Purpose of review
Here we summarize the evidence from human studies of the impairments to the structural, functional, and metabolic capacities in skeletal muscle in those with type 1 diabetes (T1D) – a condition known as diabetic myopathy. Given the importance of skeletal muscle for blood lipid and glucose management, the development and progression of diabetic myopathy would not only lead to increased insulin resistance, but also impact the ability to mitigate dysglycemic/dyslipidemic burdens.
Despite the importance of skeletal muscle in whole-body metabolic control, studies investigating diabetic myopathy are startling limited. Recent findings have demonstrated that those with T1D exhibit decreased force production, increased fatigability, loss of muscle stem cells, and a greater reliance on glycolytic metabolism, as a result of reduced mitochondrial capacity.
We propose a mechanistic model for the development of diabetic myopathy based on the human findings to date. This model suggests that repeated insulin injections in those with T1D leads to recurrent periods of intracellular hyperglycemia in myofibers. Resultant reductions in mitochondrial function lead to greater reliance on glycolytic metabolism and a concomitant shift in fiber type composition. Studies defining the scope and magnitude of diabetic myopathy and testing the veracity of this model are urgently needed in order to develop appropriate therapeutic strategies to maximize muscle health in those with T1D.