Muscles and Muscle Tissue.

Three Types of Muscle: Skeletal, Cardiac, Smooth

Characteristics of ALL muscles

  • Excitability (responsiveness)

  • Contractility 

  • Extensibility (past resting length)

  • Elasticity (recoil)


Skeletal Muscles

  • Nerve & blood supply for each muscle

  • Covered in layers of connective tissue sheaths (out to in) EPI, PERI, ENDOmysium

  • Attach to bone in at least two places

    • Origin: Immovable or less movable bone

    • Insertion: Movable bone

    • Direct attachment: Epimysium fused to periosteum/chondrium of bone

    • Indirect attachment: CT wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis to suspend the muscle


Microscopic Anatomy of Skeletal Muscle

Skeletal Muscle Fibers: Long, cylindrical cells, contain multiple nuclei 

Sarcolemma: Muscle fiber plasma membrane

Sarcoplasm: Muscle fiber cytoplasm

Glycosomes: Glycogen storage

Myoglobin: Oxygen storage

Sarcoplasmic Reticulum: Calcium storage into T tubules(Ca causes muscle contraction)

T-Tubules: Formed by protruding sarcolemma deep into cell interior, increase muscle surface area, allow electrical nerve transmission to reach into interior of each muscle fiber

Triad: Area formed from terminal cistern of one sarcomere, T tubule, and neighboring terminal cisterna


Myofibrils

  • Made up of myofilaments

  • Account for 80% of muscle cell volume

  • Repeating series of dark and light bands

  • A Bands: Dark, thick, myosin

  • I Bands: Light, thin, actin

  • H Zone: LIghter region in the middle of a dark A Band

  • M LIne: Line of protein (myomesin) that separates H Zone vertically

  • Z Disc: Sheet of proteins on midline of light I Band (zigzag line)

  • Sarcomere: From Z to Z, smallest functional unit of muscle fiber


Structural Proteins

  • Troponin: binds to tropomyosin at regular intervals to position on actin

  • Titan: Elastic filament from Z disc to thick myofilament, forms core of thick myofilament, attaches to M line to hold in place. Prevents excess stretch

  • Dystrophin: Links thin myofilaments to proteins of sarcolemma

  • Calcium: Binds to troponin, pulls on tropomyosin, exposes active sites on actin


How do muscles contract? 

  • Myosin heads bind to actin, forming cross bridges that trigger contraction

  • Cross bridges continuously form and break, pulling thin filaments closer each time towards sarcomere

  • H Zone disappears, everything contracts toward M Line

  • ATP binds to myosin head, weakening link to actin, detaching/breaking

  • Reactivation: Energy from hydrolysis of ATP moves myosin head into a high-energy state to re-bind. ATP → ADP + P


Ion Channels

  • Chemically Gated: Opened by chemical messengers (neurotransmitters)

  • Voltage Gated: Open/Close in response to electrical voltage changes in membrane potential


Neuromuscular Junction

  • Stimuli received from somatic nervous system motor neurons to axons

  • Axons branch as motor neuron enters

  • Axon branches end on muscle fiber, forming NMJ/motor end plate

  • Axon terminal and muscle fiber separated by synaptic cleft

  • Axon terminals synaptic vesicles contain acetylcholine (ACh)

  • Sarcolemma have ACh receptors

  • Acetylcholinesterase breaks down ACh

NMJ Steps

  1. Action potential arrives at axon terminal

  2. Voltage gated calcium channels open, enters motor neuron

  3. ACh released into synaptic cleft

  4. ACh diffuses across cleft and binds to Na chemical gate receptors on sarcolemma

  5. Na enters sarcolemma and generates end plate/local potential

  6. ACh is broken down by acetylcholinesterase into acetic acid and choline, stopping contraction

  7. Choline reuptake by terminal end

Regeneration of Action Potential

Action potential is all or nothing and does not stop after beginning. Caused by changes in electrical charges. Resting potential is polarized, the existing voltage across the membrane is positive compared to negative inside. 

End Plate Potential

  • ACh released from motor neuron binds to ACh receptors on sarcolemma, causes chemically gated ion channels (ligands) to open

  • Na diffuses into muscle fiber (some K diffuses outward but not much)

  • Na inward diffusion causes interior of sarcolemma to become less negative

  • Results in local depolarization called end plate potential

Depolarization

  • End plate potential causes enough change in membrane voltage to reach threshold

  • Voltage gated Na channels in membrane open

  • Na influx into cell triggers action potential and leads to contraction

  • Action potential spreads across sarcolemma from channel to channel, depolarizing

Repolarization

  • Restoring resting state

  • Na voltage gated channels close, K voltage gated channels open

  • K moves out of cell rapidly, restoring initial resting membrane voltage

  • Refractory period: Muscle fiber cannot be stimulated again until repolarization is complete. 


Whole Muscle Contraction

  • Two types of muscle contraction

    • Isometric: muscle tension increases with NO shortening

    • Isotonic: muscle tension increases WITH shortening

  • Contraction produces muscle tension, the force generated by the contraction of a muscle


Motor Unit

  • Each muscle is supported by at least one motor nerve

  • Motor unit is the nerve-muscle functional unit


Muscle Twitch

  • Three phases of muscle twitch

    • Latent period: events of excitation-contraction coupling (NO muscle tension seen)

    • Period of contraction: cross bridge formation, tension increases

    • Period of relaxation: Ca2+ re-enters into sarcoplasmic reticulum, tension goes back to zero


Graded Muscle Responses

  • Variation in the strength of contraction for different demands

  • Responses are graded by…

  1. Changing frequency of stimulation

  • Increases muscle contraction intensity

  • Additional Ca2+ released cross bridge formation

  • Unfused tetanus: muscle fibers do not completely relax due to further increase in stimulus

If stimulus frequency increases, maximal tension is reached

  • Referred to as fused tetanus

    • Prolonged muscle contractions lead to muscle fatigue, where muscle CANNOT contract

  1. Changes in stimulus strength

  • Recruitment: stimulus is sent to more muscle fibers, causing more precise control

  • Stimulus involved in recruitment…

    • Subthreshold stimulus: stimulus not strong enough, no contractions

    • Threshold stimulus: stimulus strong enough to cause first observable contraction

    • Maximal stimulus: strongest stimulus that increases maximum contractile force

  • Recruitment works on size principle

    • Smallest muscle fibers recruited first

    • Larger fibers are recruited as stimulus increases


Muscle Tone

  • Muscles are slightly contracted, even when relaxed, due to spinal reflexes


Providing Energy for Contraction

  • ATP is regenerated quickly by three mechanisms

  1. Direct phosphorylation of ADP by creatine phosphate

  • Creatine phosphate donates phosphate to ADP to form ATP

    • Creatine kinase carries out transfer of phosphate

    • CP + ADP + creatine kinase -> creatine & ATP

  1. Anaerobic pathways (NO oxygen used)

  • Glycolysis: first step in glucose breakdown

    • Glucose broken down into 2 pyruvic acid molecules

    • 2 ATPs generated for each glucose

    • In anaerobic glycolysis, pyruvic acid becomes lactic acid

  • Lactic acid

    • Diffuse into bloodstream; used as fuel for heart, liver, kidneys

    • Converted back into pyruvic acid or glucose by liver

  1. Aerobic respiration

  • 3 stages

    • Glycolysis in cytoplasm

    • Kreb cycle

    • Electron transfer phosphorylation


Energy Systems used during sports

  • Aerobic endurance

    • Length of time muscle contracts using aerobic pathways, light/moderate activity

  • Anaerobic threshold

    • Point at which metabolism converts into anaerobic pathway


Excess Postexercise Oxygen Consu (EPOC)

  • In order for muscles to return to their pre-exercise state…

    • Oxygen reserves are replenished

    • Lactic acid converted into pyruvic acid

    • Glycogen stores replaced

    • ATP & creatine phosphate reserves are resynthesized

  • All replenishing steps require extra oxygen, referred to as EPOC or oxygen debt


Factors that increase force of skeletal muscle contraction

  • Number of muscle fibers stimulated

  • Size of fibers recruited

  • Frequency of stimulation

  • Degree of muscle stretch


Muscle Fiber Types

  • Slow or fast fibers (speed of contraction)

    • Speed at which myosin ATP bases split ATP

  • Metabolic pathways used for ATP synthesis

    • Oxidative fibers: aerobic pathways

    • Glycolytic fibers: anaerobic pathways


Specific Muscle Fiber

  • Slow oxidative fibers: low-intensity activities (ex: maintaining posture)

    • High fatigue resistance, many mitochondria

    • Red in color, high in myoglobin

  • Fast oxidative fibers: medium-intensity (ex: walking, sprinting)

  • Fast glycolytic fibers: short-term intense activity (ex: hitting baseball)

    • White in color, little myoglobin

    • Fatigues quickly, few mitochondria


Actions of Muscle

  • Agonists: produce a desired movement

  • Antagonists: opposes movement of agonist (opposite sides)

  • Synergists: add extra force to movement (helping agonists)

  • Fixator: immobilizes bone or muscle’s origin (gives agonist stable base to act on)


Naming Muscles

  • Location (zygomaticus)

  • Shape (deltoideus)

  • Size (adductor magnus)

  • Direction of fibers (external obliques)

  • Number of origins (biceps brachii)

  • Location of attachments (sternocleidomastoid)

  • Muscle action (flexor digitorum superficialis)


Smooth Muscles

  • Found in walls of hollow organs

  • Spindle-shaped fibers: thin and short, only one nucleus, no striations

  • No sarcomeres, myofibrils, T-tubules, or NMJ

  • Autonomic nerve fibers innervate smooth

    • Contain varicosities, bulbous swellings, of nerve fibers

      • Store and release neurotransmitters into wide synaptic cleft (diffuse junction)

  • Lattice-like intermediate filaments present

  • Contraction: sliding myofilaments pull on intermediate filaments which pull dense bodies and sarcolemma

    • Areas of sarcolemma between dense bodies bulge outwards


Smooth Muscle Contraction

  • Slow, synchronized contractions

  • Cells electrically coupled by gap junctions (action potentials transmitted from fiber to fiber)

  • Some cells are self-excitatory, which act as pacemakers for muscle

    • Rate/intensity of contraction may be modified by neutral and chemical stimuli

  • Some Ca2+ obtained from SR, but mostly from extracellular space

  • Ca2+ binds to calmodulin, not troponin

  • Activated calmodulin activates myosin kinase

  • Activated myosin kinase phosphorylates myosin head, activating it

    • Leads to crossbridge formation with actin


Ca2+ binds to calmodulin -> mysoin kinase -> myosin head -> crossbridge formation with actin


Smooth Muscle Relaxation

  • Ca2+ detachment from calmodulin

  • Active transport of Ca2+ into SR & extracellularly

  • Dephosphorylation of myosin to inactivate myosin


Regulation of Contraction

  • Controlled by nerves, hormones, or local chemical changes

  • Neural regulation

    • Neurotransmitter binding causes either graded potential or action potential

      • Increases Ca2+ concentration in sarcoplasm, response varies

  • Hormones & local chemicals

    • Some smooth muscles have no nerve supply

      • Depolarize spontaneously or in response to chemical stimuli that bind to G protein-linked receptors

      • Chemical factors can include hormones, high CO2, pH, low oxygen

    • Some smooth muscles respond to both neutral and chemical stimuli