Life cycle of the musculotendinous unit Flashcards
embryotic development of skeletal muscle
0 to 8 weeks = embryo: initial development of each organ system Week 3: trilaminar germ disc (ectoderm > mesoderm> endoderm surface to deep) craniocaudal axis bilateral symmetry 9 to 38 weeks = fetus: period of functional maturation
Neurulation
Development of the neural tube & neural crest cells
Somites, adjacent to the neural tube, go on to form most of the vertebral column, skeletal muscle and dermis corresponding to spinal cord segments
Notochord forms from mesoderm
Development of somites from mesoderm by 3 weeks
somite
• Division of the mesoderm • Develops either side of the notochord, and developing neural tube • Develops into the different parts of the musculoskeletal system • Bilaterally paired
The somite differentiates to form dermatome (ultimately skin cells), myotome (ultimately skeletal muscle cells) and sclerotome (ultimately connective tissue / bone cells).
myoblasts
Cells of the myotome differentiate into myoblasts (muscle forming cells)
Myoblasts elongate and aggregate into bundles
Fuse longitudinally and form the multinucleated fibres (myotubes)
- have no striations
Muscle development, growth and repair:
- As muscles grow in length during maturation, the number of sarcomeres increases
- hypertrophy - generally more myofibrils - increase size not more cells
- Increase in size of skeletal muscle is primarily through
a growth in size of its component cells – ie net positive protein synthesis (more synthesis than breakdown)
sataellite cells
- However, satellite cells (stem cells) that sit within endomysium can differentiate into myoblasts
- Myoblasts fuse to other muscle cells during growth and repair throughout the life-span
- So satellite cells are also important for hypertrophy during maturation
Muscle development: Muscle tone
At birth – consider “muscle tone” rather than “muscle strength”
‘A slight constant tension of healthy muscles’
Muscle tone is a product of both neural (with input from the nervous system), and non-neural (passive structures within the musculotendinous tissue), components
Neural components of “muscle tone”:
With prolonged high excitatory drive to muscles (spasticity) > changes in connective tissue ECM > non neurally driven increases in muscle tone also (contractures).
A degree of muscle tone remains without muscle activation by neural contributors. Generated by inherent viscoelastic characteristic of the musculotendinous unit.
Dystrophin
is protein located in the intercellular surface of muscle fibres.
Stabilises muscle fibres during contraction and relaxation by binding to other proteins within the ECM.
TITIN
Titin links myosin filaments to the z-disc within each sarcomere, and facilitates the
return of the myosin filament to its initial position after stretch. Contributes to passive
force in muscle.
down syndrome
abnormal collagen formation
- low tone
People with low tone tend to fatigue quickly during everyday tasks as not getting passive muscle contrivution therefore increase in energy so increase fatiguw
fibrosis
the thickening of connective tissue in CP > high tone.
*The Modified Ashworth scale (MAS
measures resistance during passive soft-tissue stretching and is used as a simple measure of spasticity.
hypertonia
Hypertonia (high tone) – clinical example - Cerebral palsy (neuromuscular condition), damage to the brain
at or around birth. Altered neural drive to muscles. Higher drive. Associated with pain & impedes participation in everyday activities
- Secondary alterations in muscle structure during development
Increased collagen content in the connective tissue matrix the surrounds muscle fibres
- Long term contracture > muscle shortening > reduced joint range of motion > bone deformities
tibial torsion and excessive femoral neck anteversion
- Reduced muscle volume during development (may be due to decreased loading/disuse/altered drive).
Some children with CP also have hypotonia/low muscle tone in regions.
hypertonia
Hypertonia (high tone) – clinical example - Cerebral palsy (neuromuscular condition), damage to the brain
at or around birth. Altered neural drive to muscles. Higher drive. Associated with pain & impedes participation in everyday activities
- Secondary alterations in muscle structure during development
Increased collagen content in the connective tissue matrix the surrounds muscle fibres
- Long term contracture > muscle shortening > reduced joint range of motion > bone deformities
tibial torsion and excessive femoral neck anteversion
- Reduced muscle volume during development (may be due to decreased loading/disuse/altered drive).
Some children with CP also have hypotonia/low muscle tone in regions.
- Hypertonia in some muscles
