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MUSCLE PHYSIOLOGY (SKELETAL (MOTOR UNIT RECRUITMENT 3 TYPES OF FIBRES…
MUSCLE PHYSIOLOGY
SKELETAL
Function: locomotion, respiration, manipulation of objects, purposeful movement, propulsion of contents through hollow internal organs and emptying contents of organs
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SARCOMEREmuscles are increased in length by adding sarcomeres. Titin provides a scaffold, allows elastic recoil os sarcomere and assists in signal transduction. Myosin has head with atp and actin receptor binding sites, plus tails which create the bare areas, they also have 2 hinge points. Actin thin filaments that consist of 3 filaments: actin, troponin( has 3 binding subunits) and tropomyosin (covers binding sites and stabilises)
Structure of the thin (actin) Filament:
They are made of different types of proteins (actin and myosin) Actins:
o Relatively small proteins o Form filaments
Tropomyosin:
o Helps to stabilize the actin filaments o Covers the myosin binding sites in resting state
Troponin:
o 3 subunits o Involved in control of contractile activation
Structure of thick (myosin) filament:
They have globulin heads and thick tails Globular heads are the motor proteins (this is where the movement will come from) ATPase site where ATP is hydrolyzed to produce energy Hinge region - allows movement also Bare zone has no heads
During sarcomere shortening, the I bands get smaller while the A bands remain relatively constant
Sliding filament mechanism: Ca2+ causes thin filaments to slide over thick = pulls z lines closer together = shortens sarcomere = H and I band shortens
CONTRACTION: EXCITATION COUPLING AND CROSS BRIDGE CYCLING Within the sarcomere, ATP binds to an ATPase receptor on the thick filament, myosin, causing it to split into adenosine diphosphate (ADP) and inorganic phosphate (Pi).2 When a skeletal muscle fibre is stimulated by a local action potential it causes the release of calcium (Ca2+) from the lateral sacs of the muscle cell’s sarcoplasmic reticulum (SR) into the cytosol of the cell.3 Increased concentration of cytosolic Ca2+ pulls the troponin-tropomyosin complex out of its blocking position, enabling binding between the myosin cross bridges and an actin molecule.4 The binding of actin and myosin causes the myosin head to rotate 45 degrees and create a strong configuration with actin.4 The rotation causes Pi to be released from its myosin binding site, resulting in a power stroke to occur within the sarcomere.5 The power stroke decreases the length of the sarcomere by pulling the thin and thick filaments towards its centre. This change in sarcomere length causes the thick filament cross bridges and the thin filament cross bridge binding sites to overlap; thus resulting in skeletal muscle tension generation and contraction
The Cross-Bridge Cycle:
- Myosin head and how they are able to push the - The cells are full of ATP (5-10mmole) - Contractions needs ATP - Myosin head attaches to the actin firmly, there are now cross bridges- Muscle contraction - the ATP attaches to the myosin heads because it is right next to it, causing it to detach. There is now a narrow ga between the two things (this is what causes rigomortis - because all the ATP hydrolyses, ATO disconnects the filaments after death) - ATP Hydrolysis - ADP + P they do not move away. Moves the head into a new position and moves it straight up. Potential energy into the new position, straight up. The P comes off, it changes the part of the molecule, which changes in shape and attaches the filament. ADP comes of and a power stroke occurs. This power stroke pushes the actin, after that the ATP attaches and it’s repeated
Excitation contraction coupling: (events that link muscle excitation and contraction) = ap depolarises & activates V gates DHPR on the t-tubule > DHPR interact with ryanodine receptors (RYR) on the SR > Ca flows down its concentration gradient into Sacroplasm > Ca binds to tnc > initiates criss bridge cycling. Ca levels decrease after electrical stimulation due to increase action of the SERCA pump (actively pumps Ca from cytosol into SR)
RELAXATION The sarcoplasmic (also known as endoplasmic) reticulum has an energy consumer carrier known as the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) pump (Sherwood, 2015). This specialised pump actively transports Ca2+ from the cytosol of a muscle cell and concentrates it back into the lateral sacs of the SR. The end plate potential and muscle fibre action potential ceases when acetylcholinesterase removes acetylcholine from the neuromuscular junction (Sherwood, 2015). When a local action potential ceases it is no longer able to trigger a release of Ca2+, the SERCA pump returns Ca2+ back into the lateral sacs of the SR. the resulting decrease in Ca2+ allows the troponintropomyosin complex to move back into its original blocking position. This prevents actin and myosin from binding at the cross bridges. The thin filaments of the sarcomere passively return back into their original position and the muscle fibre becomes relaxed (Sherwood, 2015).
RELAX LONGER>CONTRACT During muscular contraction, the cell uses facilitated diffusion to pump Ca2+ down its concentration gradient from the lateral sacs into the cytosol. During relaxation, the SERCA pumps use active transport to pump Ca2+ from a low concentration to a high concentration, back out of the cytosol and into the sarcoplasmic reticulum. Facilitated diffusion is faster than active transport (The Pennsylvania State University, 2017) and so relaxation of a muscle fibre takes longer than contraction of the muscle fibre.
TWITCH SUMMATION When a skeletal muscle fibre is stimulated by a local action potential, it causes the release of Ca2+ from the lateral sacs of the muscle cell’s sarcoplasmic reticulum (SR) into the cytosol of the cell.3 Increased Ca2+ concentration allows the number of actin-myosin cross-bridges that form within the muscle cell to increase.5 With each stimulus, Ca2+accumulates in the muscle fibres until all possible actin myosin crossbridges have been formed. With increased stimulation maximal tension is achieved by the sustained elevation in cytosolic calcium, causing the skeletal muscle to remain in a maximal contracted state
Isotonic (constant load) contraction: muscle shortens, while load remains constant Isometric (constant length) contraction: muscle develops tension but does not shorten Two types of contractile force:
o Twitch - the force you get form one action potential o Tetanic - bigger force response. Produces forces that are normally used. More action potentials in a smaller amount of time, causing them all to summate o Calcium does not bind to troponin in sufficient quantities during the short-lived twitch respons
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Tension: Active tension refers to the tension produced by the degree of overlap between actin and myosin filaments within a sarcomere increases and declines with stretch, whilst passive tension reflects the tension produced when non-contractile proteins, such as titan, are stretched, continues to increase with stretch. Total tension is both passive and active tension combined
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LENGTH TENSION RELATIONSHIP . Maximum active tension was produced due to the optimal level of overlap of the thick filament cross bridges of the sarcomere and the thin filament cross bridge binding sites. When exceeded its optimal length fewer thin filament binding sites were available for interaction and binding with thick filament cross bridges. Overstretching the muscle length causes thin filaments to be pulled out from between the thick filaments and thus reduces the number of actin sites available for cross bridge binding.When shortened less tension was produced as a result of the overlap of thin filaments from opposite sides of the sarcomere.
Tension is influenced by frequency of stimulation, the recruitment of muscle fibres and resting muscle length (increased levels of these=increase tension
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Refractory period after contraction determines how muscles can contract at dif strengths > Latency: time delay between the stimulation and onset of contraction > binding of calcium to troponin is the rate limiting part of the process
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CARDIAC
DESCRIPTION one nucleus per cell, tubular, striated, branches connected by intercalated discs: allow AP transfer, sarcomeres arent aligned, contain hella lots of mitochonidria,
INTERCALLATED DISCS Contain: gap junctions which form a port and allow the AP to travel, and desmossomes with link the intermediate filaments with the cytoskeleton and transmits force:
MOVEMENT OF AP Ap cell has a +ve and cell next to it is -ve = in depol potential dif exists = k flows into the -ve cell (adjacent one) and cl flows in the +ve cell = current movement = voltage movement = depolarisation = movement of AP
TIGHT JUNCTIONS made of KISS, stops movements between cells epithelium and surface
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PACEMAKER ACTIVITY OF PM CELLS Resting MP of PM cells isnt stable. Depolarisation until threshold open v gated Ca channels (l type) = repolarisation from delayed closing of L type and opening of voltage gated K channels > closure of Kv channels = decreased K permeability = depolarisation > repolarisation opens the funny channels HCN (Na) = lets Na in = depolarises the cell
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