title: Muscle oxygen supply impairment during exercise in poorly controlled type 1 diabetes.
abstract: OBJECTIVE
  Aerobic fitness, as reflected by maximal oxygen (O2) 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 (HbA1c) influence O2 supply including O2 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, HbA1c <7.0%; T1D-I, n = 12 with inadequate glycemic control, HbA1c >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 O2 transport and factors able to shift the oxyhemoglobin dissociation curve.
  
  
  RESULTS
  Arterial O2 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 O2 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.
authors.affiliation: 1Physical Activity, Muscle and Health, Lille, EA 4488, University of Lille 2, FRANCE; 2Department of Kinesiology and Health Science, Faculty of Health, York University, Toronto, Ontario, CANADA; 3Department of Diabetology, Lille University Hospital, EA 4489, Lille, FRANCE; 4Department of Physiology, EA 2689 and IFR 22, Lille, FRANCE; and 5Regional Hospital Centre of Roubaix, FRANCE.
authors.forename: Semah
authors.initials: S
authors.lastname: Tagougui
authors.forename: Erwan
authors.initials: E
authors.lastname: Leclair
authors.forename: Pierre
authors.initials: P
authors.lastname: Fontaine
authors.forename: Régis
authors.initials: R
authors.lastname: Matran
authors.forename: Gaelle
authors.initials: G
authors.lastname: Marais
authors.forename: Julien
authors.initials: J
authors.lastname: Aucouturier
authors.forename: Aurélien
authors.initials: A
authors.lastname: Descatoire
authors.forename: Anne
authors.initials: A
authors.lastname: Vambergue
authors.forename: Kahina
authors.initials: K
authors.lastname: Oussaidene
authors.forename: Georges
authors.initials: G
authors.lastname: Baquet
authors.forename: Elsa
authors.initials: E
authors.lastname: Heyman
mesh_terms: D000293:Adolescent; D000328:Adult; D001810:Blood Volume; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D015444:Exercise / Q000502:physiology*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply*; D010101:Oxygen Consumption; D010108:Oxyhemoglobins / Q000378:metabolism; D055815:Young Adult
chemical_list: D006442:Glycated Hemoglobin; D006454:Hemoglobins; D010108:Oxyhemoglobins; C100003:deoxyhemoglobin