Chapter 9.3 Cheat Sheet (DRAFT) by jjovann

•Nerve impulse reaches axon terminal volta­ge-­gated calcium channels open ACh released to synaptic cleft
•ACh binds to its receptors on sarcolemma  opens ligand­-gated Na+ and K+ channels  end plate potential  Opens voltag­e-gated Na+ channels  AP and AP propag­ation across the sarcolemma down into the t-tubules
•Volta­ge-­sen­sitive proteins in T tubules (DHP receptors) change shape in response to AP and activate the Ryanodine recept­orsSR releases Ca2+ to cytosol

•Ca2+ binds to tropon­in-­Cwhich changes the shape of the tropon­in-­tro­pom­yosin complex and uncovers the myosin binding sites on actin
–Myosin heads of the thick filament will then attach to the myosin binding sites of the thin filament as long as the proper molecules are present

•Continues as long as sarcop­lasmic Ca2+co­nce­ntr­ations remain high and adequate ATP present
•Cross­-bridge format­ion­—hi­gh-­energy myosin head (has ADP and inorganic phosphate bound to it) attaches to thin filament
•Power Stroke­—myosin head pivots and pulls thin filament toward M line
–Releases ADP and Pi in the process

•The tension a muscle fiber is capable of producing is dependent upon the amount of overlap between thick and thin filaments
–Too short (under­str­etched)
•Too much overlap between thick and thin filaments
•Tension generation decreases the more a muscle shortens
•Thin filaments begin to overlap

•Rigor Mortus
–Muscles can become stiff shortly after death
•Can begin 3-4 hours after expiration
•Maximum stiffness at around 12 hours post expiration
•Can take 48-60 hours to subside
–Caused by lack of ATP post death
•Heart stops, blood flow stops, no oxygen­/nu­trient delivery and waste removal from tissue
–ATP production declines and then ends as cells die
•ATP is not available to bind to the myosin head
–This means the head does not dissociate from the active site of the actin
ATP no longer available to power calcium pumps that pump calcium out of the sarcoplasm and into terminal cisternae
–This means that intrac­ellular calcium concen­tration stays high enough to allow the active sites of the thin filament to stay unblocked
–Can be used to determine time of death

•At low intrac­ellular Ca2+ concen­tration
–Tropo­myosin blocks active sites (myosin binding sites) on actin of thin filaments
–Myosin heads of thick filaments cannot attach when binding sites of thin filament are blocked
–Muscle fiber in relaxe­d/r­esting state

•In this graphic the tropon­in-­tro­pom­yosin complex has shifted into the “gutters” of the actin molecule unblocking the myosin binding site
•The tropon­in-­tro­pom­yosin complex can slide back and forth depending on the concen­tration of Ca2+ in the sarcoplasm

•Cross bridge detach­men­t—ATP attaches to myosin head and cross bridge detaches
•"Co­cki­ng" of myosin head—e­nergy from hydrolysis of ATP into ADP and inorganic phosphate (Pi) cocks myosin head into high-e­nergy state

–Too long (overs­tre­tched)
•Too little overlap between thin and thick filame­nts•Not enough actin/­myosin crossb­ridges are able to be formed
•Tension decreases the more a muscle is stretched

•At higher intrac­ellular Ca2+ concen­tra­tio­ns–Ca2+ binds to troponin C of the tropon­in-­tro­pom­yosin complex
•Troponin changes shape and moves tropom­yosin away from myosin­-bi­nding sites
–Unblocks the myosin binding sites
•Myosin heads bind to actin and undergo power stroke causing sarcomere shortening and muscle contra­ction
–When nervous stimul­ation ceases (no more ACh release and AP stimul­ation), the majority of Ca2+in the sarcoplasm is pumped back into SR by SERCA pumps (active transport)
•This causes intrac­ellular calcium concen­tration to decrease and contra­ction to end
–Muscle fiber begins to relax
•Some calcium is pumped out of the cell by Ca pumps (active transport) in the sarcolemma

•Myosin heads bind to actin (cross bridge formation)
•Sliding of the thin filaments with respect to the thick begins as power stroke of the myosin heads take place
•Cross bridges form and break several times, ratcheting thin filaments toward center of sarcom­ere­–Causes shortening of muscle fiber
–Pulls Z discs toward M line
•I bands shorten; Z discs closer; H zones disappear; A bands of adjacent sarcomeres move closer together (A band length stays same)

•Sarcomere shortening produces tension within a muscle

–Optimal resting length
•The ideal thin and thick filament overlap that allows for the maximum number of actin/­myosin cross bridge formations
•Maximum tension (force) generated during contra­ction
•Your muscles actually rest at this length!