Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.99.3 (PRE)
 1,923 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether exercise intensity influences acute HDL-C responses, 12 male recreational runners (24.8 +/- 4 yr) who ran 15-30 miles.wk-1 exercised on a motor driven treadmill at 60% (L) and 75% (H) VO2max. A counterbalanced experimental design was utilized and energy expenditure was 800 Kcal. Fasting blood samples were obtained 24 h before exercise (24 PRE), immediately post-(IPE), 1 h post- (1 h PE), 6 h post- (6 h PE), and 24 h post- (24 h PE) exercise and analyzed for HDL-C and HDL2&3-C. In addition, postheparin plasma samples, obtained 24 h PRE, 6 h PE, and 24 h PE were analyzed for lipolytic activity--LPLA and HTGLA. An exercise trial by time interaction was observed for HDL-C (P < 0.01). Post-hoc analysis revealed no change in HDL-C following the L trial. However, an increase in HDL-C was observed 24 h PE (P < 0.01) following the H trial. The increase in HDL-C was attributed to an elevated HDL3-C (P < 0.01), with no change in HDL2-C. Analysis of plasma lipolytic activity revealed an increase in LPLA 24 h PE (P < 0.05) which may be responsible for the postexercise alterations in HDL-C. However, HTGLA decreased 6 h PE (P < 0.01) and 24 h PE (P < 0.05). We conclude that increases in HDL-C levels following endurance activity are influenced, in part, by the exercise intensity.
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PMID:The acute effects of exercise intensity on HDL-C metabolism. 805 5

Recent research has demonstrated that lymphocyte apoptosis sensitivity appears to be related to training status and exercise intensity. This work investigated the effect of prolonged, submaximal treadmill running on percentage (%) apoptosis, % necrosis and DNA strand breaks in lymphocytes and related these to changes in total lymphocyte and blood cortisol concentrations in well-trained runners. Venous blood samples (n = 14) were taken immediately before (PRE), immediately after (IPE) and 3 h after (3PE) 2.5 h of treadmill running at 75% of VO2 max from eight well-trained male endurance athletes (age 34.2 +/- 2.44 years) and analysed for cellular content and serum cortisol concentrations. Lymphocytes were isolated from whole blood and % apoptotic and necrotic cell were detected by flow cytometry using Annexin V-FITC and propidium iodide uptake. DNA strand breaks were measured by single-cell gel electrophoresis. Despite a significant (P < 0.001) exercise-induced increase in mean serum cortisol concentrations and reduction in lymphocyte counts, the mean % Annexin-V positive cells (13.3 +/- 6.78 in PRE, 11.3 +/- 5.51 in IPE and 12.8 +/- 6.75 in 3PE samples) were not significantly different at the three time-points (P > 0.05). Mean DNA strand breaks in the lymphocytes also did not change significantly (P > 0.05) rising from 25.7 +/- 2.16 to 26.9 +/- 1.89 and 27.1 +/- 1.38 microm in IPE and 3PE samples, respectively. The exercise-induced changes in total blood lymphocyte counts and cortisol concentrations did not result in a significant change in % apoptotic lymphocytes or DNA strand breaks in the endurance-trained athletes during this prolonged, submaximal exercise.
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PMID:Prolonged exercise does not cause lymphocyte DNA damage or increased apoptosis in well-trained endurance athletes. 1694 Nov 79