|Figure 1: Molecular structure of Stanozolol|
The scientists tested the effect of Stanozolol administration on markers of mitochondrial oxidative stress in rats after an acute bout of exhaustive exercise and found:
Stanozolol treatment markedly reduced the extent of exercise-induced oxidative damage to mitochondrial proteins, as indicated by the lower levels of the specific markers of protein oxidation, glycoxidation, and lipoxidation, and the preservation of the activity of the superoxide-sensitive enzyme aconitase. This effect was not due to an enhancement of antioxidant enzyme activities. Acute exercise provoked changes in mitochondrial membrane fatty acid composition characterized by an increased content in docosahexaenoic acid. In contrast, the postexercise mitochondrial fatty acid composition was not altered in stanozolol-treated rats.Those of you who frequent the Mind & Muscle Forum, may already have read my comment on the changes in plasma fatty acid composition of the cell membranes in the respective thread: These changes vaguely remind me of a recent study on the effects of fish oil supplementation in elite athletes (Omega-3 Fatty Acids PRO(!)-Inflammatory in Athletes) where an increase in DHA (docosahexaenoic acid) also increased oxidative stress in the participants. The finding that Winstrol (Stanozolol) protects against acute exercise-induced oxidative stress by reducing mitochondrial ROS production, in association with a preservation of mitochondrial membrane properties by inhibiting the increase in DHA in the cell membrane may thus also be of relevance in view of the benefits / pitfalls of fish oil supplementation. Since (manageable) structural damage and super-compensatory repairs are also a prerequisite at the heart of training adaptation and muscle growth, the decrease in cellular integrity induced by increases in long-chain PUFAs in the cell membranes could also explain the "anabolic" effect of fish oil that has been observed in a handful of studies.