Smooth muscles: involountary contractions, control movement of fluids through inner organs
Cardiac muscles: involountary contraction, striated/striped, moves the blood through the body
Describe the structure of skeletal muscle from fascia → muscle fibre
Out → In: Fascia, Epimysium, Perimysium, Fascicle, Endomysium, Muscle fibre/Cell
Describe the structure of skeletal muscle from Muscle fibre → myofibrils
Out → In: Muscle fibre, Sarcolemma (the membrane), Myoplasm/Sarcoplasm, Myofibrils
Describe the T-tubules
T-tubules = Transverse tubules
Increases the surface are of a muscle cell
Provides signals from the surface of the cell down into the cell, specifically to the sarcoplasmic reticulum (SR)
Allow the AP to reach all parts of the muscle cell almost simultaneously. Wthout this, problems would occur in signaling into the cell.
Adequate exchange of nutrients
Describe the SR
Sarcoplasmic Reticulum (SR):
Like ER but in the cell
Stores Ca2+ ions
Has pumps for transport of Ca2+ from sarcoplasm --> SR
Ca2+ gates through which Ca2+ flows out at impuls
Terminal cisternaes, one at each side of the T-tubule, where Ca2+ is stored
Triad = 2 cistarnaes, 1 T-tubule
Describe the Myofibril
The Contractive element of a muscle cell
Composed of 2 types of filaments (thin & thick)
Many subunits composed of filaments (sacromeres = smallest subunit in a muscle)
Name 2 contractile proteins
Myosin (head & tail)
Actin - has a myosin binding site onto which the head attaches (bead)
Name 2 structural proteins
Titin (anchor thick filament to the Z-disc)
Name 2 regulatory proteins
Tropomyosin: regulaes muscle contraction by interfiering with the binding og myosin & actin (moves & exposes the myosin binding site of the actin → myosin head can bind!). Has 3 subunits, I = inhibitatory, C = calcium binding, T = tropomyosin
Troponin: Ca2+ binds to it when a contraction of a muscle is initiated
Describe the cross bridge cycle (skeletal muscle contraction)
1. AP causes a Ca2+ influx through the voltage-gated calcium channels.
2. The Ca2+ influx causes vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine out into the extracellular space between the motor neuron terminal and the motor end plate of the skeletal muscle fiber.
3. The calcium binds to the troponin → conformational change (troponin moves and exposes the myosin binding sites of the actin) → myosin can bind.
4. Myosin (which has ADP and inorganic phosphate bound to its nucleotide binding pocket and is in a ready state) binds to the newly uncovered binding sites on the thin filament (binding to the thin filament is very tightly coupled to the release of inorganic phosphate). Myosin is now bound to actin in the strong binding state. The release of ADP and inorganic phosphate are tightly coupled to the power stroke (actin acts as a cofactor in the release of inorganic phosphate, expediting the release). This will pull the Z-bands towards each other, thus shortening the sarcomere and the I-band.
5. ATP binds myosin, allowing it to release actin and be in the weak binding state (a lack of ATP makes this step impossible, resulting in the rigor state characteristic of rigor mortis). The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" conformation. In general, evidence (predicted and in vivo) indicates that each skeletal muscle myosin head moves 10-12 nm each power stroke, however there is also evidence (in vitro) of variations (smaller and larger) that appear specific to the myosin isoform.
6. Steps 4-5 repeat as long as ATP is available and calcium is present on thin filament.
7. While the above steps are occurring, calcium is actively pumped back into the sarcoplasmic reticulum. When calcium is no longer present on the thin filament, the tropomyosin changes conformation back to its previous state so as to block the binding sites again. The myosin ceases binding to the thin filament, and the contractions cease.
Describe the excitation phase
1: Somatic motor neuron releases ACh at neuromuscular junction.
2: Net entry of Na+ into the cell through ACh receptor channels --> muscle AP
3: AP in T-tubule --> conformational change of DHP-rec.
4: DHP opens RyR on SR --> Ca2+ enters the cytoplasm due to low [Ca2+] in the cytoplasm at rest.
5: Ca2+ binds to troponin --> strong actin-myosin binding.
6: Myosin heads execute power stroke = pulls actin fil. past myosin fil.
7: Actin fil. slides toward the center of sacromere
Ending: Stop of NT/ACh release --> no signal/AP --> closure of RyR channel
Problem: High [Ca2+] in myoplasm, has to go back to where it came from. Does so by active transport: ATP --> ADP + Pi. Energy released, used to move Ca2+ back to SR
Name 4 types of contractions
Isometric: no work is performed, no diff in muscle length
Isotonic: tension or force generated by the muscle i greater than load = muscle shorten. The same resistance throughout the whole movement/contraction
Concentric: muscle is shortening
Eccentric: muscle is actively lengthening
Isokinetic: musce contracts & shortens at a constant speed
Describe twitch, tetanus, wave summation & motor unit summation
Twitch: The response of a skeletal mscle to a single stimulation (or AP)
Three phases of a muscle twitch:
1. Latent period: the sarcolemma and the T tubules depolarize, calcium ions are released into the cytosol, cross bridges begin to cycle but there is no visible shortening of the muscle
Dephosphorylation at attached state:"latch" state = much slower cycling → force generation during long time
Contraction of smooth muscle is generated by posphorylation of crossbridge. This phosphorylation is not needed to maintan force. Once phosphorylated, the muscle keeps on cycling and generation force but slower.