title: Metabolic adaptations of skeletal muscle to voluntary wheel running exercise in hypertensive heart failure rats.
abstract: The Spontaneously Hypertensive Heart Failure (SHHF) rat mimics the human progression of hypertension from hypertrophy to heart failure. However, it is unknown whether SHHF animals can exercise at sufficient levels to observe beneficial biochemical adaptations in skeletal muscle. Thirty-seven female SHHF and Wistar-Furth (WF) rats were randomized to sedentary (SHHFsed and WFsed) and exercise groups (SHHFex and WFex). The exercise groups had access to running wheels from 6-22 months of age. Hindlimb muscles were obtained for metabolic measures that included mitochondrial enzyme function and expression, and glycogen utilization. The SHHFex rats ran a greater distance and duration as compared to the WFex rats (P<0.05), but the WFex rats ran at a faster speed (P<0.05). Skeletal muscle citrate synthase and beta-hydroxyacyl-CoA dehydrogenase enzyme activity was not altered in the SHHFex group, but was increased (P<0.05) in the WFex animals. Citrate synthase protein and gene expression were unchanged in SHHFex animals, but were increased in WFex rats (P<0.05). In the WFex animals muscle glycogen was significantly depleted after exercise (P<0.05), but not in the SHHFex group. We conclude that despite robust amounts of aerobic activity, voluntary wheel running exercise was not sufficiently intense to improve the oxidative capacity of skeletal muscle in adult SHHF animals, indicating an inability to compensate for declining heart function by improving peripheral oxidative adaptations in the skeletal muscle.
authors.affiliation: Department of Integrative Biology, University of Colorado Denver, Denver, USA. john.swallow@ucdenver.edu
authors.forename: R L
authors.initials: RL
authors.lastname: Schultz
authors.forename: E L
authors.initials: EL
authors.lastname: Kullman
authors.forename: R P
authors.initials: RP
authors.lastname: Waters
authors.forename: H
authors.initials: H
authors.lastname: Huang
authors.forename: J P
authors.initials: JP
authors.lastname: Kirwan
authors.forename: A M
authors.initials: AM
authors.lastname: Gerdes
authors.forename: J G
authors.initials: JG
authors.lastname: Swallow
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000235:genetics / Q000378:metabolism; D001275:ATP Citrate (pro-S)-Lyase / Q000235:genetics / Q000378:metabolism; D000222:Adaptation, Physiological; D000818:Animals; D004195:Disease Models, Animal; D004734:Energy Metabolism; D005260:Female; D006003:Glycogen / Q000378:metabolism; D006019:Glycolysis; D006333:Heart Failure / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D006614:Hindlimb; D006973:Hypertension / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000503:physiopathology; D005082:Physical Exertion; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011920:Rats, Inbred WF; D012420:Running; D013997:Time Factors
chemical_list: D012333:RNA, Messenger; D006003:Glycogen; D015094:3-Hydroxyacyl CoA Dehydrogenases; D001275:ATP Citrate (pro-S)-Lyase