title: Acute hypoxia and exercise improve insulin sensitivity (S(I) (2*)) in individuals with type 2 diabetes.
abstract: BACKGROUND
  hypoxia has been shown to increase glucose uptake in skeletal muscle using the contraction-stimulated pathway, independent of the actions of insulin. Yet, the same stress has also been linked with causing insulin resistance and hyperglycaemia. The aim of this study was to examine the effects of acute hypoxia with and without exercise on insulin sensitivity (S(I)(2*) in individuals with type 2 diabetes.
  
  
  METHODS
  eight type 2 diabetic patients completed 60 min of the following: (1) normoxic rest; (2) hypoxic rest [O(2) = 14.6 (0.4)%]; (3) normoxic exercise and (4) hypoxic exercise [O(2) = 14.6 (0.4)%]. Exercise trials were set at 90% of lactate threshold. Each condition was followed by a labelled intravenous glucose tolerance test to provide estimations of insulin sensitivity (S(I)(2*) and β-cell function.
  
  
  RESULTS
  Two-compartmental analysis showed that insulin sensitivity (S(I)(2*) was higher following hypoxic rest compared with normoxic rest (p = 0.047). Insulin sensitivity (S(I)(2*) was also higher following hypoxic exercise [4.37 (0.48) × 10(-4) /min (µU/mL)] compared with normoxic exercise [3.24 (0.51) × 10(-4) /min (µU/mL)] (p = 0.048). Acute insulin response to glucose was reduced following hypoxic rest versus normoxic rest (p = 0.014).
  
  
  CONCLUSIONS
  this study demonstrated that (1) hypoxic-induced improvements in glucose tolerance in the 4 h following exposure can be attributed to improvements in peripheral insulin sensitivity (S( I)(2*) and (2) exercise and hypoxia have an additive effect on insulin sensitivity (S(I)(2*) in type 2 diabetic patients. Acute hypoxia may therefore improve short-term glycaemic control in individuals with type 2 diabetes. The application of these findings in the clinic will require further investigation.
authors.affiliation: School of Life Sciences, Department of Human and Health Sciences, University of Westminster, London, United Kingdom. r.mackenzie@westminster.ac.uk
authors.forename: Richard
authors.initials: R
authors.lastname: Mackenzie
authors.forename: Neil
authors.initials: N
authors.lastname: Maxwell
authors.forename: Paul
authors.initials: P
authors.lastname: Castle
authors.forename: Gary
authors.initials: G
authors.lastname: Brickley
authors.forename: Peter
authors.initials: P
authors.lastname: Watt
mesh_terms: D000208:Acute Disease; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control*; D005081:Exercise Therapy; D005951:Glucose Tolerance Test; D006801:Humans; D007004:Hypoglycemic Agents / Q000378:metabolism; D000860:Hypoxia; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin