Low-intensity voluntary running lowers blood pressure with simultaneous improvement in endothelium-dependent vasodilatation and insulin sensitivity in aged spontaneously hypertensive rats.
Our objective is to examine the effects of voluntary running at different intensity levels on blood pressure, endothelium-dependent vessel dysfunction and insulin resistance in aged spontaneously hypertensive rats (SHR) with severe hypertension. Ten-month-old male and female SHR with severe hypertension were assigned to voluntary running at either low intensity (30% of maximal aerobic velocity) or moderate intensity (60% of maximal aerobic velocity) on a motor-driven treadmill for 6 weeks, 20 min per day and 7 days per week. Age-matched Wistar-Kyoto rats and SHR were kept under sedentary conditions as controls. Blood pressure and heart rate were measured by the tail-cuff method. At the end of the exercise training, blood samples were collected for glucose, insulin and lipids assay, and aortae were isolated to examine their function in vitro. Low-intensity but not moderate-intensity running significantly lowered blood pressure in both male and female SHR (p<0.01). There was significant impairment in acetylcholine-induced vasorelaxation in SHR (p<0.01), which was improved by low-intensity training (p<0.05). Nitric oxide synthase blockade abrogated the improvement in endothelium-dependent relaxation. Hypertensive rats had elevated blood glucose and insulin levels with lowered insulin sensitivity that was ameliorated by low-intensity running. A significant increase in blood high-density lipoprotein (HDL)-cholesterol and a significant decrease in triglycerides were found in exercised SHR. In conclusion, low-intensity voluntary exercise lowers hypertension in aged SHR with severe hypertension. Exercise-induced simultaneous improvement in endothelium-dependent vessel relaxation and insulin sensitivity may act concomitantly in attenuating cardiovascular risk factors in aged hypertensive rats with significantly high blood pressure.
Sun
Meng-Wei
MW
Shanghai Research Institute of Sports Science, Shanghai, PR China.
Qian
Feng-Lei
FL
Wang
Jian
J
Tao
Tao
T
Guo
Jing
J
Wang
Lie
L
Lu
Ai-Yun
AY
Chen
Hong
H
D000109:Acetylcholine / Q000494:pharmacology; D000375:Aging / Q000502:physiology*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006973:Hypertension / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D000109:Acetylcholine