Poor muscle health a complication of type 1 diabetes

Type 1 diabetes can lead to poor muscle health even in active young adults, according to research from Canada. The researchers in the study, which is published today in Diabetologia, found the disease had caused alterations in mitochondrial structure and function that impaired their capacity to produce energy, as well as increased autophagic remnants in muscles. They said further research is needed to find out whether or not more rigorous exercise could help to prevent metabolic deficiencies in skeletal muscle.

The team, from McMaster and York universities, recruited 12 physically active young men and women with type 1 diabetes (mean HbA1c 7.9%) and a control group of 12 without type 1 diabetes matched for sex, age, body mass index and level of physical activity. They took microbiopsies from participants’ vastus lateralis muscle and assessed mitochondrial respiration, site-specific mitochondrial H2O2 emission and Ca2+ retention capacity, as well as mitochondrial content, muscle ultrastructure and microvasculature.

They reported that there were no differences in mitochondrial content between groups – but compared with the control group, people with type 1 diabetes had significantly lower mitochondrial oxidative capacity. The muscles of those with diabetes also exhibited increased mitochondrial H2O2 emission and decreased Ca2+ retention capacity compared with controls, and an increase in the size and number of autophagic remnants. Muscle capillary density and platelet aggregation were similar between the groups.

The study authors noted that these alterations in mitochondrial ultrastructure and bioenergetics within the skeletal muscle of active young adults with type 1 diabetes – which they pointed out could result in reduced metabolism, greater difficulty controlling blood glucose and, if left unchecked, an accelerated rate of developing disability – indicate that recreational physical activity might not be enough to prevent skeletal muscle metabolic deficiencies in type 1 diabetes.

They said: “A major clinical concern in this study is that the mitochondrial/metabolic alterations observed were in young adults with type 1 diabetes, who had self-reported moderate-to-vigorous activity levels above the American and Canadian diabetes associations’ recommendations. In addition, these changes occurred in large, proximal muscle groups without a detectable loss of capillary density.”

They added: “Further studies are required to elucidate whether more rigorous exercise may help to prevent skeletal muscle metabolic and ultrastructural abnormalities.”