Exercise for Weight Loss: Further Evaluating Energy Compensation with Exercise

Kyle D. Flack, Harry M. Hays, Jack Moreland, Douglas E. Long

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Purpose This study assessed how individuals compensate for energy expended during a 12-wk aerobic exercise intervention, elucidating potential mechanisms and the role exercise dose plays in the compensatory response. Participants and Design Three-arm, randomized controlled trial among sedentary adults age 18 to 40 yr, body mass index of 25 to 35. Groups included six exercise sessions per week, two sessions per week, and sedentary control. Methods Rate of exercise energy expenditure was calculated from a graded exercise test averaged across five heart rate zones. Energy compensation was calculated as the difference between expected weight loss (based on exercise energy expenditure) and changes in fat and fat-free mass (DXA). Resting energy expenditure was assessed via indirect calorimetry and concentrations of acylated ghrelin, leptin, insulin, and Glucagon-like peptide 1 (GLP-1) were assessed fasting and postprandial (six timepoints over 2 h). Results The 6-d·wk-1 group expended more energy (2753.5 kcal) and exercised longer (320.5 min) per week than the 2-d·wk-1 group (1490.7 kcal, 1888.8 min, P < 0.05), resulting in greater fat loss compared with the 2-d or control groups (P < 0.05). Exercise groups did not differ in the % or total kcal compensated. Greater decreases in area under the curve (AUC) for acylated ghrelin predicted greater fat loss, regardless of group, energy expended per week, exercise duration, or exercise intensity. Changes in leptin AUC was the only independent predictor for energy compensation, with a greater decrease in leptin AUC predicting less energy compensation. Exercise frequency, energy expended, duration, or intensity did not influence energy compensation. Conclusions Leptin is an important factor in successful weight loss through exercise, with greater postprandial decreases promoting less compensation. Greater amounts of exercise do not influence the compensatory response to an exercise-induced energy deficit.

Original languageEnglish
Pages (from-to)2466-2475
Number of pages10
JournalMedicine and Science in Sports and Exercise
Volume52
Issue number11
DOIs
StatePublished - Nov 1 2020

Bibliographical note

Publisher Copyright:
© Lippincott Williams & Wilkins.

Funding

The authors would like to thank the staff of the University of Kentucky’s Center for Clinical and Translational Science (CCTS), specifically the inpatient nursing staff who performed the blood draws and sample processing. Additional gratitude is extended toward CCTS Biomarker Analysis Lab, directed by Dr. Jen Moylan, and the graduate and undergraduate students assisting in data processing. The authors would also like to thank the participants for their time and effort in performing the intervention and willingness to be assessed and comply with study protocol. The project described was supported by the NIH National Center for Advancing Translational Sciences through grant number UL1TR001998. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

FundersFunder number
National Center for Advancing Translational Sciences (NCATS)UL1TR001998

    Keywords

    • ENERGY COMPENSATION
    • EXERCISE
    • GHRELIN
    • LEPTIN
    • WEIGHT LOSS

    ASJC Scopus subject areas

    • Orthopedics and Sports Medicine
    • Physical Therapy, Sports Therapy and Rehabilitation

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