Excitation-contracting coupling

7 important questions on Excitation-contracting coupling

What are the calcium concentrations outside and inside?

Extra: 1.2 mM (1200 µM)
Intra: 100 nM (0.1 µM)

What happens during phase 2 of the AP?

Ca2+ enters the cell via L-type Ca channels --> myosin binding sites are available

Where is the developed force of the muscle dependent on?

Free [Ca]i
The more calcium is present, the more binding sites are available --> more cross-bridges --> higher force
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What is the calcium-induced calcium release (CICR)?

The amount of Ca2+ entering the cell during phase 2 of the AP is relatively small --> not sufficient to increase concentration to generate high forces. Therefore, Ca2+ is released from an intracellular calcium store (sarcoplasmic reticulum) through the ryanodine receptors (stimulated by calcium in the cytoplasm).
Calcium is taken up by SR via ATP pumps to enable relaxation

How is the calcium reuptake regulated?

Via phospholamban, normally this protein inhibits the pump (SERCA). When phospholamban is phosphorylated, it is no more inhibited. Inside the SR, calsequestrin binds to several Ca2+

How is calcium removed from the intracellular space?

- SERCA (SR-ATPase)
- Na/Ca exchange (NCX)
- SL-ATPase (SL = sarcollema)

What is the effect of sympathetic activation on the muscle cells?

Release of norepinephrine stimulates the ß receptors (GPCR) which in turn activate adenylate cyclase. Then, cAMP is produced which activates PKA. PKA phosphorylates:
- L-type Ca channels (increased Ca influx)
  • Inotropic effect => stronger contraction

- Phosphorylation of phospholamban (PLB)
  • lusitropic (improvement of relaxation)

- phosphorylation of troponin I (TnI)
  • lusitropic (improvement of relaxation)

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