Impact of Sex and Exercise on Femoral Artery Function: More Favorable Adaptation in Male Rats

Abstract

Blood flow increases in arteries of the skeletal muscles involved in active work. Our aim was to investigate the gender differences as a result of adaptation to sport in the femoral arteries. Vascular reactivity and histology of animals were compared following a 12-week swimming training. Animals were divided into sedentary male (MS), trained male (MTr), sedentary female (FS), and trained female (FTr) groups. Isolated femoral artery rings were examined by wire myography. Contraction induced by phenylephrine (Phe) did not differ between the four groups. The contractile ability in the presence of indomethacin (INDO) was decreased in both sedentary groups. However, we found a specific cyclooxygenase-2 (COX-2) role only in FS rats. After exercise training, we observed increased vasoconstriction in both sexes, when nitro-L-arginine methyl ester (L-NAME) was present. The COX-dependent vasoconstriction effect disappeared in MTr animals, and the COX-2-dependent vasoconstriction effect disappeared in FTr ones. Relaxation was reduced significantly, when L-NAME was present in MTr animals compared to in FTr rats. The training was associated with greater endothelial nitric oxide synthase (eNOS) protein expression in males, but not in females. The present study proves that there are gender differences regarding adaptation mechanisms of musculocutaneous arteries to sports training. In males, relaxation reserve capacity was markedly elevated compared to in females.

Keywords: exercise training; favorable males; femoral artery; immunohistochemistry; sex differences; vascular adaptation.

Figure 1

Phenylephrine induced contraction. Data are shown as means ± SEM; n = 18–20 in each group; analysis: two-way repeated measures ANOVA; test: the Tukey’s post hoc test. Abbreviations: MS—sedentary male; MTr—trained male; FS—sedentary female; FTr—trained female.

Figure 2

Phenylephrine induced contraction in the presence of NS398, INDO, L-NAME, or DMSO in sedentary male rats (A), in trained male rats (B), in sedentary female rats (C), and in trained female rats (D). Data are shown as means ± SEM; n = 5–17 in each group; analysis: two-way repeated measures ANOVA; test: the Tukey’s post hoc test. † p < 0.05, ††† p < 0.001: DMSO vs. INDO; $$ p < 0.01, $$$ p < 0.001 DMSO vs. L-NAME; § p < 0.05 DMSO vs. NS398. Abbreviations: MS—sedentary male; MTr—trained male; FS—sedentary female; FTr—trained female; DMSO—diluted dimethyl-sulfoxide; NS398—the cyclooxygenase-2 specific inhibitor; L-NAME—nitro-L-arginine methyl ester; INDO—indomethacin.

Figure 3

Acetylcholine induced relaxation. Data are shown as means ± SEM; n = 15–19 in each group; analysis: two-way repeated measures ANOVA; test: the Tukey’s post hoc test. Abbreviations: MS—sedentary male; MTr—trained male; FS—sedentary female; FTr—trained female.

Figure 4

Acetylcholine induced relaxation in the presence of NS398, INDO, L-NAME, or DMSO in sedentary male rats (A), in trained male rats (B), in sedentary female rats (C), and in trained female rats (D). Data are shown as means ± SEM; n = 5–19 in each group; analysis: two-way repeated measures ANOVA; test: the Tukey’s post hoc test. $$ p < 0.01, $$$ p < 0.001, $$$$ p < 0.0001 DMSO vs. L-NAME. Abbreviations: MS—sedentary male; MTr—trained male; FS—sedentary female; FTr—trained female; DMSO—diluted dimethyl sulfoxide; NS398—the cyclooxygenase-2 specific inhibitor; L-NAME—nitro-L-arginine methyl ester; INDO—indomethacin.

Figure 5

(A) Optical density of eNOS labeling in the intimal layer of femoral arteries. Data are presented as individual data points, and lines represent means ± SEM; n= 5–10 in each group; analysis: two-way ANOVA; test: the Tukey’s post hoc test. (B) Representative images of vessels labeled with an anti-eNOS antibody. Scale bar, 50 µm. aa, p < 0.01 MS vs. MTr; bb, p < 0.01 MTr vs. FTr. Abbreviations: MS—sedentary male; MTr—trained male; FS—sedentary female; FTr—trained female; OD—optical density.

Figure 6

Summary of vascular function changes experienced during a12-week sports adaptation of the femoral artery in a rat model.