J. Kyle Taylor

The influence of sex, body composition, and nonesterified fatty acids on serum adipokine concentrations

Serum adiponectin concentrations are higher in women than men. The sexual dimorphism for adiponectin has been attributed to the direct effects of testosterone on adipose tissue adiponectin secretion. However, serum testosterone and adiponectin concentrations are generally lower in obese men than lean men, suggesting that sex steroids may not be the only factor that contributes to sex differences in serum adiponectin. The primary objective of this study was to examine the influence of sex, body composition, and nonesterified fatty acids (NEFAs) on serum adiponectin concentrations. Women and men between the ages of 18 and 35 years were consecutively accrued into the study. Sixty-one participants were partitioned into normal-weight (15 female and 16 male) or obese (14 female and 16 male) groups. Blood samples were obtained after a 12-hour fast. Differences between groups were determined by analysis of variance with Tukey-Kramer post hoc testing. Serum adiponectin was 26% higher in women compared with men. Body mass index was associated with total serum adiponectin in men (r = -0.63, P < .05) but not women. Adiponectin was correlated with the homeostasis model assessment index in women (r = -0.56, P < .05) and men (r = -0.58, P < .05) and with NEFAs (r = -0.68, P < .05) in men only. After partitioning men and women into normal-weight and obese groups, serum adiponectin was lower and NEFAs were higher in obese men only. Homeostasis model assessment was similar between obese women and men despite higher NEFAs in the obese men. Leptin and plasminogen activator inhibitor-1 were higher in obese participants but were not associated with serum NEFAs. These results suggest that serum NEFAs may reduce adiponectin concentrations independent of their effects on insulin sensitivity in obese young men.

The effect of exercise intensity and excess post-exercise oxygen consumption on postprandial blood lipids in physically-inactive men

Reductions in postprandial lipemia have been observed following aerobic exercise of sufficient energy expenditure. Increased excess postexercise oxygen consumption (EPOC) has been documented when comparing high- versus low-intensity exercise. The contribution of EPOC energy expenditure to alterations in postprandial lipemia has not been determined. The purpose of this study was to evaluate the effects of low- and high-intensity exercise on postprandial lipemia in healthy, sedentary, overweight and obese men (age, 43 ± 10 years; peak oxygen consumption, 31.1 ± 7.5 mL·kg-1·min-1; body mass index, 31.8 ± 4.5 kg/m2) and to determine the contribution of EPOC to reductions in postprandial lipemia. Participants completed 4 conditions: nonexercise control, low-intensity exercise at 40%-50% oxygen uptake reserve (LI), high-intensity exercise at 70%-80% oxygen uptake reserve (HI), and HI plus EPOC re-feeding (HI+EERM), where the difference in EPOC energy expenditure between LI and HI was re-fed in the form of a sports nutrition bar (Premier Nutrition Corp., Emeryville, Calif., USA). Two hours following exercise participants ingested a high-fat (1010 kcals, 99 g sat fat) test meal. Blood samples were obtained before exercise, before the test meal, and at 2, 4, and 6 h postprandially. Triglyceride incremental area under the curve was significantly reduced following LI, HI, and HI+EERM when compared with nonexercise control (p < 0.05) with no differences between the exercise conditions (p > 0.05). In conclusions, prior LI and HI exercise equally attenuated postprandial triglyceride responses to the test meal. The extra energy expended during EPOC does not contribute significantly to exercise energy expenditure or to reductions in postprandial lipemia in overweight men.

3-nitrotyrosine And Soluble Vascular And Intracellular Adhesion Molecule Responses To High-intensity Interval And Steady-state Moderate-intensity Exercise: 626 Board #22 May 27, 2

Vascular endothelium may respond differently to high-intensity interval exercise (HIIE) when compared to moderate-intensity steady state exercise (SSE). We hypothesized that greater sympathetic stimulation of soluble vascular adhesion molecule-1 (sVCAM-1) and intracellular adhesion molecule-1 (sICAM-1) and greater oxidative and nitrative stress on the vascular endothelium may transiently result from HIIE. PURPOSE: Determine the influence of HIIE on sVCAM-1, sICAM-1 and 3-nitrotyrosine (NT), a marker of nitric oxide-dependent reactive nitrogen species and nitrative stress, relative to a comparable amount of moderate-intensity SSE and a dose that is half that of SSE. METHODS: Seventeen male participants (age 27.8 + 6.4 yr; weight 80.6 + 9.0 kg; BMI 25.1 + 2.4 kg/m2; %fat = 19 + 5; VO2max 52.1 + 7.5 ml/kg/min) underwent HIIE by treadmill running (90% and 40% of VO2reserve in 3:2 min ratio) to expend 500 kcals (H500); HIIE to expend 250 kcals (H250), and; SSE at 70% VO2reserve to expend 500 kcals (M500) in a randomized crossover design. Intensities of all exercise conditions averaged 70% VO2reserve. Blood measures of sVCAM-1 (ng/mL), sICAM-1 (ng/mL), NT (nM), epinephrine (EPI) and norepinephrine (NE) in pg/mL, were obtained just before, immediately after, 2 hr and 24 hr after exercise. Significant differences were determined using 3 by 4 repeated measures ANOVAs. Effect sizes were calculated to determine the magnitude of dependent variable responses to exercise. RESULTS: HIIE resulted in 2 to 2.5 fold greater EPI responses immediately after exercise versus SSE (p = 0.0059, H250 ES = 1.89; H500 ES = 3.04). NE increased an average of 5.4 times above pre-exercise values across all exercise conditions (p < 0.0001). NT decreased immediately after HIIE (H250 ES = 0.39; H500 ES = -0.97) and returned to baseline by 2 hr post-exercise; whereas, NT was elevated 111% 2 hr (ES = 2.46) and remained 24 hr after SSE (p = 0.0001). sVCAM-1 was unchanged with HIIE but increased 6% immediately following moderate-intensity SSE and remained elevated 24 hr post-exercise (p < 0.0005, ES = 1.01). SUMMARY: Our results are in direct opposition to our hypothesis. Transient elevations in NT and sVCAM-1 after moderate-intensity SSE but not HIIE of similar average intensity and duration may indicate unique effects of interval exercise. NT and sVCAM-1 were not elevated after HIIE in spite of a greater sympathetic response than what was observed after moderate-intensity SSE.