People with T2D have lower cardiorespiratory fitness (CRF) than those without diabetes contributing to increased cardiovascular morbidity and mortality. People with T2D have impaired oxidative flux associated with lower CRF. Yet, reports on muscle mitochondrial dysfunction in T2D are mixed. As diabetes duration and age are predictors of poor outcomes, we hypothesized that T2D and increased age associate with impaired mitochondrial function. We assessed post-exercise calf mitochondrial function in overweight sedentary participants (45 with and 54 without T2D) ages 30-50 and 51-70y. Mitochondrial function was measured in vivo by 31Phosphorous magnetic resonance spectroscopy (31P-MRS) before, during and after 90 seconds of isotonic calf press at 70% maximal force and ex vivo by mitochondrial respiration in muscle fibers using the Oroboros Oxygraph-2k. There was no significant effect of age or T2D on ex vivo measures. MRS-measured phosphocreatine synthesis, apparent maximum rate of oxidative ATP synthesis and ADP time constant were worse in those with T2D or age >50 (Figure) . Age and T2D interact to significantly decrease apparent maximum rate of oxidative ATP synthesis. These data suggest that age and T2D decrease in vivo oxidative capacity. Given that impairment is only found in in vivo mitochondrial measures, factors such as micro- and macrovascular function and blood flow, combined with cardiac function, are likely implicated.


L.Abushamat: None. J.G.Regensteiner: None. R.L.Scalzo: None. D.Ramirez: None. I.E.Schauer: None. L.Knaub: None. E.Clark: None. Y.Garcia reyes: None. M.Cree-green: None. J.Reusch: Advisory Panel; Medtronic.


American Diabetes Association (1-21-CMF-003) (1-12-CT-64) ; Department of Veterans Affairs (BX002046, CX001532)

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