Matrix metalloproteinases (MMPs), also known as matrixins, are involved in the degradation of extracellular matrix of the tissue. Cigarette smoking and exercise may influence these molecules in the circulation. PURPOSE: The current study investigated the responses of MMP-1, -2, and -9 before and after a single bout of exercise performed at lower- and higher-intensity in smokers and non-smokers. METHODS: Physically inactive (N=18, physical activity < 2 days per week) male smokers (N=8, carbon monoxide ≥ 16 ppm, smoking history > 2 years, smoking > 10 cigarettes per day) and non-smokers (N=10), the ages between 20 and 30, participated in the study. Participants exercised on a treadmill for 3 miles at two different intensities in random order (lower-intensity: 55% VO2max and higher-intensity: 75% of VO2max). Overnight fasting blood samples were collected before (PRE), immediately post-exercise (IPE), and 1-hr PE to examine the responses of MMP-1, -2, and -9. All data were analyzed using an ANOVA with repeated measure. If necessary, the Sidak’s pairwise multiple comparisons and a follow-up simple effects test were used as post-hoc tests (p < 0.05). RESULTS: Only smokers significantly increased MMP-1 at IPE (1.88±0.19 ng/mL) by 22.08% from PRE (1.54±0.16 ng/mL, p=0.014), which then returned to the baseline value at 1-hr PE (1.45±0.15 ng/mL, p=0.001). The significant main effect for time indicated that MMP-2 at IPE (43.71±5.65 ng/mL) was significantly higher than PRE (25.68±3.27 ng/mL, p= 0.011) and 1-hr PE (28.04±3.34 ng/mL, p=0.036). Additionally, smokers had significantly higher MMP-9 (45.77±6.48 ng/mL, p=0.037) as compared with non-smokers (31.17±3.41 ng/mL). CONCLUSION: Regardless of exercise intensity, a single bout of exercise acutely increased both MMP-1, particularly in smokers, and MMP-2. However, this exercise-induced acute elevation of MMP-1 and MMP-2 returned to baseline values at 1-hour post exercise. A significantly higher level of MMP-9 observed in smokers may indicate that habitual cigarette smokers, as compared with non-smokers, may be more susceptible to a structural damage of extracellular matrix, endothelial inflammation, and an atherosclerotic event.



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