title: Role of chronic exercise in decreasing oxidized LDL-potentiated platelet activation by enhancing platelet-derived no release and bioactivity in rats.
abstract: This study investigates how chronic exercise affects Ox-LDL mediated-platelet activation. Five-week-old male Wistar rats were assigned to either control or trained groups. Trained rats were treadmill-trained for 10 weeks after familiarization. The following measurements were taken in both control and trained groups: plasma lipid profile, oxidation of LDL, platelet adhesiveness, aggregability, cGMP contents, plasma and platelet-NO metabolite (nitrite plus nitrate) levels, and urinary 8-iso-prostaglandin F2alpha (8-iso-PG F2alpha) levels. Based on those measurements, major findings in this study can be summarized as follows: 1) the trained group prolonged the lag time of isolated LDL subjected to copper-induced in vitro oxidation significantly longer than the control group; 2) although having higher plasma and platelet derived-NO metabolite levels, the trained group had lower urinary excretion of 8-iso-PGF2alpha than the control group; 3) the trained group had a lower platelet adhesiveness and aggregability and higher platelet derived-NO metabolite and cGMP productions than the control group; 4) the trained group had a lower Ox-LDL-potentiated platelet adhesiveness and aggregability and Ox-LDL-attenuated NO metabolite and cGMP productions in platelet than the control group; and 5) treating the platelet with L-arginine inhibited Ox-LDL-potentiated platelet activation in both control and trained groups. Results in this study demonstrate that amounts of preformed lipid peroxides decrease while NO production (which acts as an antioxidant) is significantly increased after chronic exercise. Moreover, exercise training decreases Ox-LDL-potentiated platelet activation most likely by enhancing platelet-derived NO release and bioactivity.
authors.affiliation: Department of Physical Therapy, Chang Gung University, Taoyuan, Taiwan. s5492@mail.cgu.edu.tw
authors.forename: J S
authors.initials: JS
authors.lastname: Wang
authors.forename: C C
authors.initials: CC
authors.lastname: Lin
authors.forename: J K
authors.initials: JK
authors.lastname: Chen
authors.forename: M K
authors.initials: MK
authors.lastname: Wong
mesh_terms: D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D028441:F2-Isoprostanes; D006439:Hemodynamics; D006801:Humans; D008054:Lipid Peroxides / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology*; D010973:Platelet Adhesiveness / Q000502:physiology; D010974:Platelet Aggregation / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D028441:F2-Isoprostanes; D008054:Lipid Peroxides; D008055:Lipids; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; C075750:8-epi-prostaglandin F2alpha; D009569:Nitric Oxide; D001120:Arginine; D015237:Dinoprost; D006152:Cyclic GMP