1
Q
What does the energy source for muscle contraction depend on?
A
Source of the ATP depends on the type of muscle fibres involved and the duration of contraction.
2
Q
Describe ATP immediately available as an energy source.
A
The amount of ATP immediately available in a muscle fibre is only sufficient to sustain contraction for a couple of seconds at most. This ATP needs to be replenished from other energy stores in the muscle fibres.
3
Q
Describe phosphocreatine as an energy source.
A
The next most readily available source is phosphocreatine, which can replenish ATP very short term but this will be depleted in less than 10 seconds.
4
Q
Describe glycolytic metabolism as an energy source.
A
For short bursts of muscle contraction, such as in sprints, the main source of ATP is provided by glycolytic metabolism that produces lactic acid as a by-product and is therefore known as the lactic acid system. This can sustain muscle contraction for up to a minute.
5
Q
Describe oxidative metabolism as an energy source.
A
For longer periods of muscle contraction, over a minute, the muscles become increasingly dependent on aerobic mechanisms – oxidative metabolism for ATP production.
6
Q
Distinguish the energy available for shorter and longer duration exercise.
A
There is much more energy available for short burst of muscular activity, which can sustain high amounts of cross bridge cycling and therefore higher levels of force production than longer duration activity.
7
Q
What is the role of creatine kinase?
A
Creatine effectively stores energy from ATP in the form of high energy phosphate bon in phosphocreatine, a reaction that is catalysed by the enzyme creatine kinase.
Many factors can influence the activity of creatine kinase but majorly is the ratio of ATP: ADP.
8
Q
When is there increased and decreased ATP production from phosphocreatine?
A
When high ATP levels inhibit the production of further ATP from phosphocreatine, whereas high levels of ADP will push the equilibrium to the right by receiving the high energy phosphate from phosphocreatine.
9
Q
What is the ATP-phosphocreatine system?
A
- Muscles contain 3-4 times more phosphocreatine than ATP.
- Functions as an ATP buffer, providing an immediate energy reserve that smooths out change in ATP in muscle fibres, especially at the onset of exercise.
- Depleted phosphocreatine stores can be replenishes to 70% of maximum levels in only 30 seconds.
- Important for providing energy for high intensity but short bouts of exercise of the order of seconds, such as jumping, rapid escapes or birds taking off.
10
Q
Name the 3 main fuel sources for ATP generation.
A
- Carbohydrates mobilised from glycogen stores, either locally or in the liver.
- Proteins can be catabolised to amino acids and following deamination by the liver and can either be converted to glucose in gluconeogenesis or can feed into glycolysis ad citric acid cycles.
- Oxidative metabolism of fats
11
Q
How are carbohydrates mobilised from glycogen stores?
A
Can be catabolised to monosaccharides and feed into glycolysis and then via acetyl coenzyme A into ethe citric acid cycle and oxidative phosphorylation.
12
Q
How can fats be metabolised?
A
Fats are catabolised into the glycerol backbone which can enter the glycolysis and fatty acids. This can be metabolised to acetyl coenzyme A to enter the citric acid cycle.
13
Q
Compare efficiencies of glycolysis and oxidative metabolism.
A
For every molecule of glucose, only 2 ATP molecules are produced by glycolysis/anaerobic metabolism. 36 ATP can be produced by oxidative metabolism. So oxygen delivery to muscles is a limiting factor to oxidative ATP production, which generates more energy for muscles to sustain high work rates.
14
Q
What are the properties of fast twitch fibres?
A
- Can contract rapidly, achieving maximum tension in 30-50ms.
- Fast speed required high myosin ATPase activity, with an efficient sarcoplasmic reticulum to handle the rapid calcium ion release and reuptake.
- Have low myoglobin levels, so do not have much of an oxygen store but highly active glycolytic metabolism.
- They are active during high and rapid force demands such as printing and jumping.
15
Q
Distinguish type IIa and type IIb fast twitch fibres.
A
Type IIa are rapid shortening fibres with well developed glycolytic and oxidative metabolism and are fatigue resistant.
Type IIb are the most powerful and fastest contracting and have the highest glycolytic capacity but fatigue rapidly.
16
Q
What are the properties of slow twitch fibres?
A
- Take longer to contract reaching peak tension in 50-110ms.
- This is due to low myosin ATPase activity, which is associated with slower calcium handling and a less well developed glycolytic system.
- Instead, they have a metabolism that is adapted to oxidative phosphorylation, with high myoglobin levels, providing a high muscle store for oxygen and high capillary density for delivery of oxygen and a high density of large mitochondria.
17
Q
When are slow twitch fibres utilised?
A
- Used in activities that require sustained low levels of force production, such as standing and walking.
- Their resistance to fatigue makes them particularly important for prolonged endurance exercise.
18
Q
What is the muscle fibre composition of ocular muscles?
A
Need to contract rapidly and briefly to generate eye movements. They rapidly achieve maximum tension and have a high proportion of fast twitch type II fibres.
19
Q
Describe the muscle fibre composition of soleus muscle.
A
Major antigravity muscle of the leg that requires sustained, but slow contraction to maintain standing posture and during walking. High proportion of slow twitch, type I muscle fibres, which reaches 100% in some species such as cats.
20
Q
Describe the muscle composition of gastrocnemius muscle.
A
Intermediate in contraction speed between the 2 extremes an more typical of most muscles. It has a more balanced mix of different fibre types and is important for running and jumping.
21
Q
What is the link between species and fibre type?
A
Different species have different adaptations of their muscle fibre compositions to match their lifestyle requirements. For instance, there is a general linear relationship between the sprinting speed of different species and the percentage of fast twitch, glycolytic, type IIb fibres in tehri muscles.
22
Q
What is the importance and limitations of glycolytic/lactate system?
A
Important for rapid, forceful muscle contractions that require lots of ATP quickly. ATP production by glycolysis rises over the first 10 seconds of activity, peaks at around 2 minutes into exercise.
But energy production by glycolysis will ultimately be limited to lactate production, which will eventually build up and result in metabolic acidosis.
23
Q
What is the process of lactate shuttle?
A
- Muscles with a high oxidative capacity can take up the lactate that is being produced by the fibres with low oxidative capacity via monocarboxylate transfer proteins.
- Lactate is transported into the mitochondria again via MCT where it is oxidised to pyruvate via lactate dehydrogenase.
- Pyruvate can enter the citric acid cycle and oxidative phosphorylation, which spares the consumption of other fuels.
- This redistributes lactate from cells that can’t use it to those that can. so, during intense exercise, the sole fuel source for cardiac muscle comes from circulating lactate.
24
Q
What is the Cori cycle?
A
- Can regenerate glucose and glycogen a pyruvate.
- In exercise, circulating adrenaline is going to be high and so glucose will be released back into the bloodstream, where it is available to be taken up by active muscles as a fuel.
- It may seem wasteful that this cycle effectively has a net consumption of 4 ATP but it effectively shifts the metabolic burden from the muscles to the liver.
25
How is lactate correlated with exercise intensity?
At low exercise, the blood level of lactate is low and remains constant.
As intensity of exercise increases, the capacity of the body to metabolise the circulating lactate us exceeded and it starts to accumulate in the blood.
26
How can training increase lactate threshold?
- Training results in a variety of changes, which increase the body’s ability to take up and metabolise lactate.
- Blood lactate concentration can be measured directly form blood samples.
- Alternatively and more commonly, respiratory variable can be monitored to provide an indication of lactate threshold.
- This is because the lactate accumulation in the blood leads to metabolic acidosis, which drives an increase in ventilation rate and increase in expired CO2.
27
Explain oxygen deficit.
This difference between demand and supply of ATP is made up from short term ATP stores, such as the phosphocreatine system and by glycolytic metabolism. Leads to an oxygen deficit and the lactate produced by glycolysis will need oxygen to be metabolised. So rate of oxygen uptake will remain elevated after exercise stops and only recovers gradually over time as the oxygen deficit is repaid.
28
What is the VO2 max?
The rate of oxygen uptake during exercise, which involves the whole body, increases as intensity of exercise increases until it reaches a maximum level. This is the maximum rate of consumption of oxygen by the body and is an estimate of an individual’s capacity of aerobic ATP synthesis.
29
What are the VO2 max values for humans, thoroughbred horses and greyhounds in mL/kg/min?
Human = 40-50
Human athlete = 94
Thoroughbred = 220
Greyhound = 240
30
Do differences in fibre type contribute to thoroughbred high oxidative capacity?
No – thoroughbreds still need the mix of muscle types that give the optimum combination of speed and endurance. Instead, the explanation is that thoroughbred muscles have a greater muscle mass. This is due to more and larger mitochondria in type I and IIa fibres. The greater surface area for oxidative phosphorylation provides increased ATP generating capacity and therefore increased oxygen requirements to sustain higher intensities of exercise.
31
Describe the contribution of different fibre types during locomotion.
- Low levels of activity: force generation is low and primarily provided by type I slow twitch fibres using fat fuel.
- Speed increases: more type IIa fibres recruited to provide the greater force required using fats and lactate as fuel.
- Speed increases further: type IIb glycolytic fibres recruited to provide maximum force. Unable to utilise lactate or fats due to low oxidative metabolism so primarily uses carbohydrates from glycogen stores and blood glucose form the Cori cycle.
- Lactate produced: used by other muscle fibres to maintain high rates of ATP production in type IIa and type I fibres.
- Fast speed cannot be maintained for long before muscle glycogen stores begin to be depleted and fatigue sets in.
32
What is the mechanism of fatigue?
1. Increased transmural pressure on blood vessel sin the muscle, which can decrease blood flow.
2. Resulting ischaemia can lead to the accumulation of metabolites.
3. Muscle fibre swelling and mitochondrial swelling, impairing the ability of muscle fibres to contract.
4. Prolonged anaerobic metabolism of type IIb fibres can also lead to a decrease in ATP substrates, again limiting contractile function.
33
Describe fatigue on a muscular level.
- Can result in depletion of muscle glycogen stores, which limits the work rate.
- Extracellular potassium ion accumulation can also impair action potential firing and muscle contractility, as can an increase in muscle temperature in hyperthermia.
- Prolonged exercise can lead to dehydration and electrolyte loss due to sweating, which is needed to avoid hyperthermia.
Horses are more prone to this than other species.
34
What is central fatigue?
- Results from a decrease in drive to exercise from eth brain.
- Due to inhibitory feedback from group III (A-delta) and group IV (C) afferents within the muscle.
- These can signal the work being done by the muscle, as well as the accumulation of metabolites, which decrease performance by decreasing the central motivation to keep going.
35
Describe the phases of increased ventilation at steady state exercise.
- At the onset of exercise, the pulmonary ventilation increases steeply within a single respiratory cycle.
- This is far too rapid to be a results of any changes resulting from the exercise itself.
- If the animal is expecting exercise, there is often an anticipatory phase, in which pulmonary ventilation increases before the start of exercise, driven by activity in motor cortex and respiratory centres in the medulla to directly increase ventilation rate.
- Initial phase of respiration may be followed by a dip before the second pages of the ventilatory response.
- This gradually increases over a period of several minutes to match pulmonary ventilation with the oxygen carrying capacity and oxygen demand.
- Mammalian respiratory system is very good at this matching and pulmonary ventilation is never a limiting factor to exercise performance in normal animals.
- This increase is not driven by a change in blood glasses, which remain pretty stable in most species.
- Instead this matching phase of the increase in pulmonary ventilation is driven by the mechanoreflex and metaboreflex.
36
What is mechanoreflex?
- Driven by increased activity in type III (A-delta) sensory afferents from the body of the muscle.
- These afferents have free nerve endings which are squeezed and distortion by muscle contractions.
- Provide information that the muscle are doing work to drive the medullary ventilatory response.
- Afferent information from joint receptors also contribute, as passive movement of limbs have to be sound to increase pulmonary ventilation in the absence of muscle contractions.
37
What is metabolreflex?
- Mediated by increased activity in the type IV (C type) sensory afferents.
- These respond to chemicals in the interstitial environment, including K+ and H+ ions.
- Signal the metabolic activity of the muscle fibres and drive increased ventilation via the brainstem respiratory centres.
38
In addition to mechanoreflex and metaboreflex, what else drives pulmonary ventilation?
Central command. Can control this matching phase of increase in ventilation as previous experience with a certain exercise activity induces learning in the central command system, so that the matching occurs more rapidly for subsequent periods of the same exercise.
39
When is minute ventilation proportional and disproportionate to oxygen consumption?
Proportional: low to moderate exercise intensity. No change in the alveolar partial pressures of oxygen or carbon dioxide and there is no change in the arterial blood gases.
Disproportionate: onset of blood lactate accumulation. Due to increased circulating CO2.
40
What causes the ventilatory threshold?
1. Increase in blood lactate at high intensity exercise.
2. Decrease in blood pH due to lactic acid accumulation results in a metabolic acidosis.
3. Drives the increase in ventilation via peripheral chemoreceptors in the carotid body.
4. Lactic acid is buffered by bicarbonate in the blood, which produces carbonic acid.
5. This is converted to water and carbon dioxide by the action of carbonic anhydrase, which limits the effects of lactate accumulation on blood pH.
6. The increased PaCO2 increases the diffusion gradient driving more CO2 across the lungs, which also explains the increased concentration of CO2 in the expired air.
7. Increase in CO2 exhalation during intense exercise results in a respiratory exchange ratio of above 1. The increase in this ratio can be used to estimate lactate threshold and an indicator of aerobic capacity during training.
41
Describe ventilation and locomotion coupling in gallop of horses and dogs.
In gallop, there is one phase at the same time as the hindlimbs are moving forwards in their swing phase. These movements compress the thoracic cavity, reducing the volume of the lungs.
42
Describe ventilation and locomotion coupling in swing phase of horses and dogs.
The hindlimbs are fully extended at the end of their stance phase at the same time that the forelimbs are moved forwards at the end of their swing phase. These movements reduce pressure on the thoracic cavity allowing the lungs to expand.
43
What is the piston-pendulum effect of ventilation and locomotion coupling in horses and dogs?
- This expansion and contraction of the lungs during galloping is known as the piston-pendulum effect. It reduces the work of ventilating the lungs, but is not essential for lung ventilation and may be decoupled – for instance, an animal with chronic obstructive pulmonary disease.
- Coupling means that for horses galloping at a fixed speed, with a fixed stride length, the ventilatory frequency will be fixed and any changes in minute ventilation come from changes in tidal volume,
- This fixes respiratory frequency, so increase in minute ventilation comes from increases in tidal volume.
44
Distinguish the alveolar pressure during exercise in humans and horses.
Humans: upper airways do not limit ventilation during exercise.
Horses: nasal breathing is more resistant to slow through airways. More negative alveolar pressures.
45
What is exercise induced pulmonary haemorrhage?
The rupture of the alveolar blood vessels and haemorrhage into the lung alveoli.
Particularly common in horses, nearly 100% in thoroughbreds have some sign of bleeding into their lungs and may be found in greyhounds.
May be able to see external signs in epistaxis.
46
What caused exercise induced pulmonary haemorrhage?
- Causation unclear but horses have enormous blood supply and high pulmonary pressures expanding blood capillaries.
- If coupled with high negative pressure during inspiration, this is thought to lead to bursting of the thin-walled vessels and bleeding into the lung alveoli.
- More frequent in the dorsal caudal quadrant, under the saddle. Bleeding starts at the tip if the lungs and progresses cranially over repeated occurrences.
- So a theory is a pressure wave in the lung tissue, stretching tissue and tearing delicate alveolar capillaries.
47
What is the relationship between cardiac output and oxygen demand?
- There is a linear increase in cardiac output as exercise intensity increases as measured by oxygen uptake.
- Increased oxygen demands by the exercising muscle needs to be delivered by the CVS system and as the blood is well oxygenated in the lungs the only way of getting more oxygen to the tissue us increased by increased flow and that means increased cardiac output.
48
Explain the contributions of stroke volume and heart rate to cardiac output during exercise.
At low work rates, the increase in cardiac output is largely due to the increase in stroke volume with little change in heart rate.
As exercise intensity and therefore cardiac output increases, the stroke volume reaches its maximum limit and further increases in cardiac output are primarily due to increases in heart rate.
49
What is the Frank-Starling Law of the heart?
Stroke volume is dependent on the left ventricular end-diastolic pressure.
This is increased by an increase in venous return and increases ventricular filling > increases LVEDV > stretches the cardiac myocytes > increasing cross bridge formation > more force is generated during contraction to expel more blood > increase stoke volume > increased stoke volume > positive chronotropic effect of sympathetic nerve activity > increase heart rate > onotropic effect > increase myocardial contractility.
This changes the shape of the Frank-Starling relationship, increasing stroke volume for a given LVEDP.
50
Describe the distribution of cardiac output at rest.
- 10% of blood flow is to the brain
- Muscles are not exercising, but still remain a basal level of muscle tone and receive 15% of blood flow.
- Kidneys receive 20% of blood flow
- Splanchnic circulation, including the liver, receives 30% of resting blood flow, and is also under parasympathetic control in digestive absorptive mode.
51
Describe the distribution of cardiac output at exercise.
Total cardiac output is dramatically increased.
- So although blood flow to the brain decreases as a proportion, it has not changed that much.
- The maintenance of 5% flow to the heart and the skin actually present an absolute increase in blood flow, which is required to meet the metabolic demands of the heart and increased blood flow to skin for thermoregulation.
- There is redistribution of blood from the kidneys splanchnic bed and other tissues to the muscles.
52
What 2 factors cause distribution of blood from the kidney splanchnic bed to muscles?
Massive vasodilation of the arterioles in the muscles, dramatically decreasing their resistance and therefore increasing blood flow to the active muscles.
Increased sympathetic activity, along with increased adrenaline release from the adrenal medulla results in general vasoconstriction. This increases resistance of the splanchnic and renal blood vessels, reducing blood flow to these non-essential tissues and helping to limit the drop in total peripheral resistance.
53
What is functional hyperaemia?
- Blood flow to a tissue is regulated at a local level by the vasodilatory effects of metabolic products.
- This autoregulation automatically matches blood flow to a tissue bed with its metabolic requirements.
- Vasodilation in response to adenosine, ATP, K+. lactate, CO2, H+ and increased temperature is known as functional hyperaemia.
54
What is functional sympatholysis?
- Local metabolite mediated vasodilation is against the general vasoconstriction being mediated by sympathetic activity and circulating adrenaline via alpha adrenoreceptors.
- Some, such as intraluminal ATP have a distinct effect to reduce alpha receptor mediated vasoconstriction that is independent of their effects on functional hyperaemia.
55
What does functional sympatholysis allow for?
Vasodilation to be restricted to just active muscles that require the extra blood flow, while the blanket vasoconstriction due to alpha adrenergic receptors reduces blood flow to inactive muscles. This optimises the redistribution of blood flow.
56
What is the relationship between flow mediated dilation and nitric oxide?
Nitric oxide release stimulated by shear stress. Shear stress is a frictional force parallel to the wall at the surface of the endothelium directly related to blood flow velocity. Increased shear stress causes increased endothelial nitric oxide synthase activity. Increases nitric oxide production.
57
What is the formula for shear wall stress?
4nBFR / pi x (kr)^3
58
Describe how systemic blood pressure changes in exercise.
- Increased blood flow through the skeletal muscle vascular beds will itself lead to further flow mediated dilation,
- This is due to frictional forces between the blood cells and the plasma that induces shear stress in the endothelial cells.
- This results in the production of nitric oxide by the endothelial cells and is a paracrine vasodilator.
- The greater the blood velocity to the arteriole, the greater the dilation, which helps to reduce blood velocity enabling sufficient time for gas exchange to occur.
59
Distinguish the haemoglobin and myoglobin dissociation curves in exercise.
- Even though the oxygen us largely unloaded from haemoglobin at 20 mmHg in exercising muscle, the different shape of the myoglobin O2 dissociation curve compared to the haemoglobin dissociation curve means that there is still sufficient PO2 to keep the myoglobin oxygen stores more than 80% saturated.
- These myoglobin stores help to buffer local O2 levels to smooth out local changes in supply and demand.
60
What is different about the PaO2 level in horse compared to a human?
Arterial PO2 decreases as the exercise intensity increases and this is associated with an increase in PCO2.
61
What are the effects of the enormous cardiac output in horses? How is this linked to a horse's decreased PaO2 in exercise?
- Increased blood flow must go through the lungs.
- Some of this will flow through previously underused vessels and the total volume if the pulmonary blood flow will be to increase the speed and decrease the transit time for erythrocytes in the alveolar capillaries.
- As the pulmonary blood flow increases, the erythrocytes travel further along the alveolar capillary before they equalise with the 100mmHg PaO2.
- At the highest cardiac outputs, the transit time is too short for the blood to fully load with the oxygen, despite the increased diffusion gradient due to the increased arterio-venous O2 differences.
- This lack of time for gas exchange is why PaO2 falls giving an exercise-induced hypoxaemia and PaCO2 increases in horses at the most intense exercise rates.
62
How does spleen contraction in the horse increase circulating red blood cells?
- The total oxygen content in the horse’s blood at high exercise intensity does not change.
- This is due to the sympathetic mediated contraction of the spleen which is particularly important in horses in elevating haemotocrit and haemoglobin concentration.
- At rest, a third of a horse’s red blood cells are stored in its spleen and when they are ejected into the circulation cause a notable increase in viscosity of the blood.
63
How are plasma volume and haemoconcetration related during exercise?
- The haematocrit and the viscosity of blood is further increased by a decrease in plasma volume during intense exercise.
- This is due to a build-up of metabolites in the interstitial space, which changes the balance of the Starling’s forces determining trans-endothelial water flux.
- More water diffuses into the interstitial fluid compartment by osmosis reducing plasma volume and increasing haematocrit.
64
Describe the control of cardiac blood flow during exercise.
- Muscles contract and the increased transmural pressure collapses blood vessels and restricts blood flow.
- Around 75% of O2 is delivered to cardiac muscle via the coronary arteries.
- Blood flow to cardiac muscle occurs during diastole and the total flow of blood increases as intensity of exercise increases, despite the reduction in total time in diastole due to the increases heart rate.
- Local accumulation of metabolites result in vasodilation of the arterioles supplying cardiac muscle.
- The increased sympathetic activity that increases the heart rate and myocardial contractility is associated with a vasodilation of cardiac blood vessels.
- This is because circulating adrenaline from the adrenal medulla acts on beta-2 adrenergic receptors on the coronary blood vessels causing vasodilation.
65
What is the effect of training on VO2 max?
Endurance training can increase VO2 max by up to 25%.
66
What is the effect of training on cardiac output?
- At rest, there is no difference in the cardiac output between trained and untrained individuals as they have the same metabolic rate at rest.
- The effect of training is to increase the maximal cardiac output.
67
What is the effect of training on heart rate?
Training substantially decreases resting heart rate.
68
What is the effect of training on stroke volume?
Training increases the main stroke volume at both rest and at VO2 max. endurance athletes, who both have an existing genetic predisposition to endurance and have been trained, have far greater stroke volumes.
69
Explain the effect of training on heart rate, cardiac output and stroke volume.
- The increased cardiac output following training increases oxygen delivery to the exercising muscles, enabling higher work rates.
- Although increasing heart rate is important for increasing cardiac output as exercise intensity increases, there is a natural limit.
- This is because increasing heart rate decreases the duration of diastole available for ventricular filling, which limits stroke volume.
- So maximum heart rate is not increased by training and the increase in cardiac output comes from the increase in stroke volume.
70
What is the effect of training on left ventricular volume?
- Increased stroke volume reflects both an increase in venous return and changes in the morphology and physiology of the heart.
- Human and animal athletes hearts have a larger end diastolic volume than non-athlete’s hearts.
- This is associated with remodelling of the heart giving a larger left ventricular muscle mass.
71
Why does plasma volume expansion increase preload as an effect of training?
- The cause for this increase in plasma volume is increased albumin production by the liver in response to training, which causes more water retention by the kidneys due to its effect on blood osmolarity.
- This training related expansion in blood volume results in the increased preload increases ventricular end-diastolic volume and therefore force of contraction via the Frank-Starling mechanism.
72
What is the effect of training on systolic function?
Training also increasing myocardial contractility by directly increasing the sensitivity of the cardiac myocytes to intracellular calcium ions. This increases contractility as sub-maximal activation of cardiomyocytes, increasing the tension developed at a given level of intracellular calcium ions.
73
What is the effect f training on oxygen extraction? Why is this?
Training does have an effect to increase the difference in arterio-venous O2 content, as the system becomes more efficient at extracting oxygen from the blood.
There are 2 main reasons for this:
- The redistribution of blood flow to active muscle becomes more efficient
- There are local metabolic changes in the skeletal muscle that increase their oxidative capacity
74
What is the effect of training on blood flow and distribution? Why is this?
The increase in cardiac output following endurance training is primarily flowing to skeletal muscle, this is due to a more efficient redistribution of blood flow to active skeletal muscle. This is partly due to increased vasoconstriction to non-active tissue beds, such as the splanchnic and renal beds. But this is also due to angiogenesis, increasing the capillarisation of the oxidative muscle fibres to increase blood flowing to them.
75
What are the 3 main theoretical ways that training can increase the size of a muscle?
Hyperplasia – increase in the number of muscle fibres in a muscle.
Lengthening of muscle fires – particularly during growth and this is greater in anaerobic training.
Hypertrophy – main way. Occurs by the fusion of stem cells with the muscle fibre, which adds further sarcomeres in parallel with existing ones, along with nuclei to the existing fibres. The tension generated by a muscle fibre is dependent on its cross sectional area of sarcomeres. So force of contraction increases. In response to endurance training, hypertrophy occurs to slow twitch type I fibres with no hypertrophy of type II fibres.
76
What is the effect of training on the number and size of mitochondria in oxidative fibres?
Low intensity endurance training predominantly increases the mitochondrial content of the slow twitch type I muscle fibres, without affecting type II fibres.
But as the endurance training becomes more intense, the mitochondrial content of the fast twitch, type II fibres also increases.
Increase the surface area available for oxidative phosphorylation for greater oxygen utilisation.
77
What is the effect of training on gene expression?
Increases in gene expression levels for enzymes involved in oxidative metabolism. For instance, there are increased expression levels of the citric acid cycle enzymes citrate synthase and succinate dehydrogenase going from untrained to medium trained to high intensity endurance trained human athletes.
78
Contrast with anaerobic training with endurance training.
- Anaerobic occurs during short burst of fast and forceful muscle contraction with activity that is not maintained for more than a few minutes at a time.
- There are not the same extent of CVS changes that are seen in endurance training, but training is vital to improve performance and the training needs to be specific to the movements and muscle groups that will be used in competition.
- The faster and stronger the contraction, the more effective it will be as a training condition.
79
Distinguish concentric and eccentric muscle contractions.
Concentric, isotonic contractions, contractions when shortening the muscle. Such as the extensor muscles when jumping.
Eccentric contractions occur in the leg extensor muscles during landing to act as shock as absorbers and to prevent collapse. Eccentric contractions are less effective training and also have a higher risk of muscle damage then concentric contractions.
80
What is the effect of anaerobic training on muscle fibres?
Anaerobic training for strength, speed and agility is more effective than aerobic training in causing hypertrophy and it is the fast twitch type IIa and IIb fibres that undergo hypertrophy, with the slow twitch type I fibres remaining unaffected by anaerobic training.
81
What is the effect of anaerobic training on anaerobic substrates?
- Phosphocreatine can donate its high energy phosphate bond to ADP to generate ATP and so acts as a local store and buffer of muscle fibre ATP.
- Anaerobic training increases the levels of creatine in the fast twitch, type II muscle fibres along with phosphocreatine, ATP and glycogen stores.
- Increases in enzymes of glycolytic metabolism such as phosphofructokinase.
82
What is overtraining?
Overtraining reduced overall fitness, leading to poorer performance, increased injury risk, greater risk of infection and psychological impacts, including depression.
83
What is deconditioning?
The loss of fitness, when training is reduced or stopped altogether.
84
Why can turtles dive for longer than humans?
Humans and turtles have the same oxygen stores but turtles can dive for longer. This is because turtles are ectotherms and humans are homeothermic. They do not burn through ATP as quickly and so are able to use oxygen more efficiently.
85
What is the most important sources of oxygen for diving mammals?
Haemoglobin in muscle
86
Why do Weddell seals breathe out before diving? What is the role of the lungs in diving animals?
To reduce buoyancy and to decrease gas exchange in the alveoli. Decreasing gas exchange in the alveoli as increased pressure when diving increases the partial pressure of gases, O2 and CO2 but also of nitrogen oxide. Pushes air into dead space so nitrogen us not absorbed.
87
What are the physiological challenges associated with acute ascent to altitude?
Impact on ability to exercise at higher altitudes due to reduced partial pressures of oxygen. Barometric pressure decreases. Blood will be less efficient at oxygen loading.
88
What happens to alveolar ventilation at altitude and what drives this change?
Increases. This is because of decreased arterial pressure of oxygen/PaO2.
89
What will happen to arterial pH at altitude?
Increases. Increase ventilation rate so more CO2 is removed and so pH will remove.
90
How would you expect the oxygen dissociation curve for haemoglobin in arterial blood to shift with acute ascent to altitude?
Leftwards shift. Increased pH increases affinity of haemoglobin for oxygen and they can load more oxygen.
91
Is the EMG is a direct recording of the force of contraction of the stimulated muscle?
No. EMG represents the action potentials occurring in the muscle fibres innervated by the motor neurones which make up the population of motor units whose activation leads to contraction of the muscle. In this experiment, the triceps surae muscle group.
92
The stimulus to induce the reflex contraction of the triceps surae group of muscle activates which sensory receptors?
Muscle spindles
Physiology Y2
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