Muscle Oxygen Supply Impairment during Exercise in Poorly Controlled Type 1 Diabetes

Purpose Aerobic fitness, as reflected by maximal oxygen (O-2) uptake (VO2max), is impaired in poorly controlled patients with type 1 diabetes. The mechanisms underlying this impairment remain to be explored. This study sought to investigate whether type 1 diabetes and high levels of glycated hemoglobin (HbA(1c)) influence O-2 supply including O-2 delivery and release to active muscles during maximal exercise. Methods Two groups of patients with uncomplicated type 1 diabetes (T1D-A, n = 11, with adequate glycemic control, HbA(1c) <7.0%; T1D-I, n = 12 with inadequate glycemic control, HbA(1c) >8%) were compared with healthy controls (CON-A, n = 11; CON-I, n = 12, respectively) matched for physical activity and body composition. Subjects performed exhaustive incremental exercise to determine VO2max. Throughout the exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin, deoxyhemoglobin, and total hemoglobin in the vastus lateralis. Venous and arterialized capillary blood was sampled during exercise to assess arterial O-2 transport and factors able to shift the oxyhemoglobin dissociation curve. Results Arterial O-2 content was comparable between groups. However, changes in total hemoglobin (i.e., muscle blood volume) was significantly lower in T1D-I compared with that in CON-I. T1D-I also had impaired changes in deoxyhemoglobin levels and increase during high-intensity exercise despite normal erythrocyte 2,3-diphosphoglycerate levels. Finally, VO2max was lower in T1D-I compared with that in CON-I. No differences were observed between T1D-A and CON-A. Conclusions Poorly controlled patients displayed lower VO2max and blunted muscle deoxyhemoglobin increase. The latter supports the hypotheses of increase in O-2 affinity induced by hemoglobin glycation and/or of a disturbed balance between nutritive and nonnutritive muscle blood flow. Furthermore, reduced exercise muscle blood volume in poorly controlled patients may warn clinicians of microvascular dysfunction occurring even before overt microangiopathy.