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How A Muscle Fiber Contracts????
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.
Sliding of the thin filaments toward the center of the sarcomere causes the unit to shorten or contract.
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.
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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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.
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.
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
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
the muscle fiber must then rely on other mechanisms to convert ADP to ATP
Energy Stored as
Utilised through
Initial Quantity
ATP CP
3 mmol 20 mmol
2 sec 15 sec
Glycogen
Glycolysis (anaerobic)
Aerobic metabolism
100 mmol
670
12,000
130 sec
2400 sec (40 min)
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
Muscle Recovery
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;
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????