Exercise training does not mitigate high-phosphate diet induced mitochondrial dysfunction in skeletal muscle

We reported previously that mice fed high-Pi diet (HPD) for 12 weeks exhibited reduced VO2max, altered metabolic gene expression, and mitochondrial dysfunction in skeletal muscle. Exercise is a common intervention for metabolic diseases as it improves metabolic flexibility and mitochondrial function, so we tested the hypothesis that exercise training reverses the negative consequences of HPD.

Male mice were fed HPD for five weeks to induce muscle mitochondrial dysfunction and were subsequently subjected to HPD and voluntary exercise training for nine weeks. Serum, urine, and fecal Pi were increased within one day of HPD feeding which was sustained throughout the study. No differences in food intake, body weight, or body composition were detected between NPD- and HPD-fed mice, in either sedentary or exercised trained groups.