properties of muscle contractility –ability of a muscle to shorten with force excitability...

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 MuscleFour 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 FilamentsMyosin - 2 heavy chains, 4 light chains

• Heavy chains - 230 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 Ca2+ channel

DHPR

DHPR = dihydro-pyridine receptor

Ca2+

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 ReceptorIn 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 Ca2+ channel

• In skeletal muscle, DHP receptor is apparently a voltage-sensing protein and probably undergoes voltage-dependent conformational changes

Ryanodine ReceptorThe "foot structure" in terminal cisternae of SR

• Foot structure is a Ca2+ channel of unusual design

• Conformation change or Ca2+ -channel activity of DHP receptor apparently gates the ryanodine receptor, opening and closing Ca2+ channels

Ca2+ Controls Contraction

• Release of Ca2+ from the SR triggers contraction

• Reuptake of Ca2+ into SR relaxes muscle

• So how is calcium released in response to nerve impulses?

• Answer has come from studies of antagonist molecules that block Ca2+ channel activity

This gap is actually only

~10 nm.

Ca2+-ATPase

Function of Neuromuscular Junction

acetate + cholineNa+

- -

+ +

end-plate potential (EPP)

~ -15 mV

~ -15mV+ + + + +– – – – –

~ +40mV

Summation of skeletal muscle tension; tetanus

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, [Ca2+] 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 Ca2+.

– 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.

Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings.

Cardiac Muscle

Figure 12.37

Treppe

• Graded response• Occurs in muscle rested

for prolonged period• Each subsequent

contraction is stronger than previous until all equal after few stimuli