A diet high in saturated fat leads to skeletal muscle deteriorations including
insulin resistance,
mitochondrial dysfunction and muscle fiber
atrophy. Consumption of long-chain
polyunsaturated fatty acids and exercise have shown promise in ameliorating high-fat diet (HFD)-induced oxidative stress and
inflammation. However, the impact of extra virgin
olive oil (EVOO) on mitochondrial homeostasis in muscle is largely unknown. This study aimed to investigate whether 12 wks of EVOO feeding alone and in conjunction with
endurance training could protect against metabolic and
mitochondrial dysfunction rat muscle with HFD. Female Sprague-Dawley rats were divided into 4 groups fed a control diet (C), HFD, EVOO diet, and EVOO diet with training (EVOO+T). Mitochondrial
enzyme activity and
protein content decreased with HFD compared to C, but were restored with EVOO and EVOO+T. EVOO+T elevated muscle
cytochrome c and PGC-1α levels. HFD increased muscle proteolytic markers and
protein ubiquitination, whereas these effects were not seen in EVOO and EVOO+T. HFD suppressed mitochondrial fusion
protein level while increasing fission
protein levels, but were restored with EVOO and EVOO+T. Mitophagy marker PINK1 content decreased with HFD, but was unchanged in EVOO and EVOO+T. EVOO+T upregulated autophagy markers, along with decreased phosphorylated/dephosphorylated FoxO3 ratio.
Antioxidants enzyme levels were upregulated by EVOO and EVOO+T, and EVOO+T reduced HFD-induced lipid peroxidation. In conclusion, HFD impaired muscle oxidative capacity, promoted
protein ubiquitination and mitochondrial fission, and upregulated autophagy markers. Replacement of HFD with EVOO corrected the observed adverse effects, while exercise training in conjunction with EVOO provided additional protection to the muscle.