902 resultados para Treadmill running


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The aim of this study was to examine the effect of endurance training on skeletal muscle phospholipid molecular species from high-fat fed rats. Twelve female Sprague-Dawley rats were fed a high-fat diet (78.1% energy). The rats were randomly divided into two groups, a sedentary control group and a trained group (125 min of treadmill running at 8 m/min, 4 days/wk for 4 weeks). Forty-eight hours after their last training bout phospholipids were extracted from the red and white vastus lateralis and analyzed by electrospray-ionization mass spectrometry. Exercise training was associated with significant alterations in the relative abundance of a number of phospholipid molecular species. These changes were more prominent in red vastus lateralis than white vastus lateralis. The largest observed change was an increase of similar to 30% in the abundance of 1-palmitoyl-2-linoleoyl phosphatidylcholine ions in oxidative fibers. Reductions in the relative abundance of a number of phospholipids containing long-chain n-3 polyunsaturated fatty acids were also observed. These data suggest a possible reduction in phospholipid remodeling in the trained animals. This results in a decrease in the phospholipid n-3 to n-6 ratio that may in turn influence endurance capacity.

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We have determined the effect of two exercise-training intensities on the phospholipid profile of both glycolytic and oxidative muscle fibers of female Sprague-Dawley rats using electrospray-ionization mass spectrometry. Animals were randomly divided into three training groups: control, which performed no exercise training; low-intensity (8 m/min) treadmill running; or high-intensity (28 m/min) treadmill running. All exercise-trained rats ran 1,000 m/session for 4 days/wk for 4 wk and were killed 48 h after the last training bout. Exercise training was found to produce no novel phospholipid species but was associated with significant alterations in the relative abundance of a number of phospholipid molecular species. These changes were more prominent in glycolytic (white vastus lateralis) than in oxidative (red vastus lateralis) muscle fibers. The largest observed change was a decrease of ∼20% in the abundance of 1-stearoyl-2-docosahexaenoyl-phosphatidylethanolamine [PE(18:0/22:6); P < 0.001] ions in both the low- and high-intensity training regimes in glycolytic fibers. Increases in the abundance of 1-oleoyl-2-linoleoyl phopshatidic acid [PA(18:1/18:2); P < 0.001] and 1-alkenylpalmitoyl-2-linoleoyl phosphatidylethanolamine [plasmenyl PE (16:0/18:2); P < 0.005] ions were also observed for both training regimes in glycolytic fibers. We conclude that exercise training results in a remodeling of phospholipids in rat skeletal muscle. Even though little is known about the physiological or pathophysiological role of specific phospholipid molecular species in skeletal muscle, it is likely that this remodeling will have an impact on a range of cellular functions.

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Purpose: Exercise training restores innate immune system cell function in post-myocardial infarction (post-MI) rats. However, studies of the involvement of lymphocyte (Ly) in the setting of the congestive heart failure (CHF) are few. To address this issue, we investigated the function of Ly obtained from cervical lymph nodes from post-MI CHF rats submitted to treadmill running training. Methods: Twenty-five male Wistar rats were randomly assigned to the following groups: rats submitted to ligation of the left coronary artery, which were sedentary (MI-S, N= 7, only limited activity) or trained (MI-T, N= 6, on a treadmill (0% grade at 13-20 m.m(-1)) for 60 min.d(-1), 5 d.wk(-1), for 8-10 wk); or sham-operated rats, which were sedentary (sham-S, N = 6) or trained (sham-T, N = 6). The incorporation of [2-C-14]-thymidine by Ly cultivated in the presence of concanavalin A (Con A) and lipopolysaccharide (LPS), cytokine production by Ly cultivated in the presence of phytohemagglutinin (PHA), and plasma concentration of glutamine were assessed in all groups, 48 h after the last exercise session. Results: Proliferative capacity was increased, following incubation with Con-A in the MI groups, when compared with the sham counterparts. When incubated in the presence of PHA, MI-S produced more IL-4 (96%) than sham-S (P < 0.001). The training protocol induced a 2.2-fold increase in the production of interleukin-2 (P < 0.001) of the cells obtained from the cervical lymph nodes of MI-T, compared with MI-S. Conclusion: The moderate endurance training protocol caused an increase in IL-2 production, and a trend toward the reversion of the Th-1/Th-2 imbalance associated with IL-4 production increased in the post-MI CHF animal model.

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

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O objetivo principal deste estudo foi verificar se diferentes formas de indução à acidose interferem na determinação da intensidade do lactato mínimo (LACmin) em corredores de longa distância. Desse modo, 14 corredores de provas fundas do atletismo participaram do estudo. Os atletas realizaram três protocolos: 1) teste incremental em esteira rolante, com incrementos de 1km.h-1 a cada três minutos até a exaustão, para a determinação das intensidades de limiar anaeróbio (OBLA), de limiar aeróbio (Laer), consumo máximo de oxigênio (VO2max) e intensidade de consumo máximo de oxigênio (vVO2max); 2) teste de lactato mínimo em pista de atletismo (LACminp), que consistiu de dois esforços máximos de 233m na pista de atletismo com intervalo de um minuto entre cada repetição, com oito minutos de recuperação passiva, seguido de um teste incremental semelhante ao do protocolo 1; e 3) teste de lactato mínimo em esteira rolante (LACmine), constituído de dois esforços máximos de um minuto e 45 segundos com intervalo de um minuto, na intensidade de 120% da vVO2max, seguido dos mesmos procedimentos do protocolo 2. Foram coletadas amostras de sangue do lóbulo da orelha ao final de cada estágio em todos os protocolos e no 7º minuto de recuperação passiva dos testes de LACmine e LACminp. A análise de variância (ANOVA) mostrou que ocorreram diferenças significativas entre as intensidades de LACmine (13,23 ± 1,78km.h-1) e OBLA (14,67 ± 1,44km.h-1). Dessa maneira, a partir dos resultados obtidos no presente estudo, é possível concluir que a determinação da intensidade correspondente ao lactato mínimo é dependente do protocolo utilizado para a indução à acidose. Além disso, o LACmine subestimou a intensidade correspondente ao OBLA, não podendo ser utilizado para a mensuração da capacidade aeróbia de corredores fundistas.

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O objetivo do presente estudo foi comparar as intensidades do ponto de compensação respiratório (PCR), limiar anaeróbio de concentração fixa (OBLA3,5) e limiar anaeróbio de lactato de aumento abrupto lactacidêmico (LAnLAC) determinadas em diferentes ergômetros. Para isso, onze mesatenistas (19±1 anos) realizaram testes incrementais máximos no cicloergômetro, ergômetro de braço, esteira e em teste específico para o tênis de mesa. Durante esses esforços, foram mensuradas as repostas lactacidêmica e respiratória. Na análise intraergômetro, não foram encontradas diferenças significativas entre o PCR, LAnLAC e OBLA3,5 no ergômetro de braço (63,4±4,8W, 66,9±4,5W e 64,5±6,1W, respectivamente), esteira (11,4±0,4km.h-1, 11,3±0,3km.h-1 e 11,1±0,3km.h-1, respectivamente) e teste específico (40,5±1,8bolas.min-1, 42,6±3,6bolas.min-1 e 42,8±5,6bolas.min-1, respectivamente); apenas no cicloergômetro foi verificado menor valor de OBLA3,5 (131,9±6,6W) em relação ao PCR (149,3±4,9W) e o LAnLAC (149,3±4,7W). No entanto, fortes e significativas correlações foram verificadas no teste específico entre todos esses métodos (r entre 0,83 a 0,95), entre o PCR e OBLA3,5 no ergômetro de braço (r=0,78) e entre OBLA3,5 e LAnLAC na esteira (r=0,76). Desse modo, podemos concluir que o PCR, OBLA3,5 e LAnLAC parecem corresponder ao mesmo fenômeno fisiológico, principalmente, no teste específico para o tênis de mesa.

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The main purpose of this study was to analyze the effects of exercise mode, training status and specificity on the oxygen uptake ((V)over dot O-2) kinetics during maximal exercise performed in treadmill running and cycle ergometry. Seven runners (R), nine cyclists (C), nine triathletes (T) and eleven untrained subjects (U), performed the following tests on different days on a motorized treadmill and on a cycle ergometer: (1) incremental tests in order to determine the maximal oxygen uptake ((V)over dot O-2max) and the intensity associated with the achievement of (V)over dot O-2max (I(V)over dot O-2max); and (2) constant work-rate running and cycling exercises to exhaustion at I(V)over dot O-2max to determine the effective time constant of the (V)over dot O-2 response (tau(V)over dot O-2). Values for (V)over dotO(2max) obtained on the treadmill and cycle ergometer [R=68.8 (6.3) and 62.0 (5.0); C=60.5 (8.0) and 67.6 (7.6); T=64.5 (4.8) and 61.0 (4.1); U=43.5 (7.0) and 36.7 (5.6); respectively] were higher for the group with specific training in the modality. The U group showed the lowest values for VO2max, regardless of exercise mode. Differences in tau(V)over dot O-2 (seconds) were found only for the U group in relation to the trained groups [R=31.6 (10.5) and 40.9 (13.6); C=28.5 (5.8) and 32.7 (5.7); T=32.5 (5.6) and 40.7 (7.5); U=52.7 (8.5) and 62.2 (15.3); for the treadmill and cycle ergometer, respectively]; no effects of exercise mode were found in any of the groups. It is concluded that tauVO(2) during the exercise performed at I(V)over dot O-2max is dependent on the training status, but not dependent on the exercise mode and specificity of training. Moreover, the transfer of the training effects on tau(V)over dotO(2) between both exercise modes may be higher compared with (V)over dot O-2max.

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This study analyzed the influence of recovery phase manipulation after hyperlactemia induction on the lactate minimum intensity during treadmill running. Twelve male runners (24.6 +/- A 6.3 years; 172 +/- A 8.0 cm and 62.6 +/- A 6.1 kg) performed three lactate minimum tests involving passive (LMT(P)) and active recoveries at 30%vVO(2max) (LMT(A30)) and 50%vVO(2max) (LMT(A50)) in the 8-min period following initial sprints. During subsequent graded exercise, lactate minimum speed and VO(2) in LMT(A50) (12.8 +/- A 1.5 km h(-1) and 40.3 +/- A 5.1 ml kg(-1) min(-1)) were significantly lower (P < 0.05) than those in LMT(A30) (13.3 +/- A 1.6 km h(-1) and 42.9 +/- A 5.3 ml kg(-1) min(-1)) and LMT(P) (13.8 +/- A 1.6 km h(-1) and 43.6 +/- A 6.1 ml kg(-1) min(-1)). In addition, lactate minimum speed in LMT(A30) was significantly lower (P < 0.05) than that in LMT(P). These results suggest that lactate minimum intensity is lowered by active recovery after hyperlactemia induction in an intensity-dependent manner compared to passive recovery.

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The maximal oxygen uptake (VO2max) is the maximal quantity of energy that can be produced by the aerobic metabolism in certain time unity. It can be determined direct or indirectly by predictive equations. The objective of this study was to make a specific predictive equation to determine the VO 2max from boys aged 10-16 years-old. Forty-two boys underwent a treadmill running ergospirometric test, with the initial velocity set at 9 km/h, until voluntary exhaustion. By the multiple linear regression was possible to develop the following equation for the indirect determination of the VO 2max: VO2max (ml/min) = -1574.06 + (141.38 x Vpeak) + (48.34 * Body mass), with standard error of estimate = 191.5 ml/min (4.10 ml/kg/min) and coefficient of determination = 0.934. We suggest that this formula is appropriate to predict VO2max for this population.

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Dynamic exercise evokes sustained cardiovascular responses, which are characterized by arterial pressure and heart rate increases. Although it is well accepted that there is central nervous system mediation of cardiovascular adjustments during exercise, information on the role of neural pathways and signaling mechanisms is limited. It has been reported that glutamate, by acting on NMDA receptors, evokes the release of nitric oxide through activation of neuronal nitric oxide synthase (nNOS) in the brain. In the present study, we tested the hypothesis that NMDA receptors and nNOS are involved in cardiovascular responses evoked by an acute bout of exercise on a rodent treadmill. Moreover, we investigated possible central sites mediating control of responses to exercise through the NMDA receptor-nitric oxide pathway. Intraperitoneal administration of the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK-801) reduced both the arterial pressure and heart rate increase evoked by dynamic exercise. Intraperitoneal treatment with the preferential nNOS inhibitor 7-nitroindazole reduced exercise-evoked tachycardiac response without affecting the pressor response. Moreover, treadmill running increased NO formation in the medial prefrontal cortex (MPFC), bed nucleus of the stria teminalis (BNST) and periaqueductal gray (PAG), and this effect was inhibited by systemic pretreatment with MK-801. Our findings demonstrate that NMDA receptors and nNOS mediate the tachycardiac response to dynamic exercise, possibly through an NMDA receptor-NO signaling mechanism. However, NMDA receptors, but not nNOS, mediate the exercise-evoked pressor response. The present results also provide evidence that MPFC, BNST and PAG may modulate physiological adjustments during dynamic exercise through NMDA receptor-NO signaling. © 2013 Elsevier B.V.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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