title: Age is no barrier to muscle structural, biochemical and angiogenic adaptations to training up to 24 months in female rats.
abstract: Ageing is associated with reduced transport and utilization of O(2), diminishing exercise tolerance. Reductions may occur in cardiac output (delivery), and skeletal muscle oxidative capacity (utilization). To determine the reversibility of the declines in the muscular determinants of these limitations, skeletal muscle morphological, angiogenic and biochemical responses to acute exercise and endurance training were investigated in female Fischer 344 rats (n = 42; seven groups of six rats) aged 6 (Y) and 24 (O) months compared with resting untrained controls (Y(C), O(C)). Treadmill training lasted 8 weeks (10 deg incline, 1 h per day, 5 days per week). Two groups ran at maximum tolerated speeds (Y(TR), O(TR)), while an additional Y group (Y(TM)) trained at O(TR) speed. There was no effect of age on vascular endothelial growth factor gene expression in gastrocnemius muscles after acute exercise. Similarly, age did not impair the effects of training, with increases (P < 0.05; +/-s.e.m.) occurring in all of the following: 1 h exercise running speed (Y(TR) 92 +/- 4% versus O(TR) 140 +/- 25%); citrate synthase (Y(TR) 37 +/- 8% versus O(TR) 97 +/- 33%) and beta-hydroxyacyl-CoA-dehydrogenase (Y(TR) 31 +/- 7%, versus O(TR) 72 +/- 24%) activities; and capillary-to-fibre ratio (Y(TR) 5.2 +/- 0.2% versus O(TR) 8.1 +/- 0.2%). However, Y(TM) muscle was unchanged in each measure compared with Y(C). In conclusion, these muscular responses to training were (1) not reduced by ageing, but (2) dependent on relative and not absolute work rate, since, at the same speed, O(TR) rats showed greater changes than Y(TM). Therefore, increases in exercise tolerance and muscle adaptations are not impaired in female rats up to 24 months of age, and require a smaller absolute exercise stimulus (than young) to be manifest.
authors.affiliation: Department of Medicine, Division of Physiology, University of California, San Diego, La Jolla 92093-0623, USA. h.b.rossiter@leeds.ac.uk
authors.forename: H B
authors.initials: HB
authors.lastname: Rossiter
authors.forename: R A
authors.initials: RA
authors.lastname: Howlett
authors.forename: H H
authors.initials: HH
authors.lastname: Holcombe
authors.forename: P L
authors.initials: PL
authors.lastname: Entin
authors.forename: H E
authors.initials: HE
authors.lastname: Wagner
authors.forename: P D
authors.initials: PD
authors.lastname: Wagner
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000222:Adaptation, Physiological / Q000502:physiology*; D000375:Aging / Q000502:physiology*; D000818:Animals; D002950:Citrate (si)-Synthase / Q000378:metabolism; D005260:Female; D008928:Mitochondria / Q000201:enzymology; D018485:Muscle Fibers, Skeletal / Q000201:enzymology; D018482:Muscle, Skeletal / Q000098:blood supply / Q000166:cytology / Q000502:physiology*; D018919:Neovascularization, Physiologic / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger; D051381:Rats; D011916:Rats, Inbred F344; D012420:Running / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D015094:3-Hydroxyacyl CoA Dehydrogenases; D002950:Citrate (si)-Synthase