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Adiponectin is necessary for exercise training‐induced muscular hypertrophy and vascular adaptation
Author(s) -
Gorman Katherine,
Ghosh Payal,
Behnke Bradley,
Borodunovich Kyle,
Lucero Tiffani,
Alarcon David,
Cowan Morgan,
Hotta Kazuki,
Starr Kaleb,
Delp Michael,
MullerDelp Judy M
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1240.23
Subject(s) - endocrinology , medicine , muscle hypertrophy , adiponectin , soleus muscle , skeletal muscle , treadmill , gastrocnemius muscle , plantaris muscle , aerobic exercise , physical exercise , obesity , insulin resistance
Adiponectin has been reported to be produced by skeletal muscle fibers and to influence muscle phenotype. We tested the hypothesis that adiponectin is necessary for exercise training‐induced muscular hypertrophy and alterations of the resistance vasculature in skeletal muscle. Adult C57BL/6 wild‐type (WT) or homozygous adiponectin knockout (Adipo KO) mice were obtained at 10 weeks of age and underwent treadmill exercise training (12 m/min, 5° incline, 1 hr/day, 5 days/wk for 8 wks) or remained sedentary in cages. Body mass was recorded weekly during the training/cage confinement period. At the end of the training/cage confinement period, the gastrocnemius‐plantaris‐soleus complex was isolated, and soleus muscle feed arteries were isolated for study of vascular responses to increasing intraluminal pressure (the myogenic response). The body mass of WT mice increased significantly over the training/cage confinement period, by 11.7% in sedentary mice and by 13.9% in exercise trained mice. In Adipo KO mice, body mass increased by 15.1% in sedentary mice (P<0.01 wk 8 vs wk 1), but increased by only 7.2% in exercise trained mice (P=0.07). In WT mice, the masses of both the soleus muscle (20.4±2.3 mg vs. 12.2mg; exercise trained vs. sedentary; P<0.01) and the gastrocnemius muscle (248.8 mg vs. 178.5 mg; exercise trained vs. sedentary; p<0.01) were greater in exercise trained mice as compared to sedentary mice. When expressed relative to body mass (muscle weight:body weight), these increases in mass persisted in the muscles of the exercise trained mice. In Adipo KO mice, exercise training did not increase the mass of either the soleus (12.5±1.5 mg vs. 12.1±1.5 mg; exercise trained vs. sedentary; P=0.62) or gastrocnemius muscle (195.2±11.2 mg vs. 182.7±18.9 mg; exercise trained vs. sedentary; P=0.12), whether expressed as absolute muscle mass or relative to body mass. Exercise training increased myogenic responsiveness of soleus muscle feed arteries significantly in WT mice (P<0.01, WT exercise trained vs. WT sedentary), but did not alter myogenic responsiveness of soleus muscle feed arteries in Adipo KO mice (P=0.87, Adipo KO exercise trained vs. Adipo KO sedentary). These results indicate that exercise training‐induced hypertrophy of skeletal muscle and associated improvement of vascular function does not occur in mice deficient in adiponectin. These results suggest that adiponectin is vital to the vascular and metabolic adaptations that occur in skeletal muscle in response to aerobic exercise training.