MYOSIN HEAVY-CHAIN ISOFORM TRANSFORMATION IN SINGLE FIBERS FROM M-VASTUS LATERALIS IN SPINAL-CORD INJURED INDIVIDUALS - EFFECTS OF LONG-TERM FUNCTIONAL ELECTRICAL-STIMULATION (FES)

Citation
Jl. Andersen et al., MYOSIN HEAVY-CHAIN ISOFORM TRANSFORMATION IN SINGLE FIBERS FROM M-VASTUS LATERALIS IN SPINAL-CORD INJURED INDIVIDUALS - EFFECTS OF LONG-TERM FUNCTIONAL ELECTRICAL-STIMULATION (FES), Pflugers Archiv, 431(4), 1996, pp. 513-518
Citations number
24
Categorie Soggetti
Physiology
Journal title
ISSN journal
00316768
Volume
431
Issue
4
Year of publication
1996
Pages
513 - 518
Database
ISI
SICI code
0031-6768(1996)431:4<513:MHITIS>2.0.ZU;2-G
Abstract
The myosin heavy chain (MHC) composition of single fibres from m. vast us lateralis of five spinal-cord-injured (SCI) individuals was analyse d by Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-P AGE) before, and after 6 and 12 months of functional electrical stimul ation (FES)-training, administrated for 30 min three times per week. P rior to FES training 37.2% of the fibres contained only MHC IIB, 21.2% only MHC IIA, and 40.7% co-expressed MHC IIA and MHC IIB. After 6 mon ths of FES-training the number of fibres containing only MHC IIB was r educed to 2.6% (P < 0.05), the number of fibres containing only MHC II A was increased to 44.3% (P < 0.05), and the number of fibres co-expre ssing MHC IIA and MHC IIB was 50.9% (ns). After 12 months almost all f ibres (91.2%, P < 0.05) contained only MHC IIA. The number of fibres c ontaining only MHC IIB was 2.3% and the fibres co-expressing MHC IIA a nd IIB had decreased to 4.6% (P < 0.05). The amount of fibres containi ng only MHC I never exceeded 0.5%. Likewise, the number of fibres coex pressing MHC I and MHC IIA was below 2% throughout the study period. I n total, the MHC composition of 1596 single fibres was determined. Thi s study shows that FES-training of paralysed human skeletal muscle adm inistrated over a prolonged period of time, can lead to a marked switc h in MHC expression from about equal amounts of MHC IIA and MHC IIB to an almost total dominance of MHC IIA.