title: Na+,K+-ATPase concentration and fiber type distribution after spinal cord injury.
abstract: Complete spinal cord injury (SCI) is characterized, in part, by reduced fatigue-resistance of the paralyzed skeletal muscle during stimulated contractions, but the underlying mechanisms are not fully understood. The effects of complete SCI on skeletal muscle Na(+),K(+)-adenosine triphosphatase (ATPase) concentration, and fiber type distribution were therefore investigated. Six individuals (aged 32.0 +/- 5.3 years) with complete paraplegia (T4-T10; 1-19 years since injury) participated. There was a significantly lower Na(+),K(+)-ATPase concentration in the paralyzed vastus lateralis (VL) when compared to either the subjects' own unaffected deltoid or literature values (from our laboratory, utilizing the same methodology) of VL Na(+),K(+)-ATPase concentration for the healthy able-bodied (141.6 +/- 50.0, 213.4 +/- 23.9, 339 +/- 16 pmol/g wet wt., respectively; P < 0.05). There was also a significant negative correlation between the Na(+),K(+)-ATPase concentration in the paralyzed VL and years since injury (r = -0.75, P < 0.05). These findings are clinically relevant as they suggest that reductions in Na(+),K(+)-ATPase contribute to the fatigability of paralyzed muscle after SCI. Unexpectedly, the VL muscles of our subjects had a higher proportion of their area represented by type I fibers compared to literature values for the VL of the healthy able-bodied (52.6 +/- 25.3% vs. 36 +/- 11.3%, respectively; P < 0.05). As all our subjects had upper motor neuron injuries and, therefore, experienced muscle spasticity, our findings warrant further investigation into the relationship between muscle spasticity and fiber type expression after SCI.
authors.affiliation: Department of Kinesiology, McMaster University, 1280 Main St. West, Hamilton, Ontario L8S 4K1, Canada.
authors.forename: D S
authors.initials: DS
authors.lastname: Ditor
authors.forename: S
authors.initials: S
authors.lastname: Hamilton
authors.forename: M A
authors.initials: MA
authors.lastname: Tarnopolsky
authors.forename: H J
authors.initials: HJ
authors.lastname: Green
authors.forename: B C
authors.initials: BC
authors.lastname: Craven
authors.forename: G
authors.initials: G
authors.lastname: Parise
authors.forename: A L
authors.initials: AL
authors.lastname: Hicks
mesh_terms: D000328:Adult; D015536:Down-Regulation / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D009121:Muscle Denervation / Q000009:adverse effects*; D018656:Muscle Fibers, Fast-Twitch / Q000201:enzymology / Q000473:pathology; D018485:Muscle Fibers, Skeletal / Q000201:enzymology* / Q000473:pathology; D018908:Muscle Weakness / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D010264:Paraplegia / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013119:Spinal Cord Injuries / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology
chemical_list: D000254:Sodium-Potassium-Exchanging ATPase