Study Material on Muscle Physiology and Related Diseases

1. The cross bridge cycle
A cross bridge is formed by attachment of activated myosin to actin in the muscle cell. This is
the first step. Inorganic phosphate is then released strengthening the bond between actin and
myosin.
The second step is formation of a power stroke. This involves release of ADP which causes
activated myosin heads to pivot, hence sliding thin myofilaments to the sarcomere center.
Another ATP is then bound to the head of the myosin filament. This weakens the link between
the actin and myosin head. This causes the myosin head to detach and therefore, cross-bridge
detachment.
The last step is myosin head reactivation to the initial cocked position. This process requires
energy. The energy is obtained by hydrolysis of ATP to inorganic phosphate and ADP.
2. How and why muscle force, shortening velocity and power are normalized
The cross sectional area of the muscle normalizes the force produced by the muscle. This helps
in reduction of strain to the different muscle filaments. This also masks the differences in force
production between different muscle fibers. The resting length of the muscle normalizes the
velocity or length of the muscle. Each contractile unit has to contract less in a longer muscle
fiber to produce the same reduction in length that a shorter muscle produces with more
contraction. The volume or weight of a muscle normalizes the power produced. The more muscle
fibers (volume), the more powerful and resistant to tear they are. Lighter or low volume muscles
produce less power to match their combined tensile strength.

3. Cause of exercise-induced muscle fatigue
The major cause of exercise induced muscle fatigue is lactic acid production from anaerobic
respiration. Switching to anaerobic respiration by a muscle depends on the maximum rate of
oxygen consumption by that muscle. When exercise is performed for a longer time exceeding the
rate at which a muscle can take up oxygen, an oxygen deficit develops and for continued
production of energy, anaerobic respiration is turned on which leads to production of lactic acid.
Excessive lactic acid production beyond breakdown capabilities of the liver leads to
accumulation of the acid in the muscles reducing energy production and causes pain (muscle
cramps). Long distance runners and athletes with higher rates of oxygen consumption take longer
to form significant lactic acid via anaerobic respiration hence withstand higher working limits.
4. Duchene muscular dystrophy
It’s a genetic, most common form of muscular dystrophy characterized by progressive muscle
weakness and degeneration. Absence of dystrophin that maintains the integrity of the muscle’s
membrane is cause of the disease. Dystrophin associated glycoproteins and dystrophin are the
important elements that maintain stability of the sarcolemma. A mutation in the gene that codes
for dystrophin causes the absence of the protein. This gene is located on chromosome X, the
short arm close to the p21 locus. This explains the disease affecting more boys than girls due to
the singularity of the X chromosome in boys. Symptoms begin early in childhood at about age 3
to 5. Later stages of the disease are marked by severe heart and breathing problems which cause
death.