Skeletal muscle of trained and untrained paraplegics and tetraplegics.
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.
Schantz
P
P
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Sjöberg
B
B
Widebeck
A M
AM
Ekblom
B
B
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
D015094:3-Hydroxyacyl CoA Dehydrogenases; D008291:Malate Dehydrogenase; D010732:Phosphofructokinase-1