The purpose of the present study was to determine the effect of low level laser therapy (LLLT) treatment before knee extensor eccentric exercise on indirect markers of muscle damage. Thirty-six healthy men were randomized in LLLT group (n = 18) and placebo group (n = 18). After LLLT or placebo treatment, subjects performed 75 maximal knee extensors eccentric contractions (five sets of 15 repetitions; velocity = 60° seg(-1); range of motion = 60°). Muscle soreness (visual analogue scale--VAS), lactate dehydrogenase (LDH) and creatine kinase (CK) levels were measured prior to exercise, and 24 and 48 h after exercise. Muscle function (maximal voluntary contraction--MVC) was measured before exercise, immediately after, and 24 and 48 h post-exercise. Groups had no difference on kineanthropometric characteristics and on eccentric exercise performance. They also presented similar baseline values of VAS (0.00 mm for LLLT and placebo groups), LDH (LLLT = 186 IU/l; placebo = 183 IU/l), CK (LLLT = 145 IU/l; placebo = 155 IU/l) and MVC (LLLT = 293 Nm; placebo = 284 Nm). VAS data did not show group by time interaction (P = 0.066). In the other outcomes, LLLT group presented (1) smaller increase on LDH values 48 h post-exercise (LLLT = 366 IU/l; placebo = 484 IU/l; P = 0.017); (2) smaller increase on CK values 24 h (LLLT = 272 IU/l; placebo = 498 IU/l; P = 0.020) and 48 h (LLLT = 436 IU/l; placebo = 1328 IU/l; P < 0.001) post-exercise; (3) smaller decrease on MVC immediately after exercise (LLLT = 189 Nm; placebo = 154 Nm; P = 0.011), and 24 h (LLLT = 249 Nm; placebo = 205 Nm; P = 0.004) and 48 h (LLLT = 267 Nm; placebo = 216 Nm; P = 0.001) post-exercise compared with the placebo group. In conclusion, LLLT treatment before eccentric exercise was effective in terms of attenuating the increase of muscle proteins in the blood serum and the decrease in muscle force.

In this study, we investigated the effect of biological maturation on maximal oxygen uptake ([Vdot]O(2max)) and ventilatory thresholds (VT(1) and VT(2)) in 110 young soccer players separated into pubescent and post-pubescent groups.. Maximal oxygen uptake and [Vdot]O(2) corresponding to VT(1) and VT(2) were expressed as absolute values, ratio standards, theoretical exponents, and experimentally observed exponents. Absolute [Vdot]O(2) (ml · min(-1)) was different between groups for VT(1), VT(2), and [Vdot]O(2max). Ratio standards (ml · kg(-1) · min(-1)) were not significantly different between groups for VT(1), VT(2), and [Vdot]O(2max). Theoretical exponents (ml · kg(-0.67) · min(-1) and ml · kg(-0.75) · min(-1)) were not properly adjusted for the body mass effects on VT(1), VT(2), and [Vdot]O(2max). When the data were correctly adjusted using experimentally observed exponents, VT(1) (ml · kg(-0.94) · min(-1)) and VT(2) (ml · kg(-0.95) · min(-1)) were not different between groups. The experimentally observed exponent for [Vdot]O(2max) (ml · kg(-0.90) · min(-1)) was different between groups (P = 0.048); however, this difference could not be attributed to biological maturation. In conclusion, biological maturation had no effect on VT(1), VT(2) or [Vdot]O(2max) when the effect of body mass was adjusted by experimentally observed exponents. Thus, when evaluating the physiological performance of young soccer players, allometric scaling needs to be taken into account instead of using theoretical approaches.

The need to study cardiovascular diseases (CVD) has become more and more relevant as their prevalence has increased over the years. An intact endothelial wall is essential to vascular health. Certain factors are responsible for maintaining this tissue intact, including nitric oxide (NO), which provokes dilation of blood vessels in response to shear stress. Expression of the endothelial nitric oxide synthase (eNOS) enzyme, which produces nitric oxide in response to increases in blood flow, is of fundamental importance to maintenance of the vascular system. When this enzyme is inhibited, nitric oxide production is reduced, causing endothelial dysfunction. Since C-reactive protein inhibits production of nitric oxide by the eNOS enzyme, it is one of the causes of endothelial dysfunction and cardiovascular events. The objective of the present study was to review scientific articles in the literature related to the subject 'inflammatory markers and endothelial function' . A wide-ranging review of the current literature was conducted, using systematic analysis of bibliographic references indexed in PubMed, Scielo, Medline and LILACS database, for the years 1992 to 2013. The studies reviewed show that increases in inflammation causes reductions in NO and increases in cardiovascular events. Increased inflammation is associated with higher incidence of cardiovascular diseases.Keywords: inflammation; nitric oxide; endothelium. ResumoA necessidade de estudo das Doenças Cardiovasculares (DCV) vem à tona pelo aumento da sua prevalência ao longo dos anos. Uma parede endotelial íntegra é essencial para a saúde vascular. Alguns fatores são responsáveis pela integridade deste tecido, como o óxido nítrico (NO), que provoca a dilatação do vaso sanguíneo em resposta ao estresse de cisalhamento. A expressão da enzima óxido nítrico sintase endotelial (eNOS), que produz óxido nítrico em resposta ao incremento do fluxo sanguíneo, é fundamental para a manutenção do sistema vascular. Quando há inibição desta enzima, ocorre diminuição da produção de óxido nítrico, causando disfunção endotelial. A PCR inibe a produção de óxido nítrico pela enzima eNOS, sendo então uma causadora de disfunção endotelial e eventos cardiovasculares. O presente artigo tem como objetivo revisar artigos científicos na literatura relacionados ao tema 'marcadores inflamatórios e função endotelial' . Foi realizada uma ampla revisão de literatura atual, utilizando-se análise sistemática das referências bibliográficas nas bases de dados PubMed, Scielo, Medline e Lilacs, no período de 1992 a 2013. Os estudos revisados mostram que o aumento da inflamação causa uma diminuição de NO e aumento de eventos cardiovasculares. O aumento da inflamação está associado ao aumento da incidência de doenças cardiovasculares.Palavras-chave: inflamação; óxido nítrico; endotélio.

The objective was to evaluate the metabolic and vascular effects of lifestyle interventions involving a healthy diet and either a moderate- or a high-intensity exercise regimen in nondiabetic subjects with metabolic syndrome. The effects of these interventions on flow-mediated vasodilation (FMD) and risk profiles were compared with a standard low-fat diet and engaging in daily walking (standard of care). Seventy-five healthy adults with metabolic syndrome (30-55 years old) were randomized to a 10,000-steps-a-day exercise program, a 3-times-a-week fitness (>75% peak VO(2)) program, or a 1-hour-walking-a-day program for 12 weeks. The first 2 interventions were combined with an accessible healthy, no-sugar diet; and the third was combined with a tailored low-fat diet. The outcomes, including FMD and risk factors, were examined at 12 weeks and at 1-year reassessment. Significant increase in FMD (mean difference = 1.51%, 95% confidence interval = 1.05%-3.017%, P = .0007) and decrease in arterial pressure (mean difference = 19.3 ± 2.3/-12.6 ± 1.8 mm Hg, P = .0001) were observed in all groups. However, the FMD changed most favorably in the high-intensity, low-sugar group (mean difference = 1.56%, 95% confidence interval = 0.1%-3.02%, P = .036). Significant improvements in body mass index, waist, insulin-like growth factor-1, homeostasis model assessment of insulin resistance, insulin, glucose, urinary albumin excretion, and lipid profiles occurred in all groups. Metabolic syndrome was resolved in 64%. One year later, weight loss (-9.1 ± 2.3 kg, P = .0001) and arterial pressure decrease (-18.5 ± 2.3/-12.3 ± 2.1 mm Hg, P = .0001) were maintained. Practical, health-centered diet combined with high-intensity exercise is associated with enhanced vascular protection. These data suggest that more intense exercise combined with a low-sugar diet modulates endothelium-dependent vasodilation.

A 5 % weight loss improves lipid profile and reduces inflammation in obese individuals. Endothelial function did not change significantly. Weight loss has a significant impact on these cardiovascular risk factors, and this is independent of physical training.