Abstract
Caffeine is presented in many commercial products and has been proven to induce ergogenic effects in exercise, mainly related to redox status homeostasis, inflammation and oxidative stress-related adaptation mechanisms. However, most studies have mainly focused on muscle adaptations, and the role of caffeine in different tissues during exercise training has not been fully described. The aim of this study was therefore, to analyze the effects of chronic caffeine intake and exercise training on liver mitochondria functioning and plasma inflammation markers. Rats were divided into control, control/caffeine, exercise, and exercise/caffeine groups. Exercise groups underwent four weeks of swimming training and caffeine groups were supplemented with 6 mg/kg/day. Liver mitochondrial swelling and complex I activity, and plasma myeloperoxidase (MPO) and acetylcholinesterase (AChE) activities were measured. An anti-inflammatory effect of exercise was evidenced by reduced plasma MPO activity. Additionally, caffeine intake alone and combined with exercise decreased the plasma AChE and MPO activities. The per se anti-inflammatory effect of caffeine intake should be highlighted considering its widespread use as an ergogenic aid. Therefore, caffeine seems to interfere on exercise-induced adaptations and could also be used in different exercise-related health treatments.
Highlights
Aerobic physical training demands great amounts of energy turnover, which is mainly promoted by increased oxygen consumption
We demonstrated that exercise training presents anti-inflammatory effects evidenced by decreased and MPO activity
We have found a per se anti-inflammatory effect of caffeine intake through reduction on both MPO and AChE activities on control animals. These are interesting findings since caffeine has long been used as an antioxidant molecule, in spite of the anti-inflammatory role it may exert
Summary
Aerobic physical training demands great amounts of energy turnover, which is mainly promoted by increased oxygen consumption In this sense, it is well known that exercise induces several metabolic changes, which can disrupt the mitochondrial functioning in different ways [1]. Among them the oxygen uptake rate during exercise training is considered an important factor to the mitochondrial excessive reactive oxygen species production (ROS) [2] In this context, mitochondrial dysfunction seems to be closely related to oxidative damage caused by exercise in different tissues [3]. Considering the complexity of exercise-induced cell damage, more comprehensive strategies to understand the associated mechanisms are of interest In this line, mitochondria are the major site of cellular ROS production while at the same time are ROS targets [4,5], indicating that mitochondrial dysfunction play a key role in exercise performance [6]. Mitochondria could bring to light relevant information on exercise mediated-cell antioxidant adaptation
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