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1. Contraction of Heart Muscle

2. Mechanism Of Muscle Contraction
1. An action potential, induced by the pacemaker cells in the sinoatrial (SA)
and atrioventricular (AV) nodes, is conducted to contractile cardiomyocytes
through gap junctions.
2. As the action potential travels between sarcomeres, it activates the calcium
channels in the T-tubules, resulting in an influx of calcium ions into the
cardiomyocyte.
3. Calcium in the cytoplasm then binds to cardiac troponin-C, which moves
the troponin complex away from the actin binding site. This removal of the
troponin complex frees the actin to be bound by myosin and initiates
contraction.
4. The myosin head binds to ATP and pulls the actin filaments toward the
center of the sarcomere, contracting the muscle.
5. Intracellular calcium is then removed by the sarcoplasmic reticulum,
dropping intracellular calcium concentration, returning the troponin
complex to its inhibiting position on the active site of actin, and effectively
ending contraction as the actin filaments return to their initial position,
relaxing the muscle.

3. Mechanism Of Muscle Contraction
 Muscle contraction occurs when
calcium is pumped back into the
sarcoplasmic reticulum, away from the
actin and myosin.
 When Calcium moves in this way, the
actin and myosin cannot interact, and
the muscle relaxes.

4. SLIDING FILAMENT

5. CONTRACTION
In Contraction
 I- band disappear
 H- band disappear
 M- band disappear
 Length of sarcomere decreases.

6. Sarcomere Relaxed

7. Sarcomere Partially contracted

8. Sarcomere completely contracted

9. Sarcomere relaxed

10. Stages Of Muscle Contraction

11. 02-04-2021
Jipmer Physiologist 11

12. Control of muscle contraction

13. Muscle contraction controlled by:
 A. Neuromuscular junction
 B. Sarcoplasmic reticulum (SR)
 C. Regulation by calcium ions

14. Neuromuscular junction
 Muscle contraction is triggered by motor neurons that
release the neurotransmitter acetylcholine. The
transmitter diffuses through the narrow synaptic cleft
and binds to nicotinic acetylcholine receptors on the
plasma membrane of the muscle cell (the sarcolemma),
thereby opening the ion channels integrated into the
receptors .
 This leads to an inflow of Na+, which triggers an action
potential in the sarcolemma. The action potential
propagates from the end plate in all directions and
constantly stimulates the muscle fiber.
 With a delay of a few milliseconds, the contractile
mechanism responds to this by contracting the muscle
fiber.

16. Sarcoplasmic reticulum (SR)
 The action potential (A) produced at the neuromuscular
junction is transferred in the muscle cell into a transient
increase in the Ca2+ concentration in the cytoplasm of the
muscle fiber (the sarcoplasm).
 In the resting state, the Ca2+ level in the sarcoplasm is very
low (less than 10–7 M). By contrast, the sarcoplasmic
reticulum (SR), which corresponds to the ER, contains
Ca2+ ions at a concentration of about 10-3 M.

17.  The transfer of the action potential to the SR is made
possible by transverse tubules (T tubules), which
are open to the extracellular space and establish a
close connection with the SR.
 At the point of contact with the SR, the action
potential triggers the opening of the Ca2+ channels
on the surface of the sarcolemma.
 Calcium ions then leave the SR and enter the
sarcoplasm, where they lead to a rapid increase in
Ca2+ concentrations. This in turn causes the
myofibrils to contract

19. C. Regulation by calcium ions
 The biochemical effects of Ca2+ in the cytoplasm are
mediated by special Ca2+-binding proteins (“calcium
sensors”).
 These include the annexins, calmodulin, and troponin C
in muscle.
 Calmodulin is a relatively small protein (17 kDa) that
occurs in all animal cells. Binding of four Ca2+ ions (light
blue) converts it into a regulatory element. Via a
dramatic conformational change , Ca2+-calmodulin
enters into interaction with other proteins and modulates
their properties. Using this mechanism, Ca2+ ions
regulate the activity of enzymes, ion pumps, and
components of the cytoskeleton.

20.  In relaxed muscle, the complex consisting of troponin and
tropomyosin blocks the access of the myosin heads to actin .
 Troponin consists of three different subunits (T, C, and I).
 The rapid increase in cytoplasmic Ca2+ concentrations caused
by opening of the calcium channels in the SR leads to binding
of Ca2+ to the C subunit of troponin,which closely resembles
calmodulin
 This produces a conformational change in troponin that
causes the whole troponin– tropomyosin complex to slip
slightly and expose a binding site for myosin.
 This initiates the contraction cycle. After contraction, the
sarcoplasmic Ca2+ concentration is quickly reduced again by
active transport back into the SR.

24.  When triggering of contraction in striated muscle occurs,
the following sequence of processes thus takes place:
1. The sarcolemma is depolarized.
2. The action potential is signaled to Ca2+ channels in the SR.
3. The Ca2+ channels open and the Ca2+ level in the
sarcoplasm increases.
4. Ca2+ binds to troponin C and triggers a conformational
change.
5. Troponin causes tropomyosin to slip, and the myosin heads
bind to actin.
6. The actin–myosin cycle takes place and the muscle fibers
contract.

25.  Conversely, at the end of contraction, the following
processes take place:
1. The Ca2+ level in the sarcoplasm declines due to
transport of Ca2+ back into the SR.
2. Troponin C loses Ca2+ and tropomyosin returns to its
original position on the actin molecule.
3. The actin–myosin cycle stops and the muscle relaxes.