312
UNIT 2
Covering, Support, and Movement of the Body
9
distal direction. In other words, a baby can lif its head beFore it can
walk, and gross movements precede fine ones.
All through childhood, our control oF our skeletal muscles
becomes more and more sophisticated. By midadolescence, we
reach the peak oF our natural neural control oF muscles, but can
improve it by athletic or other types oF training.
A Frequently asked question is whether the strength difference
between women and men has a biological basis. It does. Individuals
vary, but on average, women’s skeletal muscles make up approxi-
mately 36% oF body mass, whereas men’s account For about 42%.
Men’s greater muscular development is due primarily to the effects
oF testosterone on skeletal muscle, not to the effects oF exercise.
Body strength per unit muscle mass, however, is the same in both
sexes. Strenuous muscle exercise causes more muscle enlargement
in males than in Females, again because oF the influence oF testoster-
one. Some athletes take large doses oF synthetic male sex hormones
(“steroids”) to increase their muscle mass.
A Closer Look
discusses
this illegal and physiologically dangerous practice.
Because oF its rich blood supply, skeletal muscle is amazingly
resistant to inFection. Given good nutrition and moderate exer-
cise, relatively Few problems afflict skeletal muscles. However,
muscular dystrophy, the world’s most common genetic disorder,
is a serious condition that deserves more than a passing mention.
Homeostatic Imbalance
9.4
Te term
muscular dystrophy
reFers to a group oF inherited mus-
cle-destroying diseases that generally appear during childhood.
Te affected muscles initially enlarge due to deposits oF Fat and
connective tissue, but the muscle fibers atrophy and degenerate.
Te most common and serious Form is
Duchenne muscular
dystrophy (DMD)
, which is inherited as a sex-linked recessive dis-
ease. It is expressed almost exclusively in males (one in every 3600
male births). Tis tragic disease is usually diagnosed when the boy
is between 2 and 7 years old. Active, normal-appearing children be-
come clumsy and Fall Frequently as their skeletal muscles weaken.
Te disease progresses relentlessly From the extremities upward, fi-
nally affecting the head and chest muscles and cardiac muscle. Vic-
tims rarely live beyond their early 20s, dying oF respiratory Failure.
DMD is caused by a deFective gene For
dystrophin
, a cytoplas-
mic protein that links the cytoskeleton to the extracellular matrix
and, like a girder, helps stabilize the sarcolemma. Te Fragile sar-
colemma oF DMD patients tears during contraction, allowing en-
try oF excess Ca
2
1
. Te deranged calcium homeostasis damages
Developmental Aspects
of Muscles
Describe embryonic development of muscle tissues and the
changes that occur in skeletal muscles with age.
With rare exceptions, all three types oF muscle tissue develop
From embryonic mesoderm cells called
myoblasts
. In Forming
skeletal muscle tissue, several myoblasts Fuse to Form multinu-
clear
myotubes
(Figure 9.29)
. Integrins (cell adhesion proteins)
in the myoblast membranes guide this process and soon Func-
tional sarcomeres appear. Skeletal muscle fibers are contracting
by week 7 when the embryo is only about 2.5 cm (1 inch) long.
Initially, ACh receptors “sprout” over the entire surFace oF the de-
veloping myoblasts. As spinal nerves invade the muscle masses, the
nerve endings target individual myoblasts and release the growth
Factor
agrin
. Tis chemical activates a muscle kinase (MuSK),
which stimulates clustering and maintenance oF ACh receptors at
the newly Forming neuromuscular junction in each muscle fiber.
Ten, the nerve endings release a different chemical that eliminates
the receptor sites not innervated or stabilized by agrin.
Electrical activity in the neurons serving the muscle fi-
bers also plays a critical role in muscle fiber maturation. As the
somatic nervous system assumes control oF muscle fibers, the
number oF Fast and slow contractile fiber types is determined.
Myoblasts producing cardiac and smooth muscle cells do not
Fuse but develop gap junctions at a very early embryonic stage.
Cardiac muscle is pumping blood just 3 weeks afer Fertilization.
Specialized skeletal and cardiac muscle cells stop dividing early
on but retain the ability to lengthen and thicken in a growing
child and to hypertrophy in adults.
Satellite cells,
myoblast-like cells associated with skeletal mus-
cle, help repair injured fibers and allow limited regeneration oF
dead skeletal muscle, a capability that declines with age.
Cardiac muscle was thought to have no regenerative capabil-
ity whatsoever, but recent studies suggest that cardiac cells do
divide at a modest rate. Nonetheless, injured heart muscle is
repaired mostly by scar tissue.
Smooth muscles have a good regenerative capacity and smooth
muscle cells oF blood vessels divide regularly throughout liFe.
At birth, a baby’s movements are uncoordinated and largely re-
flexive. Muscular development reflects the level oF neuromuscular
coordination, which develops in a head-to-toe and proximal-to-
Embryonic
mesoderm cells
Myoblasts
Myotube
(immature
multinucleate
muscle fiber)
Satellite cell
Mature skeletal
muscle fiber
1
Embryonic
mesoderm cells called
myoblasts undergo cell
division (to increase
number) and enlarge.
2
Several
myoblasts fuse
together to form
a myotube.
Myotube
matures into
skeletal muscle
fiber.
3
Figure 9.29
Myoblasts fuse to form a multinucleate skeletal muscle fiber.
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