Skeletal muscle fibre type transformation following spinal cord injury

Abstract

Following spinal cord injury (SCI), upper motor neuron paralysed muscles lose the normal type I (slow) and II (fast) ®bre mosaic pattern and become predominantly composed of type II (fast glycolytic) ®bres). The majority of the research demonstrating this ®bre type shift was based on pH sensitive myo®brillar ATPase staining techniques on muscle from longstanding paraplegics and quadriplegics. The purpose of this study was to describe muscle ®bre type changes over a wide time spectrum post SCI using immuno¯uorescent techniques which may be more sensitive to change. A total of 19 vastus lateralis muscle biopsy specimens were obtained from 12 SCI subjects representing time points of 0.5 ± 219 months post SCI. Fast and slow myosin heavy chain isoform distribution was determined on single muscle ®bres for each of the biopsy specimens. Early post SCI (51 month) myosin heavy chain (MCH) isoform composition remained relatively stable. A transitional period was seen between 1 and 20 months post SCI wherein there was a progressive drop in the proportion of slow MHC isoform ®bres and a rise in the proportion that co-expressed both the fast and slow MHC isoform. By approximately 70 months post SCI a new steady state had been reached characterized by almost exclusively fast MHC isoform expression. This research has demonstrated that post SCI muscle type II transformation occurs in stages and commences earlier than previously appreciated. Interventions aimed at preventing or minimizing the transformation would need to be instituted within weeks post SCI.

The length–tension relationship of human dorsiflexor and plantarflexor muscles after spinal cord injury

“…RTD is dependent on myosin ATPase activity and is directly related to the proportion of type IIb fibres. 12 Previous studies have shown that muscles undergo a fibre-type transformation towards a greater representation of type IIb fibres in vastus lateralis 1,13,14 and soleus muscles 2 after SCI. There is some suggestion that the degree of fibre-type transformation may be influenced by the amount of spasticity in a particular muscle after SCI.…”

Comparison of muscular and articular factors in the progression of contractures after spinal cord injury in rats

“…6 Following SCI, it is well documented in humans [28][29][30][31] and animals 24,32,33 that skeletal muscles below the level of an upper motor neuron lesion undergo marked changes in their morphological, metabolic, and contractile properties. 34 Changes in spastic skeletal muscle generally include atrophy, loss of elasticity and relative increase in the connective tissue within the muscles, ingravescent accumulation of lipid, interstitial fibrosis and microcirculatory alteration. 7,24,29,34 Spastic muscles develop involuntary tetanic contraction, which produced a marked loss of sarcomeres in this muscles, which was greater than that from immobilization alone.…”

“…34 Changes in spastic skeletal muscle generally include atrophy, loss of elasticity and relative increase in the connective tissue within the muscles, ingravescent accumulation of lipid, interstitial fibrosis and microcirculatory alteration. 7,24,29,34 Spastic muscles develop involuntary tetanic contraction, which produced a marked loss of sarcomeres in this muscles, which was greater than that from immobilization alone. 7,35 In SCI patients, slow-to-fast conversion that is the major effect of a spinal cord transection 36 occurred in early stages (o4 weeks) postinjury, and reached gradually the new steady state characterized by a predominance of fibers expressing only the fast by 73 months.…”

Electrical Stimulation During Gait Promotes Increase of Muscle Cross-sectional Area in Quadriplegics: A Preliminary Study

“…Decrease in average muscle cross-sectional area (CSA) [8], replacement of Type I muscle fibers by Type II fibers [4], infiltration of adipose tissue inside muscles, reduction in the oxidative enzyme level, mitochondria concentration, and number of capillaries are observed in muscles located below the injury level [3,18,21].…”