title: The effect of exercise training on transverse tubules in normal, remodeled, and reverse remodeled hearts.
abstract: The response of transverse (T)-tubules to exercise training in health and disease remains unclear. Therefore, we studied the effect of exercise training on the density and spacing of left ventricle cardiomyocyte T-tubules in normal and remodeled hearts that associate with detubulation, by confocal laser scanning microscopy. First, exercise training in normal rats increased cardiomyocyte volume by 16% (P < 0.01), with preserved T-tubule density. Thus, the T-tubules adapted to the physiologic hypertrophy. Next, we studied T-tubules in a rat model of metabolic syndrome with pressure overload-induced concentric left ventricle hypertrophy, evidenced by 15% (P < 0.01) increased cardiomyocyte size. These rats had only 85% (P < 0.01) of the T-tubule density of control rats. Exercise training further increased cardiomyocyte volume by 8% (P < 0.01); half to that in control rats, but the T-tubule density remained unchanged. Finally, post-myocardial infarction heart failure induced severe cardiac pathology, with a 70% (P < 0.01) increased cardiomyocyte volume that included both eccentric and concentric hypertrophy and 55% (P < 0.01) reduced T-tubule density. Exercise training reversed 50% (P < 0.01) of the pathologic hypertrophy, whereas the T-tubule density increased by 40% (P < 0.05) compared to sedentary heart failure, but remained at 60% of normal hearts (P < 0.01). Physiologic hypertrophy associated with conserved T-tubule spacing (~1.8-1.9 µm), whereas in pathologic hypertrophy, T-tubules appeared disorganized without regular spacing. In conclusion, cardiomyocytes maintain the relative T-tubule density during physiologic hypertrophy and after mild concentric pathologic hypertrophy, whereas after severe pathologic remodeling with a substantial loss of T-tubules; exercise training reverses the remodeling and partly corrects the T-tubule density.
authors.affiliation: Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK. ole.kemi@glasgow.ac.uk.
authors.forename: Ole J
authors.initials: OJ
authors.lastname: Kemi
authors.forename: Morten A
authors.initials: MA
authors.lastname: Hoydal
authors.forename: Niall
authors.initials: N
authors.lastname: Macquaide
authors.forename: Per M
authors.initials: PM
authors.lastname: Haram
authors.forename: Lauren G
authors.initials: LG
authors.lastname: Koch
authors.forename: Steven L
authors.initials: SL
authors.lastname: Britton
authors.forename: Oyvind
authors.initials: O
authors.lastname: Ellingsen
authors.forename: Godfrey L
authors.initials: GL
authors.lastname: Smith
authors.forename: Ulrik
authors.initials: U
authors.lastname: Wisloff
mesh_terms: D000818:Animals; D048430:Cell Shape; D022081:Cell Surface Extensions / Q000473:pathology*; D005583:Fourier Analysis; D006333:Heart Failure / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D006334:Heart Function Tests; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000473:pathology; D010101:Oxygen Consumption; D010805:Physical Conditioning, Animal; D051381:Rats; D020257:Ventricular Remodeling / Q000502:physiology*