title: Skeletal muscle of trained and untrained paraplegics and tetraplegics.
abstract: The effect of physical conditioning on skeletal muscle of individuals with spinal cord injuries (SCI) has been investigated. The anterior portion of the deltoid muscle (active in wheel-chair propulsion) of untrained and endurance-trained paraplegics and tetraplegics, as well as that of untrained able-bodied subjects, was studied. The characterization involved fibre type distribution, capillarization, fibre areas and also oxidative and glycolytic enzyme levels. A general trend towards a successively higher proportion of type I fibres and lower proportion of type IIB fibres was noted in the order of able-bodied subjects (type I, 42%; type IIB, 41%, n = 8), paraplegics (type I, 57%; type IIB, 13%, n = 13) and tetraplegics (type I, 74%; type IIB, 4.5%, n = 11). The trained SCI groups had significantly higher levels of the citric acid cycle marker enzyme citrate synthase (34% and 63%) than the untrained SCI groups and able-bodied subjects, respectively. The glycolytic marker enzyme 6-phosphofructokinase was 32% lower in the tetraplegic groups than in the other groups. In contrast, the fatty acid oxidation marker enzyme 3-hydroxyacyl-CoA dehydrogenase was markedly higher in the tetraplegic group than in the able-bodied subjects (58%) and tended to be higher (21%, P < 0.1) than in the paraplegic group. The trained SCI groups displayed significantly higher (28%) levels of capillaries per fibre than the untrained SCI groups, which had about the same levels as the untrained able-bodied subjects. It is concluded that several of the findings are in line with normal muscular adaptation, whereas others are unexpected and support a hypothesis that some of the findings might be due to differences between the groups in, for instance, hormone levels or in types of muscular load.
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Schantz
authors.forename: B
authors.initials: B
authors.lastname: Sjöberg
authors.forename: A M
authors.initials: AM
authors.lastname: Widebeck
authors.forename: B
authors.initials: B
authors.lastname: Ekblom
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000222:Adaptation, Physiological / Q000502:physiology; D000328:Adult; D001706:Biopsy; D002196:Capillaries / Q000502:physiology; D006019:Glycolysis / Q000502:physiology; D006801:Humans; D008291:Malate Dehydrogenase / Q000378:metabolism; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000201:enzymology / Q000473:pathology; D018482:Muscle, Skeletal / Q000098:blood supply / Q000473:pathology / Q000502:physiology*; D010084:Oxidation-Reduction; D010264:Paraplegia / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D010732:Phosphofructokinase-1 / Q000378:metabolism; D010807:Physical Endurance; D011782:Quadriplegia / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D013119:Spinal Cord Injuries / Q000150:complications / Q000503:physiopathology / Q000628:therapy
chemical_list: D015094:3-Hydroxyacyl CoA Dehydrogenases; D008291:Malate Dehydrogenase; D010732:Phosphofructokinase-1