An acute bout of endurance exercise (EE) enhances insulin sensitivity, but the effects of sprint interval exercise (SIE) have not yet been described. We sought to compare insulin sensitivity at baseline and after an acute bout of EE and SIE in healthy men (n = 8) and women (n = 5) (age, 20.7 +/- 0.3 years; peak oxygen consumption (VO2 peak), 42.6 +/- 1.7 mL.kg(-1).min(-1); <1.5 days.week(-1) structured exercise; body fat, 21.1 +/- 1.9%). Subjects underwent 3 oral glucose tolerance tests (OGTT(s)) the day after each of the following 3 conditions: no exercise, baseline (OGTT(B)); SIE at approximately 125% VO(2 peak) (OGTT(SIE)); and EE at approximately 75% VO(2 peak )(OGTT(EE)). SIE and EE sessions were randomized for each subject. Subjects consumed identical meals the day preceding each OGTT. Two insulin sensitivity indices - composite whole-body insulin sensitivity index (ISI-COMP) and ISI-hepatic insulin sensitivity (HOMA) - were calculated, using previously validated formulas (ISI-COMP = 10 000/ radical(glucose(fasting)) x insulin(fasting) x glucose(mean OGTT) x insulin(mean OGTT)); ISI-HOMA = 22.5/(insulin(fasting) x glucose(fasting)), and the plasma concentrations of cytokines interleukin-6 and tumor necrosis factor-alpha were measured. There were no differences by sex for any condition (men vs. women, p > 0.05). Pearson's correlation coefficients between ISI-COMP and ISI-HOMA for each condition were highly correlated (p < 0.01), and followed similar patterns of response. ISI-COMP(EE) was 71.4% higher than ISI-COMP(B) (8.4 +/- 1.4 vs. 4.9 +/- 1.0; p < 0.01) and 40.0% higher than ISI-COMPSIE (8.4 +/- 1.4 vs. 6.0 +/- 1.5; p < 0.05), but there was no difference between ISI-COMP(B) and ISI-COMP(SIE) (p = 0.182). VO(2 peak) was highly correlated with both ISI-COMP and ISI-HOMA during baseline and SIE test conditions (p < 0.02). These findings demonstrate that an acute bout of EE, but not SIE, increases insulin sensitivity relative to a no-exercise control condition in healthy males and females. While these findings underscore the use of regular EE as an effective intervention strategy against insulin resistance, additional research examining repeated sessions of SIE on insulin sensitivity is warranted.
Administration of conjugated estrogens resulted in potentially antiatherogenic changes in levels of non-HDL-C, HDL-C, and calculated LDL-C. The HDL-C response to combined treatment was similar to that observed in women taking conjugated estrogens alone, while the non-HDL-C and LDL-C responses to combined treatment were similar to those produced by pravastatin therapy alone. These findings support the position of the National Cholesterol Education Program that estrogen replacement, with a progestin where indicated, should be given consideration as a therapeutic option for the management of hypercholesterolemia in postmenopausal women.
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