Exercise Physiology

Question	Answer
Define Breatholding:	'The voluntary or concious suppression of breathing' But there is a breatholding break point whereby involuntary mechanisms take over and force breathing.
Define Breatholding:	'The voluntary or concious suppression of breathing' But there is a breatholding break point whereby involuntary mechanisms take over and force breathing.
What is the average breatholding time? Are there any ways in which we can increase breathold time?	Approximately 1.1mins. Training and Distraction can both increase Breath Hold time.
What happens to PaCO2 and PaO2 when Breatholding?	PaO2 falls and PaCO2 increases. When we exercise breath holding time decreases.
True or False, the Breatholding Break Point is where PaO2 falls to a certain level.	False. When inhaling Hyperoxic air (high O2) BHT increased but the point at which inhalation occurred was at a higher PaO2. Additionally as peripheral arterial chemoreceptors detect O2 levels if they were removed BHT would be infinite, but this isnt the case.
Is there a PaCO2 Breathing Break Point?	No. After breathing high CO2 mixed air this caused PaCO2 to increase, but after a breath hold rebreathing caused PaCO2 to rise further.
Is Breath Hold Time simply effected by Lung Volume limits or Arterial Chemoreceptors?	No. Max Lung Volume is not the reason as you can perform several breath holds with intermittent exhalations. Additionally Arterial Chemoreceptors do not set breathing break point as if they were removed then breath hold time should be infinite which is not the case.
What is Central Respiratory Rhythm and how is it affected when breath holding?	CRR is how breathing is voluntarily controlled to the rhythm of movement. This shows that humans have voluntary control over our breathing, it has been found that humans can only 'detect' emergency breathing (such as inhalation after maximal breath hold). BUT CRR continues during BH, we merely suppress it to enable the BH, so the breathing break point is where suppression of CRR cannot be maintained due to involuntary mechanisms. It has also been found that the diaphragm plays a large role in BH. When the Phrenic Nerve (controls the diaphragm) was blocked BHT increased greatly- thus plays a major role in modulating BH.
What is PaCO2 and PaO2?	PaO2 is the partial pressure of oxygen in arterial blood. PaCO2 is the partial pressure of carbon dioxide in the arterial blood. The control of PaCO2 in the blood is very strictly controlled at approximately 40Hg, whereas control of PaO2 (approximately 100Hg) is not as strictly controlled as it is much more stable with changing P02 (partial pressure of oxygen in the air).
What happens to oxygen saturation when PO2 decreases?	O2 saturation remains very stable, even with a very large decrease in PO2- thus it does not have a great effect on Ventilation. PO2 only effects breathing when it falls greatly (hypoxia) which occurs at altitude, thus we increase ventilation to increase O2 supply.
Why do we hyperventilate in Hypoxic air?	To increase O2 supply. Additionally it alters the composition of alveolar air (reservoir of air in between breaths) which maintains PaO2- which without it would cause acidity to rise dangerously. Hyperventilating hypoxic air causes a decrease in alveolar PaCO2 through hyperventilation is replaced with atmospheric O2 which slightly increases PaO2 to maintain the pressure gradient which allows O2 delivery to the muscles and tissues.
How greatly does Hypoxia effect breathing?	Not very as we are not very sensitive to hypoxic air.
What happens to breathing as PaCO2 increases?	it increases greatly. Similar to what is seen during exercise- BUT PaCO2 is maintained during exercise. Soo how is breathing in exercise controlled. Aortic Chemoreceptors have been found to be un-important in ventilation as when removed minute ventilation remained the same (only thing that changed was that Ventilation did not increase when PO2 decreased, thus they detect changes in environmental air) BUT the Carotid Arterial Chemoreceptors when removed caused a 50% decrease in sensitivity to increasing PaCO2 levels (much slower to increase breathing) thus they play a minor function in how breathing is controlled.
How are Minute Ventilation and Metabolic Rate linked?	VE (Min Vent) increases linearly with with VCO2 (amount of carbon dioxide produced through metabolism) But VE always followed with a slight delay, but PaCO2 remains the same- thus does not control breathing in relation to Metabolic Rate. Additionally as we know PaO2 and PaCO2 do not change with exercise these cannot also cause Min Vent increase with Metabolic Rate. But Mixed Venous PCO2 does increase, but this cant be the signal to increase breathing as peripheral chemoreceptors are in the wrong place to detect this change.
So what does increase Breathing?	Voluntary Will Power, Training, Catecholamines, Proprioreceptors, Muscle Chemoreceptors
So what does increase Breathing?	Voluntary Will Power, Training, Catecholamines, Proprioreceptors, Muscle Chemoreceptors
How is breathing Controlled?	Obvious guess would be that as Metabolic Rate increases this causes a decrease in Oxygen and an Increase in Carbon Dioxide and this change would be detected by chemoreceptors which would then increase ventilation. BUT ARTERIAL O2 AND CO2 DO NOT CHANGE DURING EXERCISE.
What factors vary Lung Volumes and how can we measure them?	Age, Gender and size. We measure lung volumes with a Spirometer.
What is Tidal Volume?	TV is the amount of air that goes in and out of the lungs (0.4-1L)
What is Inspiratory Reserve Volume?	Max volume that can be inspired? 2.5-3.5L
What is Expiratory Reserve Volume?	Max volume that can be expired (1.0-1.5L)
What happens to IRV and ERV during exercise?	As Tidal Volume Increases (with exercise) both IRV and ERV decreases.
What is Vital Capacity?	Total Lung Capacity minus Residual Volume- approximately 3.5L.
What type of volumes are Tidal Volume, IRV, ERV and Vital Capacity?	Static Lung Volumes (Not influenced by lung compliance)
What are Dynamic Lung Volumes?	Dynamic Lung Volumes depend on Maximal Forced Vital Capacity of lungs and flow velocity (in other words Lung Compliance)
What is the Forced Respiratory Volume-to- Forced Vital Capacity Ratio?	It indicates pulmonary airflow capacity (airflow to the heart) Healthy people manage 85% Forced Vital Capacity in 1 second.
What is Max Voluntary Ventilation?	MVV is the amount of times we can breathe in a minute. We can breathe maximally greater than will ever be reached during exercise.
How does Lung Function differ between genders?	Females have smaller lung function thus they work harder to maintain sufficient Oxygen exchange from the alveoli into the arterial blood. Additionally Ventilation and Oxygen uptake vary greatly from person to person.
What happens to VO2 Max as Ventilation increases?	VO2 Max decreases as ventilation increases as we use more of our VO2 Max to maintain elevated ventilation.
Is maximal exercise limited by Ventilation?	No.
What is Minute Ventilation?	Ve is the volume of air breathed in per min (which significantly increases during exercise). During Exercise despite large increase in Minute Ventilation it rarely exceeds 6% of Vital Capacity.
What is Alveolar Ventilation?	Is the amount of air that enters the alveoli. It is approximately 500ml BUT due to anatomical dead space (un-functional area) only 350ml enters the alveoli.
What is Alveolar Ventilation?	Is the amount of air that enters the alveoli. It is approximately 500ml BUT due to anatomical dead space (un-functional area) only 350ml enters the alveoli.
What happens to both Rate and Depth of Breathing during Exercise?	They both increase. There is an initial larger increase in Depth (Tidal Volume) followed by an increase in both rate and depth. During moderate exercise TV rarely exceeds 60% of Vital Capacity.
What is the theory behind a Ventilatory Break Point?	This is where Ventilation increases linearly until the VBP is reached where Oxygen Consumption and Oxygen Use our even- NOT THE CASE. NOT THE LIMIT TO PERFORMANCE.
What is the Respiratory Control Centre?	The Medulla Oblongata. The MO receives input from the peripheral chemoreceptors, skeletal muscle chemoreceptors and the mechanoreceptors. It is driven by the higher brain centers and then controls the respiratory muscles.
What is Arterial Hypoxaemia?	Low oxygen content in arterial blood which in turns lowers max Oxygen uptake by the muscles.
What is Physiologic Dead Space?	The volume of the respiratory tract not used in gaseous exchange between the lungs and the arterial blood. It is affected by Inadequate ventilation and inadequate blood flow.
Why does Blood Pressure Increase during exercise?	Because increased Blood Pressure Increases profusion.
What is Muscle Fiber Necrosis?	Death of MUscle Fibers.
What are some causes of Muscle Fiber Necrosis?	Alcohol, Drugs, Disease, Radiation, Ischemia, Mechanical Injuries, Excessive Heating/Cooling, Exercise
What is DOMS?	DOMS stands for Delayed Onset of Muscle Soreness. This usually follows 24-48hours after Muscle Fiber Necrosis (usually caused by exercise).
What are the consequences of DOMS?	Pain when touched, Takes longer fully extend muscle, decreased Max Voluntary Contraction, Restricted ROM, Increased limb circumference.
What is a Plasmalemma Tear? and what sequence follows?	A Plasmalemma tear is a tear in the muscle plasma membrane. Following a tear: 1) Plasmalemma tears and Ca enters. 2) Macrophages enter and engulf dead parts. 3) Macrophages remove debris and t-cells arrive. 4) Uninjured parts retract and form stump with new membrane which protects against further Ca entry.
What is a Plasmalemma Tear? and what sequence follows?	A Plasmalemma tear is a tear in the muscle plasma membrane. Following a tear: 1) Plasmalemma tears and Ca enters. 2) Macrophages enter and engulf dead parts. 3) Macrophages remove debris and t-cells arrive. 4) Uninjured parts retract and form stump with new membrane which protects against further Ca entry.
How is Pain Sensed?	Pain is sensed by activation of fiber afferent's (type 3 and 4) these become active during exercise, metabolites, increased temperature, and increased muscle force generation.
What causes DOMS (activates the pain sensing afferents)?	The metabolite Bradykinin was thought to trigger development of DOMS- however this is not the case. What Bradykinin does is upregulate Nerve Growth Factors which increase the response to the muscles lengthening contraction thus causing DOMS.
What is Fatigue caused by?	Fatigue is caused by Pre-synaptic failure of the AP's. Synapses up-regulate the strength of the AP. To overcome this failure more AP's are sent which causes a build up of potassium which prevents a gradient change (as sodium potassium pump cannot work) and thus prevents contraction.
What types of fatigue are there?	High Frequency and Low Frequency.
What is High Frequency Fatigue?	This refers to the decrease of force at high stimulus frequency followed by a rapid recovery when stimulus frequency is reduced. (Like after Sprinting)
What is Low Frequency Fatigue?	Low Frequency Fatigue is a relative loss of force at a low frequency and a slow recovery which can takes hours or days (Like after long distance running)
How does the body protect against High Frequency Fatigue?	By decreasing the excitability of the motor neuron- this occurs through Feedback from the muscles.
Define the term Central Fatigue:	Central Fatigue is where we are physically inhibited to fully contract the muscle prevent causing damage to the muscle.
Describe- giving frequency intensities force generation when one is suffering from Low Frequency Fatigue:	At 20Hz stimulation force would be markedly lower, however at between 50-100Hz the force generate would be the same as in fresh muscle.
What causes Low Frequency Fatigue?	Ultimately caused by reduced levels of Ca release per AP, thus more AP's are required to generate same Ca level release, thus it takes more effort to produce force- BUT IT IS ABLE TO. LFF is most associated with eccentric exercise and causes DOMS, which is why it takes longer to recover than HFF.
What does fatigue cause?	Slower muscle relaxation through slower Ca active transport back into the SR thus X-bridges remain formed for longer. Additionally X-bridge sensitivity when fatigued is reduced (thus why we increase number of AP's to increase Ca release) Thus because we compensate for this (through more AP's) a change is Ca kinetics does not explain a slowing in muscle relaxation. Additionally as X-bridge formation and VO2 max are linked this explains why VO2 max is decreased when fatigued. Power is also decreased as both force and velocity are decreased.
What causes fatigue during high intensity?	Characterized by a reduction in force and slower muscle relaxation which is caused by Acidosis. Lactate (H+) builds up in high intensity exercise. H+ competes with Ca for troponin binding sites- thus a low pH (high H+) interferes with X-bridge formation as lower amounts of Ca is released. But through testing this only accounts for a 30% decrease in force- this means that when fatigued increasing Ca is not as effective as it would be in fresh muscle. Additionally a low pH inhibits Glycolysis (through inhibition of PFK) which thus protects against further lactate build up.
Does PCr effect Fatigue?	PCr maintains ATP turnover rate so people believe it could fully contribute BUT it doesnt. PCr does decline with force but PCr recovers before force does- indicates not fully responsible.
What effect does ATP/ADP ratio have on Fatigue?	The ratio is maintained through the deamination of AMP to IMP. High IMP (through high AMP levels- low ATP) levels cause down-regulation of ATP usage (slows X-bridge formation) which decreases force. Additionally high Pi (bi-product of ATP breakdown to ADP) causes a decrease in force. These factors in part cause fatigue.
What is the most important point to remember with regard to muscular fatigue?	THAT IT IS MULTI-FACTORIAL. Caused by lower sensitivity to Ca causing slower X-bridge breaking. Acidosis (H+ build up causing reduced Ca release and competing with Ca on Troponin binding sites. PCr declines. and High IMP.
What are the characteristics of immature Muscle Fibers?	Slow Contracting, Contain Embryonic Myosin (un-differentiated myosin heavy chain isoform) and immature ATPase. The embryonic myosin becomes either type 1 or type 2 dependent on gene expression.
What determines Muscle Fiber Type Composition?	50% genetic and 50% is determined through training. It is more difficult to 'make' (change myosin heavy chain isoform) to type II. Training type, intensity and duration effects differentiation.
What affects does Resistance Training Have on Muscle Fiber Changes?	Trained weight lifters have no different amounts (in %) of type 1 muscle fibers than untrained, however they are larger through hypertrophic adaptation. Additionally the resistance caused a decrease in Mitochondria but an increase in structural proteins.
How easily can you type Muscle Fiber Type?	It is very hard to change Type I MF into Type II but it can be done between Type IIa and Type IIx (endurance training they IIx --> IIa- more oxidative)
What effects do Sprint Training have on the Muscle Fibers?	Sprint Training caused an increase in MF size in both types I and II. Additionally Type IIa became Type IIb (more glycolytic)
Does the Nerve that innervates the MF have an effect?	Yes. The nerve which innervates the MF determine the MF type through differences in firing frequency and firing pattern. Nerves that innervate Slow Twitch MF's fire constantly at 10Hz, whereas nerves that innervate Fast twitch MF's fire intermittently at 30-60Hz. It is through this principle that allows us to change muscle fiber type, this is known as Cross Innervation.
What effects do Altitude have on MF's?	MF composition does not change in altitude but they decrease in size and oxidative capacity is decreased by approximately 30%.
What effects do Nutritional/Hormonal factors have on MF's?	Activities such as smoking or alcohol decrease MF size but Creatine has been found to increase MF size.
What effects do ageing and disuse have on the MF's?	Disuse and ageing both lead to muscle atrophy, which causes a decrease in strength. Additionally more specifically to ageing MF type composition changes with Typ II becoming Type I.
What is Muscular Atrophy?	A decrease in muscle mass. Caused by a decrease in protein synthesis and an increase in protein degradation causing a negative protein balance.
What methods can be used to measure muscle mass?	Weigh It, Anthropometry, DEXA, MRI scanners.
What effects does muscular Disuse have on the muscle?	A decrease in MF CSA, conversely training increases MF CSA.
What is Steady State Protein Turnover?	This is where Protein Synthesis and Protein Degradation are equal. It approximately takes 70 days to breakdown and re-synthesize all structural proteins and approximately 25 days for all Sarcoplasmic Proteins.
How does Disuse effect the Motor Neuron?	When limb is immobilized the EMG activity of the motor neuron decreases to approximately 5-15% of normal values. In postural muscles (muscles used in posture) the immobilization causes a change in Motor Neuron firing pattern from tonic (continuous firing) to phasic (fast bursts) causing change in MF type. Type II (phasic) is default and thus the change to tonic firing pattern causes Type II to become Type I.
How does fixation in both lengthened and shortened positions effect MF's?	When a limb is fixed in a lengthened position we increase the number of sarcomeres in the muscle thus leading to hypertrophy. When lengthened it changes the Motor Neuron firing pattern from phasic to tonic which causes an increase in Type 1 MF. Conversely when fixed in a shortened position this causes a change from tonic to phasic increasing Type 11 MF's.
What other effects does immobilization have on on the joint and the limbs enzymatic activity?	With Immobilization we see increased amounts of collagen thus causing an increase in stiffness, however stretching can help this. Additionally enzymatic activity decreases with immobilization- additionally Type I MF are affected more.
What is a twitch and what effect does muscle atrophy have on it?	A twitch is the sum of the force of all Motor Units which are activated by the Stimulus. We see preferential atrophy of Type I MF's which does not cause a change in total twitch time course BUT the time to peak force is quicker BUT only because peak force is lower.
What effect does Ageing have on the Muscles?	Ageing causes a decrease in muscle CSA (decrease in MF's) and an increase in fat.
Are larger or smaller nerves (and thus Motor Units) recruited first?	Largest Nerves are recruited first as they have the lowest threshold. Smaller nerves have higher thresholds thus are recruited last.
Explain the principle of Cross Innervation:	With ageing Motor Neurons die, thus we have fewer Motor Units. But because of Cross Innervation the Motor Units are bigger. Cross Innervation is where when a Motor Neuron dies a surrounding Motor Neuron Cross Innervates the now unattached MF's. The newly attached MF's adapt to the new Motor Neuron firing pattern which causes a change in Myosin Isoform (from Fast Twitch to Slow Twitch). This priniciple causes a Mosaic Pattern- where MF types are grouped.
Are both Slow Twitch and Fast Twitch Muscle Fibers lost equally as we age? and how is power output affected with age?	No we lose more Type II MF. Power declines with age, but regular physical activity can somewhat delay this. It is also worth noting that total twitch to,me decreases with age due to slower release and re-uptake of Calcium, which in turn causes a greater response in tetanic stimulation (quicker to fatigue) as the muscle cant relax as calcium uptake is slower.
Define Weakness:	Weakness is the failure to generate required force on the first attempt
Define Fatigue:	Fatigue is the failure to maintain force.
What are the possible Central Locations for Fatigue?	Excitatory Input to the Motor Cortex, Excitatory Drive to the lower Motor Neuron, Motor Neuron Excitability.
What are the possible Peripheral Locations for Fatigue?	Neuromuscular transmission, Sarcolemma Excitability, Excitation-Contraction Coupling, Contractile Mechanism, Metabolic Energy Supply.
How can we test Fatigue?	We can test fatigue by Comparing Electrically evoked Force and Voluntary Contraction force- (removes motivational factors and tests explicitly whether the muscle is physically able to generate the required force). We can also look at the M-wave (muscle mass AP size) and the Hoffman Reflex (excitability of the alpha motor neuron)
What Neurophysiological changes arising from Resistance Training cause an increase in strength?	Increased Motor Neuron excitability, Increased Motor Unit firing (and synchronization), Greater efficiency in neural recruitment patterns, decreased neural inhibitory reflexes, Reflex potentiation in some muscles and increased CNS activation.
How greatly can MVC increase due to neural changes?	Greatly, through greater muscle utilization. This is proven by hypnosis and being startled being found to increase MVC through greater muscle utilization (proved as you are not any physically stronger)
Is force higher in Voluntary contraction or when it is electrically stimulate?	Voluntary Contraction due to co-contraction of muscle (whereas in electrical stimulation muscles are isolated). If you train through electrical stimulation you will see an increase in muscle size but no increase in force as we haven't learnt to contract more forcefully.
Is the improvement in Weightlifting ability proportionate to physical strength gain?	No. Weightlifting leads to being able to lift more weight but physical strength did not increase to the same extent, this shows that the increase in weight lifting ability is partially due to the learnt skill of weight lifting not muscular hypertrophy.
What is the Cross Over Effect?	It is the principle by which if we solely train our right bicep our left bicep will also improve in physical strength but only the right bicep will exhibit muscular hypertrophy.
In fast movements, what trained aspects can increase force?	Technique and Timing
How does stimulus frequency affect force generation and magnitude?	A higher frequency stimulus causes a more rapid increase in force but max force is no different.
How does stimulus frequency affect force generation and magnitude?	A higher frequency stimulus causes a more rapid increase in force but max force is no different.
How does training affect EMG signals from muscles?	Training increases EMG response which is a result of better neural recruitment and increased firing rate, thus we get a quicker maximal voluntary contraction.
How does training affect Motor Units?	Training causes individual Motor Units in ballistic (fast and voluntary actions) to be much more explosive, thus the rate of tension generation is much quicker. Additionally a high firing frequency can be sustained for longer- as shown by trained weight lifters being able to sustain force much longer than untrained.
What relationship do Neurological and Hypertrophic adaptations have as a training regime progresses?	Initially increases in strength are mainly due to neural adaptation, but as the regime continues the increases in strength come more from muscular hypertrophy.
What determines Muscle Fiber Type?	The Myosin Heavy Chain Isoform determines speed of contraction and thus muscle fiber type. Myosin Heavy Chain 1= Slow Twitch, MHC IIa= Fast Twitch Oxidative, MHCIIx= Fast Twitch Glycolytic
How can we visually determine type of muscle?	Through Myoglobin content, the more myoglobin the darker the muscle (chicken is low in myoglobin, steak is high)
What size Motor Units will be recruited first? and is there a link between Motor Unit Size and Muscle Fiber type?	Smaller Motor Units are easier to recruit as they have a lower threshold stimulus than Larger Motor Units. Additionally smaller MU's are Slow Twitch, whereas larger MU's are Fast Twitch.
Explain why Fast Twitch Muscle Fibers generate more force than Slow Twitch:	Fast Twitch Muscle Fibers produce more force due to Hyperplasia, which is the increased number of Muscle Fibers, which are larger through Muscle Fiber Hypertrophy.
How important is Muscle Fiber CSA in force production?	Extremely important. Force generating capacity is not due to MF type it is due to Muscle Fiber CSA, as the larger the CSA the more X-bridge formation, thus greater tension (thus force) can be generated.
What is flexibility and what factors effect it?	Flexibility refers to the Range of Motion available at a joint or group of joints. The shape of the bones and cartilage of the joint effects flexibility, additionally the length of the muscles, tendons, ligaments and fascia across the joint.
What factors limit the Range of Motion available?	Age, Gender, Genetics, Posture, Disease
How are Flexibility and Injury Linked?	The greater the deviation from 'normal' flexibility the greater the risk of injury. Additionally good flexibility of the lower back significantly decreases the chance of injury.
How are Flexibility and Injury Linked?	The greater the deviation from 'normal' flexibility the greater the risk of injury. Additionally good flexibility of the lower back significantly decreases the chance of injury.
What is Osteoperosis?	Loss of bone mineral density, the vertebrae is usually affected. Lordosis is the forward concave curve of the spine and Scolliosis is an abnormal lateral curve of the spine.
How does Flexibility effect Energy Efficiency:	The more flexible the less energy efficient our movement is (greater O2 consumption). The opposite is also true the less flexible the more energy efficient our movements become.
How do muscle adapt when they are fixed in a shortened position?	They shorten. Sarcomeres loosen and the Muscle Fibers shorten, thus the range of motion available is reduced. Additionally shorter Muscle fibers are less powerful.
Explain the Tendon Normal Stress-Strain Curve:	Refers how the stiffness of tendons are effected by increased loads. As load increases as does the stiffness of the of the tendon due to the stretch of the tendon. So when tendons are naturally shorter the same absolute stretch causes greater stress and strain. Disuse causes deformation and thus decreased force production- Resistance Training offers protection against this.
What is energy storage?	This is the principle through which we store energy in muscles before contraction which allows for a greater force production. An example is how we can jump higher when we start from a crouched position or perform rebound jumps.
How can we improve Connective Tissue ability to stretch?	Through Stretch Training we can improve there Viscoelastic Stiffness. There are 2 types of stretch we can perform. Static stretches mean that a lower force is required to maintain the same stretch of the tendon. Ballistic Stretches allow for a more rapid application of force through a quicker application of stiffness, thus we get a greater amount of force for the same muscle elongation.
What is Thixotrophy?	This is the principle that the bodies tissues are stiff when they are unused but loose when used, thus the warming of tissues decreases stiffness. Creep is the lengthening of connective tissue over time with the same amount of force exertion and Stress Relaxation is the decrease in force when the length is help.
Are the muscles elastic in nature?	Yes. Cross bridge formation causes stiffness in the muscle. When more cross bridges are attached the more stiff the muscle. This explains why we can generate more force when we store energy in the muscle- there are more cross bridges attached.
What is speed of muscular contraction dependent on?	ATPase. Speed of contraction is dependent on the speed at which ATP cab be broken down, this is performed by the enzyme ATPase.
Describe both Eccentric and Concentric Muscular Contractions:	Concentric- Muscle Shortens during contraction. Eccentric- Muscle Lengthens during contraction.
Describe what an Isometric Twitch is, and explain how it is formed:	An Isometric twitch is a single muscular contraction. Contraction in this twitch is faster than relaxation as Ca release is faster than active transport of Ca back into the SR.
What is Series Elasticity?	Series elasticity refers to the effect of consecutive stimuli on the muscular reaction. Summation occurs when the second stimuli arrives before the COMPLETE tension dissipation of the muscle, thus force increases. Tetanus occurs when there is NO dissipation of tension between stimuli so force builds. We generate much greater force through tetanus than through muscular twitches.
Does force increase exponentially with tetanus?	No. Force does not increase exponentially with increasing stimulus frequency. Optimal firing rate is approximately 100Hz any stimulus frequency above or below this causes a reduction in tension and thus reduced force output.
What is Twitch Potentiation (Post Tetanic Protensation)?	This is where after a MVC a subsequent twitch contraction is much more forceful.
How does load effect the speed of contractions?	No load= Very fast contraction whereas a Heavy Load= Slow contraction.
Describe the Force Velocity Relationship:	The Force Velocity Relationship is based on the principle: Power= Force x Velocity. We can generate more force from a muscle that is lengthening.
What is a Motor Unit?	A Motor Unit consists of a Motor Neuron and all of the Muscle Fibers it innervates. There are 3 types of Motor Unit- Slow Oxidative, Fast Oxidative, Fast Glycolytic
Describe the Muscle Contraction Cycle:	1) AP travels along neuron axon until it reaches a myo-neural junction (synapse) where it releases Acetylcholine which diffuses over to the sarcolemma and t-tubules. 2) SR releases Calcium which binds to Tropomyosin causing it to shift exposing the Myosin Binding sites on the Troponin of the Actin. 3) The Myosin globular heads (contain ADP + Pi) attach to the exposed sites causing the expulsion of the Pi 4) The ADP is expended causing the power stroke (flexes causing movement of Actin) 5) ATP enters the Myosin head and is broken down to ADP + Pi to break formation of the X-bridge. 6) To relax the AP's stop and through Active transport the Calcium is returned to the SR.
What is the optimal muscle length for optimal force production?	Optimal muscle length is roughly 100% (so not flexed or extended- so at a 90 degree angle) If any longer sarcomeres are stretched, if any shorter sarcomeres are squashed- both bad as optimal tension cannot be generated.
What is the Latent Period?	The Latent Period is the delay between the sending of the AP and the muscular contraction.
What is Electro-Chemical Coupling and at what stage does it occur in the Muscular contraction cycle?	It is the system responsible for Ca release from the SR. When the action potential enters the t-tubules this causes the coupling of Dihydropyridine (DHP) Receptors and Ryanodine which allows Ca release from SR (thus this system is the mediator of Ca release)
What makes up Muscle?	Actin, Myosin and other proteins (eg- Titin). The Actin and Myosin form X-bridges which generate tension (force). X-bridge formation is dependent on Calcium availability.
How many types of Skeletal Muscle Arrangement are there?	4- Parrallel, Unipennate, Bipennate, Multipennate
What is a Sarcomere?	A Sarcomere is formed of Myosin (thick filament) which is anchored in place by Titin (which prevent Sarcomere collapse) and Actin (thin filament) which are anchored to z-lines by the protein Nebulin.
Give some basic information about Actin:	Actin is 42kDa which is wrapped in tropomyosin in a double helix formation.
Give some basic details about Myosin:	Myosin is 500kDa which has 2 globular heads and 3 chains. There are 2 light chains and 1 heavy chain. The Globular heads repeat approximately every 43nm. Myosin is stabilized in place by Titin.
Describe the pathways of both the Afferent and Efferent Nervous Systems:	Afferent is towards the Central Nervous System and Efferent is from the Central Nervous System to the Target (muscle etc)
At rest is the charge of a cell positive or negative?	Negative. Charge is determined by the permeability of the plasma membrane to Sodium and Potassium which are maintained by the Sodium/Potassium Pump.
How do Excitatory and Inhibitory Post-synaptic Potentials Differ?	Excitatory cause depolarization (can be spatial or temporal) whereas Inhibitory cause Hyperpolarization.
What are the two components of the Peripheral Nervous System?	Somatic and Autonomic. The Somatic Nervous System controls voluntary muscular contractions. The Autonomic Nervous System controls involuntary muscles such as smooth and cardiac muscles.
What sources of Sensory Information does the Somatic Nervous System Receive?	Joint Proprioreceptors- Free Nerve Endings (touch, pressure), Golgi type receptors (surround ligaments) and Pacinian Corpuscles (around joints and in skin). Muscle Proprireceptors- Muscle Spindles and Golgi Tendon Organs. Muscle Chemoreceptors
What do Muscle Spindles, Golgi Tendon Organs and Muscle Mechanoreceptors/Chemoreceptors monitor?	Muscle Spindles: Respond to changes in length, also cause the stretch reflex. Golgi Tendon Organ: Monitors muscle tension and thus prevents damage from excessive force generation by causing relaxation through Inhibitory Postsynaptic Potentials. Muscle Chemoreceptors: Sense changes in chemical environment and thus inform the CNS of the required Metabolic Rate based on Muscular activity. Muscle Mechanoreceptors: Are sensitive to Muscle Contraction.
What is the function of the Central Nervous System?	The CNS is the processing centre of the Nervous System, which processes all information from the Peripheral Nervous System.
As we know the CNS controls Motor Function (How we make movement) but what systems allow this?	Subcortical and Cortical Motivation Area's- Send a rough draft of required movement. Cerebellum and Basal Ganglia- Convert the rough draft into movement. The Cerebellum converts slow movements and the Basal Ganglia converts fast movements. The Motor Cortex through the Thalamus- Sends message down the spine to the muscles and FB is given from Muscle Receptors and Proprioreceptors for fine tuning of the movement.
What does the Autonomic Nervous System do?	Controls Involuntary muscles (cardiac and smooth). Additionally it is divided into 2 divisions- The Parasympathetic and Sympathetic systems. The Parasympathetic through AcH inhibits the effector organ to conserve energy expenditure whereas the Sympathetic through Nor-adrenaline excites the effector organ that increases energy expenditure.
How does the Endocrine system 'control' the body?	Through hormone producing glands, with the primary function of Communication with cells to regulate the cells function.
How does the Nervous System 'control' the body?	The Nervous System uses transmitters for direct cell to cell communication to regulate there behavior.
What has the greatest effect on the effectiveness of hormone response?	The Plasma Concentration of the hormone- the amount of the hormone. Soo the rate of secretion and excretion effects hormone effectiveness.
Explain what Down-regulation and Up-regulation refer to in Hormone control:	Hormones only effect specific receptors, thus amount of receptors and amount of hormone determine the magnitude of the hormones effect. Down-regulation is Receptors decrease with increased levels of the hormone and Up-regulation is where receptors increase with decreased amount of hormone.
In what ways can Hormones Act?	Hormones can act by: Altering membrane transport, alter DNA activity thus protein synthesis, activate second messengers, and modulate enzyme activity (increase/decrease activity, stimulate production, change enzyme shape, activate inactive enzyme forms)
Name some Endocrine Glands:	Pituitary Gland, Thyroid and Parathyroid Glands, Adrenal Glands, Pancreas, Testes and Ovaries.
What higher control system controls the Pituitary Glands and what hormones does the Pituitary Gland release?	The Hypothalamus. The Pituitary Gland is split into the Anterior and Posterior. The Anterior PG secretes Growth Hormone (Stimulates Insulin Like Growth Factors which cause muscle growth, tissue growth, Long Bone growth, and Glucose Sparing through increasing Gluconeogenesis and Fatty Acid mobilization) The Posterior PG secretes ADH which acts to retain plasma volume by reducing water excretion.
What hormones do the Adrenal Medulla and Adrenal Cortex secrete?	The Adrenal Medulla secretes Adrenaline and Nor-adrenaline. The Adrenal Cortex secretes Aldosterone (Maintains plasma Sodium and Potassium, regulates Blood Pressure and Blood Volume) and Cortisol (Maintains Plasma Glucose through increasing gluconeogenesis, glycogenesis and Free Fatty Acid Mobilization)
What hormones do the Ovaries and Testes secrete?	The Ovaries secrete Estrogen and Progesterone to maintain reproductive function and the Testes secrete Testosterone which promotes muscle growth.
What happens with O2 Uptake with Incremental Exercise?	O2 uptake increases with intensity until VO2 Max is reached- VO2 Max is limited by ability to deliver O2 to the muscle and the muscle's ability to use O2.
At what point do we reach the Lactate threshold?	We reach the Lactate Threshold (OBLA) when blood lactate reaches 4mmol. This occurs at approx 50-65% VO2 max for untrained and between 65-80% in trained athletes.
Why does Lactate build during exercise?	The decreased oxygen, the acceleration in Glycolysis (in response to increased energy requirement) which causes excess NADH which is converted to Lactate. Additionally Lactate removal decreases during exercise.
Define Metabolism:	Sum of all chemical reactions, both anabolic (Synthesis) and catabolic (Breakdown)
Define Bioenergentics:	The conversion of food into energy.
What do enzymes do?	Catalyze reactions. Changes in environment (for example pH change) can increase or decrease enzymatic activity.
At rest where does are energy come from?	Almost 100% comes from aerobic pathways.
As we go from rest to exercise what happens?	Immediate increase in both ATP and Oxygen intake. Oxygen consumption reaches steady state after 4 minutes (in this 4 min period our energy comes from anaerobic pathways- this is known as the Oxygen Defecit) Trained athletes have less Oxygen Deficit than untrained.
As we go from Exercise to Recover what happens?	We must repay our Oxygen Debt (Comes from Oxygen Deficit-4mins) thus we keep Oxygen consumption elevated (EPOC-only 20% of increased O2 consumption goes to repayment of O2 debt)
What are the 2 phases of the Oxygen Debt?	Rapid Phase (Replenishment of PCr and Oxygen in both the muscle and blood) and the Slow Phase (Increased HR, Breathing, Body Temp, Epinephrine/Norepinephrine and Gluconeogenesis)
What is Homeostasis, and explain the principle of gain and how we respond to it?	Homeostasis is the maintenance of a constant and normal internal environment. Gain is the term given for any change in the internal environment, for example a fall in body temperature from 37-35 is a gain of 2 degrees. We use both Positive and Negative FB Systems to make changes to our internal environment. An example Of Negative FB would be to begin shivering to warm the body. Positive FB is where we amplify the change, for example when we get hotter Positive FB would cause us to become hotter.

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	Created by Mark Arsenal over 11 years ago