Skeletal muscle mitochondrial capacity is reduced in both aging and diabetes. Whether diabetes further impairs mitochondrial capacity in older adults and how this relates to cardiorespiratory fitness (VO2peak) and glycemic control (HbA1c) remains uncertain. We examined muscle mitochondrial capacity of those with diabetes (self-reported, including Type 1 and 2) and without diabetes in the Study of Muscle Mobility and Aging (SOMMA) (273 men, 194 women; mean±SD age: 76.8±5.3 years) . Mitochondrial capacity was assessed by 31P magnetic resonance spectroscopy (ATPmax) and respirometry of vastus lateralis biopsy specimens. ATPmax (diabetes; 0.48 ± 0.1, nondiabetes; 0.54 ± 0.1 mM/sec, p=0.07) and fatty acid oxidation (FAO) supported OXPHOS (FAO: diabetes; 11.5 ± 4.5, nondiabetes; 12.5 ± 4.4 pmol/min/mg, p=0.01) were lower in those with diabetes compared to those without. VO2peak, assessed by a graded exercise test, was lower in those with diabetes (diabetes; 1478.8± 399.9, nondiabetes; 1495.5 ± 431.3 mL/min, p=0.01) . In all participants, ATPmax (r2=0.07, p=<0.01) and FAO (r2=0.04, p=0.14) explained a small proportion of variance in HbA1c. VO2peak significantly related to mitochondrial capacity (ATPmax: r2=0.66, p=<0.01, FAO: r2=0.64, p<0.01) , but the relationships do not vary by diabetes status.

In summary, older adults with diabetes have marginally lower fitness and mitochondrial capacity. Mitochondrial capacity is related to both glycemic control and cardiorespiratory fitness regardless of diabetes status.


S. V. Ramos: None. P. M. Coen: None. G. Distefano: None. P. Cawthon: None. S. M. Marshall: None. P. Kramer: None. A. Molina: None. M. J. Jurczak: None. F. Toledo: None. B. H. Goodpaster: None.


Study of Muscle, Mobility and Aging (SOMMA) RO1 AG059416

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