CHAPTER 6
Muscle
103
Figure 6-3A.
Longitudinal section of striated muscle.
H&E,
3
400
The cellular units of skeletal muscle are called
muscle ± bers
. Each
F ber is a long, roughly cylindrical cell bounded by a plasma mem-
brane, the
sarcolemma
. Muscle F bers range from 10 to 100
μ
m in
diameter and may be many centimeters in length in mature mus-
cles. This large size presents a problem for a single cell nucleus
serving far distant cytoplasm and cell membrane. In skeletal
muscle, this problem is solved by the formation of a
syncytium
,
resulting from the fusion of several
myoblasts
, during develop-
ment. A single muscle F ber will therefore have many nuclei.
A distinctive feature of skeletal muscle, visible in this section, is a
repeating pattern of dark and light bands oriented at right angles
to the length of the F ber. These bands are designated
A bands
and
I bands
(see ±ig. 6-4A). Capillaries and myelinated nerve F bers
are often observed in sections of skeletal muscle tissue.
Nuclei
Sarcolemma
Capillary
A
Nuclei
Sarcolemma
Capillary
B
Figure 6-3B.
Transverse section of skeletal muscle (ton -
gue).
H&E,
3
272
Muscle ±
bers in the tongue
run in several different directions,
so, although most F
bers in this section are cut transversely
(in cross section), some are cut diagonally. Skeletal muscle
F bers are round or polygonal in cross section, and, in a nor-
mal muscle, the F ber diameter is relatively uniform. The nuclei
are fl
attened and lie peripherally in each F
ber, just beneath the
sarcolemma
.
CLINICAL CORRELATION
Figure 6-3C.
Muscular Dystrophy.
H&E,
3
136
The
muscular dystrophies
are a group of inherited
myogenic
disorders characterized by progressive degeneration and
weakness of skeletal muscle without associated abnormality
of the nervous system. They can be subdivided into various
groups based on the distribution and severity of muscle weak-
ness and genetic F ndings.
Duchenne muscular
dystrophy
([DMD] illustrated here) is the most common and severe
form of the disease. It is carried by mutation of an X-linked
recessive gene, the
dystrophin
gene. The lack of the dystro-
phin protein impairs the transfer of force from actin F la-
ments to the cell wall and causes the progressive weakness.
Pathological changes include
large variations in muscle ± ber
diameter
, extensive
endomysial ± brosis
between the F bers,
degeneration and regeneration of F bers with
necrosis
and
phagocytosis,
centrally displaced nuclei
, and replacement of
muscle by fat and connective tissue. Steroids are the primary
drugs used to treat DMD. Gene therapy using a functioning
dystrophin protein has not yet been successful.
Centrally displaced
nuclei
Abnormally large
range of fiber
diameters
Endomysial fibrosis
Necrotic fiber
Inflammatory
cells
C
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