Introduction: Data on the metabolic effects of resistance exercise (strength training) in adolescents are limited.
Purpose: The objective of this study was to determine whether a controlled resistance exercise program without dietary intervention or weight loss reduces body fat accumulation, increases lean body mass, and improves insulin sensitivity and glucose metabolism in sedentary obese Hispanic adolescents.
Methods: Twelve obese adolescents (age = 15.5 ± 0.5 yr, body mass index = 35.3 ± 0.8 kg·m−2; 40.8% ± 1.5% body fat) completed a 12-wk resistance exercise program (two times 1 h·wk−1, exercising all major muscle groups). At baseline and on completion of the program, body composition was measured by dual-energy x-ray absorptiometry, abdominal fat distribution was measured by magnetic resonance imaging, hepatic and intramyocellular fat was measured by magnetic resonance spectroscopy, peripheral insulin sensitivity was measured by the stable-label intravenous glucose tolerance test, and hepatic insulin sensitivity was measured by the hepatic insulin sensitivity index = 1000/(GPR × fasting insulin). Glucose production rate (GPR), gluconeogenesis, and glycogenolysis were quantified using stable isotope gas chromatography/mass spectrometry techniques.
Results: All participants were normoglycemic. The exercise program resulted in significant strength gain in both upper and lower body muscle groups. Body weight increased from 97.0 ± 3.8 to 99.6 ± 4.2 kg (P < 0.01). The major part (∼80%) was accounted for by increased lean body mass (55.7 ± 2.8 to 57.9 ± 3.0 kg, P ≤ 0.01). Total, visceral, hepatic, and intramyocellular fat contents remained unchanged. Hepatic insulin sensitivity increased by 24% ± 9% (P < 0.05), whereas peripheral insulin sensitivity did not change significantly. GPR decreased by 8% ± 1% (P < 0.01) because of a 12% ± 5% decrease in glycogenolysis (P < 0.05).
Conclusions: We conclude that a controlled resistance exercise program without weight loss increases strength and lean body mass, improves hepatic insulin sensitivity, and decreases GPR without affecting total fat mass or visceral, hepatic, and intramyocellular fat contents.
1Department of Pediatrics, Baylor College of Medicine, Houston, TX; 2Children's Medical Center and University of Texas Southwestern Medical Center, Dallas, TX; 3Department of Electronics and Informatics, University of Padua, ITALY; and 4Department of Pediatrics, Beatrix Children's Hospital, University Medical Center Groningen, University of Groningen, Groningen, THE NETHERLANDS
Address for correspondence: Agneta L. Sunehag, M.D., Ph.D., Children's Nutrition Research Center, 1100 Bates St., Houston, TX 77030; Email: firstname.lastname@example.org.
Submitted for publication December 2009.
Accepted for publication March 2010.