BACKGROUND: Baroreflex sensitivity (BRS) impairment has been associated with endothelial dysfunction and oxidative stress. METHODS: Because exercise training could improve endothelial function in spontaneously hypertensive rats (SHR), the effect of moderate exercise training on oxidative stress and BRS was investigated. Groups were divided into sedentary and trained Wistar-Kyoto rats (S-WK, n = 7 and T-WK, n = 6) and SHR (S-SHR and T-SHR, n = 9 each). Exercise training was performed on a treadmill (5 days/week, 60 min, 10 weeks), and the lactate threshold (20 m/min) was used to determine moderate intensity. RESULTS: Exercise training reduced mean arterial pressure in WK and SHR (S-WK 127 +/- 4, T-WK 105 +/- 5, S-SHR 169 +/- 4 versus T-SHR 140 +/- 4 mmHg; P < 0.01). Baroreflex bradycardic (S-WK -1.89 +/- 0.15, T-WK -2.11 +/- 0.37, S-SHR -0.80 +/- 0.09 versus T-SHR -1.29 +/- 0.10 bpm/mmHg; P < 0.0001) and tachycardic (S-WK 2.57 +/- 0.19, T-WK 2.73 +/- 0.21, S-SHR 1.18 +/- 0.07 versus T-SHR 2.02 +/- 0.10 bpm/mmHg; P < 0.0001) responses were significantly different between groups. Lipoperoxidation in erythrocytes (S-WK 11 320 +/- 739, T-WK 10 397 +/- 765, S-SHR 20 511 +/- 1627 versus T-SHR 10 211 +/- 589 counts per second (cps)/mg haemoglobin; P < 0.0001) and aortas (S-WK 12 424 +/- 2219, T-WK 7917 +/- 726, S-SHR 26 957 +/- 1772 versus T-SHR 17 777 +/- 1923 cps/mg protein; P < 0.0001) was reduced in T-SHR compared with S-SHR. Inverse correlations were observed between both bradycardic and tachycardic responses and lipoperoxidation in erythrocytes (r = 0.56 and r = -0.77, respectively; P < 0.01) and aortas (r = 0.77 and r = -0.80, respectively; P < 0.0001). CONCLUSION: Our results indicate that exercise training decreases oxidative stress, which is related to an improvement in BRS in SHR.
BACKGROUND: Baroreflex sensitivity (BRS) impairment has been associated with endothelial dysfunction and oxidative stress. METHODS: Because exercise training could improve endothelial function in spontaneously hypertensiverats (SHR), the effect of moderate exercise training on oxidative stress and BRS was investigated. Groups were divided into sedentary and trained Wistar-Kyoto rats (S-WK, n = 7 and T-WK, n = 6) and SHR (S-SHR and T-SHR, n = 9 each). Exercise training was performed on a treadmill (5 days/week, 60 min, 10 weeks), and the lactate threshold (20 m/min) was used to determine moderate intensity. RESULTS: Exercise training reduced mean arterial pressure in WK and SHR (S-WK 127 +/- 4, T-WK 105 +/- 5, S-SHR 169 +/- 4 versus T-SHR 140 +/- 4 mmHg; P < 0.01). Baroreflex bradycardic (S-WK -1.89 +/- 0.15, T-WK -2.11 +/- 0.37, S-SHR -0.80 +/- 0.09 versus T-SHR -1.29 +/- 0.10 bpm/mmHg; P < 0.0001) and tachycardic (S-WK 2.57 +/- 0.19, T-WK 2.73 +/- 0.21, S-SHR 1.18 +/- 0.07 versus T-SHR 2.02 +/- 0.10 bpm/mmHg; P < 0.0001) responses were significantly different between groups. Lipoperoxidation in erythrocytes (S-WK 11 320 +/- 739, T-WK 10 397 +/- 765, S-SHR 20 511 +/- 1627 versus T-SHR 10 211 +/- 589 counts per second (cps)/mg haemoglobin; P < 0.0001) and aortas (S-WK 12 424 +/- 2219, T-WK 7917 +/- 726, S-SHR 26 957 +/- 1772 versus T-SHR 17 777 +/- 1923 cps/mg protein; P < 0.0001) was reduced in T-SHR compared with S-SHR. Inverse correlations were observed between both bradycardic and tachycardic responses and lipoperoxidation in erythrocytes (r = 0.56 and r = -0.77, respectively; P < 0.01) and aortas (r = 0.77 and r = -0.80, respectively; P < 0.0001). CONCLUSION: Our results indicate that exercise training decreases oxidative stress, which is related to an improvement in BRS in SHR.
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