R. It was concluded that the two forms of active recovery determine an increase in the blood lactate removal, regardless of the mode of high-intensity exercise performed previously. Active recovery performed by the muscle groups that were not previously fatigued, can improve the blood lactate removal.