Histology of Muscle

Skeletal Muscle Tissue

Muscle Histology Elongated cylindrical cells = muscle fibers Plasma membrane = sarcolemma Transverse (T) tubules tunnel from surface to center of each fiber Multiple nuclei lie near surface of cell Cytoplasm = sarcoplasm

Muscle Histology Throughout sarcoplasm is sarcoplasmic reticulum Stores calcium ions Sarcoplasm contains myoglobin Red pigmented protein related to Hemoglobin that carries oxygen Along entire length are myofibrils Myofibrils made of protein filaments Come in thick and thin filaments

The Sarcomere Filaments overlap in repeating patterns Unit structure is called sarcomere Separated by Z discs Darker area = A band associated with thick filaments H zone has no thin filaments I band has thin filaments no thick filaments

Functional Anatomy Thick filament (myosin) has moveable heads (like “heads” of golf clubs) Thin filaments (actin) are anchored to Z discs Contain myosin binding sites for myosin head Also contain tropomyosin & troponin Tropomyosin blocks myosin binding site when muscle is at rest

Sliding Filament Mechanism During contraction myosin heads bind actin sites Myosins pull and slide actin molecules (and Z discs) toward H zone I bands and H zones become more narrow Sliding generates force and shortens sarcomeres and thus fibers

Neuromuscular Interaction Nerve signal triggers muscle action potential Delivered by motor neuron One neuron can trigger 1 or more fibers at the same time Neuron plus triggered fibers = motor unit

Neuromuscular Interaction Neuronal ending to muscle fiber = neuromuscular junction (NMJ) Synaptic end bulbs (at neuron terminal) Release neurotransmitter Muscular area = Motor end plate Between is synaptic cleft

1 Axon terminal Axon collateral of somatic motor neuron Sarcolemma Myofibril ACh is released from synaptic vesicle ACh binds to Ach receptor Junctional fold Synaptic vesicle containing acetylcholine (ACh) Synaptic cleft (space) Motor end plate (a) Neuromuscular junction (b) Enlarged view of the neuromuscular junction (c) Binding of acetylcholine to ACh receptors in the motor end plate Synaptic end bulb Neuromuscular junction (NMJ) Synaptic end bulb Motor end plate Nerve impulse Muscle action potential is produced Na+ 2 3

Action at NMJ Release of acetylcholine (ACh) Diffuses across cleft Activation of ACh receptors Generation of Muscle Action Potential Repeats with each neuronal action potential Breakdown of ACh

Contraction Trigger Muscle action potential → Ca2+ release from Sacroplasmic Reticulum (SR) Ca2+ binds to troponin → Moves tropomyosin off actin sites → Myosin binds & starts cycle

Contraction Cycle Myosin binds to actin & releases phosphate group (forming crossbridges) Crossbridge swivels releasing ADP and shortening sarcomere (power stroke) ATP binds to Myosin → release of myosin from actin ATP broken down to ADP & Pi → activates myosin head to bind and start again Repeats as long as Ca2+ concentration is high

Relaxation Breakdown of ACh to stop muscle action potentials Ca2+ ions transported back into SR lowering concentration → This takes ATP Tropomyosin covers actin binding sites

ACh diffuses across synaptic cleft, binds to its receptors in the motor end plate, and triggers a muscle action potential (AP). Nerve impulse arrives at axon terminal of motor neuron and triggers release of acetylcholine (ACh). Synaptic vesicle filled with ACh ACh receptor Acetylcholinesterase in synaptic cleft destroys ACh so another muscle action potential does not arise unless more ACh is released from motor neuron. Ca2+ Muscle action potential Nerve impulse SR Contraction: power strokes use ATP; myosin heads bind to actin, swivel, and release; thin filaments are pulled toward center of sarcomere. Troponin–tropomyosin complex slides back into position where it blocks the myosin binding sites on actin. Muscle relaxes. Ca2+ active transport pumps Ca2+ release channels in SR close and Ca2+ active transport pumps use ATP to restore low level of Ca2+ in sarcoplasm. Ca2+ binds to troponin on the thin filament, exposing the binding sites for myosin. Muscle AP travelling along transverse tubule opens Ca2+ release channels in the sarcoplasmic reticulum (SR) membrane, which allows calcium ions to flood into the sarcoplasm. Elevated Ca2+ 1 2 3 4 9 5 6 7 8 Transverse tubule

Muscle Tone Even at rest some motor neuron activity occurs = Muscle Tone Keeps muscle in a state of readiness If nerves are cut fiber becomes flaccid (very limp)

Production of ATP for Muscle Contraction

Aerobic Cellular Respiration Production of ATP in mitochondria Requires oxygen and carbon substrate Produces CO2 and H2O and heat.

Fatigue Inability to contract forcefully after prolonged activity Limiting factors can include: Ca2+ Creatine Phosphate Oxygen Build up of acid Neuronal failure

Oxygen Use After Exercise Convert lactic acid back to glucose in liver Resynthesize creatine phosphate and ATP Replace oxygen removed from myoglobin

Control of Muscle Contraction Single action potential(AP) → twitch Smaller than maximum muscle force Total tension of fiber depends on frequency of APs (number/second) Maximum = tetanus Total tension of muscle depends on number of fibers contracting in unison Increasing numbers = Motor unit recruitment