572 12 Meat
Fig. 12.10.A schematic representation of a thin filament. (according toKarlsson, 1977)
12.3.2.1.6 Contraction and Relaxation
Muscle stimulation by a nerve impulse triggers
depolarization of the outer membrane of the mus-
cle cell and thus release of Ca^2 +ions from the
sarcoplasmic reticulum. The Ca^2 +concentration
in the sarcoplasm of the resting muscle increases
quickly from 10−^7 to 10−^5 mole/l. The binding
of this Ca^2 + to the troponin complex causes
a conformational change in this protein. As
a consequence, displacement of the tropomyosin
fibrils occurs along the F-actin filament. Thus,
the sterically hindered sites on the actin units
are exposed for interaction with the myosin
heads. The energy required for the shifting of
the unbound myosin heads is obtained from the
hydrolysis of ATP. The hydrolysis products of
ATP, ADP and inorganic phosphate (Pi), remain
on the myosin heads, which then bind to the
actin monomers (Fig. 12.11a). Consequently, the
myosin heads, now bound to actin, are forced to
undergo a conformational change, which forces
the thin filament to move relative to the thick
filament (Fig. 12.11b).
The thin filaments and the heads of the thick
filaments reverses half way between the Z lines.
Therefore, the two thin filaments which interact
with one thick filament are drawn toward each
other, resulting in a shortening of the distance be-
tween the Z lines.
When the myosin heads release ADP and P 1
and become detached from the thin filaments
(Fig. 12.11c), the heads are ready to take up
a fresh charge of ATP (Fig. 12.11d). If the Ca^2 +
concentration in the sarcoplasm remains high,
the ATP will again hydrolyze and the interaction
of the myosin heads with the thin filament is
repeated (Fig. 12.11a). However, if the Ca^2 +
concentration drops in the meantime, no ATP
hydrolysis occurs, tropomyosin again blocks the
access of myosin heads to the actin binding sites
Fig. 12.11.Molecular processes involved in muscle
contraction (see text; according toKarlsson, 1977)and the muscle returns to its resting state. The
decrease in Ca^2 + concentration when muscle
excitation has ceased, as well as the increase
in Ca^2 + during stimulation, i. e. the flow of
calcium ions, is controlled by the sarcoplasmic
reticulum. The Ca^2 + concentration is low in
the sarcoplasm of the resting muscle, while
it is high within the sarcoplasmic reticulum.
When the ATP level is low, detachment of the
myosin and actin filaments does not occur. The
muscle remains in a stiff, contracted state called
rigor mortis (cf. 12.4). Hence, relaxation of
muscle depends on the presence of regenerated
ATP.