Recently, aerobic exercise stimulating the sympathetic nervous system was shown to promote thermogenic uncoupling protein-1 (UCP-1) induced white adipose tissue (WAT) browning (i.e., conversion of white adipocyte cells into brown-like thermogenic beige fat cells) [1] thereby increasing energy expenditure [2], [3], [4]. Despite the existence of several homologues such as uncoupling protein-2 and uncoupling protein-3, UCP-1 is the only member of the family that performs a true thermogenic function [5]. Beige adipocyte is a distinct thermogenic fat cell type in both mouse and human [6] and highly expresses UCP-1 which generates heat by uncoupling mitochondrial respiration from adenosine triphosphate (ATP) synthesis [7]. Therefore, browning can be targeted to prevent the development of metabolic diseases related to obesity and can be considered as a promising strategy against weight gain [8]. However, whether exercise-induced browning occurs consistently in humans is far from being established [2]. In the meantime, even though UCP-1 is an intracellular (mitochondrial) protein, low serum UCP-1 was demonstrated to be an important predictor for insulin resistance in humans [9]. Thus, in this context, we may suggest that an increased serum UCP-1 levels due to exercise may also be a key indicator for human health. However, as far as we know, no study has investigated the effects of any kind of exercise (aerobic or anaerobic) on serum UCP-1 levels.

Exercise-induced WAT browning process is mediated by increased serum levels of myokines such as irisin and interleukin-6 (IL-6) which increase UCP-1 mRNA expression in WAT [2], [3]. To be more precise, exercise causing inflammation stimulates the gene expression of fibronectin type III domain-containing protein 5 (FNDC5) and irisin is cleaved from FNDC5 and released in circulation [10]. However, research about the effects of acute and/or chronic anaerobic exercises on irisin and IL-6 are contradictory [1], [10], [11], [12]. Moreover, endothelial nitric oxide synthase (eNOS) expressed in brown adipose tissue (BAT) in response to inflammatory stimuli [13] produces nitric oxide (NO) which has antioxidant features [14] and is found to be closely related with UCP-1 as training was proven to increase UCP-1 mRNA expression only in wild type mice and not in eNOS knockout mice [15], [16]. Speaking of which, acute and chronic aerobic and anaerobic exercises consistently increase serum NO levels [14]. Thus, increased NO, irisin and IL-6 due to exercise may play together an important role in the exercise-induced WAT browning process which in turn may also contribute to the increase of serum UCP-1 levels. However, the increase in free radicals occurring primarily during strenuous exercise such as acute and chronic anaerobic exercises was reported to downregulate UCP-1's activity in BAT [2]. Moreover, an imbalance between the production of ROS and the antioxidant system occuring during acute and chronic anaerobic exercises is well known to cause oxidative stress (OS) [17]. Therefore, chronic anaerobic training (CAT) may lead to excessive OS and thus may affect negatively UCP-1 and browning related myokines. Likewise, an acute maximal exercise (AME) with maximal oxygen comsumption such as the YO-YO intermittent recovery test level 1 (YO-YO IR-1) [18] may have CAT-like effects on OS, UCP-1 and browning related myokines.

Furthermore, UCP-1 is thought to be a gene associated with weight gain due to impaired thermogenesis. Researchs were held especially with UCP-1-3826 A/G polymorphism (UCP1P) which is revealed as an adenine to guanine (A–G) point mutation in –3826 position from the TATA box at the 5′ flanking region of the UCP-1 gene. Indeed, people from GG genotype group are demonstrated to be more prone to gain weight [19]. In addition, G allele was associated with the development of insulin resistance in Italian obese patients [20]. Furthermore, it is well known that the effects of exercise on weight loss differ from person to person and the important reason for this difference is presumed to be mainly hereditary. In this context, a mutation in UCP1P may also influence the possible effect of anaerobic exercises on UCP-1, OS, NO and the above mentioned myokines levels in some genotype groups. One plausible reason of the impaired thermogenesis may be an UCP1P induced modification of OS. However, to the best of our knowledge, no research studying the association between UCP1P and the effects of anaerobic exercise on OS was found in the literature. Therefore, the purpose of the present study was to investigate the role of UCP1P on the effects of AME and CAT on serum levels of UCP-1, OS markers, irisin, NO and IL-6 in healthy young men. The present study may shed light on how people with different phenotypes in terms of UCP-1 may be affected by anaerobic exercise and may provide new data to adjust training periodization according to the phenotype characteristics if a phenotypically negative effect may exist for especially UCP-1 and OS parameters.