Muscle Contraction by the Sliding Filament Model

Muscle Contraction by the Sliding Filament Model: Muscle Contraction by the
Sliding Filament Model:
Action potential triggers an influx of Ca2+:
When an impulse arrives at a neuromuscular junction, it
causes Ca2+ to be released from the sarcoplasmic
reticulum into the sarcoplasm.
Ca2+ binds to troponin, causing it to change shape.
Thos moves the tropomyosin, exposing the binding sites
on the actin.
The myosin heads attach to the actin binding sites,
forming cross-bridges.
Hydrolysis of ATP provides the energy needed to move the
myosin head:
2+
Ca activate ATPase, which breaks down ATP to provide
the energy needed for muscle contraction.
This takes the form of the energy released moving the
myosin head, pulling the active filament along in a rowing
action – the power stroke.
ATP provides the energy needed to break the crossbridge:
ATP attaching to the myosin head causes them to detach
from the actin binding sites & move back into their
previous positions.
The head can bind to new sites, repeating the process as
long as the muscle continues to be stimulated (if there are
Ca2+ present).
Each bridge will go through the cycle, moving 5-10nm, 50-
100 times.
Relaxing muscles:
When the muscle stops being stimulated, Ca2+ leave the
troponin & are removed by active transport into the
sarcoplasmic reticulum.
Troponin changes shape again, pulling tropomyosin
molecule back over the actin-myosin binding sites.
Without cross-bridges, the actin filaments slide back into
their original position, lengthening the sarcomere.