Increased levels of adhesion molecules or metalloproteinases (MMPs) may indicate endothelial dysfunction. Exercise mobilizes circulating angiogenic cells (CACs) from bone marrow in healthy subjects, improving vascular function. However, it is unclear whether this mechanism is preserved in the early stages of metabolic syndrome (early MetS). We aimed to evaluate the acute effects of exercise on adhesion molecules, angiogenic factors, MMPs, and CACs in early MetS. Fifteen subjects with early MetS and nine healthy controls underwent an exercise session and a nonexercise session, randomly. Adhesion molecules, angiogenic factors, CACs, and MMPs were evaluated before and after exercise or nonexercise sessions. At baseline, levels of sE-selectin, sICAM-1, and MMP-9 were higher in early MetS than in controls (P ≤ 0.03). After exercise, sE-selectin, sICAM-1, and MMP-9 levels were still higher in early MetS (P < 0.05). Subjects with early MetS presented less CACs (P = 0.02) and higher MMP-9 activity (P ≤ 0.04), while healthy controls presented higher MMP-2 activity after exercise. There was no difference between moments in nonexercise session (P > 0.05). In conclusion, subjects with early MetS already presented impaired endothelial function at rest along with a decrease in CACs and an increase in MMP-9 activity in response to exercise.

Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene reduce shear stress-induced nitric oxide production. Thus, we investigated the individual and combined impact of 3 variants in the eNOS gene (-786T>C, intron 4b4a, and 894G>T) on vascular reactivity before and after exercise. Sedentary, healthy subjects were studied (105 women/26 men, age 32 ± 1 years [mean ± standard error of the mean]). Genotypes were determined by polymerase chain reaction restriction fragment length polymorphism, and haplotypes were determined by a Bayesian-based algorithm. Vascular reactivity was evaluated by the percentage of change in forearm vascular conductance provoked by 5 minutes of circulatory occlusion before (baseline) and 10, 60, and 120 minutes after a maximal cardiopulmonary exercise test. Vascular reactivity increased 10 minutes after exercise in the entire sample (baseline: 218 ± 11% vs 10 minutes: 284 ± 15%, P < 0.001), remained increased at 60 minutes (239 ± 12%, P = 0.02 vs baseline), and returned to baseline at 120 minutes (210 ± 10%, P = 0.83 vs baseline). Genotype analysis showed that subjects with the 894G>T polymorphism had lower vascular reactivity than wild counterparts (group effect, P = 0.05). Furthermore, subjects with haplotype 2 (H2), containing the -786T>C and 894G>T polymorphisms, had lower vascular reactivity than wild counterparts (haplotype 1 [H1]) (group effect, P = 0.05), whereas subjects with haplotype 4 (H4), containing only the 894G>T polymorphism, had vascular reactivity similar to that of wild counterparts (H1) (group effect, P = 0.35). Altogether, these results indicate that the 894G>T polymorphism reduced exercise-mediated increase in vascular reactivity, particularly when it occurred concomitantly with the -786T>C polymorphism.

Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene (NOS3) have been associated with lower eNOS expression and activation, which can lead to impairment in eNOS related traits. Thus, we investigated the individual (genotype analysis) and combined (haplotype analysis) impact of three polymorphisms in the NOS3 (−786T>C, 4b4a and 894G>T) on hemodynamic variables. Sedentary, non‐obese, healthy subjects were enrolled [n = 93, age 31 ± 9 years (mean ± SD)]. Genotypes were determined by PCR‐RFLP and haplotypes were inferred by a Bayesian based algorithm. Heart rate (ECG) and blood pressure (BP; finger photoplethismography) were continuously measured during 10 min in the supine position before [baseline (BL)], 10, 60 and 120 min after a maximal cardiopulmonary exercise test. Stroke volume was estimated by the Model Flow method. Then, cardiac output (CO) and total peripheral resistance (TPR) were calculated. There was no difference between subjects in genotype analysis. However, subjects with haplotype containing the polymorphisms −786T>C and 4b4a had higher systolic BP at 10, 60 and 120 min after exercise than subjects with wild haplotype (P < 0.05), which occurred due to higher CO (P < 0.05), while TPR was similar between groups (P > 0.05). In conclusion, NOS3 haplotype containing the polymorphisms −786T>C and 4b4a was associated with impaired hemodynamic response after a bout of maximal dynamic exercise.

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