Muscle Contraction:
Muscle contraction is tightening or shortening of a
muscle based on variation in tension or length
respectively.
Action potential from nerve impulse to sarcolemma
spreads through sarcoplasmic reticulum through T-tubules which
results in release of calcium ions (Ca+2) from the sarcoplasmic
reticulum.These calcium ions stimulate the regulatory proteins and
binds with Troponin C (regulatory protein). The other regulatory
proteins Troponin T and Troponin I also plays major role in masking
myosin binding site of actin.
As calcium ions binds to Troponin C, the active site of
actin gets unmasked and results in interaction of active site of
actin with myosin head forming a cross bridge. There by utilising
the ATP myosin drags actin filament thus contracting sarcomere,
ultimately muscle contraction takes place.
Skeletal Muscle:
- Ca+2-ATPase pumps calcium ions (Ca+2) into longitudinal
part of sarcoplasmic reticulum and then Ca+2 is transferred into
cisternae and get stored.
- When action potential arrives at T-tubule and gets
transmitted deep into the tubule which opens voltage-gated Ca+2
channels, located in dihydropyridine receptor.
- Conformational changes occurs in ryanodine receptors,
results in Ca+2 release into sarcoplasm which diffuses to bind with
troponin C to cause muscle contraction by forming actin-myosin
cross-bridge cycle.
- Auto-activation of Ca+2-ATPase pumps Ca+2 from
sarcoplasm to sarcoplasmic reticulum.
- Ca+2 then binds with calsequestrin in cisternae and
stored there.
- Ultimately, ends in muscle relaxation due to decrease
in sarcoplasmic Ca+2 concentration.
Smooth Muscle:
- Calcium ions (Ca+2) influx into the smooth muscle cell,
makes it bind with calmodulin-dependant myosin light chain
kinase.
- This causes phosphorylation of myosin by increasing
myosin ATPase activity.
- Myosin binds with actin resulting in cross-bridge
formation.
- Later dephosphorylation of myosin by myosin light chain
phosphatase occurs resulting in latch-bridge state which means
sustained contraction followed by slow relaxation.
Cardiac Muscle:
- Na+ is required for action potential of cardiac
muscle and increase in extracellular calcium increases the force of
contraction.
- When the cardiac muscle is depolarized, through the
T-tubules, Ca+2 is released into sarcoplasmic
reticulum.
- Ca+2 entry into the cell from intestinal fluid triggers
Ca+2 release from sarcoplasmic reticulum which then binds to
Troponin C forming a calcium troponin complex which interacts with
tropomyosin that uncovers the active site of myosin and
actin.
- This allows cross-bridge cycling, which causes muscle
contraction.