Poor glycaemic control is associated with increased risk of microvascular disease in various organs including the eye and kidney, but the relationship between glycated haemoglobin (HbA(1c)) and microvascular function in skeletal muscle has not been described. We tested the association between HbA(1c) and a measure of microvascular exchange capacity (K-f) in skeletal muscle in people with central obesity at risk of developing Type 2 diabetes.
Microvascular function was measured in 28 women and 19 men [mean (+/- sd) age 51 +/- 9 years] with central obesity who did not have diabetes. We estimated insulin sensitivity by hyperinsulinaemic-euglycaemic clamp, visceral and total fatness by magnetic resonance imaging, fitness (VO2 max by treadmill testing), physical activity energy expenditure [metabolic equivalents of tasks (METS) by use of the SenseWear Pro armband] and skeletal muscle microvascular exchange capacity (K-f) by venous occlusion plethysmography.
In regression modelling, age, sex and fasting plasma glucose accounted for 30.5% of the variance in HbA(1c) (r2 = 0.31, P = 0.001). Adding K-f to this model explained an additional 26.5% of the variance in HbA(1c) (r2 = 0.57, P = 0.0001 and K-f was strongly and independently associated with HbA(1c) (standardized B coefficient -0.45 (95% confidence interval -0.19, -0.06), P = 0.001).
We found a strong negative independent association between a measure of skeletal muscle microvascular exchange capacity (K-f) and HbA(1c). K-f was associated with almost as much of the variance in HbA(1c) as fasting plasma glucose.