Muscular tissue

Ch. 11

Universal Characteristics of Muscle• Responsiveness (excitability)

• Conductivity

• Contractility

• Extensibility

• Elasticity

Mechanical tension used to:1) produce movement

 

2) maintain body position

 

3) regulate organ volume

sphincters regulate outflow of organ contents.

4) generate heat to maintain body temperature

 

5) propel fluids and food material through compartments

Skeletal Muscle: Voluntary, striated, neurogenic muscle

Series and parallel elastic components

a myofiber

Figure 11.3a

Figure 11.3b

Figure 11.3c

Figure 11.4

The sliding filament theory

Figure 11.6b

Motor end plate

Muscle Contraction & Relaxation

• Four phases involved in this process– excitation where action potentials in the nerve lead to

formation of action potentials in muscle fiber.– excitation-contraction coupling: an action potential

on the sarcolemma leads to contraction.– contraction is shortening of muscle fiber (or at least

generation of tension).– relaxation is return of fiber to its resting length or

tension.

Components of excitation-contraction coupling

• Acetylcholine (the neurotransmitter)

• Acetylcholine receptors (ligand-gated ion channels)

• Acetylcholinesterase

• Voltage-gated channels

• Calcium

• Ca++ ATPase

• Troponin, tropomyosin, and myosin

• ATP

Excitation (steps 1 & 2)

• Voltage-gated calcium channels open triggering exocytosis of acetylcholine (ACh) from synaptic vesicles.

Excitation (steps 3 & 4)

• Binding of ACh opens Na+ and K+ channels resulting in an end-plate potential (EPP)

Excitation (step 5)

• Voltage change in end-plate region (EPP) opens nearby voltage-gated channels producing an action potential.

Excitation-Contraction Coupling(steps 6&7)

• Action potential spreads over sarcolemma and down into T tubules causing SR calcium gates to open.

Excitation-Contraction Coupling(steps 8&9)

• Calcium causes binding of myosin to active sites on actin.

Contraction (steps 10 & 11)

• Myosin head with an ATP molecule bound to it initiates contraction- hydrolysis of ATP to ADP cocks the head of the myosin.

• Cocked myosin binds to actin

Contraction (steps 12 & 13)

• Power stroke; then a new ATP is bound resulting in release of myosin from actin.

Relaxation (steps 14 & 15)

• Acetylcholinesterase breaks down ACh in synaptic cleft.

Relaxation (step 16)

• Active transport (Ca++ ATPase) pumps calcium back into SR

Relaxation (steps 17 & 18)

• Loss of calcium from sarcoplasm results in removal from troponin, hiding of active sites and relaxation.

Length-Tension Curve

Production of Variable Contraction Strengths

• 1. Recruitment of motor units. – Stimulation of more motor units by the CNS produces

a stronger contraction.– Experiment: Stimulating a nerve with higher voltage

(an artificial process) produces a stronger contraction.• Mimics activation of more motor units by brain.

• 2. Stimulate the muscle at higher frequencies (stimuli/sec)– Each muscle fiber produces a stronger contraction

when stimulated repeatedly.

Figure 11.6a

• Fine control– small motor units contain as few as

20 muscle fibers per nerve fiber (eye muscles)

• Strength control– Big muscles may have 1000 fibers per nerve fiber

(gastrocnemius muscle)

Motor unit recruitment:

Experiment: expose a nerve and stimulate it with an electrical charge while measuring strength of muscle contraction.

Fig. 8-16, p.330

Effects of stimulation frequency on contraction strength

Isometric & Isotonic Contractions

Fig. 8-20, p.334

Muscle Contraction Phases

• Isometric: Tension (red) builds even though the weight is not moving

• Isotonic: Length (blue) begins to change, muscle maintains the same tension from then on.

Sources of ATP for muscle contraction

Figure 11.18

Long-Term Energy

• After 40 seconds of exercise, aerobic respiration– oxygen consumption rate increases for first 3-4

minutes & then levels off to a steady state– ATP production keeps pace with demand

• Limits are set by:– depletion of glycogen & blood glucose– loss of fluid and electrolytes through sweating– little lactic acid buildup occurs – Fatigue: inability to contract further

Types of skeletal muscle fibers• Red muscle fibers (slow oxidative):

– Less powerful, fatigue resistant• high myoglobin content

• lots of mitochondria

• lots of blood capillaries

• White muscle fibers (fast glycolytic):– High power output, fatigues quickly

• lower myoglobin content

• fewer mitochondria

• fewer blood capillaries

Figure 11.19

Smooth Muscle

• Fusiform cells with one nucleus– no visible striations, sarcomeres or Z discs– thin filaments attach to dense bodies scattered

throughout sarcoplasm & on sarcolemma– Not much SR, & has no T tubules

• calcium for contraction comes from extracellular fluid

• Autorhythmic; may be myogenic or neurogenic.• Nerve supply is autonomic, if any is present.• May respond to local conditions- chemicals and

stretch etc.

Figure 11.20

Figure 11.23

Slow, efficient, and fatigue resistant

• Contraction & relaxation very slow in comparison to other muscle types

• Little influence of length on tension

• Uses l0-300 times less ATP to maintain the same tension– latch-bridge mechanism maintains tetanus (muscle

tone) with little energy expenditure.– keeps arteries in state of partial contraction

(vasomotor tone)– Does not fatigue easily

Cardiac Muscle

• Autorhythmic, myogenic

• Uses aerobic respiration almost exclusively.

• Action potential is sustained.

• Does not fatigue easily

Cardiac Muscle

Regeneration of muscle tissues:Ability differs between types of muscle tissue.

• Cardiac muscle cells: no repair or replacement of damaged cardiac muscle cells.– repair occurs by fibrosis– cardiac muscle fibers can undergo hypertrophy.

Skeletal muscle:

• some repair of damaged muscle fibers can occur through actions of satellite cells and cells from red bone marrow.

– can’t repair significant loss of muscle fibers.– repair occurs by fibrosis.– can occur through disuse (disuse atrophy)– Followed by hypertrophy of remaining cells.

Smooth muscle cells:

– hypertrophy– cell division of existing smooth muscle cells – new cells form from pericytes