Key result
Insulin resistance, as estimated by HOMA2-IR above the median, was associated with a 3.26-fold increased odds of having below-median exercise capacity in patients with type 2 diabetes and coronary artery disease.
Cross-Sectional (n=137)
No
Odds Ratio: 3.26 (95% CI 1.35–7.83)
p-value: p=0.008
Insulin resistance is inversely associated with exercise capacity in patients with type 2 diabetes and CAD, particularly in those with exercise-induced ischemia.
Association between higher HOMA2-IR and reduced exercise capacity in T2D-CAD; hypothesis-generating and should not yet change practice.
BACKGROUND: Previous studies on type 2 diabetes have shown an association between exercise capacity and insulin resistance. In patients with coronary artery disease (CAD) exercise capacity is often reduced due to exercise-induced ischemia. We have investigated the association between glucometabolic control, including the homeostatic model assessment (HOMA) of insulin resistance, and exercise capacity in patients with type 2 diabetes and CAD with and without exercise-induced ischemia. METHODS: In 137 patients (age 63.1 ± 7.9) cardiopulmonary exercise testing on treadmill was performed using a modified Balke protocol. The highest oxygen uptake (VO2peak) was reported as 30-s average. Fasting blood samples were drawn for determination of glucose, insulin and HbA1c. Insulin resistance (IR) was assessed by the HOMA2-IR computer model. Exercise-induced ischemia was defined as angina and/ or ST-depression in ECG ≥ 0.1 mV during the exercise test. RESULTS: HOMA2-IR was inversely correlated to VO2peak (r = -0.328, p < 0.001), still significant after adjusting for age, gender, smoking and BMI. Patients with HOMA2-IR above the median value (1.3) had an adjusted odds ratio of 3.26 (95 % CI 1.35 to 7.83, p = 0.008) for having VO2peak below median (23.8 mL/kg/min). Insulin levels were inversely correlated to VO2peak (r = -0.245, p = 0.010), also after adjusting for age and gender, but not after additional adjustment for BMI. The correlation between HOMA2-IR and VO2peak was also significant in the subgroups with (n = 51) and without exercise-induced ischemia (n = 86), being numerically stronger in the group with ischemia (r = -0.430, p = 0.003 and r = -0.276, p = 0.014, respectively). Fasting glucose and HbA1c were not correlated with VO2peak or AT. CONCLUSIONS: Insulin resistance, as estimated by fasting insulin and the HOMA index, was inversely associated with exercise capacity in patients with type 2 diabetes and CAD, the association being more pronounced in the subgroup with exercise-induced ischemia. These results indicate that insulin resistance is related to exercise capacity in type 2 diabetic patients with CAD, possibly even more so in patients with exercise-induced ischemia compared to those without.
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Byrkjeland et al. (2014) conducted a cross-sectional in Type 2 diabetes and coronary artery disease (n=137). Insulin resistance (HOMA2-IR above median) vs. Lower insulin resistance (HOMA2-IR below median) was evaluated on VO2peak below median (23.8 mL/kg/min) (OR 3.26, 95% CI 1.35-7.83, p=0.008). Insulin resistance, as estimated by HOMA2-IR above the median, was associated with a 3.26-fold increased odds of having below-median exercise capacity in patients with type 2 diabetes and coronary artery disease.
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