Hsu-Ko Kuo1, Joel M Gore. 1. Division of Cardiology, Department of Medicine, University of Massachusetts, Worcester, MA, USA, hsuko.kuo@umassmemorial.org.
Abstract
OBJECTIVE: Insulin resistance (IR) and chronic inflammation are inversely related to heart rate recovery (HRR), a marker of cardiac autonomic function. Little is known, however, about the joint effects of IR and inflammation on HRR. METHODS: The study sample consisted of 2649 healthy individuals aged 12-49 years with measures of submaximal cardiopulmonary fitness testing from the National Health and Nutrition Examination Survey 1999-2004. HRR 1-min (HRR1) and 2-min (HRR2) after recovery were recorded (bpm). IR was defined if homeostasis model assessment (HOMA-IR) was ≥ 2.73. C-reactive protein (CRP) was quantified by latex-enhanced nephelometry. RESULTS: In the fully adjusted model, participants with IR had attenuated HRR compared to those without (mean HRR1 11.8 vs. 12.7, p = 0.011; mean HRR2 31.2 vs. 33.4, p < 0.001). Mean HRR1 for participants with CRP >0.3 mg/dL, CRP 0.1-0.3 mg/dL, and CRP <0.1 mg/dL were 11.6, 12.0, and 12.8 (p for trend 0.002), respectively. Mean HRR2 in the three corresponding groups were 33.0, 32.5, and 31.8 (p for trend 0.033), respectively. Participants with IR and CRP elevation had slower HRR than those without IR and with normal CRP. The mean HRR1 comparing participants with IR/CRP >0.3 mg/dL to those with no IR/CRP <0.1 mg/dL were 10.5 and 13.1 (p < 0.001), while the mean HRR2 for the same comparison were 29.1 and 33.8 (p < 0.001). HRR (especially HRR2) was inversely correlated with various metabolic risks. CONCLUSIONS: Insulin resistance and CRP levels were inversely associated with HRR in healthy adolescents and adults. Participants with IR and elevated CRP had the worst HRR. Our findings suggest a joint effect of IR and inflammation on cardiac autonomic dysfunction.
OBJECTIVE:Insulin resistance (IR) and chronic inflammation are inversely related to heart rate recovery (HRR), a marker of cardiac autonomic function. Little is known, however, about the joint effects of IR and inflammation on HRR. METHODS: The study sample consisted of 2649 healthy individuals aged 12-49 years with measures of submaximal cardiopulmonary fitness testing from the National Health and Nutrition Examination Survey 1999-2004. HRR 1-min (HRR1) and 2-min (HRR2) after recovery were recorded (bpm). IR was defined if homeostasis model assessment (HOMA-IR) was ≥ 2.73. C-reactive protein (CRP) was quantified by latex-enhanced nephelometry. RESULTS: In the fully adjusted model, participants with IR had attenuated HRR compared to those without (mean HRR1 11.8 vs. 12.7, p = 0.011; mean HRR2 31.2 vs. 33.4, p < 0.001). Mean HRR1 for participants with CRP >0.3 mg/dL, CRP 0.1-0.3 mg/dL, and CRP <0.1 mg/dL were 11.6, 12.0, and 12.8 (p for trend 0.002), respectively. Mean HRR2 in the three corresponding groups were 33.0, 32.5, and 31.8 (p for trend 0.033), respectively. Participants with IR and CRP elevation had slower HRR than those without IR and with normal CRP. The mean HRR1 comparing participants with IR/CRP >0.3 mg/dL to those with no IR/CRP <0.1 mg/dL were 10.5 and 13.1 (p < 0.001), while the mean HRR2 for the same comparison were 29.1 and 33.8 (p < 0.001). HRR (especially HRR2) was inversely correlated with various metabolic risks. CONCLUSIONS:Insulin resistance and CRP levels were inversely associated with HRR in healthy adolescents and adults. Participants with IR and elevated CRP had the worst HRR. Our findings suggest a joint effect of IR and inflammation on cardiac autonomic dysfunction.
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