Lipid peroxides, prostacyclin, and thromboxane A2 in runners during acute exercise.
We studied the effect of physical activity on lipid peroxidation and on the production of antiaggregatory, vasodilatory prostacyclin (epoprostenol, PGI2) and its endogenous antagonist, thromboxane A2 (TxA2) in 10 well-trained long-distance runners before, during, and after maximal exercise on a cycle ergometer. Pre-exercise levels of lipid peroxides (2.0 +/- 0.4 mumol X l-1, means +/- SD), plasma immunoreactive 6-keto-prostaglandin F1 alpha (i 6-keto-PGF1 alpha, a metabolite of PGI2) (192.8 +/- 51.7 pmol X l), and serum immunoreactive thromboxane B2 (i TxB2, a metabolite of TxA2) (703.3 +/- 290.1 nmol X l) did not differ from those of 10 non-athletic controls. Plasma i 6-keto-PGF1 alpha was increased at the seventh minute of the exercise test, but not any more at the end of the exercise or 30 min later. Lipid peroxides or i TxB2 did not change. Our data suggest that the changes of the PGI2/TxA2-ratio induced by long-term or acute physical exercise are too small to explain the protective effect of physical fitness against coronary heart disease.
D000293:Adolescent; D000328:Adult; D011464:Epoprostenol / Q000097:blood*; D005260:Female; D006801:Humans; D008054:Lipid Peroxides / Q000097:blood*; D008297:Male; D005082:Physical Exertion; D012420:Running; D013928:Thromboxane A2 / Q000097:blood*; D013931:Thromboxanes / Q000097:blood*
D008054:Lipid Peroxides; D013931:Thromboxanes; D013928:Thromboxane A2; D011464:Epoprostenol