MUSCLE
Campbell and Reece - the last half of chapter 49
HOW MUSCLE WORKS MOLECULARLY-
this has been a real success story in cell-molecular biology
TRANSPARENCY Fig. 49.31
skeletal (striated) muscle cell ("fiber") 10- 100 microns (huge)
and long (from tendon to tendon)
There are smaller units within "fiber" called "myofibrils"
(1-2 microns in cross section)
Thus 1000-2000 myofibrils/fiber
Sarcomeres are units along the length of myofibrils
Interestingly, the striped (striated) pattern of myofibrils is in register
for all the myofibrils in the fiber giving the whole muscle fiber a striated
appearance.
Within the myofibrils are the filaments
Actin - G (globular) polymerizes to F (filamentous) actin - the thin filament
Myosin - (2 heavy chains and 4 light chains) - the thick filament
I-band (isotropic - light), A-band (anisotropic, dark) based on actin and
myosin, see figure
here is a picture
from our histology
course, but watch out because the arrows for A, I, and H do not point
accurately
TRANSPARENCY Fig 49.32 Sliding filament explanation of muscle contraction
TRANSPARENCY Fig. 49.33 - picture myosin as a boat rowing through a sea
of surrounding actin molecules. Interestingly ATP binding unhooks myosin
from actin. This can be remembered by thinking about rigor mortis - a "stiff"
in a detective show - has been dead long enough so that ATP has run out
and actin and myosin are locked together. ATP -> ADP and a phosphate
added to the myosin and this is like the rower taking another stroke. When
the phosphate gets kicked off of the myosin, the myosin and actin bind.
Ca2+ ions are released to make muscle contract (explained later)
tropomyosin on actin TRANSPARENCY Fig. 49.34
troponin has a Ca2+ binding site like calmodulin
Ca2+ binding to troponin pulls tropomyosin off of actin's binding sites
for myosin
HOW MUSCLE WORKS ELECTRICALLY (AND IONICALLY)
TRANSPARENCY Fig. 49.35
here is a picture
from our histology
course of the neuromuscular junction
Action potential from nerve opens channels at acetylcholine synapse at neuromuscular
junction, then action potential goes down muscle cell. But cell is too big.
So T tubules get action potential into cell at numerous locations (for each
sarcomere and for each myofibril). Proximity with a specialized smooth endoplasmic
reticulum called the sarcoplasmic reticulum causes release of Ca2+.
TRANSPARENCY Fig. 49.38 Motor units
(how many muscle cells per motor neuron)13 eye, 1730 calf
In summary:
ACh to synapse Ecxitation to spike
Final common pathway - motor neuron carries integrated information from
nervous system
1 - 1 spike, tetanus for sustained TRANSPARENCY Fig. 49.37
action potential in membrane and t-tubules, t=transverse
Ca++ release from sarcoplasmic reticulum (ER)
T at A-I junction in Skeletal muscle but it is at the z line in cardiac
muscle and in frog skeletal muscle
Types of skeletal muscle: Difference obvious in turkeys
Fast twitch, strong, anaerobic, white meat
Slow twitch, enduring, aerobic, dark meat
capillaries (hemoglobin), myoglobin, cytochromes in mitochondria
can alter with training
Metabolism:
phosphocreatine (creatine phosphate [backup, battery]) makes ATP using
phosphpcreatine kinase
glycogen
hemoglobin -> myoglobin
TRANSPARENCY Fig 40.4 -i.e. look back to introductory structure-function
chapter
striated - skeletal, volontary (best for study)
initiate-precentral gyrus, control via basal ganglia control (damaged in
Parkinson's) and cerebellum
smooth muscle - arterioles, gut, uterus - involontary, autonomic
Ca++ activates myosin light chain kinase, phosphorylation contraction
cardiac muscle - automatic
gap junctions at intercalated disc
here is a picture
from our histology
course of heart muscle cells joined at intercalated discs
Dr. Fisher is our muscle
expert, and he teaches a course in exercize physiology
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this page was last updated 1/19/04