potential propagated into T-tubules
binding to troponin
removes blocking action
removal from troponin
and generate force
from lateral sac
Release and uptake of calcium by the sarcoplasmic reticulum during contraction and relaxation of a skeletal muscle ﬁ ber.
calcium channel. During a T-tubule action potential, charged
amino acid residues within the DHP receptor protein induce a
conformational change, which acts via the foot process to open
the ryanodine receptor channel. Calcium is thus released from
the lateral sacs of the sarcoplasmic reticulum into the cytosol,
activating cross-bridge cycling. The rise in cytosolic calcium
in response to a single action potential is normally enough to
brieﬂ y saturate all troponin binding sites on the thin ﬁ laments.
A contraction is terminated by removal of calcium from
troponin, which is achieved by lowering the calcium concentra-
tion in the cytosol back to its prerelease level. The membranes
of the sarcoplasmic reticulum contain primary active-transport
-ATPases—that pump calcium ions from the
cytosol back into the lumen of the reticulum. As we just saw,
calcium is released from the reticulum when an action poten-
tial begins in the T-tubule, but the pumping of the released
calcium back into the reticulum requires a much longer time.
Therefore, the cytosolic calcium concentration remains ele-
vated, and the contraction continues for some time after a
single action potential.
To reiterate, just as contraction results from the release
of calcium ions stored in the sarcoplasmic reticulum, so con-
traction ends and relaxation begins as calcium is pumped back
into the reticulum (see Figure 9–12). ATP is required to pro-
vide the energy for the calcium pump—the third major role of
ATP in muscle contraction (