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Creado por sophietevans
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| During exercise, many physiological processes are repeated in cycles which may be altered in frequency and/or magnitude. These are continually modified by the brain, and to some extent peripheral CO2/pH receptors, and some functions have anatomical reserves if necessary. Name three of these physiological processes. | Locomotion, heart function, and respiration. |
| Elite marathon runners run at what percentage of their VO2-max compared with average marathon runners? What enables them to do this? | Elite marathon runners are able to run at >80% of their VO2-max, compared with the 50-60% VO2-max that average marathon runners are able to run at. This is a result of being able to oxidise a greater extent of muscle glycogen (Coyle, 2007, Physiological Regulation of Marathon Performance). |
| True or false: lactate seems to be generated from glycogen in inactive muscle fibres? | True (Coyle, 2007, Physiological Regulation of Marathon Performance). |
| Which organelles do well-trained endurance athletes possess greater concentrations of? | Mitochondria. |
| Before exercise even begins in a marathon, what are the five anticipatory processes that occur in the body? | 1. Autonomic nervous system input (fight or flight -> release of adrenaline). 2. Energy sources are mobilised (by hormones). 3. Cardiovascular adjustments anticipate the needs. 4. Respiratory responses - reserves recruited. 5. Temperature regulation. |
| As an anticipatory measure before a marathon begins, sympathetic autonomic nervous activity is increased, resulting in adrenaline being released. What physiological effects does this have? | It acts on the sinoatrial node to increase the heart rate, as well as on the ventricular myocardium to increase the contractility and therefore stroke volume. Together, these increase the cardiac output and, along with increasing the venomotor tone by acting on vascular smooth muscle of veins to contract them which also increases stroke volume, this acts to marginally increase mean arterial blood pressure. Lastly, the adrenaline acts on the pancreatic islets of Langerhans to increase glucagon secretion from α cells (to liberate energy sources) and to decrease insulin secretion from β cells (to create a pro-liberation environment) -> this acts to increase blood glucose concentration. |
| Is the first mile of a marathon aerobic or anaerobic? | Anaerobic - it results in the formation of increased lactate and H+ ions (from both lactic acid and carbonic acid formation), but trained athletes switch to aerobic metabolism within a mile to most efficiently use precious glucose/glycogen stores. |
| What are the two initial fuels for increased activity? | Muscle ATP stores and creatinine. |
| Respiratory and cardiovascular functions increase immediately upon the onset of exercise - but can they increase before? | Yes, there is a feedforward mechanism which is separate from the anticipatory sympathetic response but governed by central nervous command. |
| What is the 'aim' of the respiratory feedforward mechanism before exercise begins? And the respiratory feedback mechanism once exercise has started? | The feedforward mechanism aims to maintain arterial pO2 and pCO2 by increased ventilation (under both central control and control by mechanoreceptors and chemoreceptors which input to respiratory centres), whereas the feedback mechanism aims to decrease ventilation when pCO2 drops in order to prevent hyperventilation and respiratory alkalosis. |
| Where in the brain are the cardiorespiratory centers? | The brain stem. |
| Tidal volume and rate increase during exercise. Which predominately increases in low-moderate intensity exercise, and which predominately increases in high intensity exercise? | Low-moderate intensity exercise: increased tidal volume. High intensity exercise: increased tidal rate (volume stabilises ~65% of vital capacity). These preferences are to work towards maintaining pO2/pCO2 while not exhausting the lungs, but rather maximising their efficiency. |
| Which organs predominately control the body temperature at rest? | The heart and liver generate the most heat at rest. |
| What is the leg muscle temperature at rest? | ~35 degrees Celsius, just slightly less than the core temperature at the peripheries are further from the heat generating organs, and have a greater surface area:volume ratio from which to lose heat. |
| Around 10 minutes into a marathon (assuming the environment temperature has stayed the same), what are the temperature changes in the overall body temperature and the leg muscle temperature from rest? | Overall body temperature at rest = 37 degrees Celsius; 10 minutes into a marathon = 38.5 degrees Celsius. Leg muscle temperature at rest = 35 degrees Celsius; 10 minutes into a marathon = 39 degrees Celsius. Now, the legs are the primary heat-generating organs as a greater extent of biochemistry is occurring during their activity. |
| What environmental factor might make it difficult to lose body heat during a marathon? | Humidity - this prevents sweat from evaporating as efficiently and removing heat as the energy required for this evaporation. |
| What are three ways in which the body tries to lose heat during a marathon? | There is an increase in blood flow to the skin (aided by vasodilation), as much as 7 L/min maximum skin blood flow during exercise compared with 0.15 L/min at rest. There is increased sympathetically induced vasodilation in certain vascular beds in response to increased core temperature, as well as a decrease in sympathetically induced vasoconstriction as heat decreases the sensitivity of adrenergic receptors in the veins. |
| What distance of a marathon is the 'long haul' or 'steady state'? | ~the first 20 miles |
| Why is there an increased in blood glucose in the first ~6 miles of a marathon? | Adrenaline concentration increases, resulting in increased glucagon concentration which results in glycogenolysis and gluconeogenesis. |
| Why does the blood glucose concentration tend to fall below the resting value in the last ~6 miles of a marathon? | Muscle glycogen stores, plasma glucose, and newly formed glucose are depleted, and oxidation of carbohydrates is reduced. |
| What is the main fuel source during the latter half of a marathon? | Free plasma fatty acids. |
| Why is there a surge in epinephrine in the last ~4 miles of a marathon? | Glucose is depleted below the resting plasma concentration at this point, and epinephrine is released in response to this physiological distress in order to mobilise further glucagon from the pancreas, and to promote gluconeogenesis in the liver, as well as lipolysis in adipose tissues to provide further substrate-level energy sources for respiration. |
| Mean arterial pressure increases during the marathon, both as a result of increased venomotor tone and compression of blood vessels by muscles. By how much does it increase from the resting value? | ~20% increased |
| The baroreceptor reflex is not effective during exercise, as blood pressure is supposed to be increased in order maintain activity so seeing to lower it would be pointless. However, at what point during exercise might it become active again? | When blood volume decreases due to dehydration. |
| What role do metaboreceptors play in increasing blood pressure during high intensity exercise? | They feedback to the cardiorespiratory control centres in the brain stem to further increase blood pressure in order to remove more accumulated metabolites from the muscle. |
| How does the orderly recruitment of respiratory muscles in order to maximise their efficiency and minimise overall work during exercise come about? | Stretch receptors in lung tissue can result in activation in a certain order and varied force of contraction of respiratory muscles to ease work. |
| Despite gastrointestinal function being decreased during exercise (due to increased sympathetic activity as well as blood flow diverted to other organs) so that gastrointestinal motility is decreased, the physical activity of the body during exercise increases the movement of contents through the gastrointestinal tract. Why doesn't this result in diarrhoea? | Because water absorption lags behind motility. |
| Most marathons start in the morning, so by the latter stages of the race the ambient temperature has risen to around 30 degrees Celsius, for instance, reducing the ability to lose heat by convection. Assuming the humidity is low, heat loss via sweat is still effective. Why would this increased need to reduce body heat result in competition between organs for blood? | Because there is increased blood flow to the skin which reduces the amount of blood available to the rest of the body, resulting in competition for the remainder between organs. |
| If blood distribution is considered to always be a competition between the skin, the muscles, the viscera, and the vital organs, where is the majority of the blood in the following conditions: 1) at rest in a neutral environment? 2) at rest in a warm environment? 3) during moderate exercise in a cool environment? 4) during moderate exercise in a hot environment? | 1) Distributed relatively evenly between the viscera and vital organs. 2) Distributed relatively evenly between the skin and the vital organs. 3) Distributed relatively evenly between the muscle and the vital organs. 4) Blood is distributed to the vital organs (always) but there is competition for it between the skin and skeletal muscles - this will either result in fatigue or hyperthermia. |
| During exercise, sweat production can reach up to what rate? | Up to 1.8 L/hour - 10% of sweat is lost from the plasma volume. |
| The fluid volume of the body is finite and fluid is lost during exercise, so conservation is critical to the maintenance of a healthy internal environment. What can the body do to conserve fluid during exercise? | Decrease urine production by lowering the glomerular filtration rate and increasing water re-absorption. |
| Increased sympathetic activity and decreased glomerular filtration rate stimulate the release of what from the kidney juxtoglomerular cells? What effect does this have? | This stimulates renin release from the kidney juxtoglomerular cells. Renin converts angiotensinogen to angiotensin I. This is converted by ACE to angiotensin II which has multiple physiological effects, including stimulating aldosterone release. Aldosterone stimulates sodium re-absorption - water follows sodium, resulting in a decreased urine output, so the combination of increased sympathetic activity and decreased GFR results in conserved fluids during exercise. |
| Is sweat hypo-osmotic or hyper-osmotic? | It is hypo-osmotic so its loss results in plasma becoming hyper-osmotic. This is detected by osmoreceptors, which leads to increased anti-diuretic hormone being released which increases water reabsorption. This complements the action of aldosterone, the release of which results from increased sympathetic activity and decreased glomerular filtration rate. |
| Why is the thirst response not sufficient for hydration in a marathon? | Drinking voluntarily, you will only take in ~2/3 of what you actually need so it is not sufficient to rely on thirst - by the time you are thirsty, you are already dehydrated. |
| What is better for hydration during exercise: a sports drink or water? | In exercise under an hour, the glucose in sports drinks will not contribute to the energy needs of a person doing exercise, so water is sufficient. In exercise over an hour, the glucose will contribute to the energy needs, so a sports drink may be more appropriate. The flavourings may increase consumption in either case, which can only a be a good thing for hydration, unless the drink is hyperosmotic, as this will decrease water absorption across the intestinal tract. There is minimal evidence for the use of sports drinks containing ions affecting activity performance. |
| What is 'hitting the wall'? | Exercise at 70–85% V-dotO2max cannot be maintained without sufficient carbohydrate oxidation and thus the severe lowering of muscle glycogen, often coupled with hypoglycaemia, results in the need to reduce intensity to [almost equal to]40–60% V-dotO2max. This phenomenon has been termed ‘hitting the wall’ and the subsequent velocity appears to be that which can be maintained largely by oxidation of fat, blood glucose and lactate. (Coyle, 2007, Physiological regulation of marathon performance) The primary directive is to protect the brain (provide it with sufficient O2 and glucose). |
| Fatigue is the 'early warning system' of the body that exertion is too high and energy reserves cannot support the activity much longer. Is the somatic or the autonomic nervous system in control in fatigue? | In extreme fatigue, the autonomic nervous system predominates in order to preserve life/homeostasis. Fatigue has both physical and psychological aspects to it, and elite athletes can 'push through' fatigue for a short while in order to continue exercise. |
| Which three broad factors does fatigue towards the end of the marathon result from? | Intrinsic factors within exercising muscles, systemic factors influenced by metabolic and environmental stresses, and psychological factors e.g. pain. |
| List some of the intrinsic factors of fatigue within exercising muscle towards the end of a marathon. | Depletion of glycogen (in fatigue, there are depleted carbohydrate intermediates so fat stores cannot be utilised efficiently in the Krebs cycle); production of lactic acid (the H+ ions produced by its dissociation act on local and distal muscle to cause fatigue, but the lactate can at least be used for gluconeogenesis in the liver); accumulation of phosphate from the breakdown of ATP (can inhibit enzymes such as glucofructokinase from glycolysis); calcium accumulation in the mitochondria; and increased plasma K+ ion levels (if these increase to 7 mmol/dm^3 an individual can have a cardiac arrest). |
| How do H+ ions result in fatigue? | Within muscle cells, H+ ions inhibit phosphofructokinase (from glycolysis), displace Ca2+ ions from troponin (which inhibits muscle contraction - weakness), and stimulates nociceptors. In the brain, H+ ions cause the sensations of pain and nausea. In adipose tissue, H+ ions disturb lipase which reduces the mobilisation and availability of fats for metabolism. |
| During normal exercise, muscle pH decreases quickly with increasing exercise intensity, and arterial pH decreases slowly until high intensity exercise. What is different in marathon/endurance exercise? | The arterial pH decreases quickly but is recovered by the respiratory buffering system as a result of increased ventilation. |
| What is syncope? Why should you not stop exercising straight away after running a marathon? | Syncope ('fainting') is an insufficient blood supply to the brain. This is a risk after endurance exercise as the vessels are dilated in an attempt to lose heat and to best perfuse the muscles, and stopping exercise stops the skeletal muscle pump, resulting in blood pooling in the extremities. As a result, there is less venous return and a decreased stroke volume, leading to decreased cardiac output and a decreased mean arterial pressure - so pressure to carry blood to the brain is not maintained and less blood is being returned anyway. In order to prevent it, light exercise (a 'cool down') should be maintained for a period after the marathon ends. |
| What are the benefits to the body of fainting i.e. why does it resort to this drastic measure? | There is decreased competition between organs for blood (because there is decreased skeletal muscle activity and decreased heat production), and venous pooling as a result of gravity can no longer occur (because you are horizontal!) so venous return to the heart is increased, thus increasing stroke volume + cardiac output. |
| What is water intoxication? How does one avoid it? | In high intensity exercise, it is important to stay hydrated. However, the consumption of large volumes of hypo-osmotic fluids can result in decreased plasma osmolarity and an uptake of this fluid by the more hyper-osmotic cells. The brain cells swell against the fixed volume of the cranium, which increases the intracranial pressure, resulting in symptoms such as headaches, vomiting, and convulsions. The hyponatraemia that results causes multiple effects, up to death as a result of ion imbalance in vital tissues such as the myocardium. To avoid it, individuals should regularly drink small amounts of electrolyte-containing (ideally isotonic) fluid. |
| What is post-exercise fever? Why isn't a raised temperature during exercise a fever? | The hyperthermia during exercise does not alter the 'set point' in the hypothalamus, but an elevated temperature after exercise is a true hyperthermia because the hypothalamic 'set point' has been increased as a result of release of proinflammatory cytokines, such as IL-1 and IL-6, from damaged skeletal muscle, resulting in individuals feeling cold while actually having a dangerously raised core temperature. |
| What does DOMS stand for? | Delayed Onset Muscle Soreness |
| What is delayed onset muscle soreness? | There is sarcomere damage at the Z lines (the points of attachment of myosin via titin) as a result of strenous muscle activity. The plasma membrane permeability increases, and creatinine kinase and Ca2+ enter (these intracellular measures are a signal that damaged has occurred). It is repaired by phagocytosis and cytokine release by macrophages, hence the delay in soreness - their migration, proliferation and secretion of pro-inflammatory cytokines and hence result in dolor/function laesa takes time. |
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