title: Skeletal muscle characteristics predict body fat gain in response to overfeeding in never-obese young men.
abstract: The associations between skeletal muscle morphological and metabolic properties and the changes in body composition and metabolic rates in response to long-term overfeeding were investigated in 24 healthy young male identical twins (12 pairs). The proportions of muscle fiber types (type I, type IIA, and type IIB) and the activities of creatine kinase (CK), oxoglutarate dehydrogenase (OGDH), and phosphofructokinase (PFK) were determined from biopsies of the vastus lateralis before and after the overfeeding protocol. Body weight, fat mass (FM), fat-free mass (FFM), percent body fat (%FAT), resting metabolic rate (RMR), and thermic effect of a standardized meal (TEM) were also measured before and after 100 days of overfeeding. Type I muscle fiber proportions correlated inversely with the changes of FM and %FAT (r = -0.43, P =.035; r = -0.49, P =.01), and type IIA positively with the same overfeeding-induced changes (r = 0.43, P =.035; r = 0.47, P =.021). Baseline CK and PFK activities correlated negatively with the changes of RMR (r = -0.49, P =.017; r = -0.53, P =.01). OGDH activity at baseline correlated negatively with the changes of FM (r = -0.47, P = 0.02) but the ratio of PFK/OGDH correlated positively with the change of FM (r = 0.46, P =.02). We conclude that overfeeding induced a lower gain of FM in individuals with higher proportions of type I fiber, lower proportions of type IIA fiber, and higher OGDH activities at baseline. CK and PFK activities at baseline were associated with an attenuated increase in RMR when challenged by overfeeding. The significant correlations range from 0.43 to 0.53, and account for 18% to 28% of the variance in the response to overfeeding. The results suggest that an elevated skeletal muscle oxidative capacity plays a protective role in the response to long-term positive energy balance.
authors.affiliation: Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA.
authors.forename: Guang
authors.initials: G
authors.lastname: Sun
authors.forename: Olavi
authors.initials: O
authors.lastname: Ukkola
authors.forename: Tuomo
authors.initials: T
authors.lastname: Rankinen
authors.forename: Denis R
authors.initials: DR
authors.lastname: Joanisse
authors.forename: Claude
authors.initials: C
authors.lastname: Bouchard
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology / Q000502:physiology*; D000818:Animals; D015992:Body Mass Index; D001835:Body Weight; D003402:Creatine Kinase / Q000378:metabolism; D005247:Feeding Behavior; D007655:Ketoglutarate Dehydrogenase Complex / Q000378:metabolism; D008297:Male; D051379:Mice; D018485:Muscle Fibers, Skeletal / Q000502:physiology*; D018482:Muscle, Skeletal / Q000201:enzymology / Q000502:physiology*; D025203:Phosphofructokinase-1, Muscle Type / Q000378:metabolism; D012044:Regression Analysis
chemical_list: D007655:Ketoglutarate Dehydrogenase Complex; D025203:Phosphofructokinase-1, Muscle Type; D003402:Creatine Kinase