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

PURPOSE: Aerobic fitness, as reflected by maximal oxygen (O(2)) uptake (V˙O(2max)), 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 V˙O(2max). 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, V˙O(2max) 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 V˙O(2max) 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.