Exhaustive Training Increases Uncoupling Protein 2 Expression and Decreases Bcl-2/Bax Ratio in Rat Skeletal Muscle

Abstract

This work investigates the effects of oxidative stress due to exhaustive training on uncoupling protein 2 (UCP2) and Bcl-2/Bax in rat skeletal muscles. A total of 18 Sprague-Dawley female rats were randomly divided into three groups: the control group (CON), the trained control group (TC), and the exhaustive trained group (ET). Malondialdehyde (MDA), superoxide dismutase (SOD), xanthine oxidase (XOD), ATPase, UCP2, and Bcl-2/Bax ratio in red gastrocnemius muscles were measured. Exhaustive training induced ROS increase in red gastrocnemius muscles, which led to a decrease in the cell antiapoptotic ability (Bcl-2/Bax ratio). An increase in UCP2 expression can reduce ROS production and affect mitochondrial energy production. Thus, oxidative stress plays a significant role in overtraining.

Hyperlipidemia exacerbates cerebral injury through oxidative stress, inflammation and neuronal apoptosis in MCAO/reperfusion rats

“…4d, f). MDA, which indirectly reflects the degree of ROS on membrane lipid peroxidation, is one of the products of membrane lipid peroxidation (Liu et al 2013). Currently, there was no significant change on MDA level in the experimental groups before the surgical operation of cerebral I/R, but sensitively induced by MCAO/R injury both in I/R and HL + I/R rats.…”

Efectos de un protocolo de entrenamiento de alta intensidad sobre marcadores fisiológicos de estrés en ratas. [Physiological effects of the stress induced by a high-intensity exercise protocol in rats].

“…Finalmente, el EAI, como es el de fuerza hipertrofia, puede provocar hipoxia, hipoglucemia o estrés oxidativo, situaciones que podrían inducir estrés del retículo endoplásmico, induciendo daño renal a nivel glomerular y tubular (Dickhout y Krepinsky, 2009;Inagi, 2009). En línea con estos resultados, recientemente algunos autores han encontrado una asociación entre sobreentrenamiento y estrés oxidativo (Liu, He, y Li, 2013).…”

Implementation of the ergogenic action of antioxidative agents

“…Therefore, it is unquestionable that the antioxidants can be also used for a modification of such process significant for live organisms as the programmed cellular death (Park et al, 2014). It is shown that an increase in the level of reactionable forms of oxygen in the course of training, for example, in red fibbers of skeletal muscles, causes a decrease in the antiapoptotic ability of cells (index Bcl-2/Bax) (Liu, He, 2013). Moreover, irrespective of the genesis of apoptosis (hypertonia, electromagnetic oscillations, malignant neoplasms, Нelicobacter pylori-associated diseases), the application of various antioxidants such as melanin and vitamins C, A, and E is accompanied by a decrease in the number of apoptotically changed cells and in the activity of the enzymes caspases, in particular, caspase-8 (Magenta et al, 2011).…”