Biomechanics Flashcards
Motor unit and the role of neurotransmitters in stimulating skeletal muscle contraction
The central nervous system and the motor neurons connect with the muscles to send messages from brain to muscle in order to contract.
The motor neuron is the deliverer of that message.
DENDRITES: The tentacles that receive that information that’s being sent down the central nervous system.
CELL BODY.
NUCLEUS: Where the cell’s activities are coordinated and calculated.
AXON: Long transportation device. Can be between 2 cm and 1 meter. The impulse travels through here. It travels down through the ACTION POTENTIAL method (electrical, meaning this potential has not happened yet). Sodium ions and potassium ions interact with each other to transport this impulse down the axon.
AXON TERMINAL: end point before it branches off somewhere else.
SYNAPTIC END BULBS: They are attached to a muscle. They are a part of the NEUROMUSCULAR JUNCTION.
NEUROMUSCULAR JUNCTION
It involves the Synaptic end bulb, the muscle itself and the receptors that sit on the muscle tissue.
This Action potential has traveled down the axon. It has now depolarized the Synaptic end bulb.
Calcium ions gates have opened and have rushed in the Synaptic end bulb and they have pushed sacks containing ACETYLCHOLINE towards the end of the Synaptic end bulb. It has merged into the membrane and acetylcholine rushes into the Synapse and it finds the receptors to sit on, of the muscle.
These receptors are vital because they allow the Sodium ions into the muscle cell and this transports the impulse from the neuron into the muscle.
So, the calcium ions allow the acetylcholine to enter the synapse, they attach to the receptors and sodium ions can rush into the muscle cell.
Acetylcholine is a neurotransmitter that allows the impulse to pass from the neuron into the muscle. Binds the receptors on the muscle cells.
When this needs to stop, CHOLINESTERASE is released. Catabolic reaction. It catalyzes acetylcholine so it can no longer bind receptors. No impulse can pass across into the muscle. No more muscle contraction.
The Synaptic end bulb depolarizes, the neuromuscular junction depolarizes and this allows the acetylcholine to sit on the receptors to allow sodium ions into the muscle cell which triggers the start of the SLIDING FILAMENT THEORY.
The sliding filament theory
The skeletal muscle contracts by this theory.
“Prison break” analogy:
Releasing hundreds of inmates.
Get into the prison.
Get to each cell.
Open each cell door at once.
Release all of these inmates.
Five defendants. They are responsible for different aspects of the prison break.
EXHIBIT A:
Sodium ions.
Potassium ions.
Calcium ions.
Acetylcholine.
Depolarization of the motor end plate.
Where the acetylcholine is released from the Synaptic end bulb across the synapse, sits onto the receptors, the sodium receptors on the muscle cell, allowing a rush of sodium ions into the muscle to allow the muscle Action potential to go further into the muscle to SARCOMERES.
Cholinesterase:
Covers the tracks of the acetylcholine, so it is undetectable.
Breaks down the acetylcholine, so no more contraction can occur from that moment on.
EXHIBIT B:
SARCOPLASMIC RETICULUM
This sits around the muscle fiber. The muscle fiber is attached to the neuron. Every single filament and myofibril within that muscle fiber is stimulated by this impulse, and the weight stimulated by this impulse is how it is transported around the muscle fiber. The sarcoplasmic reticulum sits around the outside of the muscle fiber, so the impulse can spread to every myofibril within that muscle fiber.
T-TUBULES
They go on the length ways of each myofibril. Every sarcomere can be impacted by the sodium ions released into the muscle fiber.
EXHIBIT C:
SARCOMERE
Each sarcomere is separated, this is why a muscle is striated in color. Each end of a sarcomere can be seen.
EXHIBIT D:
MYOFILAMENTS = ACTIN AND MYOSIN.
Which are within the myofibril within the sarcomere.
The section in the middle: When the muscle contracts, the H zone disappears as the actin and myosin pull over each other.
The Z-disk on the side of each sarcomere also shortens as each sarcomere shortens, and when each sarcomere in the whole muscle fiber shortens, the whole muscle shortens, and therefore we have a concentric contraction.
EXHIBIT E:
TROPONIN and TROPOMYOSIN.
Bodyguards. The aim is to move them out of the way, so that the actin and myosin can access each other.
CHAIN OF EVENTS.
Depolarisation of the motor end plate.
Action potential from the neuron into the muscle, in order for the muscle to be stimulated.
Acetylcholine is released, assisted by calcium ions, which is triggered by the influx of sodium ions into the motor end plate which depolarizes it and allows the acetylcholine to pass into the synapse, sit on the receptors, allowing sodium ions into the muscle.
In the muscle cell: MUSCLE ACTION POTENTIAL. All or nothing. The whole of that muscle fiber will either be stimulated or not stimulated at all.
It will spread throughout the muscle cell, traveling around the sarcoplasmic reticulum, and the sodium passes down the t-tubules until it arrives at each and every sarcomere in each myofibril.
Get rid of troponin and tropomyosin, the bodyguards.
We allow the calcium ions in there, the calcium ions bind with the troponin, which is connected to the tropomyosin, so when a protein binds with something, the shape changes. So, the calcium ions bind with the troponin and change the shape of the troponin and tropomyosin. This allows them to move out of the way, exposing the active sites of the actin for the myosin to grab hold of them.
Taking the bodyguards out of the cell block, unlocking the cell gates and allowing all of the cell mates to escape.
Cross Bridge.
Actin and myosin form together to create a Cross Bridge. This is where the myosin grabs hold of the actin and it is ready to initiate a power stroke. The power stroke comes when the atp releases the energy, turns it into adp + p, but the energy is released and this allows the slide to happen.
Then, the myosin lets go of the actin. As long as the atp is present, it can continue to do this again.
The power stroke pulls the actin filament past the myosin, shortening the sarcomere between the Z lines, the H zone disappears. This happens in every single sarcomere within the muscle fiber. That’s when we have a concentric contraction. This continues as long as there are enough calcium ions and atp present within the sarcomere, for this to take place. It will continue, and continue, and continue.
All of the inmates escape.
If this continues to happen we get muscular contraction until further notice.
SYNOPSIS:
Sodium and potassium interact with the axon depolarizing the motor end plate, calcium rush into the motor end plate, forcing acetylcholine to blend through the membrane into the synapse, sit on the receptors, open up the sodium ion gates, allowing sodium ions into the muscle. Cholinesterase breaks down the acetylcholine and no more sodium ions can pass into the muscle. This causes a muscle action potential. Sodium ions spread throughout the whole muscle fiber until they get to the sarcomeres where they release calcium ions once more. Calcium ions allow the change of shape to the troponin which in turn changes the tropomyosin as well. This reveals the active site of the actin. As long as calcium ions and atp is present, we can keep creating the Cross Bridge, we can keep creating the power strokes and we can keep shortening the sarcomere. This continues until the calcium ions or atp are not present and then there is no more muscular contraction and we can stop.
Slow and fast twitch fibers: Structure and function
Muscle fiber RECRUITMENT.
The neuron is attached to each of the muscle fibers. So the sliding filament theory will occur in each four of the muscle fibers. If an action potential was initiated, the bigger the recruitment, the more forceful the outcome. The smaller the recruitment, the less force. More resistance to fatigue so it can go a longer duration.
SLOW TWITCH FIBERS/TYPE 1 are slower, more steady contraction. Is not going to generate all the power, but it is going to last longer. They are called OXIDATIVE FIBERS, because oxygen is present within that muscular contraction.
The muscle fibers that are attached to the neuron are a small motor unit. There are not too many fibers attached.
Large capillary density, if we have more capillaries we have more oxygen, passing through into the muscle by gaseous exchange.
Very large mitochondrial density.
High oxidative capacity, because oxygen is required. Atp takes place in the mitochondria for aerobic respiration. Therefore, the density is high.
Low glycolytic capacity: capacity to use glycogen.
Very high resistance to fatigue, because of the oxidative capacity.
Low force production, because of the size of the motor unit and it recruits less muscle fibers. Jog, not sprint. One feels the muscles less when jogging because less muscle fibers are being recruited.
Distance events, duration sports.
Triglycerides.
FAST TWITCH FIBERS.
TYPE 2B FIBERS: Explosive fibers, no oxygen present, big, powerful, short contraction.
Very large size of motor unit. One needs all the help one can get. It recruits as many as possible.
Low mitochondrial density. No oxygen required.
Low capillary density.
Low oxidative capacity.
High glycolytic capacity. Glycogen and glucose is the main fuel source, so the capacity to use that is high.
Low resistance to fatigue. Low mitochondrial, capillary and oxidative capacity. No oxygen.
Very high force production, because the motor unit is large. Therefore, we generate a forceful contraction and movement.
Activity used for short sprints, explosive actions.
The fuel source is CP and glycogen.
TYPE 2A FIBERS: A love child of type 2b fiber and slow twitch fiber. Oxidative glycolytic fiber type.
Large size of motor unit. Not as large as type 2b.
Large mitochondrial density. Not as large as the type 1. It has some oxidative capacity.
Large capillary density. Oxygen is required.
High oxidative capacity.
High glycolytic capacity. Glycogen is used as the source.
Medium resistance to fatigue. Not as much as type 1. Lactic acid will build up, but it has got some resistance to fatigue.
High force production. Not as much as type 2b.
Activity used for 400m, 800m, prolonged anaerobic outbursts. You cannot go 100% for that long.
Fuel sources are fats and glycogen.
An athlete does not have just one type. There are going to be certain muscles within his body that are dominated by a type.
Movement of synovial joints
FLEXION: Flexion is forwards. Takes place at the hinge joint and the ball and socket joints.
Elbow and knee (hinge).
Hip and shoulder (ball and socket).
EXTENSION: Backwards. After flexing, it is necessary to go back to the starting position, by extending. If not, stuck. Takes place at hinge joints and ball and socket joints.
Knee and elbow (hinge).
Hip and shoulder (ball and socket).
The shoulder can go backwards. Hyper extension.
ABDUCTION: Lateral movement. Movement away from the midline. Ball and socket joint.
Shoulder and hip (ball and socket).
ADDUCTION: Lateral movement. Movement towards the midline. After abduction, getting back to the starting position. Back in.
Shoulder and hip back to the midline (ball and socket).
CIRCUMDUCTION: A combination of flexion, extension, abduction and adduction. Drawing a big circle with an arm or leg. Hip and shoulder.
Butterfly technique.
ROTATION: The joint rotates.
Football kick.
Spin bowler in cricket. Rotate shoulder as the ball releases from the hand.
Swimming backstroke. Rotate at the top of the little finger to enter the water first.
ELEVATION: Referring to the neck. When one elevates the shoulders, the trapezius muscles are contracting at the back.
DEPRESSION: Going back to the starting position.
PLANTARFLEXION: Feet, hinge joint. Go onto the tiptoe.
DORSIFLEXION: Gets the feet back to the starting position. Also from the starting position, like a ski jumper. Pushing forward.
INVERSION: Inside line of the food, big toe, is pointing inwards towards the midline. Hinge joint. Subtalar and transverse tarsal joints.
EVERSION: When the big toe and inside of the foot start to move outwards. Hinge joint. Away from the midline. Outside of the foot is slightly elevated off the ground. Subtalar and transverse tarsal joints.
SUPINATION: When the palm of the hand faces the sky.
Forehand topspin (tennis). From a pronated position to a supinated position.
PRONATION: When the palm of the hand faces the ground.
Backhand topspin: from a supinated to a pronated position.
Types of muscle contraction
ISOTONIC
CONCENTRIC: Constrict, reduce. Bicep curl. Muscle is contracting as the joint angle is decreasing, shortening.
ECCENTRIC: Elastic, lengthening. Muscle is under stress whilst it is lengthening. Bicep curl. The bicep is still the prime mover. It looks like the elbow is extending. The bicep is eccentrically contracting.
ISOKINETIC
Help with speed, strength and speed of recovery.
Not accessible for everybody. Technology and professionals required.
During a bicep curl, there is a peak in pressure and stress on the muscle and there is a low. This does not happen in isokinetic. Is a clever machine that can make sure the pressure is consistent throughout the range of moment and also that the contraction itself is at the same speed, causing that pressure on the movement, too.
ISOMETRIC
No movement at the joint. No shortening or lengthening of muscles under tension. Same dimension, same length during tension whilst they are contracting.
Plank.
Ski sit.
Holding out dumbbells in a T position.
Reciprocal inhibition
Working in tandem to stop something from working.
Working in tandem: ANTAGONISTIC MUSCLE PAIRS.
Two opposite muscles that work together where one contracts and one relaxes.
An AGONIST (flexes) and ANTAGONIST (extensor). They can both contract but not at the same time. One of them is inhibited.
In a bicep curl, the bicep is the flexor and agonist and the tricep is the extensor, antagonist. The bicep contracts and shortens to cause flexion at the elbow. Whilst this happens, the tricep muscle relaxes and lengthens (extends). Tricep contracts to cause extension.
This can be the other way around.
Movements in relation to joint action and muscle contraction
PLANTARFLEXION: GASTROCNEMIUS muscle contracts, bring up to the tiptoes.
DORSIFLEXION: TIBIALIS ANTERIOR causes it at the ankle joint.
FLEXION (Knee): Caused by the HAMSTRING muscle contracting, reducing the joint angle behind the leg.
EXTENSION (Knee): Caused by the QUADRICEP. Allow to return to anatomical position.
FLEXION (Hip): Caused by PSOAS MAJOR (ILIOPSOAS).
EXTENSION (hip): Caused by GLUTEUS MAXIMUS. It contracts to extend the hip.
FLEXION (Elbow): Caused by the BICEP contracting.
EXTENSION (Elbow): Caused by the TRICEP contracting.
FLEXION (Shoulder): Caused by the DELTOID. ANTERIOR DELTOID.
EXTENSION (Shoulder): Caused by LATISSIMUS DORSI.
ABDUCTION (Shoulder): Caused by LATERAL DELTOID.
ADDUCTION (Shoulder): aSSISTED by PECTORALIS MAJOR.
Delayed onset muscle soreness (DOMS) in relation to eccentric and concentric muscle contraction
Microscopic damage to sarcomeres has been linekd to delayed onset muscle soreness.
1. Strenous muscular contractions damage the sarcomeres. Damage is also caused to the sarcoplasmic reticulum membrane in the muscle.
2. Calcium leaks out of the sarcoplasmic reticulum and collects in the mitochondria, the power house of the cell. Then, the muscle canot produce as much ATP, the body’s immediate energy soyrce or fuel, as it should. This buildup of calcium also activates enzymes which breakd own the proteins necessary for muscle contraction.
3. Membrane damage combined with the breakdown of muscle proteins results in inflammation, or swelling, and increased histamine (chemical that causes inflammation) and free production, which stimulates pain receptors and results in the sensation of muscle pain.
DOMS is prevented/minimized by reducing the eccentric component of muscle actions during early training, starting training at a low intensity and gradually increasing the intensity, and warming up before exercise, cooling down after exercise.
Delayed Onset of Muscle Soreness (DOMS) tends to occur as soon as 6-8 hours post-exercise, and peaks around the 48 hour mark.
Delayed Onset of Muscle Soreness (DOMS) tends to occur as soon as 6-8 hours post-exercise, and peaks around the 48 hour mark.
DOMS results primarily from eccentric muscle action and is associated with structural muscle damage, inflammatory reactions in the muscle, overstretching and overtraining.
In eccentric actions, large loads are supported by a smaller cross-sectional area than in concentric contractions.
Unaccustomed loads cause excessive muscle tension resulting in microscopic damage. After a few hours, neutrophils and macrophages accumulate around the injury site.
The products of macrophage activity and intracellular contents stimulate free nerve endings in the muscle.
The symptoms (swelling, stiffness, soreness, etc) start being obvious from 24 hours post-exercise.
Scalar and vector
Scalar: Quantity with magnitude.
Example: The mass of an object. It only has size.
Vector: Quantity with magnitude and direction.
Example: Weight. Weight is mass times the gravity force. That is pulling downwards giving a direction. 75 kg mass is 700 Newtons.
Distance
The length of the space between two points. It is measured in meters. It is a scalar.
Displacement
The action of moving an object from its position. From an object’s start place to the object’s finish. Measured in meters. Vector.
100 meter race: distance and displacement are both 100 meters. Straight line.
If the race is four laps, 400 meters in total, the distance is 400 meters but the displacement is 0. Because the athlete finished at the start point.
Force
An interaction that will change the motion of a body. Measured in Newtons. It is a vector.
Weight and gravity are a force measured in Newtons. Other forces could be a push, a pull, air resistance.
There are many forces that will interact with an object and change the motion of that object.
Speed
The rate at which an object travels a distance. Meters per second. Scalar.
Velocity
The rate at which an object travels a distance with direction. Meters per second. Vector.
Acceleration
The rate of change of velocity in a unit of time. Meters per second per second. Vector.
If an athlete’s velocity is 30 meters per second when running a race, it was not like that throughout the whole race. Firstly, it was 10, then 20 meters per second. They accelerated.
