Abstract

We have previously shown that 27% and 45% of chronic stroke survivors have impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), respectively, placing them at high risk for the development of type 2 diabetes (T2DM). These glucose abnormalities may contribute to metabolic inflexibility, which is the failure to appropriately adapt substrate oxidation to substrate availability. Thus, we tested the hypothesis that the ability to shift from fat (respiratory exchange ratio (RER)=0.7) to carbohydrate (RER=1.0) oxidation during exercise is reduced in stroke survivors with increasing fasting (G0) and 2-hr oral glucose tolerance test (G120) glucose levels. Chronic hemiparetic stroke patients without T2DM (N=18; 63±2 year old; mean±SEM) underwent a graded exercise stress test, with indirect calorimetry for measurement of peak fitness (VO 2 peak). Additionally, we measured RER at rest and during submaximal exercise (60% of VO 2 peak), and subjects completed an OGTT for measurement of G0 and G120. On average, subjects were obese (BMI: 30±2 kg/m 2 ; 19-45 ml/kg/min) and had poor VO 2 peak levels (20±1 ml/kg/min; 9-33 ml/kg/min). Thirty three percent had neither IFG nor IGT, while 33% had IFG (G0: 5.22±0.19 mmol/L), 56% had IGT (G120: 7.94±0.49 mmol/L), and 22% had both IFG and IGT. At rest, RER was 0.71±0.01 and increased to 0.78±0.01 at 60% of VO 2 peak (P<0.01). After controlling for obesity and VO 2 peak, G0 related to RER at 60% of VO 2 peak (r=-0.47) and the change in RER (60%VO 2 peak-rest; r=-0.42) (P’s<0.05). G120 also related to the change in RER (r=-0.36) (P’s<0.05). Our results indicate that lower carbohydrate oxidation and the change in carbohydrate oxidation during exercise of increasing intensity are related to hyperglycemia in chronic stroke survivors. This inflexibility may limit the capacity to fulfill the energy requirements of daily physical activity performance, thereby heightening the probability of a more sedentary lifestyle post-stroke.

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