Effect of cardiorespiratory fitness on vascular regulation and oxidative stress in postmenopausal women.
Increasing evidence exists suggesting an important role for oxidative stress in the pathogenesis and progression of hypertension in women via a decrease of NO production after menopause. Regular physical training has been shown to upregulate antioxidant enzymatic systems, which may slow down the usual increase of oxidative stress in postmenopausal women. The aims of this study were to determine the impact of fitness status on enzymatic antioxidant efficiency, oxidative stress, and NO production and to determine the associations among oxidative stress, enzymatic antioxidant and NO production, mean arterial blood pressure (MABP), and cerebrovascular conductance (CVC) in postmenopausal women (n=40; 50 to 90 years old). Physical fitness, physical activity, resting MABP, and CVC were measured. End product of NO, lipid peroxidation (malondialdehyde and 8-iso-prostaglandin F2alpha), DNA oxidation (8-hydroxy-2'-deoxyguanosine), protein nitration (nitrotyrosine), antioxidant glutathione peroxidase, and catalase activities were measured in plasma. We identified significant negative associations between oxidative stress and indices of physical fitness (malondialdehyde: r=-0.33, P<0.05; 8-iso-prostaglandin F2alpha: r=-0.39, P<0.05; 8-hydroxy-2'-deoxyguanosine: r=-0.35, P<0.05) and physical activity (malondialdehyde: r=-0.30, P<0.05; 8-iso-prostaglandin F2alpha: r=-0.41, P<0.01; 8-hydroxy-2'-deoxyguanosine: r=-0.39, P<0.05). Conversely, glutathione peroxidase was positively correlated with fitness level (r=0.55; P<0.01). Finally, MABP and CVC were significantly associated with 8-hydroxy-2'-deoxyguanosine (MABP: r=0.36, P<0.05; CVC: r=-0.36, P<0.05), nitrotyrosine (MABP: r=0.39, P<0.05; CVC: r=-0.32, P<0.05), and the end product of NO (MABP: r=-0.57, P<0.01; CVC: r=0.44, P<0.01). These findings demonstrate that, after menopause, fitness level and regular physical activity mediate against oxidative stress by maintaining antioxidant enzyme efficiency. Furthermore, these results suggest that oxidative stress and NO production modulate MABP and CVC.
Department of Physiology and Pharmacology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.
Vincent
V
Pialoux
Allison D
AD
Brown
Richard
R
Leigh
Christine M
CM
Friedenreich
Marc J
MJ
Poulin
D000368:Aged; D000369:Aged, 80 and over; D000886:Anthropometry; D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism*; D001774:Blood Chemical Analysis; D001794:Blood Pressure / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology; D003430:Cross-Sectional Studies; D015237:Dinoprost / Q000097:blood; D005080:Exercise Test; D005260:Female; D006801:Humans; D016014:Linear Models; D008315:Malondialdehyde / Q000097:blood; D008593:Menopause / Q000502:physiology*; D008875:Middle Aged; D015999:Multivariate Analysis; D009569:Nitric Oxide / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010809:Physical Fitness / Q000502:physiology; D011336:Probability; D017585:Ultrasonography, Doppler, Transcranial
D000975:Antioxidants; D009569:Nitric Oxide; D008315:Malondialdehyde; D015237:Dinoprost