Exercise HR recovery (HRR) has proven an effective clinical means to assess parasympathetic dysfunction linked to all-cause mortality, but an analogous functional assessment for sympathetic dysfunction has not been developed.
Purpose: We investigated whether exercise recovery provides additional cardiorespiratory information, beyond the initial HRR period, to index sympathetic overactivity associated with insulin resistance.
Methods: Young people (N = 20) with diverse percent body fat (9%-52%) were studied using fasting, oral glucose tolerance test (OGTT), and high-carbohydrate meal measurements. Participants also completed a graded fitness test (oxygen consumption peak test on cycle ergometer) after which HR and oxygen consumption (V˙O2) measurements were continued for 3 min into recovery. The first, rapid phase of exercise recovery was used as the clinical measurement for parasympathetic control (HRR = HR2 min − HRmax). The second, initial plateau phase of exercise recovery was used to calculate a novel functional index for sympathetic overactivity (the plateau value for the ratio of HR normalized for V˙O2 (HR/V˙O2plat)).
Results: As expected, parasympathetic function (HRR) was within the normal range in these young people (−58 ± 2 bpm). The index for sympathetic overactivity varied over a wide range from 9 to 34 bpm/(mL·kg−1·min−1), with obese adolescents having values in the highest 25th percentile. We found that this simple index was correlated to both the OGTT-derived whole-body insulin sensitivity index (r = −0.74, P < 0.001) and Homeostasis Assessment Model for Insulin Resistance (r = 0.76, P < 0.001), independent of percent body fat and parasympathetic function. Meal-induced thermogenesis was also associated with HR/V˙O2plat (r = −0.64, P < 0.01) but not with HRR.
Conclusion: In young individuals, recovery from intense exercise may provide a simple means to quantify both parasympathetic and sympathetic function. The exercise recovery index for sympathetic overactivity was linked to insulin resistance.
1John B. Pierce Laboratory, New Haven, CT; and 2Yale School of Public Health, 3Department of Internal Medicine, and 4The Yale Center for Clinical Investigation, Yale University School of Medicine, New Haven, CT
Address for correspondence: Catherine W. Yeckel, Ph.D., John B. Pierce Laboratory, 290 Congress Ave, New Haven, CT 06519; E-mail: email@example.com.
Submitted for publication November 2007.
Accepted for publication August 2008.