muscular system. outline i.skeletal muscle structure ii.muscle contraction: cell events iii.muscle...

Muscular system

Outline

I. Skeletal Muscle Structure II. Muscle Contraction: Cell EventsIII. Muscle Contraction: Mechanical EventsIV. Muscle MetabolismV. Types of Skeletal Muscle FibersVI. Smooth and Cardiac Muscles

Outline

I. Skeletal Muscle Structure II. Muscle Contraction: Cell EventsIII. Muscle Contraction: Mechanical EventsIV. Muscle MetabolismV. Types of Skeletal Muscle FibersVI. Smooth and Cardiac Muscles

1- Skeletal Muscle Structure

– Muscle fibers extend length of muscle from tendon to tendon

Motor units

• Motor unit: Composed of one motor neuron and all the muscle fibers that it innervates

• There are many motor units in a muscle

• The number of fibers innervated by a single motor neuron varies (from a few to thousand)

• The fewer the number of fibers per neuron the finer the movement (more brain power)

• Which body part will have the largest motor units? The smallest?

Components of a muscle fiber

Figure 12.2 (2 of 2)

Muscle fiber components

• Sarcolemma: muscle cell membrane

• Sarcoplasma: muscle cell cytoplasm

• Motor end plate: contact surface with axon terminal

• T tubule: cell membrane extension into the sarcoplasm (to reach the myofibrils)

• Cisternae: areas of the ER dedicated to Ca++ storage (located on each side of the T-tubules)

• Myofibrils: organized into sarcomeres

The sarcomere

• The myofibrils are organized into a repetitive pattern, the sarcomere

• Myosin: thick filament• Actin: thin filament• Bands formed by pattern: A

and I and H bands• Z line: area of attachment

of the actin fibers• M line: Myosin fiber centers

Figure 12.5d

The sarcomere

Myosin structure

• Many myosin molecules per filament, golf club shape

• Long tail topped by a thickening: the head forms crossbridges with the thin filament

• Presence of the enzyme, ATPase in the head release energy for contraction

Figure 12.4

Actin structure

• Formed by 3 different proteins:

- globular (G) actins - tropomyosin: long, fibrous

molecule, extending over actin, and preventing interaction between actin and myosin

- troponin: binds reversibly to calcium and able to move tropomyosin away from the actin active site

Outline

I. Skeletal Muscle Structure II. Muscle Contraction: Cell EventsIII. Muscle Contraction: Mechanical EventsIV. Muscle MetabolismV. Types of Skeletal Muscle FibersVI. Smooth and Cardiac Muscles

Figure 11.13

2- Muscle contraction: Cell events

Synaptic events• The AP reaches the axonal

bulb• Voltage-gated calcium

channels open• The influx of calcium in the

bulb activates enzymes the vesicles containing the neurotransmitter molecule dock and release the neurotransmitter in the synapse

• The neurotransmitter for skeletal muscles is always acetylcholine

• The receptors on the muscle fiber are cholinergic receptors

• These receptors are nicotinic (fast) acting receptors

2- The Mechanism of Force Generation in Muscle

Figure 12.7

Figure 12.6

• http://www.blackwellpublishing.com/matthews/myosin.html

• http://www.ebsa.org/npbsn41/intro_muscle.html

Muscle relaxation• Ach is removed from the

receptors by acetylcholinesterase• Ligand-gated Na+channels close• Na/K pumps reestablish the RMP• Ca++ ions leave troponin and are

brought back into the cisternae (this process needs energy)

• Tropomyosin moves back over the actin active site

• The myosin heads release their binding to actin

• The filaments passively move back into resting position

Applications• Myasthenia gravis: autoimmune disease where antibodies against the Ach

receptors are produced. Which consequences do you expect?

• Muscular dystrophy: some proteins forming the muscle fibers are abnormal. Which consequences do you expect?

• Curare binds to the Ach receptor without activating them. What are the effect of curare on the skeletal muscle?

• The botulism toxin prevents the release of the neurotransmitter into the synapse. What will be the consequence?

• Nerve gas inhibits acetylcholinerestase present in the synapse. What will be the consequence?

•

• Rigor mortis: why does the body stiffen shortly after death?

Outline

I. Skeletal Muscle Structure II. Muscle Contraction: Cell EventsIII. Muscle Contraction: Mechanical EventsIV. Muscle MetabolismV. Types of Skeletal Muscle FibersVI. Smooth and Cardiac Muscles

3- Muscle contraction: Mechanical events

• 1 stimulation 1 twitch

• Muscle twitch: 3 phases: - latent phase - contraction phase - relaxation phase

☻ do not confuse the AP and the twitch!!!

Figure 12.16

Events during the twitch• Latent phase: Stimulus to

beginning contraction: AP to myosin binding to actin active site

• Contraction phase: beginning to end of muscle tension myosin heads slide along the actin filaments

• Relaxation phase: peak tension to no tension Ca++ ions moved back into the cisternae, tropomyosin moves back over actin, myosin head release actin and the filaments move back into resting position

Figure 12.17

Summation and tetanus

• Summation: Rapid sequence of stimuli muscle twitches fuse into each other, each subsequent one being stronger that its precedent (due to Ca++?)

• Tetanus: very rapid sequence of stimuli: no relaxation

Outline

I. Skeletal Muscle Structure II. Muscle Contraction: Cell EventsIII. Muscle Contraction: Mechanical EventsIV. Muscle MetabolismV. Types of Skeletal Muscle FibersVI. Smooth and Cardiac Muscles

IV- Muscle metabolism• Muscle fibers use ATP (only first

few seconds) for contraction• ATP must then be generated by

the muscle cell: - from creatine phosphate, first - from glucose and glycogen - from fatty-acids

ATP formation from the above compound is possible if oxygen is present (oxidative phosphorylation: 36 ATP per glucose)

Oxygen is delivered to the muscle by myoglobin, a molecule with high affinity to oxygen and related to hemoglobin

Figure 12.11

If the effort is strong and sustained, the muscle might not have enough oxygen delivered to it by myoglobin anaerobic glycolysis with only 2 ATP formed per glucose and synthesis of lactic acid

Consequence of anaerobic metabolism?

Effects of exercise on the muscle

• Aerobic exercises: long sustained exercises promote increased oxidative capacity of the muscle fiber increased blood vessel supply, increased mitochondria

• High intensity, short burst exercise: increased glycolytic activity increased synthesis of glycolytic enzymes, increased synthesis of myofibrils (increased muscle size)

Outline

I. Skeletal Muscle Structure II. Muscle Contraction: Cell EventsIII. Muscle Contraction: Mechanical EventsIV. Muscle MetabolismV. Types of Skeletal Muscle FibersVI. Smooth and Cardiac Muscles

Figure 12.23

V- Types of Muscle Fibers• Various muscles contract at different speed

composed of different types of muscle fibers

Basis for classification

• Velocity of contraction: slow vs fast• Energy source: oxidative vs glycolytic

Oxidative Glycolytic

Use O2 to synthesize new ATP

– Red– Small diameter– Resistant to fatigue

Store ATP for immediate use

– Large diameter– Quick to fatigue– Pale color

• Which types of meat are chicken breast and duck breast?

• Why the difference?

Outline

I. Skeletal Muscle Structure II. Muscle Contraction: Cell EventsIII. Muscle Contraction: Mechanical EventsIV. Muscle MetabolismV. Types of Skeletal Muscle FibersVI. Smooth and Cardiac Muscles

VI- Smooth and Cardiac Muscles

Main Body muscles

Muscles of the face

• For facial expression• Attached to a bone and

to skin

Muscles of the anterior trunk

• Transverse oblique• Rectus abdominis

Intercostal musclesDiaphragm

Muscles moving the shoulder

• Trapezius• Latissimus dorsi• Erector spinae

Muscles moving the upper and lower arm

• Pectoralis major• Deltoid

Biceps brachiiTriceps brachii

Muscles moving the thigh• Psoas• Gluteus

Muscles moving the lower legs

• Quadriceps femoris • Biceps femoris

Muscles moving the foot

• Gastrocnemius

• Achille’s tendon (not a muscle)

Pathology

• Sprain / strain• Muscular dystrophy• Myasthenia gravis• Insecticide poisoning• Botox• Achille’s tendon rupture

Myasthenia gravis

• Antibodies attack Ach receptors

• Progressive weakness and paralysis

• No cure

Muscular dystrophy

• Due to a defective protein

• Progressive muscle weakness and paralysis

• No cure

Achilles’s tendon rupture