Muscle Physiology Flashcards
Skeletal Muscle and Physiology
- Responsible for creating behavior (movement)
- Metabolic regulation (think diabetes)
- Heat production (shivering)
- Adapts to various loading conditions
Two types of myofilaments
- Myosin
- Actin
Muscle Fiber Innervation
Each fiber innervated by one neuron at one location
One neuron can innervate many fibers (motor unit)
Steps in Neuromuscular Transmission (Excitation-Contraction Coupling)
Electrical stimulus (action potential) –> mechanical response (contraction)
- Action potential at neuromuscular junction
- Calcium release
- Myosin and actin interaction
- Muscle contraction (cross-bridge cycling)
- Calcium removal
- Relaxation
Step 1: Action Potential at Neuromuscular Junction
- Action potential arrives in presynaptic axon terminal
- Opening of voltage-gated Ca channels and entry of Ca
- Release of ACh from vesicles to cleft
- Diffusion of ACh to sarcolemma
- ACh binds to receptors on the motor end plate w/in sarcolemma increasing conductance of motor end plate to Na and K resulting in EPP
- Depolarization of membrane reaches threshold and opens V-G channels which initiates action potential on sarcolemma
- Degradation of ACh by acetylcholinesterase (AChE)
End Plate Potential (EPP)
- Each vesicle release of ACh causes a mini EPP (MEPP)
- Does NOT cause action potential
- Summation of multiple MEPPs produce EPP
- EPP is graded potential confined to the motor end plate
- Magnitude depends on amount and duration of ACh at end plate
Factors Affecting Magnitude of EPP
Normally: the release of Ach is more than sufficient to fire an action potential
- Amount of ACh release which is regulated by Ca present
- Activity of AChE
- Any agonist/antagonist present
Step 2: Calcium Release
Depolarization of T-tubules
Action potential travels entire sarcolemma into T tubules
Ca Release from SR:
1. Membrane depolarization opens L-type Ca channel
2. Mechanical coupling between L-type channel and Ca-release channel causes release channel to open
3. Ca exits the SR and activates troponin C, leading to muscle contraction
Step 3: Myosin and Actin Interaction
Actin in the Sarcomere: actin, tropomyosin (inhibits binding of myosin to actin), troponin (Ca sensitive molecular switch)
Ca binding to the troponin complex allows for physical repositioning of the tropomyosin filament, which exposes the myosin binding site on the actin molecules
Step 4: Muscle Contraction (Cross-bridge cycling)
Sliding of actin along the myosin filaments results in physical shortening (contraction) of the sarcomere
Excitation-Contraction Coupling in Cardiac contractile cells
- Action potential causes depolarization of membrane
- Opening of L-type voltage-gated Ca channels
- Ca from the ECF enters the cell
- Ca-induced Ca release (from SR)
- Cytosolic Ca levels increase
- Ca binds to troponin pulling the troponin-tropomysosin complex aside
- Myosin binds to actin
- Cross bridge cycling (contraction)
Ca Release in Cardiac Muscle
Ca comes from both the SR and from the outside (through L-type Ca channels)
Relaxation in Cardiac Muscles
Cytosolic Ca concentrations decrease by return of Ca into SR by SERCA
Extrusion of Ca from Cardiac Muscle cell by: sarcolemmal Na/Ca exchanger (energy for Ca against gradient is obtained via the inward driving force for Na; the Na/K ATPase maintains gradient while Sarcolemmal Ca ATPase pumps Ca out
Three mechanisms that increase Ca in smooth muscle:
- Voltage-gated Ca channels (action potential)
- Ligand-gated Ca channels (hormones & neurotransmitter)
- IP3-gated Ca channels located on SR: Hormones and neurotransmitter act on G-protein coupled receptors on sarcolemma –> phospholipase C up –> PIP2 to IP3 and DAG –> IP3 opens the Ca channel on SR –> Ca release into ICF
Ca effects in smooth muscle
-Ca diffuses into the cell across the the sarcolemma or from SR
- The Ca increases ATPase activity of the myosin head (slowly)
- Ca binds to calmodulin
- Ca-calmodulin regulates myosin-light-chain kinase up which triggers cross-bridge cycling
