Relationship of Cellular Adhesion Molecules and Stress Hormones in Obese Males Following Exercise

The development of atherosclerosis is associated with a steady accumulation of inflammatory molecules. Exercise-induced hormones such as cortisol and catecholamines (epinephrine and norepinephrine) may play a role in endothelial inflammation. Methods: Fifteen obese (BMI \u3e 30 kg/m2) sedentary (less than 2 days per week of physical activity) male volunteers, the ages between 18 and30, participated in the study. The participants performed a single bout of cycling exercise (average energy expenditure ~ 300 kcal) at two different intensities in random order [low-intensity: 50% of maximal heart rate and high-intensity: 80% of maximal heart rate]. Overnight fasting blood samples were collected at baseline, immediate post-exercise (IPE), 1-hr PE, and 24-hr PE for each intensity of exercise to determine the responses of soluble cell adhesion molecules [intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), and E-selectin (sE-selectin)] and exercise-induced stress hormones. Data were analyzed by an analysis of variance with repeated measures along with the Bonferroni multiple comparisons. The linear regression analysis was used to examine the interaction between exercise-induced hormones and vascular inflammation markers (p \u3c .05). RESULTS: There exhibited no significant change in sICAM-1, sVCAM-1, E or NE, while sE-selectin at 1-hr PE (10.25±1.07 ng/mL) significantly decreased (p = .045) from baseline (12.22±1.39 ng/mL). COR at IPE (262.12±31.09 ng/ml) was significantly higher (p = .001) than 1-hr PE (189.35±31.11 ng/ml) during high-intensity exercise. In contrast, COR at IPE (187.52±31.09 ng/ml, p = .009) and 1-hr PE (156.24±31.11 ng/ml, p = .001) were significantly lower than baseline (259.75±23.07 ng/ml) during low-intensity exercise. COR and sICAM-1 had a negative relationship at 1-hr PE during low-intensity exercise (r2 = .34, p = .02), whereas COR and sVCAM-1 had a positive relationship at IPE during high-intensity exercise (r2 = .36, p = .02). CONCLUSION: sE-selectin was favorably reduced following exercise, and changes in cortisol were exercise-intensity dependent. Although sICAM-1 and sVCAM-1 did not significantly change following exercise, a significant interaction between cortisol and these cell adhesion molecules suggests that cortisol is one of the responsible exercise-induced hormones that may be associated with cell adhesion molecule metabolism

Responses of Matrix Metalloproteinases in Obese Men after Undergoing Low and High Intensity Exercise

Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that degrade extracellular matrix proteins and play a role in various pathological conditions such as inflammation and endothelial dysfunction. PURPOSE: The current study investigated the responses of MMP-1, -2, and -9 in obese men over a 24-hour period after undergoing different intensities (low vs. high) of cycling exercise. METHODS: Fifteen sedentary (physical activity \u3c 2 days/week) obese [body mass index (BMI) \u3e 30kg/m2] men between the ages of 18 and 30 years participated in the study. Each participant completed a similar volume (average energy expenditure ~ 300 kcal) of cycling exercise at 2 different intensities in random order [low intensity: 50% of maximal heart rate and high-intensity: 80% of maximal heart rate] on a separate occasion. Fasting overnight blood samples were collected at baseline, immediate post exercise (IPE), 1-hour post exercise (1-PE), and 24-hours post exercise (24-PE) for each exercise intensity trial to examine the responses of MMP-1, -2, and -9. An analysis of variance (ANOVA) with repeated measures was used to determine the mean differences in intensity and time on MMP-1, -2, and -9. If necessary, the Sidak’s multiple pairwise comparisons and a follow-up Simple effects test were employed as a post-hot test (p \u3c 0.05). RESULTS: No change was found in MMP-1 following either low- or high-intensity exercise over the 24-hr period. During the low-intensity exercise trial, MMP-2 at 24-hr PE (72.68±6.43 ng/mL) was significantly lower than IPE (87.23±8.02 ng/mL, p=0.008) and 1-hr PE (92.01±7.99 ng/mL, p=0.011). During the high-intensity exercise trial, MMP-9 at IPE (54.19±9.16 ng/mL) was significantly higher than PRE (30.48±5.86 ng/mL, p =0.008), 1-hr PE (34.82±5.08 ng/mL, p=0.040), and 24-hr PE (31.03±4.82 ng/mL, p=0.006). Additionally, MMP-9 at 24-hr PE (31.32±4.82 ng/mL) was significantly lower than PRE (41.43±5.86 ng/mL, p=0.009) during the low-intensity exercise trial. CONCLUSION: Both MMP-2 and -9, but not MMP-1, significantly increased immediately following exercise, which then returned to its baseline values post exercise. This exercise-induced acute change in MMP-2 and MMP-9 was dependent upon exercise intensity since MMP-2 changed with low-intensity exercise, whereas MMP-9 was altered following high-intensity exercise. Additionally, MMP-9 at 24 hours decreased after 24 hours following low intensity exercise. Thus, the current study suggests that the responses of MMP-2 and MMP-9 to exercise are dependent on exercise-intensity, and low-intensity exercise may favorably influence cardiovascular health by lowering both MMP-2 and MMP-9 in obese men