32 resultados para MODERATE DEVIATIONS


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The aim of this study was to analyze the influence of aerobic fitness on the effects of prior exercise on VO2response during subsequent moderate-intensity exercise. After determination of the lactate threshold (LT) and maximal VO2 (VO2max). 14 untrained subjects (UG) and 14 well-trained cyclists (TG) performed on different days and in random order, rest to moderate-intensity exercise transitions (6 minutes at 80% of LT), preceded by either no prior exercise or prior supramaximal exercise (PSE: two bouts of 1 minute at 120% of VO2max, with a 1-minute rest in between). Baseline VO2 was significantly increased (p<0.05) by PSE in both groups (UG: 0.39 ± 0.06 vs. 0.51 ± 0.15 L·min -1;TG: 0.37 ± 0.06 vs. 0.58 ± 0.14 L·min -1). In the TG group, the steady state VO2 was significantly increased by PSE (TG: 2.21 ± 0.38 vs. 2.07 ± 0.27 L·min-1, p<0.05; UG: 1.60 ± 0.27 vs. 1.60 ± 0.29 L· min-1, p>0.05). It can be concluded that aerobic fitness level influences the effects of PSE on VO2 response during moderate-intensity exercise. [J Exerc Sci Fit • Vol 7 • No 1 • 48-54 • 2009].

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Chronic alcohol intake decreases adiponectin and sirtuin 1 (SIRT1) expressions, both of which have been implicated in various biological processes including inflammation, apoptosis and metabolism. We have previously shown that moderate consumption of alcohol aggravates liver inflammation and apoptosis in rats with pre-existing nonalcoholic steatohepatitis (NASH). This study investigated whether moderate alcohol intake alters SIRT1 activity, adiponectin/Adiponectin receptor (AdipoR)-related signaling and lipid metabolism in a pre-existing NASH status. Sprague-Dawley rats were fed with a high-fat diet (71% energy from fat) for 6 weeks to induce NASH then subsequently divided into 2 sub-groups: fed either a modified high-fat diet (HFD, 55% energy from fat) or a modified high-fat alcoholic diet (HFA, 55% energy from fat and 16% energy from ethanol) for an additional 4 weeks. We observed in comparison to HFD group, HFA increased hepatic nuclear SIRT1 protein but decreased its deacetylase activity. SREBP-1c protein expression and FAS mRNA levels were significantly upregulated, while DGAT1/2 and CPT-I mRNA levels were downregulated in the livers of HFA compared to HFD. Although hepatic AdipoR1 decreased, HFA did not alter AdipoR2 and their downstream signaling. There were no significant changes in plasma adiponectin and free fatty acids (FFA), as well as adiponectin expression in adipose tissue between the two groups. The present study indicates that suppression in SIRT1 deacetylase activity contributes to alcohol-exacerbated hepatic inflammation and apoptosis in rats with pre-existing NASH. In addition, moderate alcohol intake did not modulate adiponectin/AdipoR signaling axis in this model.