Contractility
Ability of a muscle to forcefully shorten
Excitability
Ability to respond to a stimulus, such as may be delivered from a motor nerve or a hormone
Extensibility
Ability of a muscle to be stretched
Elasticity
Ability to recoil or bounce back to the muscles original length after being stretched.
Skeletal muscle
Voluntary muscle because we can consciously or voluntarily control it in response to input by nerve cells.
Striated (striped)
Cardiac muscle
Heart. Involuntary, autorhythmic without nervous or hormonal stimulation.
Striated
Smooth muscle
Walls of hollow organs- digestive, reproductive, urinary, tubes such as blood vessels & airways.
Involuntary, Visceral, nonstriated
Voltage gated ion channel sequence
draw picture.
- Action potential arrives at axon terminal of somatic nerve.
- voltage gated Ca ch in axon membrane open & enter axon terminal from extracellular space
- ACh released into neuromuscular junction by exocytosis into synaptic terminal, synapse.
- ACh binds to nicotinic receptors in post-synaptic membrane- the sarcolemma of the muscle fiber. This specialized region of the sarcolemma = motor end plate & location of ACh receptors
- ACh binding causes ligand-gated Na in & K out to open & depolarizes sarcolemma by inducing a conformational change in voltage gate Na+ ch.’s initiating a action potential
- Action potential travels across sarcolemma and down T-tubules
- Acetylocholinesterase breaks the ACh into acetyl & choline. Choline goes back into the somatic nerve
Na+ channels
2 gates
- Activation Gate: keeps channel closed at rest & open to allow Na to diffuse into the cell reversing the resting membrane potential causing depolarization
- Inactivation gate: moves slowly, closes Na channels & ends depolarization phase of action potential
Action potential
- Activation gates of voltage-gated Na channels open causing depolarization of sarcolemma
- Inactivation gates are delayed slightly so Na can rush in to cause depolarization. Once closed, action potential peaks
- Voltage gated K+ channels open slowly during this whole time. K+ diffuse out of cell slowly causing repolarization to its resting membrane potential. (-70mV)
Dihydropyridine (DHP) Ryanodine channel (RYN)
DHP are mechanically linked to protein ch. located in the SR membrane called RYN channels. These 2 protein channels span the dis between the T-tubule & and the SR
DHP responds to voltage, causes RYN to open and the Ca to leave the SR into the sarcoplasm.
Ca binds to TnC subunit of the troponin molecules.
TnT subunit of troponin pries tropomyosin out of resting locations that hide active site of g-actin molecule
Cross bridges
Heads of myosin molecules bind to exposed G-actin active sites and form cross bridges to move the thick and thin myofilaments- fibers shorten- movement results.
Movement of myosin heads is known as the power stroke or working stroke
ATP in power stroke
Myosin head must bind an ATP molecule to use the ATPase talent to hydrolyse ATP into ADP + Pi & use its energy to cock the head back into high energy position-Recovery stroke. Cross bridge cycling.
Myosin heads have 2 phases
Power Stroke/working stroke: when myosin heads bend and ratchet the actin molecules over themselves
Recovery stroke: myosin heads detach from actin and being cocked back into high energy position to prepare for next power stroke
Physiologic contracutre
Temporary contracture that sometimes occurs with severe muscle fatigue.
Rigor mortis
Muscle stiffness by depletion of ATP. Death of body/ life. Stops ATP production which relaxation of myosin heads= constant contraction
Muscle Contracture
A muscle that has shortened and resits relaxing to its normal resting length. Electrically silent= we do not see repeated action potentials coming down motor neurons to muscle cell.
Originates because of a physiological change of the muscle fiber… not the motor neuron that innervates it.
Prolonged immobilization
Spasticity
Muscle weakness
Cramp
Sudden involuntary painful contraction. Repeated firing of action potentials in motor neurons. Common in lower leg & foot
Na+ channels
2 gates
- Activation Gate: keeps channel closed at rest & open to allow Na to diffuse into the cell reversing the resting membrane potential causing depolarization
- Inactivation gate: moves slowly, closes Na channels & ends depolarization phase of action potential
Action potential
- Activation gates of voltage-gated Na channels open causing depolarization of sarcolemma
- Inactivation gates are delayed slightly so Na can rush in to cause depolarization. Once closed, action potential peaks
- Voltage gated K+ channels open slowly during this whole time. K+ diffuse out of cell slowly causing repolarization to its resting membrane potential. (-70mV)
Dihydropyridine (DHP) Ryanodine channel (RYN)
DHP are mechanically linked to protein ch. located in the SR membrane called RYN channels. These 2 protein channels span the dis between the T-tubule & and the SR
DHP responds to voltage, causes RYN to open and the Ca to leave the SR into the sarcoplasm.
Ca binds to TnC subunit of the troponin molecules.
TnT subunit of troponin pries tropomyosin out of resting locations that hide active site of g-actin molecule
Cross bridges
Heads of myosin molecules bind to exposed G-actin active sites and form cross bridges to move the thick and thin myofilaments- fibers shorten- movement results.
Movement of myosin heads is known as the power stroke or working stroke
ATP in power stroke
Myosin head must bind an ATP molecule to use the ATPase talent to hydrolyse ATP into ADP + Pi & use its energy to cock the head back into high energy position-Recovery stroke. Cross bridge cycling.
Myosin heads have 2 phases
Power Stroke/working stroke: when myosin heads bend and ratchet the actin molecules over themselves
Recovery stroke: myosin heads detach from actin and being cocked back into high energy position to prepare for next power stroke
