Reductions in RIP140 are not required for exercise and high fat diet mediated increases in mitochondrial enzymes

The over‐expression of RIP140 reduces the expression of mitochondrial enzymes whereas the deletion of RIP140 increases mitochondrial content. Despite the importance of RIP140 in the control of mitochondrial biogenesis the effects of physiological perturbations on regulating RIP140 in skeletal muscle has not been determined. To this end, rats were exercised by 2 hours of daily swim training for 14 consecutive days or fed a high fat diet (HFD) for 6 weeks. In an additional study 6 healthy college aged males completed 6 sessions of high intensity exercise training consisting of 8–12 X 1 min sprints on a stationary bicycle at 100% of peak power. Exercise training increased the protein contents of CORE1 (48% increase), COXI (91% increase) and COXIV (30% increase) and citrate synthase activity (45% increase) while having no effect on RIP140 mRNA levels and protein content in rat triceps. Similarly, high intensity exercise training in humans did not cause reductions in the nuclear protein content of RIP140. The consumption of a HFD increased the protein contents of CORE1 (72% increase) and COXIV (53% increase) and the enzyme activities of citrate synthase (26% increase) and beta HAD (71% increase). RIP140 mRNA and protein content was not reduced by the consumption of a HFD. Collectively our results demonstrate that reductions in RIP140 are not required for the induction of mitochondrial biogenesis in skeletal muscle.