Case 9 Flashcards
what are the cells of the bone?
Bone contains four types of cells: Osteocytes, Osteoprogenitor cells (stem cells), Osteoblasts (osteogenesis) and Osteoclasts (osteolysis).
what are osteoprogenitor cells? what do they do?
- These are mesenchymal stem cells that divide and differentiate into osteoblasts.
- These maintain populations of osteoblasts and are important in the repair of a fracture.
- Osteoprogenitor cells located in the periosteum and the bone marrow (endosteum).
what are osteoblasts? what do they do?
- These originate from osteoprogenitor cells.
- Form new bone matrix in a process called osteogenesis. In other words, osteoblasts form the osteoid, which is then calcified into bone.
- Osteoblasts also assist in the calcification of osteoid into bone.
- As osteoblasts surround themselves with extracellular matrix, they become trapped in their secretion and become osteocytes.
what is osteogenesis?
- Osteoblasts secrete collagen molecules and ground substance (extrafibrillar matrix – gel-like substance surrounding the collagen molecules).
- Collagen molecules combine to form collagen fibres.
- The resultant tissue is called osteoid (non-calcified bone).
- Hydroxyapatite crystals form on the collagen fibres. The osteoid is now calcified and this is bone.
what are osteocytes? what do they occupy? what do they do?
- These are mature bone cells that cannot divide.
- Each osteocyte occupies one lacuna, occupying layers called lamellae.
- Lamellae are connected by canaliculi, providing nutrients from the central canal.
- If released from their lacunae, osteocytes can convert to a less specialized type of cell, such as an osteoblast or an osteoprogenitor cell.
what are osteoclasts? what are they derived from? what do they do?
- Derived from granulocyte/monocyte progenitor cells.
- Multinucleated cells involved in bone resorption (bone removal and recycling).
- Osteoclast membrane secretes enzymes which dissolve the matrix and release the stored minerals into the blood stream.
- This process is called osteolysis, this process is important in the regulation of calcium and phosphate concentrations in body fluids.
what is a myofibril? what is it composed of? how organised?
• Myofibril (muscle fibril) – is a basic rod-like unit of muscle.
• They are composed of long proteins such as actin, myosin and titin, and other proteins that hold them together.
• These proteins are organised into thin filaments and thick filaments, which repeat along the length of the myofibril in sections called sarcomeres.
Thin filaments are actin.
Thick filaments are myosin.
light bands
- what do they contain
- what are they called
- contain only actin filaments (+ Z discs)
- called I bands
dark bands
- what do they contain
- what are they called
- contain myosin filaments + actin filaments (where they overlap the myosin)
- called A bands
what are the ends of the actin filaments attached to?
a Z disc
what does the Z disc do?
The Z disc passes crosswise across the myofibril and also crosswise from myofibril to myofibril, attaching the myofibrils to one another all the way across the muscle fibre. Therefore, the entire muscle fibre has light and dark bands, as do the individual myofibrils. These bands give skeletal and cardiac muscle their striated appearance.
what is a sarcomere?
the portion of the myofibril that lies between two successive Z discs
what are the spaces between the myofibrils filled with? what does this comprise of?
sarcoplasm
• It comprises of: Significant amounts of myoglobin, an oxygen-binding molecule. Potassium, magnesium, phosphate ions. Sarcoplasmic reticulum Protein enzymes
• Mitochondria lie parallel to myofibrils.
what is titin?
- One end of the titin molecule is elastic and is attached to the Z disc, acting as a spring and changing length as the sarcomere contracts and relaxes.
- The other part of the titin molecule tethers it to the myosin thick filament.
what does actin consist of? (+ what is wrapped around it) and the function of different components?
- The backbone of the actin filament is a double-stranded F-actin protein molecule.
- Each strand is composed of G-actin molecules.
- Attached to each one of the G-actin molecules is one molecule of ADP – The active site.
• Tropomyosin is wrapped spirally around the sides of the F-actin helix.
• In the resting state, the tropomyosin molecules lie on top of the active sites of the actin strands so that attraction cannot occur between the actin and myosin filaments to cause contraction.
• Attached intermittently along the sides of the tropomyosin molecules are troponin.
Troponin I has a strong affinity for actin
Troponin T has a strong affinity for tropomyosin
Troponin C has a strong affinity for calcium ions.
- This complex is believed to attach the tropomyosin to the actin.
- The strong affinity of the troponin for calcium ions is believed to initiate the contraction process.
myosin
- what made up of
- what different components do
- what are cross-bridges
• The myosin filament is made up of many individual myosin molecules.
• Myosin molecules are composed of a head, neck and tail.
The myosin head binds the actin filament.
The myosin head functions as an ATPase enzyme.
The myosin neck acts as a linker and as a lever arm for transducing force generated by the motor domain.
The myosin neck can also serve as a binding site for myosin light chains, which have regulatory functions.
The myosin tail connects the myosin head to the body of the myosin molecule.
• The protruding tails and heads together are called cross-bridges.
Each cross-bridge is flexible at two points called hinges - one where the tail leaves the body of the myosin filament, and the other where the head attaches to the tail.
There are no cross-bridge heads in the centre of the myosin filament because the hinged tails extend away from the centre.
• The myosin filament itself is twisted so that each successive pair of cross-bridges is axially displaced from the previous pair by 120 degrees. This ensures that the cross-bridges extend in all directions around the filament.
describe what happens at the neuromuscular junction and after that
- Impulse (action potential) arrives at axon terminal.
- Ca2+ ions rush in (as action potential activated Ca2+ gates); Ca2+ reacts with synaptic vesicles.
- Synaptic vesicles fuse with cell membrane of axon terminal.
- ACh (acetylcholine) released through a process known as exocytosis.
ACh is synthesised in the axon terminal through the use of ATP. - ACh binds with motor end plate receptors: depolarization occurs as Na+ rushes into the muscle cell, causing an end plate potential (EPP).
ACh is destroyed by acetylcholinesterase. - Impulse travels through T-tubules which excite the sarcoplasmic reticulum (SR).
- Ca2+ ions released from the SR.
- Ca2+ binds with troponin.
- Shift of tropomyosin, which makes the binding sites available for myosin S1 units to bind.
- ATPase splits (hyrolysis) ATP = ADP + Pi + Energy
- Myosin can now bind to active sites on actin.
- Sliding action of actin over myosin called the Power Stroke.
- Impulse stops to muscle; calcium ions pumped back into SR by Ca2+ (active transport) pumps.
- Tropomyosin returns over the active sites on actin and muscle action ceases.
why is the normal neuromuscular junction said to have a high safety factor? what is fatigue of the neuromuscular junction?
- Each impulse that arrives at the neuromuscular junction causes about three times as much end plate potential as that required to stimulate the muscle fibre.
- Therefore, the normal neuromuscular junction is said to have a high safety factor.
- However, continuous stimulation of the nerve fibre at great rates diminishes the number of acetylcholine vesicles so much that impulses fail to pass into the muscle fibre. This is called fatigue of the neuromuscular junction.
what is resting membrane potential in skeletal fibres?
about -80 to -90 millivolts
what is a motor end plate?
- A motor nerve fibre forms a complex of branching nerve terminals that invaginate into the surface of the muscle fibre but lie outside the muscle fibre plasma membrane.
- The entire structure is called the motor end plate.
- It is covered by Schwann cells that insulate it.
- motor end-plate is the specialised part of muscle fibre where motor neurone innervates
describe excitation-contraction coupling
• When an action potential passes over muscle membrane, the action potential spreads to the interior of the muscle fibre along the membranes of the transverse (T) tubules.
• This action potential results in two effects:
1. The T tubule action potentials act on the membranes of the longitudinal sarcoplasmic tubules to cause release of calcium ions into the muscle sarcoplasm from the sarcoplasmic reticulum, resulting in contraction.
2. Calcium-induced calcium release:
• The T tubule action potentials also open voltage-gated calcium channels in the membranes of the T Tubules themselves, which causes calcium ions to diffuse directly into the sarcoplasm.
• The diffusion of calcium ions activates calcium release channels, also called ryanodine receptor channels, in the sarcoplasmic reticulum membrane of the longitudinal sarcoplasmic tubules.
• This triggers the release of calcium ions from the sarcoplasmic reticulum into the sarcoplasm.
• Calcium ions in the sarcoplasm then interact with troponin to initiate cross-bridge formation and contraction.
• This is called calcium-induced calcium release.
what would happen without extra calcium from the T tubules? what does strength of contraction of muscle depend on?
- Without this extra calcium from the T tubules, the strength of muscle contraction would be reduced considerably.
- The strength of contraction of muscle depends to a great extent on the concentration of calcium ions in the extracellular fluids.
what happens at the action potential (after excitation-contraction coupling)?
At the action potential, the influx of calcium ions to the interior of the muscle fibre is suddenly cut off, and the calcium ions in the sarcoplasm are rapidly pumped back out of the muscle fibres (via the Na+/Ca2+ exchanger) into both the sarcoplasmic reticulum (SERCA Ca2+ pumps) and the T tubule–extracellular fluid space through the plasma membrane (PMCA Ca2+ pumps), stopping contraction or it is stored in the sarcoplasmic reticulum.
how do the cross-bridges affect force of contraction? what is the reason for this?
- Each one of the cross-bridges is believed to operate independently of all others, each attaching and pulling in a continuous repeated cycle.
- Therefore, the greater the number of cross-bridges in contact with the actin filament at any given time, the greater the force of contraction.
describe what causes muscular contraction (power stroke)?
- the hydrolysation of ATP into ADP and inorganic phosphate allows the myosin head to return to the resting position
- ADP + Pi are bound to myosin as myosin head attaches to actin
- ADP + Pi release causes head to change position and actin filament to move
- binding of ATP causes myosin head to detach from the actin filament
- Attached state -> ATP binds to myosin head, causing the dissociation of the actin-myosin complex ->
- Released state -> ATP is hydrolysed, causing myosin heads to return to their resting conformation ->
- Cocked state -> a cross-bridge forms and the myosin head binds to a new position on actin ->
- Cross-bridge state -> phosphate is released – myosin heads change conformation, resulting in the power stroke – the filaments slide past each other ->
- Power-stroke state -> ADP is released ->
- Attached state
what happens to the sarcomere during contraction?
H & I bands shorten
A bands stay the same size
what is summation in muscular contraction?
Summation occurs in two ways:
By increasing the number of motor units contracting simultaneously, which is called multiple fibre summation.
By increasing the frequency of contraction, which is called frequency summation and can lead to tetanisation (sustained muscle contraction?).
what is the size principle?
- As the synaptic activity driving a motor neuron pool progressively increases, low threshold S motor units are recruited first, then FR motor units, and finally, at the highest levels of activity, the FF motor units.
- As a result, this systematic relationship has come to be known as the size principle.
why is there an asynchronous motor unit drive?
The different motor units are driven asynchronously (not occuring at the same time) by the spinal cord, so contraction alternates among motor units one after the other, thus providing smooth contraction even at low frequencies of nerve signals.
what are the different types of muscle contraction?
• Isometric muscle contraction – when the muscle does not shorten during contraction. The length of the muscle remains unchanged.
E.g. pushing against a wall.
• Isotonic muscle contraction – when the length of the muscle shortens but the tension on the muscle remains constant throughout the contraction.
• Concentric muscle contraction – in the direction of contraction of a muscle (towards origin of muscle).
• Eccentric muscle contraction – in the opposite direction of contraction of a muscle (towards insertion of muscle).
isotonic contractions are either concentric (working muscle shortens) or eccentric (working muscle lengthens)
Muscles contract better at their optimum length – most of our muscles are maintained within this optimum range most of the time
Contraction is stronger and faster the closer the muscle initial length is to the optimum length
muscle contraction results in energy expenditure during what?
Interaction of actin and myosin filaments during contraction.
Pumping of Ca2+ from the sarcoplasm back into the sarcoplasmic reticulum after contraction.
Restoration of the intracellular ionic environment after muscle contraction because of the actions of the Na+/K+ pump.
how is ATP generated for long activity?
Oxidative phosphorylation
This type of phosphorylation is an aerobic process in which ATP is liberated from fats, carbohydrates, and protein.
how is ATP generated for heavy activity?
Anaerobic glycolysis
This causes the breakdown of glucose to lactate and pyruvate with the release of energy.
This energy is used to convert ADP to ATP.
ATP is generated at double the rate of oxidative phosphorylation.
This is predominant in type II muscle fibres that have few mitochondria but many glycogen granules.
This is only an intermediate-term source of energy, because lactate and pyruvate accumulate in the cell.
how is ATP generated of intense activity?
• Creatine phosphokinase
Phosphocreatine contains high-energy phosphate bonds, which can be used to phosphorylate ADP to ATP by the enzyme creatine kinase.
It is located in the Z line.
• Myokinase
The enzyme myokinase catalyses the transfer of a phosphate group from one ADP molecule to another to form ATP and the by-product adenosine monophosphate (AMP).
This is known as the ‘last gasp’ of short-term energy stores.
oxidative phosphorylation
- occurs in which types of fibres
- what is it
- how much ATP
- how fast
- Occurs in slow twitch and intermediate type of fibres.
- Reduction of O2 into H20 using electrons from NADH and FADH2.
- Occurs on the inner mitochondrial membrane.
- Explained by the principle of the chemiosmotic theory.
- Involves a series of “downhill” electron transfers – exergonic.
- Energy used to drive protons through the inner membrane.
- Transmembrane chemical + electrical difference drives ATP synthesis.
- 38 ATP molecules produced per molecules of glucose
- But quite a slow process – plentiful but slow
substrate-level phosphorylation
- occurs in which types of fibres
- what is it
- how much ATP
- how fast
- Occurs in fast twitch type of fibres.
- Direct formation of ATP by phosphorylation of ADP.
- Produced by reaction with high free energy.
- These reactions do not require oxygen, therefore, it is important in tissues short of oxygen (e.g. skeletal muscles).
- Produces 2 ATP molecules
- Limited supply of ATP but fast
what happens in normal and intense muscular contraction? - what converted to what, requiring ATP via what, how much ATP, how fast is process?
- In normal muscular contraction, glucose is converted into pyruvate and then CO2.
- This requires ATP via oxidative phosphorylation.
- There is plentiful ATP but the process is slow.
- In intense muscular contraction, glycogen in converted into glucose and then lactate.
- This requires ATP via substrate level phosphorylation.
- There is limited ATP but the process is fast.
- Oxygen and nutrient supply is rate limiting.
• Muscle glycogen reserves are finite and lactate is a problem.
Oxygen is used by liver to produce glucose from lactate – Cori Cycle.
• But muscle still needs a rapid method to produce ATP from ADP.
ATP and creatine are produced from ADP and Phosphocreatine via the enzyme creatine kinase.
what is fibre hypertrophy?
muscle hypertrophy results from an increase in the number of actin and myosin filaments in each muscle fibre
increase in size of fibres?
• Along with the increasing size of myofibrils, the enzyme systems that provide energy also increase. This is especially true of the enzymes for glycolysis, allowing rapid supply of energy during short-term forceful muscle contraction.
what is fibre aplasia?
The rate of synthesis of muscle contractile proteins is far greater when hypertrophy is developing. In turn, some of the myofibrils themselves have been observed to split within hypertrophying muscle to form new myofibrils.
hyperplasia = increase in number of fibres
when does muscle atrophy occur? what is the pathway?
When a muscle remains unused for many weeks, the rate of degradation of the contractile proteins is more rapid than the rate of replacement.
Therefore, muscle atrophy occurs.
The pathway that appears to account for much of the protein degradation in a muscle undergoing atrophy is the ATP-dependent ubiquitin-proteasome pathway.
Proteasomes degrade damaged or unneeded proteins by proteolysis.
Ubiquitin is a regulatory protein that labels which cells will be targeted for proteasomal degradation.
describe the adjustment of muscle length
When muscles are stretched to greater than normal length, new sarcomeres are eventually added at the ends of the muscle fibres, where they attach to the tendons.
This increases the length of muscles.
muscle denervation
- what does loss of innervation to a muscle result in
- what happens after about 2 months
- what happens if the muscle is once again innervated
- what happens in the final stage of denervation atrophy
- what are the fibres that remain like
- Loss of innervation to a muscle results in atrophy.
- After about 2 months, proteasome degradation begins to occur, causing further muscle wastage.
- If the muscle is once again innervated, then there can be full recovery within 3 months.
• In the final stage of denervation atrophy, most of muscle fibres are destroyed and replaced by fibrous and fatty tissue.
This fibrous tissue has a tendency to continue shortening for many months, which is called contracture.
• The fibres that do remain are composed of a long cell membrane with many muscle cell nuclei but with few or no contractile properties and little or no capability of regenerating myofibrils if a nerve does regrow.
when do macromotor units form? what do they effect?
- When some but not all nerve fibres to a muscle are destroyed, the remaining nerve fibres branch off to form new axons that then innervate many of the paralyzed muscle fibres.
- This causes large motor units called Macromotor units.
- This decreases the fineness of control one has over the muscles but does allow the muscles to regain varying degrees of strength.
what can exercise increase (cellular level)?
Exercise can increase muscle mitochondrial biogenesis (i.e. gives more mitochondria per muscle cell).
This is probably via Ca2+ signalling pathways in the cell as well as via a chronic imbalance of ATP demand versus ATP production by mitochondria which causes activation of signalling protein kinases.
- Acute exercise initiates higher levels of mRNA, as observed during the recovery period following exercise
- The protein products of the mRNA are imported into pre-existing mitochondria, or be incorporated into multi-subunit complexes of the respiratory electron transfer chain
- The result is the expansion of the mitochondrial network within muscle cells and the capacity for aerobic ATP provision
- The chain of events becomes impaired with chronic inactivity and aging, which leads to a reduced muscle aerobic capacity and an increased tendency for apoptosis (driven by cytochrome-c leakage from the mitochondria)
- The resumption or retention of an active lifestyle can ameliorate this, improve endurance, and help maintain muscle mass in older age
AMPK - what does it do?
AMPK – adenosine monophosphate-activated protein kinase:
This enzyme plays a role in cellular energy homeostasis.
This is the ‘fuel gauge of the cell’.
During a bout of exercise, AMPK activity increases while the muscle cell experiences metabolic stress brought about by an extreme cellular demand for ATP.
Upon activation, AMPK increases cellular energy levels by inhibiting anabolic energy consuming pathways (fatty acid synthesis, protein synthesis, etc.) and stimulating energy producing, catabolic pathways (fatty acid oxidation, glucose transport, etc.).
AMPK + AMP -> AMPK-P = important in slow twitch muscle
AMP -> IMP +NH3 = important in fast twitch muscle
what can lack of exercise lead to?
Skeletal muscle atrophy causes a drop in:
Protein levels, fibre diameter, force production, and fatigue resistance.
A reduction in protein synthesis coupled with increased protein degradation pathways contribute to muscle loss due to disuse.
Proteolytic pathways (ubiquitin-proteasome, lysosomal, and calpain) are involved in muscle atrophy.
Transcription factor NF-κB and myostatin are important cell signallers for muscle cell atrophy. Lack of exercise leads to increase in these factors in muscle.
what does the gait cycle consist of?
one cycle of swing and stance by one limb
describe the stance phase. which muscles are involved with each part of phase?
- Heel strike (initial contact) – Gluteus maximus and Tibialis anterior
- Loading response (foot flat) – Quadriceps femoris
- Midstance – Soleus and gastrocnemius (together known as Triceps surae)
- Terminal stance (heel off) – Soleus and gastrocnemius (Triceps surae)
describe the swing phase. which muscles are involved?
The swing phase begins after push off when the toes leave the ground and ends when the heel strikes the ground.
- Preswing (toe off) – Rectus femoris
- Initial and Midswing – Iliopsoas and rectus femoris
- Terminal swing – Hamstrings, Tibialis anterior and Ankle dorsiflexers
how much of the gait cycle does each phase occupy?
- Terminal swing – Hamstrings, Tibialis anterior and Ankle dorsiflexers
• The swing phase occupies approximately 40% of the walking cycle and the stance phase, 60%.
• The stance phase is longer because it features a period of double support as the weight is being transferred from one leg to the other.
In running, there is no period of double support.
most of the change in gait cycle time is due to shortening of what?
Most of the change in cycle time is due to shortening the stance phase; the swing phase remains relatively constant over a wide range of locomotor speeds.
what is controls the timing and coordination of complex patterns of movement and adjusts them in response to altered circumstances?
local circuits in the spinal cord called central pattern generators
what are different abnormal gaits?
- apraxic gait
- waddling gait
- crossing over/scissoring gait
- parkinsonian
- hemiplegic
- cerebellar ataxia
- sensory ataxia
describe apraxic gait
- Problem with cortical integration – frontal lobe damage (e.g. hydrocephalus, infarction).
- Acquired walking skills become disorganized.
- Shuffling small steps (marche a petit pas) may be seen here.
- Patient usually has small-stepping, broad-based gait.
- Patient almost seems to have forgotten how to walk.
describe waddling gait
- Muscle / hip disease.
- Patient bends their pelvis forward and walks with a waddle.
describe crossing over/scissoring gait
- Caused by bilateral spasticity.
- Patient may walk stiffly on toe.
- Patient has problems turning.
describe parkinsonian gait
- Small paces, slow and shuffling gait (similar to marche a petit pas)
- Stooped posture, reduced arm swing usually unilateral.
- Tremor may increase on walking.
- Basal ganglia dysfunction.
describe hemiplegic gait
- Unilateral upper motor neuron lesion - caused by MS or stroke
- Classically patient has a flexed upper limb and extended lower limb on the affected side.
- To move the affected limb patient has to circumduct the leg
describe cerebellar ataxia
- Broad-based gait, patient may sway from side to side, possibly fall
- Patient may appear drunk.
- Due to cerebellar lesion.
describe sensory ataxia
- Patient over flexes hip, lifts knee high and slaps foot down on walking
- This can occur in a patient with peripheral neuropathy (bilateral) or a common peroneal nerve lesion (unilateral)
- form of ataxia (loss of coordination) caused not by cerebellar dysfunction but by loss of sensory input into the control of movement
when the eyes are open, which three sensory systems provide input into the cerebellum to maintain truncal stability?
- vision
- proprioception
- vestibular sense
what is Romberg’s test?
• Ask the subject to stand with their feet together without support, first with their eyes open and then with their eyes closed.
• Closing the eyes eliminates vision.
If the proprioception and vestibular pathways are intact the subject will not sway.
If patient sways - Romberg positive.
If the subject sways with their eyes closed this indicted a defect in their proprioception pathways.
If the patient starts to sway with their eyes open or closed, this indicates a cerebellar lesion.
stress fracture
- what is it
- how is it caused
- who normally gets it
- symptoms
- diagnosis
- treatment
- A fracture occurring in normal bone that has been subject to excessive and repeated trauma resulting in cumulative microscopic fractures.
- Over time, these microfractures exceed the capacity of the normal healing process, resulting in the development of a macrofracture.
- Patients are usually long distance runners, ballet dancers, footballers, and others who undergo regular intensive training.
- Pain, localised tenderness, and swelling gradually develop.
- Initially x-rays are normal, but a bone scan or MRI will usually allow diagnosis to be made.
• Treatment – protected weight bearing, rest, cross-training, and (less common) surgery.
what is an orthosis?
a surgical device that exerts external forces on part of the body to support joints or correcting deformity
what is a hinged ankle foot orthosis?
- The hinged ankle foot orthosis (H.A.F.O) is a moulded plastic splint to stabilize the foot and ankle.
- It may allow full up and down movement of the foot or it may have a system that will restrict the amount of ankle movement.
- The orthotist will take a cast of the ankle to have one made specifically for the patient to meet their clinical needs.
• Different foot lengths are available, some finishing behind the ball of the foot, whilst others will have a full foot to toe end.
what is an osteophyte?
- These are bony projections that occur at the sites of cartilage degeneration or destruction near joints and intervertebral discs.
- They are usually shaped like a rose-thorn.
why do oestophytes form? what do the do?
- Osteophytes form because of the increase in damaged joint’s surface area.
- This is most common from the onset of arthritis.
- Osteophytes limit joint movement and typically cause pain.
• Osteophyte formation is related to sequential and consequential changes in bone formation that is due to aging, degeneration, mechanical instability, and disease.
anterior cruciate ligament sprain/tear
- how common
- who most common in
- men or women and why
- treatment
• One of the most common knee injuries is an ACL sprain/tear.
• Athletes who participate in high demand sports are more likely to injure it.
Higher incidence in females than males
This may be due to:
Physical conditioning
Muscular strength
Neuromuscular control
Pelvis size – females have wider hips and so working their legs will cause the vastus lateralis to develop more than the vastus medialis, thus pulling the patella laterally and causing the tear in the ligament.
Lower extremity (leg) alignment
Increased looseness in ligaments
Effects of oestrogen on ligament properties
• Surgery may be required to regain full function of knee.
• This will depend on several factors such as:
Severity of injury
Activity level
• Damage to other structures in the knee are secondary:
Articular cartilage
Meniscus
Other ligaments
which bones form the knee joint
femur, tibia, patella
• The kneecap sits in front of the joint to provide protection.
what are the 4 primary ligaments in your knee?
Collateral ligaments
Medial
Lateral - These control the sideways motion of the knee and brace it against unusual movement.
Cruciate ligament
Anterior – runs diagonally in middle of knee and prevents tibia from sliding out in front of femur as well as providing rotational stability of the knee
Posterior
o These are found inside the knee joint
o They cross each other to form an “X”
o These control the back and forth motion of the knee.
what are the causes of an ACL tear?
- Changing direction rapidly
- Stopping suddenly
- Slowing down while running
- Landing from jump incorrectly
- Direct contact or collision (football tackle)
what are the symptoms of an ACL tear?
• Pain with swelling:
Within 24 hours knee swells.
Swelling and pain may resolve on its own.
However, if sports are resumed, the knee will be unstable and there’s risk of further damage to the cushioning cartilage (meniscus).
• Loss of full range motion.
• Tenderness along joint line.
• Discomfort while walking.
what are the tests for an ACL tear?
A physical examination as well as an X-ray and MRI scan will be carried out:
Physical examination – doctor will compare injured knee with non-injured knee.
X-ray – although this will not show any injury to ACL, it can show whether the injury is associated with a broken bone.
MRI – shows images of soft tissues – ACL.
what is the treatment for an ACL tear?
Nonsurgical:
- Bracing
This protects the knee from instability.
Crutches may also be given to keep prevent weight on your leg.
- Physical therapy
As the swelling goes down rehabilitation program is started.
Specific exercises will restore function to knee and strengthen the leg muscles that support it.
First, returning motion to the joint and surrounding muscles is prioritised.
This is followed by strengthening program designed to protect the new ligament.
The final phase is aimed at a functional return tailored for the athlete’s sport.
Surgical:
- Rebuilding the ligament
Most ACL tears cannot be sutured back together - to surgically repair the ACL and restore knee stability, the ligament must be reconstructed.
The doctor will replace the torn ligament with a tissue graft.
This graft acts as a scaffolding for a new ligament to grow on.
It may take up to 6 months for recovery.
what is female athlete triad syndrome? who is it seen in? how serious is it? how does one aspect affect another?
Female athlete triad is a syndrome of 3 interrelated conditions which include:
Eating disorders (low energy availability)
Menstrual Dysfunction (Amenorrhoea)
Decreased bone mineral density (osteoporosis/ osteopenia)
- This is seen in females participating in sports that emphasise leanness or low body weight.
- The triad is a serious illness with lifelong health consequences and can potentially be fatal.
- Suffering from one element predisposes to suffering from the other 2 as well.
what are the signs and symptoms of female athlete triad syndrome?
• Clinical symptoms include: Disordered eating and fatigue Noticeable weight loss Increased healing time from injuries Increased incidence of bone fracture Cessation of menses • Affected females may also struggle with low self-esteem and depression.
• Signs include:
Restrictive eating but not meeting the clinical criteria for an eating disorder.
Subtle menstrual disturbances such as a change in menstrual cycle length, anovulation, or luteal phase defects, but not yet have developed complete amenorrhea.
Athlete’s bone density may decrease, but may not yet have dropped below her age-matched normal range.
describe how an eating disorder forms from FATS and how it affects other aspects in syndrome
• Energy is taken in through food consumption and our bodies expend energy through normal functioning as well as through exercise.
• In the case of the triad, low energy availability may be due to:
Eating disorders - low caloric intake
Excess exercise and same food intake
Increase energy expenditure while also eating less
• Having low dietary energy from excessive exercise and/or dietary restrictions leaves too little energy for the body to carry out normal functions such as maintaining a regular menstrual cycle or healthy bone density.
what are the two types of amenorrhoea?
Primary amenorrhoea, which is the absence of menstruation by the age of 16.
Secondary amenorrhoea, which is the absence of menstruation for 3 months in a woman who has previously had cycles.
what are the different causes of amenorrhoea?
Polycystic ovary syndrome, where the ovaries don’t release the egg (ovulate).
The hypothalamus stops producing GnRH (needed in menstruation).
This can be triggered by excessive weight loss and exercise as well as stress.
Abnormally high levels of prolactin (hyperprolactinaemia).
Premature ovarian failure, when to ovaries stop working before menopause.
- Weight fluctuations from dietary restrictions and/or excessive exercise affect the hypothalamus’s output of gonadotropic hormones.
- Gonadotropic hormones stimulate growth of the gonads and the secretion of sex hormones.
- These gonadotropic hormones play a role in stimulating oestrogen release from the ovaries.
- Without oestrogen release, the menstrual cycle is disrupted.
• Exercising intensely and not eating enough calories can lead to decreases in oestrogen:
The hormone that helps to regulate the menstrual cycle.
As a result, a female’s periods may become irregular or stop altogether.
osteoporosis
- what is it
- what causes it
- what link with athletes
• This is a skeletal disorder characterised by compromised bone strength predisposing a person to an increased risk of fracture.
• Low oestrogen levels + poor nutrition, especially low Ca2+ intake, can lead to osteoporosis
This condition may lead to stress fractures and other injuries.
- With oestrogen deficiency, the osteoclasts live longer and resorb more bone.
- As osteoclasts break down bone, patients see a loss of bone mineral density.
- Low bone mineral density renders bones more brittle and hence susceptible to fracture.
- Athletes are active and their bones must endure mechanical stress which means the likelihood of experiencing bone fracture is particularly high.
• In terms of diet, a deficiency in the intake of calcium or vitamin D further exacerbates the problem of weak bones.
shin splints
- what are they
- who are they common among
- what do they prevent
- what characterised by
- what causes them
- This is described as pain along the inner edge of the shinbone (tibia).
- They are a common injury affecting athletes who engage in running sports or other forms of physical activity.
- Most prevalent lower leg injury.
- It is characterised by general pain in the lower region of the leg between the knee and ankle.
- They are caused by repeated trauma to the connective muscle tissue surrounding the tibia.
what is pronation and how does it link to shin splints?
Pronation occurs when the ankle bone moves downward and towards the middle to create a more stable point of contact with the ground:
i.e. the ankle rolls inwards so that more of the arch has contact with the ground.
This abnormal movement causes muscles to fatigue more quickly and unable to absorb any shock from the foot hitting the ground.
Over-pronation is the common cause for shin splints and action should be taken to offset the biomechanical irregularity.
shin splints
- what is pain associated with shin splints caused by
- what do repetitive stress, impact forces do
- how is impact worsened
- treatment
- Pain associated with shin splints is caused from a disruption of Sharpey’s fibres that connect the medial soleus fascia through the periosteum of the tibia where it inserts into the bone.
- With repetitive stress, impact forces fatigue the soleus and create repeated tibial bending.
- The impact is worsened by running uphill, downhill, on uneven terrain or on hard surfaces.
- Improper footwear, including worn-out shoes can also contribute to shin splints.
- Treatments include resting, applying ice to shin to reduce (increase?) blood flow, elevation of legs reducing swelling and pain killers/anti-inflammatory.
what are the non-interactive theories of placebo effect?
• Characteristics of individuals
Certain individuals have characteristics that make them susceptible to placebo effects.
Characteristics include emotional dependency, extroversion, neurosis, being introverted and being highly suggestible.
• Characteristics of the treatment
This depends on the effectiveness of the placebo effect in the actual process involved in the placebo treatment.
For example, larger pill size, 2 pills instead of 1 and surgery have shown to be more effective in eliciting a change.
• Characteristics of the health professional
The kind of professional administering the placebo may determine the degree of placebo effect.
what are the interactive theories of the placebo effect?
- An examination of the processes involved in the interactions between patients, the treatment and the health professionals.
- There are mechanisms to understand this multidimensional process:
- Experimenter bias
This refers to the impact that the experimenter’s expectations can have on the outcome of a study.
I.e. the doctors expect me to get better. - Patient expectations
Suggests that most patients experience spontaneous recovery following illness as most illnesses go through periods of spontaneous change and that patients attribute these changes to the treatment. - Reporting error
Patients expect to show improvement following medical intervention, want to please doctor and therefore show inaccurate reporting by suggesting that they are getting better, even when their symptoms remain unchanged.
Doctors have also shown to report errors because they would like to see improvement in patients. - Conditioning effects
Patients associate certain factors with recovery and an improvement in their symptoms.
The conditioning theory states that the unconditioned stimulus (treatment) would usually be associated with an unconditioned response (recovery).
However, if this unconditioned stimulus (treatment) is paired with a conditioned stimulus (e.g. hospital, a white coat), the conditioned stimulus can itself elicit a conditioned response (recovery, the placebo effect). - Anxiety reduction
Placebos decrease anxiety and pain reduction, thus helping the patient to recover.
Relating this to the gate control theory, anxiety reduction may close the gate and reduce pain, whereas increased anxiety may open the gate and increase pain.
Placebos may decrease anxiety by empowering the individual and encouraging them to feel that they are in control of their pain.
what are the physiological theories of the placebo effect?
- Placebos increase endorphin (opiate) release – the brain’s natural painkillers – which therefore decreases pain.
- Evidence has been shown through the dependence, withdrawal and tolerance nature of placebos which is very similar to heroin; it also causes increased opiate release.
- Placebos work because the patient and the health professionals expect them to work.
- This emphasises the role of expectations and regards placebo effects as an interaction between individuals and between individuals and their environment.
• Cognitive dissonance theory
Cognitive dissonance is the mental stress or discomfort experienced by an individual who holds two or more contradictory beliefs, ideas, or values at the same time, or is confronted by new information that conflicts with existing beliefs, ideas, or values.
(e.g. your parents tell you at a young age that kids with blue eyes = bad, as you grow, you find out that they are just like you and so they aren’t bad at all……you experience cognitive dissonance as you are confronted with two contradictory views)
Cognitive dissonance leads to either a change in behaviour (you start playing with kids with blue eyes) or a change in attitude (you ignore kids with blue eyes).
This theory argues that faith healing has lasted and homeopathic medicines are still used because they work.
This is because time, effort and money is put into them and if they were readily available, they would not be as effective.
Investment is needed and an individual needs to:
Justify their behaviour.
See themselves as rational and in control.
Leon Festinger’s theory of cognitive dissonance focuses on how humans strive for internal consistency.
When inconsistency (dissonance) is experienced, individuals tend to become psychologically uncomfortable and they are motivated to attempt to reduce this dissonance, as well as actively avoiding situations and information which are likely to increase it.
This leads to a placebo effect – “this treatment will work because I have put time and money into it” (this is a change in attitude with regards to treatment)
• The theory is supported by the following:
It can explain all placebo effects, not just pain.
It does not require patient expectations, but choice.
It suggests the individual needing commitment to the medical procedure such as investment.
• Problems with this theory are:
Unconscious regulating mechanisms are not explained.
The theory has only been tested on acute pain in labs – not in real life.
Subjects have been provided with money and persuaded to justify behaviour which may have led to their increased anxiety and therefore pain perception.
Therefore, according to cognitive dissonance theory, dissonance can be resolved by the placebo having an effect on the individual’s health status by activating unconscious regulating mechanisms.
describe the link between health beliefs and the placebo effect and illness cognition and the placebo effect
Health beliefs
• For a placebo to have an effect, the individual needs to have a belief that the intervention will be effective.
• For example, taking a placebo as a prescribed pill will be more effective, as it is a traditional medical intervention, than a placebo in the form of herbal medicine which will only be effective if the patient believes in alternative medicines.
• Patients’ beliefs may themselves be a mechanism for explaining placebo effects such as having a direct effect on health through physiological changes, or an indirect effect via behavioural change.
Illness Cognition
• For a placebo to have an effect, the individual needs to hold particular beliefs about their illness.
• If an individual believes that their illness has a medical cause then a placebo in the form of a pill would be effective.
describe the role of health belief of health professionals in the placebo effect
- A doctor may need to believe in the intervention for it to have an effect.
- Theories of health professionals’ health beliefs and their role in doctor–patient communication illustrate a useful emphasis on interaction rather than individual characteristics.
describe the role of health-related behaviours in the placebo effect
- If an individual believes that they have taken something or behaved in a way that may promote good health, they may also change other health-related behaviours (e.g. smoking, drinking, exercise), which may also improve their health.
- The choice to take a medication may itself be seen as a health-related behaviour, and may be predicted by theories of behaviour and behaviour change.
describe the role of stress in the placebo effect
- If placebos have an effect either directly (physiological change) or indirectly (behaviour change) then this is in parallel with theories of stress.
- Placebos may function by reducing any stress caused by illness.
- If an individual has taken control of their illness (perceived control) this may reduce the stress response, reducing any effects this stress may have on the illness.
what is placebo-induced pain reduction is mediated by?
- Placebo-induced pain reduction may be mediated either by physiological changes, such as opiate release, or by anxiety reduction (gate control theory) which suggests that the experience of pain is a result of an interaction between psychological (beliefs, anxiety) and physiological (opiates) processes.
- Placebo-induced pain reduction may also be mediated by patient expectations and previous experience about the efficacy of the treatment intervention.
what is patient/agent-driven decision making?
- In this, the physician presents all options and the patient makes his/her own choice.
- The physician provides expert knowledge only and makes no recommendations.
what is physician recommendation decision making?
- The physician explains all the option and also makes a recommendation.
- The physicians must base their recommendations on the patient’s values rather than on their own.
- This can require time and advanced communication skills.
- When a patient asks the physician what he/she should do, the physician mist consider the patient’s perspective and ensure he/she is neither intentionally nor unintentionally coercive.
what are the different types of fracture?
- Greenstick fracture – incomplete fracture – the broken bone is not completely separated
- Stable fracture – the broken ends of the bone line up and are barely out of place
- Open, compound fracture – the skin may be pierced by the bone or by a blow that breaks the skin at them time of the fracture – the bone may or may not be visible in the wound
- Transverse fracture – has a horizontal fracture line
- Oblique fracture – has an angled pattern
- Spiral fracture – the break spirals around the bone; common in a twisting injury
- Comminuted fracture – the bone shatters into three or more pieces
- Compression – the bone is crushed, causing the broken bone to be wider or flatter in appearance
- Segmental – the same bone is fractured in two places, so there is a ‘floating’ segment of bone
patellofemoral pain
- what is it
- what causes it
- Patellofemoral pain syndrome is a broad term used to describe pain in the front of the knee and around the patella
- Sometimes called ‘runner’s knee’
- Symptoms are often relieved with conservative treatment, such as changes in activity levels or a therapeutic exercise programme
- Occurs when nerves sense pain in the soft tissues and bone around the patella
- It’s thought to be a result of stress on the joint between your patella and your thigh
Causes:
• Overuse
-vigorous physical activities that put repeated stress on the knee
-also caused by a sudden change in physical activity
• Patellar malalignment
-caused by abnormal tracking of the patella in the trochlear groove
-the patella is pushed out to one side of the groove when the knee is bent
-this abnormality may cause increased pressure between the back of the patella and the trochlear, irritating soft tissues
runner’s knee
- what is it
- what causes it
- what symptoms
- what can contribute to it
• Common term used to describe any of several conditions that cause pain around the patella
• These conditions include: anterior knee pain syndrome, patellofemoral malalignment, chondromalacia patella, and iliotibial band syndrome
• Running is a common cause, but any activity that repeatedly stresses the knee joint can cause the disorder
• More common in women than men, particularly middle age women
• Overweight individuals are especially prone
• The hallmark of runner’s knee is a dull, aching pain around or behind the patella, especially where it meets the lower part of the femur
• Other symptoms include swelling and popping or grinding in the knee
• May be caused by irritation of the soft tissues or lining of the knee, worn or torn cartilage, or strained tendons
• Any of following can contribute:
- Overuse
- Trauma to patella
- Misalignment of patella
- Completely or partial dislocation of patella
- Flat feet
- Weak or tight thigh muscles
- Inadequate stretching before exercise
- Arthritis
- Fractured patella
what is the SNARE hypothesis? link to toxins?
SNAREs (anchors in the vesicle membrane) = synaptobrevin, synaptotagmin
t-SNAREs (target membrane) = syntaxin, SNAP-25
- Long-endings that zipper together
BOTULINUM TOXIN (BOTOX)
- Enzymatically cleaves synaptobrevin (a SNARE protein involved in formation of the SNARE complexes) –> disrupts vesicle release -> muscles relax
- Disrupts SNARE (mediate vesicle fusion with their target membrane) complex formation
- Therapeutic application for cerebral palsy
TETANUS
- Neurotoxin produced by Costridium tetani in the soil
- Spreads through extracellular fluid and enters nervous system at NMJs – spreads retrogradely into CNS
- Cleaves synaptobrevin
- Particularly active on inhibitory neurons = no inhibition of motor neurons
what is the active zone?
- Specialised regions of the presynaptic terminal where vesicle release occurs
- These areas are complex and dynamic
- Main components: Ca2+ channel (Cac), Bruchpilot (Brp)
describe excitation of the postsynaptic muscle
- Acetylcholine release
- Binds to receptor (ligand-gated - ionotropic)
- Opens receptor
- Sodium moves into cell down concentration and electro-gradient
- Small change in membrane potential which activates voltage-gated sodium channels in the membrane
- They allow considerably more sodium in
- Which is enough to start an action potential in the muscle
- Action potential travels around muscle fibre at high speed
- Depolarisation around muscle
- Voltage-gated calcium channels open in response -> calcium-induce calcium release
- Calcium coming in acts on sarcoplasmic reticulum, where calcium floods out
acetylcholine
- where is it used
- synthesis
- Neurotransmitter at the mammalian NMJ
- Choline source = extracellular fluid
- Synthesis = ChAT (choline acetyltransferase) (one step)
- Choline + acetyl CoA –> ACh -> choline + acetic acid
- Cholinergic neurons = muscle and certain circuits in the PNS and CNS
acetylcholine receptors
- what are the different types
- influences what permeability
- how quick is effect
- names of each
Type: ionotropic (form an ion channel pore)
Signal: increase cations (Na+)
Effect: excitatory ‘FAST’
Type: metabotropic (indirectly linked with ion channels on the plasma membrane through signal transduction mechanisms, often G proteins, e.g. G protein-coupled receptors)
Signal: influences K+ permeability
Effect: mixed ‘SLOW’
Nicotinic receptor – ionotropic
Muscarinic receptor – metabotropic
how quickly is ACh degraded?
quickly
what is curare?
nACh receptor antagonist (weak and reversible)
- used as muscle relaxant
what is fitness? two types?
- Physically (and psychologically) able to meet the demands of your environment
- Two basic kinds of fitness:
- ‘health-related’
- ‘skill-related’ (usually task specific)
does glycolysis need oxygen?
no
does the process of aerobic respiration starting from eating food
Stage 1: food breakdown, gut
- Breakdown of large macro-molecules to simple subunits (amino acids, simple sugars e.g. glucose, fatty acids and glycerol)
Stage 2: glycolysis, absence of O2, cell cytoplasm
- Breakdown of simple subunits of acetyl CoA accompanied by production of limited ATP and NADH
Stage 3: aerobic respiration, cell mitochondria
- Complete oxidation of acetyl CoA to H2O and CO2 involves production of much NADH, which yields much ATP via electron transport
what percentage of fibre types in sprinters and long-distance runners?
Type II > 80% - sprinters
Type I >60% - long-distance runners
aerobic system
- what does it use
- what for
- training load
- training improves what
- Uses oxygen and fuel stores to provide energy
- For prolonged low to moderate intensity work
- Training load: stead-state exercise 30 minutes or longer
- Training improves oxygen transport from lungs to active muscles and removal of waste products
anaerobic (lactate) system
- what does it produce
- training load
- improved ability to do what
- No oxygen requirements – produces lactate
- Energy for short, sharp bursts of high intensity work (1-2 minutes)
- Training load: high intensity for about 2 minutes, incomplete rest + reps
- Improved ability to generate energy quickly and without oxygen, helps sustain high-intensity exercise due to improved tolerance and buffering/removal of muscle acid build-up
anaerobic (ATP-PC) system
- what produced
- what used
- training load
- improved ability to do what
- No oxygen requirements – no lactate production
- Uses creatine phosphate (phosphocreatine) to rapidly regenerate ATP from ADP
- Immediate high energy supply for a few seconds
- Training load: high intensity sprint interval for about 5-10 seconds, complete rest and re-charge + a few reps
- Improved ability and capacity to perform short-term maximal efforts
what happens during recovery? how do different training loads affect recovery?
- Stimulus – produces fatigue
- Compensation – recovery period – depends on what energy system using
- System recovers to be more efficient – have over compensation
- So, if you completely recovery and start training again, you can train them but not over fatigue them
Different training loads have different effects on the athlete’s recovery
- Training too easy you overcompensate slightly
- Training adequate you overcompensate a good amount
- Training too hard you don’t overcompensate
Principle of progressive overload – optimal improvement
what is a common marker of aerobic endurance ability?
- Common marker of aerobic endurance ability is VO2 max
- The rate of volume of oxygen consumption while working at maximum capacity ml O2/kg/min
- Thought to indicate innate ability to perform endurance sport
- Bad news is that can only be improved by no more than 15% with endurance training (individually variable)
- Men have higher VO2 max than women generally
VO2 MAX AT ALTITUDE
- 10% fall in VO2 max for every 1000m above 1200m
- If Everest was 20-50m higher, no human could reach the top without supplementary oxygen
- Best mountaineers do not have exceptional VO2 max at sea level
what is cardio-pulmonary exercise testing (CPeX)?
measuring ability to utilise oxygen
who do best from surgery?
those who have the greatest capacity to use oxygen
anaerobic threshold
- what is it
- when is it
- what like in olympic athletes
- Anaerobic threshold – when a small increase in oxygen consumption causes a big increase in CO2 production
- Appears to be where patients move from using their mitochondrial energy pathways to their glycolytic energy pathways
- Olympic athletes have a high aerobic threshold, they can go a long way before they start producing much more CO2
what are the following:
- actin
- tropomyosin
- myosin
- troponins
- alpha actinin
- titin
- myomesins
- vinculin
- cap-Z
- tropomodulin
- desmin
- dystrophin
- nebulin
- Actin: 40kD (kilodalton – measure of mass) globular protein that associates to form filaments. It is the major component of the thin filaments.
- Tropomyosin: thin filament structural component binding to actin
- Myosin: 200kD globular head coupled to long coiled-coil tail. Plus two 20kD light chains. Binds and hydrolyses ATP, undergoing a conformational change in the head.
- Troponins: globular proteins. Troponin I binds to actin & troponin-T, and inhibits the actin-myosin interaction unless calcium is bound to troponin-C
- Alpha-actinin: cross-links actin filaments at the sarcomere Z-line/disks
- Titin: very long filamentous protein, links Z-lines to M-lines
- Myomesins: bind to titin – generate hexagonal packing of thick filaments
- Vinculin: binds to alpha-actinin
- Cap-Z: caps the +ends of actin filaments at the Z-disk/line
- Tropomodulin: caps the -ends of the thin filaments
- Desmin: links together adjacent myofibrils at the Z-disk/line
- Dystrophin: links actin filaments to the muscle cell outer membrane (mutates or absent in Duchenne Muscular Dystrophy)
- Nebulin: determines the length of the thin filaments
are the fibres in a motor unit all the same type?
yes
type 1 fibres
- describe them
- contraction speed
- motor neurone
- Slow twitch or slow oxidative fibres
- Slow contraction speed (governed by a low myosin ATPase rate)
- These fibres allow steady activity and are resistant to depletion of energy reserves
- The motor neurone will have a constant low firing frequency
- These cells are designed for good supply of nutrients, having a high surface area- to- volume ratio and good access to nearby blood capillaries
- They also have abundant mitochondria (ATP generation) and myoglobin (oxygen capture and storage) and for this reason have a reddish colour and can sustain aerobic metabolism using fat as a source of energy for long periods
- Typical or marathon runners
describe type 2A fibres
- Fast oxidative-glycolytic fibres
- General-purpose type which are similar in most respects to slow twitch fibres
- They have a faster contraction speed and a higher myosin ATPase activity than type I
- They are still relatively resistant to fatigue and adapted to a good supply of energy sources, but will utilise glucose as well as fats
- They are more expensive to operate than type I and can be co-opted when needed, e.g. in a final burst of speed for the line
- Their motor neurones characteristically show bursts of activity, but intermittently
- Common in footballers
describe type 2B fibres
- Fast twitch- or fast glycolytic fibres
- They have the highest myosin ATPase activity
- They are specialised for short maximal force efforts and easily become short of energy
- These cells are not adapted for efficient exchange of nutrients and waste products, with low surface area to volume ratio (cells are larger) and with limited blood supply
- They have a paler colour because they contain fewer mitochondria and less myoglobin
- They can generate ATP by substrate-level phosphorylation (glucose -> lactic acid)
- These types of fibres predominate in a sprinter’s muscles
- Their motor neurones transmit occasional bursts of very high frequency impulses
which fibres does balancing a ball on your head use predominantly? eyeblink reflex?
fast twitch fibres in neck muscles to make rapidly his position to balance pall – precision movements are done by the fast twitch muscles
The type of skeletal muscle fibre involved in the eyeblink reflex is type 2B
which fibres generate heat?
slow twitch fibres
what is the role of the liver in muscle biochemistry?
- Muscle glycogen reserves are finite and increase lactate concentration is a problem
- Oxygen is used by liver to produce glucose from lactate -> Cori Cycle
- Liver ATP used to synthesise glucose (gluconeogenesis)
what energy conversion happens under maximum workload over time?
- ATP-PCr system used most at beginning
- Glycolysis then increases when this used up
- Then aerobic phosphorylation in creases over time, as glycolysis decreases
what conversions happen in light, heavy and intense activity?
FAs, ketones, glucose -> CO2 = light activity
Muscle glycogen -> lactate = heavy activity
ADP + Pi -> ATP, phosphocreatine -> creatine = intense activity
what does myokinase do?
ADP represents the ‘last gasp’ of the short-term energy stores
ADP + ADP – (myokinase)> ATP + AMP
- When ADP levels rise in the muscle cells, myokinase can produce one bit more ATP
what different energy sources are available?
- ATP in muscle already: 6.8 kJ
- Creatine phosphate in muscle: 14 kJ
- Muscle glycogen (-> lactate): 200 kJ
- Muscle glycogen (-> CO2): 2500 kJ
- Liver glycogen (-> CO2): 570 kJ
- All fats (-> CO2): 120,000 kJ
what is sprinting and longer distance running powered by?
- Sprinting is powered by ATP, creatine phosphate and glycolysis
- Longer distance running requires oxidative phosphorylation (mitochondria)
what is leptin? via what does it operate?
- involved in appetite and fat deposition
- may also operate via the AMPK signalling pathway
what are the target systems that lead to muscle loss? what are triggers/signals?
Target systems:
- Decrease protein synthesis rate
- Increase protein degradation rate
Triggers & signals: - Akt - mTORr - p70S6kinase - 4E-BP1 (all above lead to decrease protein synthesis rate) - Glucocorticoids - Myostatin - NF-kappaB - Reactive oxygen species (above can target both systems)
which types of muscle are striated?
skeletal and cardiac
how do levels of calcium affect contraction of muscle?
Less calcium = not much contraction
More calcium = potential for contraction
define the following:
- muscle unit
- motor unit
- motor neurone pool
- Muscle unit – muscle fibres innervated by a single motor neurone
- Motor unit – muscle unit plus its motor neurone
- Motor neurone pool – collection of neurones innervating a single muscle
- A motor neurone innervates one set of muscle fibres
- A pool consists of many motor neurones, each of which innervates a motor unit within the muscle
what is fine control and coarse control? how many motor neurones control a muscle typically? how many muscle fibres does each motor neurone control? how can muscle fibres be changed?
- Fine control – few muscle fibres per motor unit
- Coarse control – many muscle fibres per motor unit
- typically, a muscle is controlled by about 100 motor neurones – cell bodies in the spinal cord (or brain stem)
- each motor neurone controls 100-1000 muscle fibres scattered over the muscle
- Muscle fibres can be changed by patterns of motor neurone activity and absolute levels of activity
what are the two mechanisms of gradation of muscle fibres? what happens short and long term when increasing exercise?
Two mechanisms:
- Recruitment of motor units
- Firing rate of motor units
Short-term of increasing exercise it’s the nervous system that has to get used to recruiting more fibres, then long-term you get changes in firing
what is stimulated by tendon tap?
Tendon tap -> stretch muscle -> stimulate muscle spindles
upper and lotor motor neurone lesions
- paralysis
- muscle tone
- reflexes
UMN:
- spastic (persistent spasms)
- hypertonia
- hyperreflexia
LMN:
- flaccid (muscle loses innervation)
- hypotonia
- hyporeflexia
