Contraction ends when cytosolic Ca$^{2+}$ falls. In skeletal muscle, this requires active transport of Ca$^{2+}$ back into the sarcoplasmic reticulum (SR).

The main transporter is SERCA, the sarco/endoplasmic-reticulum Ca$^{2+}$ ATPase. SERCA uses ATP hydrolysis to pump Ca$^{2+}$ from the cytosol into the SR against its electrochemical gradient.

cytosolic Ca2+
      ↓ SERCA + ATP
Ca2+ accumulated in SR

Falling calcium switches off thin-filament activation

As SERCA lowers cytosolic Ca$^{2+}$:

1. Ca$^{2+}$ dissociates from troponin C;
2. tropomyosin returns toward its inhibitory position on actin;
3. formation of new productive cross-bridges decreases;
4. existing cross-bridges complete their ATP-dependent cycles and active tension falls.

Relaxation is therefore an active molecular process, not simply contraction 'running backward.' ATP is required both for continued myosin cycling/detachment and for Ca$^{2+}$ reuptake.

The SR stores calcium for the next contraction

Inside the SR, Ca$^{2+}$-binding proteins help store a large amount of Ca$^{2+}$ while limiting the concentration of freely dissolved Ca$^{2+}$.

When the next excitation arrives, SR release channels can rapidly return some of this stored Ca$^{2+}$ to the cytosol.

Thus one contraction–relaxation cycle contains two opposite Ca$^{2+}$ fluxes:

excitation: SR → cytosol  (release)
relaxation: cytosol → SR  (ATP-driven reuptake)

The electrical signal can end quickly, but mechanical relaxation takes time because cytosolic Ca$^{2+}$ and cross-bridge activity must decay after the membrane has repolarized.