Page 190 - Anatomy and Physiology of Farm Animals, 8th Edition

Microscopic Anatomy and Physiology of Muscle / 175

at right angles in the myofibrils and sarco- horses were utilized as a primary mode
plasmic reticulum. The T system propa-
VetBooks.ir gates action potentials from the sarcolemma of transportation, this was most often
observed as “sweeny” in draft horses
into the interior of the muscle fiber (Fig. 9‐1)
to initiate contraction of the entire fiber. with ill‐fitting collars. The suprascapular
nerve would undergo repetitive damage
Skeletal muscle fibers range in diameter from the collar, causing denervation
from 10 to 100 μm. In general, the large fib- and atrophy of the supraspinatus and
ers appear to be longer and tend to be found infraspinatus muscles, and destabiliza-
in large rather than small muscles. Animals tion of the shoulder joint.
on full feed are reported to have larger fib-
ers than animals on restricted feed. It is
generally accepted that males have larger Excitation, Contraction, and Relaxation
muscle fibers than females. Length of skel-
etal muscle fibers varies widely with the Skeletal muscle contraction is triggered by
length of the muscle and arrangement of the generation of an action potential on the
muscle fibers (parallel or pennate). Some sarcolemma. This action potential is initi-
fibers in parallel muscles probably extend ated by the firing of a motor neuron whose
the entire length of the muscle. axon branch terminates at the neuromus-
It is generally believed that skeletal cular junction near the midpoint of the
muscle fibers are such specialized cells muscle fiber. The neuromuscular junction
that little if any multiplication of fibers or (Fig. 9‐4) is a type of excitatory synapse.
formation of new fibers occurs after birth. The action potential of the nerve is not
All increases in size of muscles at any stage propagated directly onto the adjacent mus-
in life following birth are due to hypertro- cle cell. Instead, depolarization of the
phy (increase in size) of individual muscle motor nerve ending releases a chemical
fibers, with the synthesis of more myofibrils neurotransmitter, acetylcholine (ACh).
and an increased vascular supply. It is well When ACh diffuses across the synaptic
known that exercise can increase muscular cleft of the neuromuscular junction, it
development, as is seen in weight lifters. binds to specific cell membrane receptors
This, of course, is accomplished by increase (nicotinic ACh receptors) on the postjunc-
in size of existing individual muscle fibers. tional membrane of the muscle fiber
If the nerve supply to a muscle is (Fig. 9‐4). The binding of ACh to its recep-
destroyed, the muscle fibers decrease to tors brings about the opening of ligand‐
practically nothing, a condition called gated membrane channels, which allow
denervation or neurogenic atrophy. When sodium ions to enter the muscle cell. The

Synaptic vesicle
with acetylcholine
Nicotinic acetylcholine
receptor and channel

Acetylcholine
molecule

Muscle cell

Figure 9-4. Structural features of a neuromuscular junction. The terminal end of the axon contains
synaptic vesicles with the neurotransmitter acetylcholine. Nicotinic acetylcholine receptors are on the cell
membrane of the skeletal muscle cell.