Presentation on theme: "Properties of Muscle Contractility –Ability of a muscle to shorten with force Excitability –Capacity of muscle to respond to a stimulus Extensibility."— Presentation transcript:
Properties of Muscle Contractility –Ability of a muscle to shorten with force Excitability –Capacity of muscle to respond to a stimulus Extensibility –Muscle can be stretched to its normal resting length and beyond to a limited degree Elasticity –Ability of muscle to recoil to original resting length after stretched
Muscle Tissue Types Skeletal –Attached to bones –Nuclei multiple and peripherally located –Striated, Voluntary and involuntary (reflexes) Smooth –Walls of hollow organs, blood vessels, eye, glands, skin –Single nucleus centrally located –Not striated, involuntary Cardiac –Heart –Single nucleus centrally located –Striations, involuntary, intercalated disks
Morphology of Muscle Four types: skeletal, cardiac, smooth and myoepithelial cells
Long multinucleated cells that respond only to motor-nerve signals, which cause Ca release from sarcoplasmic reticulum and activation of actin-myosin interaction. Shorter mononucleated cells linked to each other by intercalated disks that contain many gap junctions. Capable of independent, spontaneous contraction, with electrical depolarization transmitted from cell to cell through gap junctions. Spindle-shaped mono- nucleated cells. Contraction influenced by hormones and autonomic nerves. Contraction governed through myosin light chain kinase.
Skeletal muscle 40% of adult body weight 50% of child’s body weight Muscle contains: –75% water –20% protein –5% organic and inorganic compounds Functions: –Movement –Maintenance of posture
Structure of Thick Filaments Myosin - 2 heavy chains, 4 light chains Heavy chains kD Light chains - 2 pairs of different 20 kD chains The "heads" of heavy chains have ATPase activity and hydrolysis here drives contraction Light chains are homologous to calmodulin
RyR RyR = ryanodine receptor Ca 2+ channel DHPR DHPR = dihydro- pyridine receptor Ca 2+
Mechanism of muscle contraction
Sliding filament model of muscle contraction "Crossbridges" form between myosin and actin, with myosin pulling actin into "H zone" and shortening distance between Z disks.
Length-tension curve for skeletal muscle Full overlap between thick and thin filaments Decreasing overlap limits maximum tension No overlap (Muscles are not naturally stretched to this point) Actin poking through M line; myosin bumping into Z disk. Contraction range with normal skeletal movements
Molecular mechanisms of crossbridge action
T-tubules are NOT positioned at M lines.
Dihydropyridine Receptor In t-tubules of heart and skeletal muscle Nifedipine and other DHP-like molecules bind to the "DHP receptor" in t-tubules In heart, DHP receptor is a voltage-gated Ca 2+ channel In skeletal muscle, DHP receptor is apparently a voltage-sensing protein and probably undergoes voltage-dependent conformational changes
Ryanodine Receptor The "foot structure" in terminal cisternae of SR Foot structure is a Ca 2+ channel of unusual design Conformation change or Ca 2+ -channel activity of DHP receptor apparently gates the ryanodine receptor, opening and closing Ca 2+ channels
Ca 2+ Controls Contraction Release of Ca 2+ from the SR triggers contraction Reuptake of Ca 2+ into SR relaxes muscle So how is calcium released in response to nerve impulses? Answer has come from studies of antagonist molecules that block Ca 2+ channel activity
This gap is actually only ~10 nm. Ca 2+ -ATPase
Contractile force can also be regulated through activation of more, or fewer, motor units.
Muscle contraction Types –Isometric or static Constant muscle length Increased tension –Isotonic Constant muscle tension Constant movement » –
Time is required for maximal twitch force to develop, because some shortening of sarcomeres must occur to stretch elastic elements of muscle before force can be transmitted through tendons. By the time this maximal force is developed, [Ca 2+ ] and number of active crossbridges have greatly decreased, so an individual twitch reaches much less than the maximum force the muscle can develop.
* Mitochondria generate ~32 ATP from one glucose (slow, but efficient). * Glycolysis generates 2 ATP from one glucose (fast, but inefficient; lactate accumulates). * Creatine kinase reaction: (fastest) ADP + creatine-P ATP + creatine Generate ATP
Fatigue: * Central — involving central nervous system may involve such factors as dehydration, osmolarity, low blood sugar, and may precede physiological fatigue of actual muscles. * Peripheral — in or near muscles accumulation of lactate and pH, especially in fast-twitch fibers inorganic phosphate — may increasingly inhibit cleavage of ATP in the crossbridge cycle or in the sequestering of Ca 2+.
–Incomplete tetanus Muscle fibers partially relax between contraction There is time for Ca 2+ to be recycled through the SR between action potentials
–Complete tetanus No relaxation between contractions Action potentials come sp close together that Ca 2+ does not get re- sequestered in the SR
A skeletal muscle twitch lasts far longer than the refractory period of the stimulating action potential, so many additional stimuli are possible during the twitch, leading to summation of tension and even tetanus.
In cardiac muscle, the action potential — and therefore the refractory period — lasts almost as long as the complete muscle contraction, so no tetanus, or even summation, is possible. Sequential contractions are at the same tension, though gradual increases and decreases occur with autonomic nervous system input.