Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle

Abstract

Anabolic androgenic steroids are used in the sport context to enhance muscle mass and strength and to increase muscle fatigue resistance. Since muscle fatigue has been related to oxidative stress caused by an exercise-linked reactive oxygen species (ROS) production, we investigated the potential effects of a treatment with the anabolic androgenic steroid stanozolol against oxidative damage induced on rat skeletal muscle mitochondria by an acute bout of exhaustive exercise. Mitochondrial ROS generation with complex I- and complex II-linked substrates was increased in exercised control rats, whereas it remained unchanged in the steroid-treated animals. 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. Our results suggest that stanozolol protects against acute exercise-induced oxidative stress by reducing mitochondrial ROS production, in association with a preservation of mitochondrial membrane properties.

A Tutorial on Oxidative Stress and Redox Signaling with Application to Exercise and Sedentariness

“…complex I increases by approximately 187%, and at ETC. complex III by 138% during exhaustive muscular activity [7]. Note that while this is a sizeable increase in the rate of ROS production, it may be less than one might expect given that the metabolic rate of contracting muscle fibers increases approximately 100-fold or more from resting levels [8].…”

“…complex III (ROS formed within the mitochondrial matrix and in the inter-membrane space) [4,5]. Basal ROS production had previously been estimated to account for between 2 and 5% of oxygen consumed, but more recent evidence suggests that it is substantially less-perhaps approximately 0.15% of consumed oxygen [6,7]-and ROS production at ETC. complex I increases by approximately 187%, and at ETC.…”

Reactive oxygen species: players in the cardiovascular effects of testosterone

“…Moreover, testosterone increases mitochondrial respiratory capacity (74). Conversely, stanozolol (an anabolic androgenic steroid) decreases mitochondrial ROS and oxidative stress induced by acute exercise in rat skeletal muscle (167). Considering the anabolic effects of testosterone and its related androgens and also their effects upon mitochondrial metabolism, it is likely that androgens can modulate mitochondrial ROS generation.…”

Oxidative Stress in Muscle Growth and Adaptation to Physical Exercise

“…For instance, acute effects of nandrolone decanoate do not promote the production of ROS and even possess some anti-oxidative potential [20]. Anabolic steroid stanozolol decreases mitochondrial ROS generation during acute exercise [41]. High doses of GH also involved in detrimental effects related to energy metabolism and oxidative stress [44], whereas close-to-physiological levels prevents memory deficits in early stages of the neurodegenerative process and slow down adverse effects of immobilisation in old rats muscle tissue [5,40].…”