964 resultados para VO(2)PEAK


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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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The aim of this study was to address the question if the VO2 kinetics is further improved as the aerobic training status increases from trained to elite level athletes. Maximal oxygen uptake (VO(2)max), work-rate associated to VO(2)max (IVO(2)max) and VO2 kinetics of moderate (Mod) and maximal exercise (Max) were determined in fifty-five subjects. Then, they were assigned into three groups: low (LF), intermediate (IF) and high (HF) aerobic fitness level. In average, the VO(2)max of LF, IF and HF groups were, respectively, 36.0 +/- 3.1, 51.1 +/- 4.5 and 68.1 +/- 3.9 ml . kg . min(-1) (p <= 0.05 among each other). VO2 kinetics mean response time of both exercise intensities were significantly faster (p <= 0.05) in HF (Mod, 27.5 +/- 5.5 s; Max, 32.6 +/- 8.3 s) and IF (Mod, 25.0 +/- 3.1 s; Max, 42.6 +/- 10.4 s) when compared to LF (Mod, 35.7 +/- 7.9 s; Max: 57.8 +/- 17.8 s). We can conclude that VO2 kinetics is improved as the fitness level is increased from low to intermediate but not further improved as the aerobic fitness level increases from intermediate to high.

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

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The objective of the present study was to compare pulmonary gas exchange kinetics (VO 2 kinetics) and time to exhaustion (Tlim) between trained and untrained individuals during severe exercise performed on a cycle ergometer and treadmill. Eleven untrained males in running (UR) and cycling (UC), nine endurance cyclists (EC), and seven endurance runners (ER) were submitted to the following tests on separate days: (i) incremental test for determination of maximal oxygen uptake (VO 2max) and the intensity associated with the achievement of VO 2max (IVO 2max) on a mechanical braked cycle ergometer (EC and UC) and on a treadmill (ER and UR); (ii) all-out exercise bout performed at IVO 2max to determine the time to exhaustion at IVO 2max (Tlim) and the time constant of oxygen uptake kinetics (τ). The τ was significantly faster in trained group, both in cycling (EC = 28.2 ± 4.7 s; UC = 63.8 ± 25.0 s) and in running (ER = 28.5 ± 8.5 s; UR = 59.3 ± 12.0 s). Tlim of untrained was significantly lower in cycling (EC = 384.4 ± 66.6 s vs. UC; 311.1 ± 105.7 s) and higher in running (ER = 309.2 ± 176.6 s vs. UR = 439.8 ± 104.2 s). We conclude that the VO 2 kinetic response at the onset of severe exercise, carried out at the same relative intensity is sensitive to endurance training, irrespective of the exercise type. The endurance training seems to differently influence Tlim during exercise at IVO 2max in running and cycling. © 2003 Taylor & Francis Ltd.

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The objective was to analyze the oxygen uptake (VO2) kinetics during exercise performed at critical power (CP) in subjects with different aerobic status in cycling. Six trained cyclists (GT) and seven non-trained subjects (GNT) underwent to the following protocols in cyclergometer: (a) incremental to exhaustion to determine VO2max and its respective workload (IVO(2)max); b) three square-wave tests to exhaustion at 95-110% IVO2max to determine CP, and; (c) one square-wave test to exhaustion at 100% CP. During the exercise at CP the slow component expressed as absolute value (GT: 342.4 +/- 165.8 ml.min(-1) vs. GNT: 571.3 +/- 170.1 ml.min(-1)) and as the relative contribution to the increase of VO2 during exercise (GT: 10.0 +/- 4.6% vs. GNT: 26.6 +/- 7.3%) were lower for trained subjects. The VO2 at the end of the exercise at PC (GT: 89.8 +/- 8.4% VO(2)max vs. GNT: 97.4 +/- 2.8% VO(2)max) was significantly lower in GT (rho = 0.045), and similar to VO(2)max in GNT. Therefore, the aerobic level might influence the VO2 responses to exercise at PC

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

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Bearing in mind that cancer cachexia is associated with chronic systemic inflammation and that endurance training has been adopted as a nonpharmacological anti-inflammatory strategy, we examined the effect of 8 weeks of moderate intensity exercise upon the balance of anti-and pro-inflammatory cytokines in 2 different depots of white adipose tissue in cachectic tumour-bearing (Walker-256 carcinosarcoma) rats. Animals were assigned to a sedentary control (SC), sedentary tumour-bearing (ST), sedentary pair-fed (SPF) or exercise control (EC), exercise tumour-bearing (ET), and exercise pair-fed (EPF) group. Trained rats ran on a treadmill (60% VO(2)max) 60 min/day, 5 days/week, for 8 weeks. The retroperitoneal (RPAT) and mesenteric (MEAT) adipose pads were excised and the mRNA (RT-PCR) and protein (ELISA) expression of IL-1 beta, IL-6, TNF-alpha, and IL-10 were evaluated. The number of infiltrating monocytes in the adipose tissue was increased in cachectic rats. TNF-alpha mRNA in MEAT was increased in the cachectic animals (p < 0.05) in relation to SC. RPAT protein expression of all studied cytokines was increased in cachectic animals in relation to SC and SPF (p < 0.05). In this pad, IL-10/TNF-alpha ratio was reduced in the cachectic animals in comparison with SC (p < 0.05) indicating inflammation. Exercise training improved IL-10/TNF-alpha ratio and induced a reduction of the infiltrating monocytes both in MEAT and RPAT (p < 0.05), when compared with ST. We conclude that cachexia is associated with inflammation of white adipose tissue and that exercise training prevents this effect in the MEAT, and partially in RPAT.

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Background: Exercise training (ET) has been used as a nonpharmacological strategy for treatment of diabetes and myocardial infarction (MI) separately. We evaluated the effects ET on functional and molecular left ventricular (LV) parameters as well as on autonomic function and mortality in diabetics after MI. Methods and Results: Male Wistar rats were divided into control (C), sedentary-diabetic infarcted (SDI), and trained-diabetic infarcted (TDI) groups. MI was induced after 15 days of streptozotocin-diabetes induction. Seven days after MI, the trained group underwent ET protocol (90 days, 50-70% maximal oxygen consumption-VO(2)max). LV function was evaluated noninvasively and invasively; baroreflex sensitivity, pulse interval variability, cardiac output, tissue blood flows, VEGF mRNA and protein, HIF1-alpha mRNA, and Ca2+ handling proteins were measured. MI area was reduced in TDI (21 +/- 4%) compared with SDI (38 +/- 4%). ET induced improvement in cardiac function, hemodynamics, and tissue blood flows. These changes were probable consequences of a better expression of Ca2+ handling proteins, increased VEGF mRNA and protein expression as well as improvement in autonomic function, that resulted in reduction of mortality in TDI (33%) compared with SDI (68%) animals. Conclusions: ET reduced cardiac and peripheral dysfunction and preserved autonomic control in diabetic infarcted rats. Consequently, these changes resulted in improved VO(2)max and survival after MI. (J Cardiac Fail 2012; 18:734-744)

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The aim of this work was to evaluate the effects of low-level laser therapy (LLLT) on exercise performance, oxidative stress, and muscle status in humans. A randomized double-blind placebo-controlled crossover trial was performed with 22 untrained male volunteers. LLLT (810 nm, 200 mW, 30 J in each site, 30 s of irradiation in each site) using a multi-diode cluster (with five spots - 6 J from each spot) at 12 sites of each lower limb (six in quadriceps, four in hamstrings, and two in gastrocnemius) was performed 5 min before a standardized progressive-intensity running protocol on a motor-drive treadmill until exhaustion. We analyzed exercise performance (VO(2 max), time to exhaustion, aerobic threshold and anaerobic threshold), levels of oxidative damage to lipids and proteins, the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), and the markers of muscle damage creatine kinase (CK) and lactate dehydrogenase (LDH). Compared to placebo, active LLLT significantly increased exercise performance (VO(2 max) p = 0.01; time to exhaustion, p = 0.04) without changing the aerobic and anaerobic thresholds. LLLT also decreased post-exercise lipid (p = 0.0001) and protein (p = 0.0230) damages, as well as the activities of SOD (p = 0.0034), CK (p = 0.0001) and LDH (p = 0.0001) enzymes. LLLT application was not able to modulate CAT activity. The use of LLLT before progressive-intensity running exercise increases exercise performance, decreases exercise-induced oxidative stress and muscle damage, suggesting that the modulation of the redox system by LLLT could be related to the delay in skeletal muscle fatigue observed after the use of LLLT.

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[EN] Several weeks of intense endurance training enhances mitochondrial biogenesis in humans. Whether a single bout of exercise alters skeletal muscle mitochondrial DNA (mtDNA) content remains unexplored. Double-stranded mtDNA, estimated by slot-blot hybridization and real time PCR and expressed as mtDNA-to-nuclear DNA ratio (mtDNA/nDNA) was obtained from the vastus lateralis muscle of healthy human subjects to investigate whether skeletal muscle mtDNA changes during fatiguing and nonfatiguing prolonged moderate intensity [2.0-2.5 h; approximately 60% maximal oxygen consumption (Vo(2 max))] and short repeated high-intensity exercise (5-8 min; approximately 110% Vo(2 max)). In control resting and light exercise (2 h; approximately 25% Vo(2 max)) studies, mtDNA/nDNA did not change. Conversely, mtDNA/nDNA declined after prolonged fatiguing exercise (0.863 +/- 0.061 vs. 1.101 +/- 0.067 at baseline; n = 14; P = 0.005), remained lower after 24 h of recovery, and was restored after 1 wk. After nonfatiguing prolonged exercise, mtDNA/nDNA tended to decline (n = 10; P = 0.083) but was reduced after three repeated high-intensity exercise bouts (0.900 +/- 0.049 vs. 1.067 +/- 0.071 at baseline; n = 7; P = 0.013). Our findings indicate that prolonged and short repeated intense exercise can lead to significant reductions in human skeletal muscle mtDNA content, which might function as a signal stimulating mitochondrial biogenesis with exercise training.

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[EN] The aim of this study was to find out whether the efficiency of concentric muscle contraction is impaired by eccentric squatting exercise. The study involved 25 male physical education students in two experiments. In the first experiment 14 subjects undertook cycling exercise at 65% VO(2)max until exhaustion on two occasions. During the experimental condition their cycling was interrupted every 10 min so they could perform eccentric squatting exercise, whereas in the control condition they rested seated on the bike during the interruptions. Eccentric squatting consisted of 10 series of 25 reps with a load equivalent to 150% of the subject's body mass on the shoulders. During the first experiment gross efficiency decreased (mean +/- SE) from 17.1 +/- 0.3 to 16.0 +/- 0.4%, and from 17.2 +/- 0.3 to 16.5 +/- 0.4%, between the 2nd and 9th cycling bouts of the experimental and control conditions, respectively (both p < 0.05). The reduction in cycling efficiency was similar in both conditions (p = 0.10). Blood lactate concentration [La] was higher during the experimental than in the control condition (p < 0.05), but substrate oxidation was similar. MVC was decreased similarly (25-28%) in both conditions. The 11 subjects participating in the second experiment undertook 25 reps of eccentric squatting exercise only, each with a load equivalent to 95% of his maximal voluntary contraction (MVC), repeated every 3 min until exhaustion. One hour after the end of the eccentric squatting exercise series cycling, VO(2) and gross cycling efficiency were comparable to the values observed before the eccentric exercise. Both experimental protocols with eccentric exercise elicited similar muscle soreness 2 days later; however, at this time cycling efficiency was similar to that observed prior to eccentric exercise. The interposition of cycling exercise between the eccentric exercise bouts accelerated the recovery of MVC. We conclude that eccentric exercise does not alter or has only a marginal effect on gross cycling efficiency even in presence of marked muscle soreness.

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[EN] BACKGROUND: To determine if there is an association between physical activity assessed by the short version of the International Physical Activity Questionnaire (IPAQ) and cardiorespiratory and muscular fitness. METHODOLOGY/PRINCIPAL FINDINGS: One hundred and eighty-two young males (age range: 20-55 years) completed the short form of the IPAQ to assess physical activity. Body composition (dual-energy X-Ray absorptiometry), muscular fitness (static and dynamic muscle force and power, vertical jump height, running speed [30 m sprint], anaerobic capacity [300 m running test]) and cardiorespiratory fitness (estimated VO(2)max: 20 m shuttle run test) were also determined in all subjects. Activity-related energy expenditure of moderate and vigorous intensity (EEPA(moderate) and EEPA(vigorous), respectively) was inversely associated with indices of adiposity (r = -0.21 to -0.37, P<0.05). Cardiorespiratory fitness (VO(2)max) was positively associated with LogEEPA(moderate) (r = 0.26, P<0.05) and LogEEPA(vigorous) (r = 0.27). However, no association between VO(2)max with LogEEPA(moderate), LogEPPA(vigorous) and LogEEPA(total) was observed after adjusting for the percentage of body fat. Multiple stepwise regression analysis to predict VO(2)max from LogEEPA(walking), LogEEPA(moderate), LogEEPA(vigorous), LogEEPA(total), age and percentage of body fat (%fat) showed that the %fat alone explained 62% of the variance in VO(2)max and that the age added another 10%, while the other variables did not add predictive value to the model [VO(2)max = 129.6-(25.1x Log %fat) - (34.0x Log age); SEE: 4.3 ml.kg(-1). min(-1); R(2) = 0.72 (P<0.05)]. No positive association between muscular fitness-related variables and physical activity was observed, even after adjusting for body fat or body fat and age. CONCLUSIONS/SIGNIFICANCE: Adiposity and age are the strongest predictors of VO(2)max in healthy men. The energy expended in moderate and vigorous physical activities is inversely associated with adiposity. Muscular fitness does not appear to be associated with physical activity as assessed by the IPAQ.

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Altitude training has become very popular among athletes as a means to further increase exercise performance at sea level or to acclimatize to competition at altitude. Several approaches have evolved during the last few decades, with "live high-train low" and "live low-train high" being the most popular. This review focuses on functional, muscular, and practical aspects derived from extensive research on the "live low-train high" approach. According to this, subjects train in hypoxia but remain under normoxia for the rest of the time. It has been reasoned that exercising in hypoxia could increase the training stimulus. Hypoxia training studies published in the past have varied considerably in altitude (2300-5700 m) and training duration (10 days to 8 weeks) and the fitness of the subjects. The evidence from muscle structural, biochemical, and molecular findings point to a specific role of hypoxia in endurance training. However, based on the available performance capacity data such as maximal oxygen uptake (Vo(2)max) and (maximal) power output, hypoxia as a supplement to training is not consistently found to be advantageous for performance at sea level. Stronger evidence exists for benefits of hypoxic training on performance at altitude. "Live low-train high" may thus be considered when altitude acclimatization is not an option. In addition, the complex pattern of gene expression adaptations induced by supplemental training in hypoxia, but not normoxia, suggest that muscle tissue specifically responds to hypoxia. Whether and to what degree these gene expression changes translate into significant changes in protein concentrations that are ultimately responsible for observable structural or functional phenotypes remains open. It is conceivable that the global functional markers such as Vo(2)max and (maximal) power output are too coarse to detect more subtle changes that might still be functionally relevant, at least to high-level athletes.