Acute hypoxia and exercise improve insulin sensitivity (S(I) (2*)) in individuals with type 2 diabetes

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.

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.

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).

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.