Expression Of Markers Of Browning In White Adipose Tissue In Life-long Endurance Trained Athletes

Abstract

Physical exercise and training results in adaptations in adipose tissue. Such adaptations may in part be mediated through “cross-talk” with skeletal muscle. One of these adaptations potentially relevant to energy metabolism in endurance athletes is the beiging of white adipose tissue (WAT). Beiging is the process by which WAT shows characteristics of brown adipose tissue (BAT), possibly increasing basal metabolic rate. While the process of beiging in rodents and the existence of BAT in humans has been shown previously, it is unknown if and how life-long endurance exercise influences beiging of WAT depots. PURPOSE: To study the influence of life-long training on adipose tissue markers of beiging and metabolic performance, the uncoupling protein 1 (UCP-1), CIDEA and PPAR-γ in white adipose tissue (WAT) in sub-elite athletes. METHODS: Periumbilical subcutaneous adipose tissue biopsies were collected from 14 life-long trained sub-elite endurance athletes (8 male, 6 female; VO max performance over 90th percentile for their age group) and 13 age-matched controls (6 male 7 female). Gene expression was analyzed on extracted RNA. Fold induction was statistically analyzed by Student’s-test. RESULTS: UCP-1 gene expression was significantly higher in trained women compared with the control group (p=0.046). No significant difference was found in men when comparing UCP-1 expression (p=0.257). Expression of CIDEA was, again, significantly higher compared with controls (p=0.049), but also in men (p=0.024). Finally, expression of PPAR-γ was significantly higher in trained women (p=0.005). Again no differences were found in men (p=0.924). CONCLUSION: Life-long endurance training results in a higher expression of brown adipose tissue markers in periumbilical WAT in women, in men only in expression of CIDEA, a factory closely associated with metabolic health. Previous results in rodents show a higher susceptibility of females to upregulate BAT markers following β-adrenergic signaling. A similar mechanism might be possible in humans. This effect might also be caused by differences in body fat distribution and functionality, with women having a higher prevalence for BAT.