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Cardiovagal Modulation and Efficacy of Aerobic Exercise Training in Obese Individuals


Medicine & Science in Sports & Exercise: February 2014 - Volume 46 - Issue 2 - p 369–375
doi: 10.1249/MSS.0b013e3182a66411
Applied Sciences

Type 2 diabetes (T2D) is associated with poor exercise tolerance and peak aerobic capacity (V˙O2peak) even when compared to obese nondiabetic peers. Exercise training studies have demonstrated improvements in V˙O2peak among patients with T2D, yet there is a large amount of variability in this response. Recent evidence suggests that cardiac autonomic modulation may be an important factor when considering improvements in aerobic capacity.

Purpose: This study aimed to determine the effects of a 16-wk aerobic exercise program on V˙O2peak in obese individuals, with and without T2D, who were classified as having either high or low cardiovagal modulation (HCVM or LCVM) at baseline.

Methods: Obese individuals (38 women and 19 men; body mass index = 36.1 kg·m−2) were studied in the fasted state. ECG recordings were obtained while seated for 3 min, before and after 4 months of exercise training (4 d·wk−1, 65% V˙O2peak). The ECG recording was analyzed for HR variability in the spectral domain. Groups were split on a marker of CVM (normalized high frequency (HFnu)) at the 50th percentile, as either HCVM or LCVM.

Results: V˙O2peak only increased with exercise training among those classified as having HCVM, regardless of diabetes status (T2D: HCVM = 20.3–22.5 mL·kg−1·min−1, LCVM = 24.3–25.0 mL·kg−1·min−1; obese nondiabetics: HCVM = 24.5–26.3 mL·kg−1·min−1, LCVM = 23.1–23.7 mL·kg−1·min−1) (P < 0.05). No change in V˙O2peak was observed for the LCVM group. Changes in weight do not explain the change in V˙O2peak among the HCVM group. Glucose tolerance only improved among the LCVM group with T2D.

Conclusions: Obese individuals, with or without T2D, when classified as having relatively HCVM before exercise training, have a greater propensity to improve V˙O2peak after a 16-wk aerobic training program.

1Integrative Physiology Laboratory, Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL; 2Department of Physiology, Georgia Regents University, Augusta, GA; 3Department of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, Urbana, IL; and 4Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO

Address for correspondence: Tracy Baynard, Ph.D., Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 W. Taylor St., MC-517 Chicago, IL 60612; E-mail:

Submitted for publication June 2013.

Accepted for publication July 2013.

© 2014 American College of Sports Medicine