HOW A MUSCLE FIBER CONTRACTS????

Sarcomeres = functional units of a skeletal muscle fiber. Each myofibril contains thousand of sarcomeres The thick filaments lie in the center of the sarcomere. The thin filaments are attached to either end of the sarcomere & extend toward the center & passing among the thick filaments. The arrangement of thin & thick filaments within sarcomere produces the striped appearance of a myofibril.

As a results, the entire muscle fiber has banded/striated appearance.

Sliding of the thin filaments toward the center of the sarcomere causes the unit to shorten or contract.

This explaination of muscle contraction is called the sliding filament model.

What causes filament sliding????

Sliding occurs after the cross-bridges, or head of the thick filaments attach to the thin filaments. Each cross-bridges then pivots at its base, pulling the thin filaments towards the center of the sarcomere. This pivoting, shortens the sarcomere is called a power stroke. A molecule of ATP must bind to the myosin head before it can detach from the thin filament; the ATP will be used for the next power stroke.

What triggers a contraction???????????? Cross-bridges formation can occur only in the presence of calcium ions (Ca2+). Ca2+ - stored in the endoplasmic reticulum of the muscle fiber. Ca2+ - released into sarcoplasm when 1/> electrical impulses travel across the muscle fibers, in response to the arrival of neurotransmmiter at the motor end plate. Ca2+ - pumped back into endoplasmic reticulum as soon as the impulse/s ceased. this active process required ATP. The muscle contraction ends when Ca2+ level in sarcoplasma return to normal low level. Each time ATP is broken down, some energy is released as heat. Muscle contractions release large amount of heat responsible for maintaining body temperature.

WHAT IS RIGOR MORTIS??

When death occurs, circulation stops, and the skeletal muscles are deprived of nutrients and oxygen. Within a few hours, the skeletal muscle fibers have run out of ATP, & the endoplasmic reticulum becomes unable to remove Ca2+ from sarcoplasm. Ca2+ diffusing into the cell from the extracellular fluid or leaking out of their storage area then trigger a sustained contraction. Without ATP, the myosin cannot detach from the cross-bridges, and the muscles locks in the contracted position. All the bodys skeletal muscles are involved, and the individual becomes stiff. This physical state, called rigor mortis, lasts until the muscle fibers begin to decompose 15 25 hour later.

CONTRACTION OF SKELETAL MUSCLE

contract only under the control of the nervous system Communication between the nervous system and a skeletal muscle fiber occurs at neuromuscular junction (NMJ), or myoneural junction

The Neuromuscular Junction (NMJ) Each skeletal muscle fiber is controlled by a neuron at a single NMJ A single axon branches and ends at an expanded synaptic terminal

The cytoplasm of the synaptic terminal contains mitochondria and vesicles filled with molecules of acetylcholine (ACh).
ACh trigger the contraction of the muscle fiber. A narrow space, the synaptic cleft, separates the synaptic terminal of the neuron from the opposing sarcolemmal surface. This surface (motor end plate), contains membrane receptors that bind ACh. The synaptic cleft and sarcolemma also contain the enzyme acetylcholinesterase (AChE), or cholinesterase, which breaks down ACh.

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(1)

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Interference With Neural Control Mechanisms

Bacteria, Spiders, Snakes & U

What do the bacteria {Clostridium botulinum}, black widow spiders, cobras and humans have in common??????

They all produce toxins, that attack the chemical synaptic transmission which occurs at NMJ

Botulism is caused by the neuro- toxin botulin, which is produced by the growth of C. botulinum in improperly canned foods.
"Botulism comes from the Latin word for "sausage' because of the early association of the disease with poorly preserved meat Botulin is a very potent blocker of neuromuscular transmission; As few as 10 molecules of the toxin are enough to inhibit a cholinergic synapse. It is believed that botulin inhibits the release of ACh at the NMJ, leading to a potentially fatal muscular paralysis

Black widow spider venom also exerts its deadly effects by affecting transmitter release.
The venom first increases, and then eliminates, ACh release at the neuromuscular junction

The bite of the cobra also results in the blockade of neuromuscular transmission in its victim.

The active compound in the snake's venom, called cobratoxin, is a peptide molecule that binds tightly to the postsynaptic receptors and prevents their activation by ACh.

Humans have synthesised a large number of chemicals that poison synaptic transmission at the neuromuscular junction. Originally motivated by the search for chemical warfare agents, this effort led to the development of a new class of compounds called organophosphates. These are irreversible inhibitors of AChE, and by preventing the degradation of ACh, they probably kill their victims by causing a desensitisation of ACh receptors. The organophosphates used as insecticides, like parathion, are toxic to humans only in high doses.

Myasthenia gravis
Myasthenia gravis is an autoimmune disease [cause is a misguided attack on the ACh receptors by the immune system] Results in the loss of ACh receptors at the junctional folds

The name is derived from the Greek for severe muscle weakness.
The disorder is characterised by weakness and fatigability of voluntary muscles, typically including the muscles of facial expression, and it can be fatal if respiration is compromised.

ENERGY SOURCES FOR CONTRACTION

A single muscle fiber contain ~ 15 billion thick filaments. When actively contracting, EACH thick filament breaks down ~ 2500 ATPs/sec Even a small skeletal muscle contains thousands of muscle fibers, the ATP demands of a contracting skeletal muscle are enormous.

the demand for ATP in a contracting muscle fiber is so high

A resting muscle fiber contains only enough ATP and other high-energy compounds to sustain a contraction until additional ATP can be generated. During contraction, the muscle fiber will generate ATP at the same rate as it is used.

ATP and Creatine Phosphate (CP) Reserves At rest, a skeletal muscle fiber produces more ATP than it needs. Under these conditions, ATP transfers energy to creatine to form another highenergy compound, CP, or phosphorylcreatine:

ATP

muscle relaxed

Creatine

creatine phosphokinase (CPK)

ADP
** [CPK]blood serious muscle damage **

Creatine phosphate

During a contraction, each myosin cross-bridge breaks down ATP, producing ADP and a phosphate group. The energy stored in creatine phosphate is then used to "recharge" ADP, converting it back to ATP through the reverse reaction:

Creatine
creatine phosphokinase

ATP

Creatine phosphate

ADP Contracting muscle

Energy for muscle contraction

A resting skeletal muscle fiber contains ~ 6X as much CP as ATP.

When a muscle fiber undergoing a sustained contraction, these energy reserves are exhausted in only about 17 sec.

the muscle fiber must then rely on other mechanisms to convert ADP to ATP

Aerobic metabolism [ in mitochondria] Other mechanisms

Glycolysis [in cytoplasm] (anaerobic)

Anaerobic metabolism Aerobic metabolism

Produce 17 ATPs/molecule fed/cycle

produce 36 ATPs / glucose molecule

{2 ATP in glycolysis + 2 pyruvic acid in aerobic metabolism (34ATP)}

Sources of Energy Stored in a Typical Muscle Fiber

Energy Stored as

Utilised through

Initial Quantity

Number of Twitches Supported by Each Energy Source Alone 10 70

Duration of Contraction Supported by Each Energy Source Alone

ATP CP

ATP ADP + P ADP + CP ATP + C

3 mmol 20 mmol

2 sec 15 sec

Glycogen

Glycolysis (anaerobic)
Aerobic metabolism

100 mmol

670
12,000

130 sec
2400 sec (40 min)

Anaerobic energy production has its drawbacks:

When glycolysis produces pyruvic acid faster than it can be utilised by the mitochondria, pyruvic acid levels rise in the sarcoplasm. Under these conditions, the pyruvic acid is converted to LACTIC ACID.

lactic acid -

lower the intracellular pH. Changes in pH will alter the functional characteristics of key enzymes. The muscle fiber will then become unable to continue contracting

Muscle Fatigue A skeletal muscle is considered fatigued when it can no longer contract, despite continued neural stimulation. Can be due to : exhaustion of ATP and CP reserves

drop in pH {buildup of lactic acid}

interruption in blood supply/lack of neurotransmitter (rare)

Muscle Recovery

When a muscle fiber contracts:Energy reserves consumed

Heat released
lactic acid generated

In the recovery period, conditions inside the muscle fibers gradually returned to normal, preexertion levels. It may take several hours to a week

During recovery period, the bodys O2 demand increases. The extra O2 is used by mitochondria in;

HEPATOCYTES ATP is required for conversion of lactic acid to glucose

MUSCLE FIBERS
ATP is needed to restore ATP & glycogen reserves

The additional O2 required during recovery period is called the oxygen debt. How to pay????

the rate & depth of breathing