Physiology of Sport Performance Module Notes PDF

Physiology of Sport Performance Module Notes **MODULE 1: FACTORS AFFECTING PERFORMANCE** **Intro** Non-physiological Biomechanics Factors affecting performance - We need to have an understanding of factors of performance from a physiological and non-physiological perspective - Be able...

Physiology of Sport Performance Module Notes **MODULE 1: FACTORS AFFECTING PERFORMANCE** **Intro** Non-physiological Biomechanics Factors affecting performance - We need to have an understanding of factors of performance from a physiological and non-physiological perspective - Be able to identify sites of fatigue   Non Physiological Factors - Environment - Diet   **1.1: Non Physiological Factors Affecting Sport Performance** Factors include but aren\'t limited to (these ones are the key non physiological factors): - Biomechanics: plays an integral role in the prep and profiling of an athlete. Understanding how they function, efficiency of movement and risk of injury can be taken from this area. Plays a large role. - Skill; sub area of biomechanics. Ability of an athlete to complete a task or action or their ability to learn it. - Psychology: large area of research in sports science. Mental state of an athlete plays a role in performance. Can be viewed from different perspectives: their ability to participate, mental health, mental state from an arousal/motivated view - Nutrition: grey area. Can be physiological and non physiological. How we fuel and what we fuel with will impact performance.   How much these factors influence someone will depend on the person and their type of sport. All factors will impact an athletes ability to perform in some way.     **1.2: Physiological Sites of Fatigue** Defining fatigue: an inability to maintain power output or force during repeated muscle contractions, which is reversible with rest Sites of fatigue are specific to the activity, as each sport has different demands.   Reasons for fatigue can include: - Muscle fibre type and training state of the person - Whether the muscle was stimulated voluntarily or electrically - The use of both amphibian and mammalian muscle preparations, with some isolated from the body - The intensity and duration of the exercise and whether it was continuous or intermittent activity.   Video Notes - Fatigue can be split into central or peripheral, as outlined in the picture - Fatigue will be sport specific in how it manifests. - There is no perfect agreement on the site of fatigue due to different studies and their methods. - Central fatigue: brain. Impairments may be due to motivation, arousal, sending motor unit signals to recruit MU and sending that to the spinal cord. - Peripheral fatigue: number of sites \>\>\>\> - The actin myosin interaction results in tension and heat that should equal force and power output. - [Studies on sites of fatigue on PP notes. ] - Compared to studying muscle function in vivo, using an isolated single muscle fibre to study muscle fatigue provides the advantage of measuring both ions and metabolites within fibre possible and force production of the single fibre can be measured are correct. - Fatigue studies are not in perfect agreement due to there being an inconsistency in the intensity and duration of the exercise and whether or not that exercise was continuous or intermittent - A disadvantage of utilising isolated muscles to explore causes of fatigue in research is that the mechanisms of fatigue may become biassed due to the - presence of extracellular gradients   **1.3: Central Fatigue** Central fatigue is associated with fatigue of the CNS. It\'s suggested that if the CNS is impaired, we\'d observe: a reduction in the number of functioning Mus involved in activity and a reduction in motor unit firing frequency. There is literature both for and against this concept.   Video notes - If the issues with motor units are found, there is a case of saying it is central fatigue - There are more recent studies indicating that CNS does have a role in fatigue. - There was a study done, showing that those given active encouragement were able to beat their previously set maximum in the activity, suggesting that their mental state plays a roll in output and motivation levels. - There is evidence that the impairment of voluntary contraction of muscle may be due to impairments in the CNS and its ability to recruit motor units. - If we can reduce the depression of stimulatory drive, feedback pathways will be improved. - Fatigue has a role in excessive endurance training and can be viewed as overtraining. OT results in reduced performance capacity, fatigue, anxiety, etc. - There has been studies looking at the levels of serotonin. Increased serotonin is can be linked with fatigue but findings are mixed. More recent recent has looked the ratio of serotonin to dopamine and if serotonin is higher, it can contribute to fatigue and vice versa. - Low epinephrine may also be contributing to fatigue. - Central governor model: the CNS is intimating involved with exercise and continually feedback of the body\'s receptors and it\'s responses to the internal and external environment. The brain will automatically reduced power output that we can achieve in a self preservation response to the environment to prevent harm and maintain essential functions. - Our level of performance is limited by our higher brain centres. - The role of the CNS to overall fatigue, there\'s a 10% estimate of CNS involvement in fatigue. - Research indicates that following a series of voluntary contractions to produce skeletal muscle fatigue, electrical stimulation of the fatigued muscle group results in an increase in the maximal voluntary forced production. This suggests that the upper limit of voluntary strength   **1.4: Peripheral Fatigue** - Vast majority of evidence points to peripheral factors being the main cause of fatigue - Neural factors: increases in the CNS arousal facilitate motor unit recruitment to increase strength and alter fatigue. Under certain conditions an AP may be blocked in the T tubule and sarcolemma. The NMJ is probably not a contributing factor to neural fatigue. - Mechanical factors: the cross bridge cycle occurring is important to continue activities and tension development. Fatigue may be partly related due to high hydrogen ion concentration and the inability of the SR to rapidly uptake the calcium and results in an longer relaxation time. This then causes a fatigue effect due to muscle contraction not being able to be maintained. - Energetics of contraction: fatigue is associated with a mismatch at the rate that muscle can use ATP and the rate that ATP is supplied. An accumulation in metabolites (Pi and ADP), as a result of ATP breakdown during muscle contraction results in reduced cross bridge binding to actin, inhibits max force and inhibits calcium release from the SR. cellular homeostasis is unable to be maintained. Muscle fibres are recruited from Type 1 \> Type 2a \> Type 2b (aerobic to anaerobic). Exercises needing the more anaerobic fibres results in an increase in hydrogen ion production. - Radial production may contribute to muscular fatigue. Exercise itself promotes free radical production and may damage contraction and impact fatigue for exercise for longer than 30 minutes. May disrupt potassium homeostasis. - Supplement consumption may help reduced fatigue impairment. - The muscle redox state and isometric force production. The muscle redox state and isometric force production. In the rested state (a), the muscle is reduced. As exercise begins, the initial creation of free radicals within skeletal muscle benefits force production (b). With prolonged exercise (i.e., \> 30-minute duration), however, continuous production of radicals creates a relatively oxidized state within muscle and force production declines (c) as fatigue sets in. During recovery, the muscle returns to a relatively reduced state, absent of fatigue - Free radicals can promote muscle fatigue in events lasting longer than 30 minutes by damaging contractile proteins and limiting the number of cross bridges binding to actin - In increase in hydrogen ions will interfere with cross bridge cycling **MODULE 2: TESTING PHYSIOLOGICAL CAPACITY FOR SPORT** ***2.0 Testing Physiological Capacity for Sport*** - Origins of EP testing came from England, Scandinavia and the US. - Since the 80\'s, Australia has been the lead in sport science and physiology testing.   *Why is this topic important?* - We need to be able to know what physiological factors contribute to an athlete and their sport. - Understand how to test different capacities - Eg of factors: aerobic endurance, ability to perform a certain skill and repeat it, mental focus, technical ability, etc. - Having an understanding of this allows us to recognise the athletes strengths and weaknesses and then develop a plan to help address that. - We can\'t address if the athlete\'s physiological capacity has improved or is lacking, unless we have quantified it.   *How do we choose what to test?* - First need to identify the most important physiological capacities are for the respective sport. - We need an understanding of the sport, the movements and the demands placed upon the athlete. - We need to think about the practicalities and feasibility of running a specific test. Do we have the means and access to the appropriate equipment to test? - Does the mode of exercise being tested reflect the mode of exercise done in the sport? - There will always be more than one published method of measuring a certain physical capacity, so research is required to see comparisons between test protocols and if one is superior to another.   *What physiological capacities can be tested?* Aerobic Endurance: - max capacity - max sustainable aerobic power. Anaerobic/Sprint: - peak power - mean max power (highest average power sustained over a period of time) - work above critical power (total amount of anaerobic energy expenditure above max sustained aerobic) - repeat sprint capacity-consistency Muscle strength and power: - max force production capabilities of a muscle - max dynamic strength - \"speed-strength\" or power - combo of force and velocity - strength endurance - consistency.   What factors should be considered when deciding which capabilities to test? - How feasible is the test - Do we have access to the relevant equipment - Does the test replicate the sport or very close to - Can we repeat the test later on?   ***2.1 Aerobic Endurance Capacity and VO2max*** - Aerobic capacity is predictive of endurance capacity - VO2max is often done to test aerobic capacity, however, it depends on the event. - Generally, VO2max can predict aerobic capacity, however in elite sport it isn\'t always the best predictor due to varying factors and it is also dependent on the sport. - For longer duration aerobic events when the athlete isn\'t hitting their VO2max, than using VO2max isn\'t the best predictor, eg: extremely long running events. - When looking at an incremental exercise test, we are not looking for a peak value, but for an exercise intensity where we\'ve reached out max sustainable aerobic power. - When thinking about aerobic capacity, are we talking about VO2max or max aerobic capacity.   Max Aerobic Capacity - You can only report a result of VO2 max if you have evidence that the athlete has produced max effort. - Signs of max effort: attained HRmax, RER, lactate above 7.0 mmol/l, plateau in oxygen consumption despite an increase in exercise intensity. - If you don\'t have evidence of VO2 max, you need to report it as VO2 peak. - How is it tested: incremental test to exhaustion, done on a treadmill or bike or ramp test. The future of this is running a normal test protocol, then let them recover and then get them to work for a minute at the highest power output they can. - Max sustainable aerobic power. How is it defined? It is done through different tests: Lactate threshold, maximum lactate steady state, anaerobic threshold, maximum metabolic steady state and critical power. - Hrmax = 208 - (0.7 x age)   ***2.2 The Critical Power Concept*** *First video notes (rewatch this. Watched once without taking extensive notes, rewatch)* Power/velocity vs time to fatigue relationship - As power/velocity is increased, the time to fatigue is less - This power to time to fatigue curve has been found across multiple species. - Critical power correlates with rate of energy repletion that is linked to aerobic metabolism - CP demarcates heavy and severe exercise intensity domains with attendant whole body and intramuscular responses. - Exercise tolerance: 2 - 30 minutes is highly predictable - Crisp demarcation between heavy and severe exercise intensity domains suggest distinct fatigue mechanism. - Issues is that during very short and very long exercise bouts, tolerance can be poorly predicted. - Lack of knowledge regarding specific intramuscular processes can cause issues. The Mechanistic Bases of the Critical Power Concept - VO2max is commonly established in a RAMP exercise test and until exhaustion sets in. - CP itself can\'t be established in a single test, but must be done in a separate protocol. - Establishing critical power: you need to perform a series to tests to exhaustion. End exercise VO2 would always be the same. You would start to see a hyperbolic power/duration curve forming. - CP increases following continuous endurance and HIIT training. It decreases in hypoxia - The W prime is reduced by glycogen depletion and exercise prior to CP exercise but then increases following sprint training. - There is evidence the CP decreases due to prior exhaustive exercise resulting attainment of VO2max previously. - The W prime may be increased due to creatine loading and prior heavy intensity exercise below CP, altering response. - CP is purely aerobic and the W prime is anaerobic. - Exercise tolerance above CP is limited and is indicated by the W prime. - The physiological determinants of the W prime: intramuscular substrates (PCr and glycogen), accumulation of metabolites associated with fatigue (hydrogen ions and inorganic phosphate) and VO2 kinetic response: development of the slow component and VO2max. - It\'s becoming increasingly recognised that the W prime is associated with the kinetic response. - Intramuscular PCr and related metabolites are in control of mitochondrial respiratory, the PCr respiratory is an important determinant of the W prime.   Second Video - Definition of CP: highest exercise intensity that someone can maintain for a prolonged period of time. Synonymous with anaerobic, lactate and ventilatory threshold - Determine through a series of time trails. Doesn\'t measure VO2 or lactate - Requires curve fitting and maths. - W above critical power is the W prime. W prime is a representation of anaerobic capacity. - Asymptote: the flat part of the fitted curve represents CP How do we test it? - At least 2 time trials minimum, 5 is superior - Series of trials to determine mean max power for each effort duration - 12-20 minutes - Example of how to graph this is in this video     ***2.3 Lactate Threshold*** - Definition: inflection point in lactate exercise intensity relationship - The beginning on a non linear increase in lactate concentration. - There is an intersection point on a graph, where it goes from steady to a sudden increase and that is the lactate threshold point. - This video shows the Dmax method to give the indicated point of LT2. - To do a lactate threshold test you need to do an incremental exercise test that has three to five minute stages, blood samples need to be collected and the data analysis method needs to be chosen carefully - Needs to be a step test, not a ramp test so that data values at distinct   ***2.4 Anaerobic Threshold*** - Testing this works to determine max sustainable aerobic power - Older than testing CP or LT2 - You need to ask if this method is more practically valuable than testing CP or LT2. - This is more predictive of performance than VO2max - Definition: a change in the relationship between ventilation and oxygen consumption - Aka first ventilatory threshold (VT1) - Identified using the v-slope method. - The point of change on a graph reflects the anaerobic threshold, when it goes from constant and gradually linear increase to a sharper increase. - Better to use a step test rather than a RAMP test. - This video has a data set example. Spreadsheet downloaded. Shows how to graph find threshold - It\'s not uncommon if using the 2 different graphing methods, if the threshold point found is slightly different. It would then be written that the threshold point would be between the two values   ***2.5 Anaerobic Capacity*** - Aka sprint capacity is a key determinant in many sports - Defined: 1. peak power - instantaneous max power occurring for a second or a fraction of 2. mean max power - the average power sustained over a fixed duration 3. repeat sprint capacity - the ability to sustain performance over a set of sprint tasks. - To test it: usually done doing a single max effort on an ergometer - We have an ergometer for bikes, rowing and kayak - We have to use a treadmill for running but it doesn\'t measure power and we don\'t have an accurate method for swimming. - In the future: there is emerging technology that can be worn and used to measure power, however accuracy is debateable. Using the CP method, W prime can represent anaerobic capacity     ***2.6 Muscle Strength and Power*** - Muscle Strength Definition: 1. Max force production capabilities of a muscle 2. Max dynamic strength eg: isometric mid thigh pull - Max dynamic strength can be done assessing 1RM or 3RM - There is a specific warm up protocol for 1RM - Power: the combo of peak force and contraction velocity elicited by the muscle. - To test for power, we need a force plate - Strength endurance: consistency. Similar to repeated sprint ability. Doesn\'t look at peak force or power, but just looking at a task requiring consistent repeated effort. - To test for endurance, a mass 70% of 1RM is used and the task is repeated until failure, the quality of technique is to be maintained and contraction controlled. A metronome sets the rate. There is no set test protocol, literature needs to be used to guide testing. **MODULE 3: PHYSIOLOGICAL LIMITATIONS TO SPORTS PERFORMANCE** ***3.0 Physiological Limitations to Performance*** There are several reasons why it is important for us to understanding the factors responsible for limiting sport performance. This may include an ability to overcome or mitigate the limiting factor(s) with appropriate training and (legal) supplementation or it may be used a tool to identify talented (genetically gifted) individuals within a large cohort of potential athletes. If we understand the biological limitations, or limitations based on a specific genotype we can leverage this information to make important strategic decisions about how to train and how to compete. As exercise intensity increases, muscle fibre recruitment progresses from type I → type IIa → type IIx. This means that the ATP supply needed for tension development becomes more and more dependent upon anaerobic pathways. Suggesting, fatigue is specific to the type of task undertaken. If a task requires only type I fibre recruitment, then the factors limiting performance will be very different from those associated with tasks requiring type IIx fibres. ** ** ***3.1 Factors limiting all out anaerobic performances*** All out performances fall into 1 of 2 categories: 1. Ultra short term (less than 10 seconds): eg: 100m sprint, weightlight, 50m freestyle etc. 2. Short term (10-180 seconds) An image showing the factors affecting fatigue in ultra short-term events.      Ultra Short Term - Events less than 10 seconds - Dependent on type 2 muscle fibres - Large amount of force is needed - Motivation, skill and arousal are important - Primary energy systems are ATP-PC and glycolysis, with a focus on phosphocreatine. The energy release necessary for performance is generated by the demand generated by neuromuscular drive. Intramuscular energy supply isn\'t a limitation. - Creatine supplements may improve performance. - Fibre type distribution and recruitment: the ratios will vary between individual but in this area, we want to focus on the recruitment of type 2. - Recruitment of fibres will rely on the athletes level of motivation and arousal. It plays an integral part in our ability to develop power. - Skill and technique can affect fatigue and performance.   Short Term - Events lasting between 10-180 seconds - Shift to aerobic metabolism - 70% energy supplied anaerobically at 10 seconds - 60% supplied aerobically at 180 seconds - Fuelled primarily by anaerobic glycolysis - Results in elevated lactate and hydrogen ion levels. - Interferes with calcium binding to troponin and glycolytic ATP production - Ingestion of buffers may improve performance   ** ** ***3.2 factors limiting all out aerobic performances*** Energy fuelling bouts of exercise longer than 3 minutes comes from aerobic sources. These longer duration bouts are subject to environmental and dietary factors having a direct influence on fatigue. Exercise is split into (little diagrams on PP): - Moderate length, 3-20 minutes - Intermediate length, 21-60 minutes - Long term performance, 1-4hrs   Moderate - 3-20 minutes - 60% ATP generated aerobically at 3 minutes - 90% of ATP supplied aerobically at 20 minutes - High VO2max is advantageous - Higher stroke volume and high arterial oxygen content (haemoglobin and inspired oxygen) - requires expenditure near VO2max, this leads to a recruitment of type 2 fibres in additional to type 1 and thus, a build up of the by products   Intermediate - 21-60 minutes - Mostly aerobic - Performing just below 90% vo2max - High VO2max is important - High % of type 1 fibres (important for running economy or exercise efficiency) - Environmental factors: heat and humidity, hydration status and lactate threshold of the athlete - VO2max and running economy is a good indicator for performance - Biomechanics and bioenergetics both influence running economy - Higher proportion of type 1 fibres gives someone a high lactate threshold - Races aren\'t run at 100% of VO2. - Performance is determined by the % of VO2max that a runner can maintain as well as their running economy.   Long - 1-4hrs - Aerobic fuel only - Environmental factors more important - Maintaining rate of carbohydrate utilisation: muscle and liver glycogen stores decline so ingestion of carbohydrates are needed to help maintain carbohydrate oxidation in the muscle - If we can\'t maintain carb utilisation and stores, performance will end up in the bin. - Consumption of fluids and electrolytes are important. If only drinking water and heavy fluid loss occurs, it can result in hyponatremia which is when your blood sodium levels get too low. - Diet also influences performance ** ** ** ** ***3.3 acid base balance*** - The concentration of H+ in the body is expressed as pH, normal is 7.4 - Abnormal pH levels can effective enzymatic reactions and can lead to negative impacts of physiological function and performance - Acids: molecule that can liberate H+, increases H+ concentration, eg: lactic acid - Bases: molecules that combine with H+ and decreases their concentration, eg: bicarbonate. - High intensity exercise around 45 sec produces large amounts of H+ - Some sports have a higher risk of acid base disturbance, a spring finish in distance/endurance event increases the risk of acidosis - Acidosis can impair performance - Failure to maintain acid base homeostasis can lead to impairments in ATP production and interfere with calcium binding sites - Type 2 fibres have a higher muscle buffering capacity. This means that those with more type 2 have the greater ability to buffer. - Diets low in acids can decrease plasma pH but doesn\'t affect buffering capacity. Some sports ban some buffers. - Supplementing with sodium bicarbonate can have the side effects of nausea and vomiting and large doses can lead to alkalosis - Supplementing with sodium citrate. Improves extracellular buffering capacity and can improve performance during high intensity exercise. Large doses have the same effect as bicarbonate - Supplementation with beta alanine. Precursor to carnosine synthesis. Carnosine serves as in intracellular buffer and can increase time to exhaustion during high intensity exercise. Only know side effect is skin tingles. - H+ production depends on exercise intensity, amount of muscles involved and the duration of exercise. - Blood pH declines as exercise intensity increases and muscle pH declines with increase intensity and it\'s pH is lower than blood. - Whilst the kidneys have a role in the long term regulation of acid base balance, they don\'t have a major role in exercise.   Sources of H+ during exercise: - Production of CO2: end product of oxidative phosphorylation - Production of lactic acid: glucose metabolism via glycolysis - ATP breakdown during muscle contraction: results in a release of H+   Sources of H+ in Contracting Skeletal Muscles - Aerobic metabolism \> carbonic acid - Anaerobic metabolism \> lactate   Acid Base Buffer Systems: 1. Acid base balance maintained by buffers - Release H+ when pH is high - Accept H+ when pH is low 2. Intracellular buffers (these work collectively) (table showing action on PP) - Proteins - Phosphate groups - Bicarbonate - Histidine-dipeptides 3. Extracellular buffers - Bicarbonate: supplementing with this has shown some improvements in some sports. - Haemoglobin - Blood proteins   Buffering of H+ in the muscle. - 60% by intracellular proteins. - 20 to 30% by muscle bicarbonate. - 10 to 20% by intracellular phosphate groups. Buffering of lactic acid in the blood. - Bicarbonate is major buffer. - Increases in lactic acid accompanied by decreases in bicarbonate and blood pH. - Haemoglobin and blood proteins play minor role. ** ** ***3.4 pulmonary function and performance*** - This is an area that has been deliberated for a while - It\'s not clear the role that it plays in exercise performance. - In low to moderate intensity, the pulmonary system doesn\'t limit exercise tolerance. - In high intensity exercise, it\'s not a limit for healthy people at sea level. However respiratory fatigue can occur during high intensity exercise at 90-100% VO2max levels in prolonged bouts of high intensity. This is due to the fatigue of the respiratory muscles - If there is incomplete pulmonary gas exchange, it may limit athletes in some performances.   ***3.5 genetic limitations*** - Genetics has a role in determining our training response. - Some people will be naturally more athletic than others. - 97 different genes contribute to training improvements and responses in VO2max - The average person has improve in VO2max between 15-20% - High responders can have upward of 50% improvement with appropriate training. - Low responders may only see a 2-3% improvement. - Anaerobic capacity is more genetically determined than aerobic. - Training in anaerobic performance can only improve to a small degree, due to the % of type 2 fibres that you are born with. - Genetics will have a role in a high VO2max, superior exercise economy and lactate threshold and critical power.   Low responders - Genotype A - Have low, untrained VO2max - Exhibit limited exercise training response High Responders - Genotype E - Those with ideal genetic make up - Have a untrained yet high VO2 max - Often increase VO2max by 50% with training. **MODULE 4: RESISTANCE TRAINING ADAPTATIONS AND PERFORMANCE** ***.4.1: Resistance Training Promotes Changes in the Nervous System*** - Neural adaptations contribute to RT induced increases in muscular strength - Neural adaptations have a key role in strength gains in the early stages of training, ie: 2-8 weeks. As time goes on, it becomes more physiological adaptations. - Untrained people will see increases in strength anyway between 10-80% in the first 6 months of training, but the initial gains are neurological adaptations. - Evidence supporting neural adaptations in the first 8 weeks is that muscular strength increases in the first 2 weeks without change to muscle fibre sizer and the cross education training of one limb results in increases in strength in the untrained limb. - The exact mechanisms that lead to increases in neural drive is unclear and inconclusive. - There is some evidence that RT lowers inhibition in the motor cortex and spinal cord. - Prior to training, we have a high contraction of the antagonist muscle. Max force production is achieved when the agonist muscle isn\'t paired with co activation of the antagonist, but literature is inconclusive on this concept. *Neural Steps Leading to Muscular Contraction* 1. Process: muscular contraction begins \> higher brain centres 2. Neural message forwarded to motor cortex 3. Message is dispatched to brain steam and relayed to spinal cord 4. At the spinal cord, excitatory neural message depolarises motor neurons 5. Send waves of depolarisation down the axon to the muscle fibres contained in the motor unit.   *Neural Adaptations* Increased neural drive, this results in: - Increased number of motor units recruited - Increased firing rate - Increased synchronisation - Improved neural transmission across NMJ   ***4.2: Resistance Training Induced Changes in Muscle Structure and Function*** *RT promotes an increase in muscle fibre specific tension in type 1 fibres:* - Specific force production in muscle fibres is greater in type 2 than type 1 fibres. - Type 2 fibres have more myosin and cross bridges = greater force generation - Increases in muscle fibre specific tension in type 1 fibres is linked to increased calcium sensitivity = more cross bridges binding to actin. This is independent to changes in muscle size.   *Training induced increases in muscle mass:* - Hyperplasia: increase in a total number of fibres in the muscle, however, there is lack of evidence to support that this occurs in humans. There is a wee bit of evidence in animal models, but not much. - Hypertrophy: increased CSA of a muscle fibre. Dominant factor in RT changes in muscle mass. This is due to an increase in muscle proteins.   **Physiological Variable** **RT Effect** **Comments** ---------------------------------------- ------------------------------------------------------------------------------------ ------------------------------------------------------------------------------------------------------------- Nervous System Increased neural drive, possible changes in ratio of agonist/antagonist activation Adaptation occurs rapidly after initiation of training program Muscle Mass increased Hypertrophy detectable within 3 weeks after initiation of training. Unclear if hyperplasia occurs in humans Muscle Fibre Specific Force Production Increased Specific force increased in type 1 fibres only Muscle Fibre Type Shift from fast to slow fibres Small shift from type 2x to 2a with no evidence of % type 1 fibres increasing Muscle oxidative capacity unclear Increases in muscle oxidative capacity possible, but depends upon type of resistance training performed Muscle capillary density unclear Training adaptation possible, but depends upon type of training being performed Muscle antioxidant capacity increases 12 weeks of training increases antioxidant enzyme activity by almost 100% Tendons and ligament strength increased Harmonised increase in tendon/ligament strength to match increases in muscle strength Bone mineral content Increased Increased in bone mineral content results in stronger bones.   ***4.3: Detraining following Strength Training*** - Ceasing any RT program leads to a degree of atrophy and loss of strength. - Strength losses occur slower than endurance based adaptations. - Recovering strength loss can occur quite fast, within 6 weeks, of returning to training.   Does skeletal muscle have a memory? - Gym myths: after a prolonged period of no training, when you train again, you can make rapid gains during retraining. Supposed muscle memory. - This is a controversial topic. - Research suggests it is due to RT induced increases in myonuclei in the trained fibres that aren\'t lost during detraining. - Maintaining these myonuceli gives an edge in protein synthesis upon retraining.   Prolonged inactivity leads to rapid atrophy - 20-30 days of inactivity can lead to a 20-30% reduction in muscle fibre size - Conservation of muscle mass is dependent on balance between MPS and MPB - Increases in radial production promotes muscle atrophy   **MODULE 5: AEROBIC AND ANAEROBIC TRAINING ADAPTATIONS AND PEROFRMANCE** ***5.0: Intro*** - These concepts are important to better know the physiological responses that occur in response to different training modalities. We need to be able to explain these adaptations and why they occur.   ***5.1: Training and Changes in VO2max*** - VO2max: the measure of the maximal capacity of the body to transport and use oxygen during dynamic exercise using large muscle groups - It is defined by the Fick Equation: VO2max= max cardiac output X a-vO2 difference - The primary difference in VO2max between people is stroke volume.   Training to increase VO2max - Training large muscle groups - Working out 3+ times per week, endurance based activity above 50% VO2 max - HIIT can increase VO2max as well.   Responses to increases in VO2max - 15-20% increase in gen pop. - Smaller increases will occur in those with an already high VO2max - Up to 50% increase in those with very very low VO2max - Short duration adaptations are likely due to increases in volume. Long duration responses are changes to stroke volume and a-vO2 differences.   Factors Influencing Stroke Volume - TPR (afterload), contractility and EDV (preload) - EDV is then made up of plasma volume, filling time and venous return, and ventricular volume. - So preload will increase and then afterload will decrease with changes. - There are improvements in a-vO2. there is a decrease in SNS vasoconstriction and there is better blood flow and means that filling time is expanded. This lets the body grab oxygen better due to increases in capillary density and the number of mitochondria.   ***5.2: Training and Changes in Fibre Type and Capillarity*** Fast to slow shift muscle fibre type - Reduction in fast fibres and increases in slow fibres - Magnitude of fibre type change determined by training factors and genetics. - This leads to enhanced diffusion of oxygen and better removal of wastes. - Endurance training is responsible for this shift. - Slow myosin isoforms have lower ATPase activity meaning they can perform more work with less ATP = better efficiency = better mechanical efficiency     ***5.3: Training and Changes in Fuel Utilisation*** Endurance Training Changes - Plasma glucose is the primary fuel for the nervous system. It\'s essential in maintaining base bodily functions and also supplies blood to the brain. - Increased transport of FFA into the muscle. This is due to increased capillary density in the muscle and an increase in fatty binding protein and fatty acid translocase (FAT). - High levels of carnitine palmitoyltransferase (CPT-1) and FAT works together to increase FFA entry into the mitochondria - Mitochondrial oxidation of FFA \> increased enzymes of B oxidation = increased rate of acetyl-CoA formation and high citrate level inhibits PFK and glycolysis. - These endurance trained adaptations means that plasma glucose is spared due to the body\'s adapted ability to use fat for fuel   ***5.4: Detraining following endurance training*** - Rapid decreases in VO2max. Approx 8% lost within 12 days, 20% after 84 days. - The decrease in VO2max as a result of detraining is caused by a decrease in maximal stroke volume and oxygen extraction (the reverse of what happened when we train) - Performance at submaximal intensities also declines quickly when in a state of detraining, due to a decrease in the number of mitochondria in muscle fibres. - Other decreases: max a-vO2 difference, mitochondria, oxidative capacity of muscle, type 2a fibres but an increase in type 2x fibres.   Retraining and VO2 max - Muscle mitochondria adapt quickly to training and will double within the first 5 weeks. - Mitochondrial adaptations lost quickly with detraining, 50% of that is lost in the first week and then the majority is lost within 2 weeks. It would take 3-4 weeks of training to regain what was lost. - Muscle memory is and isn\'t a thing. During retraining, because the mitochondrial developments are there, it means that the muscles will rapidly add the mitochondria when retraining.   ***5.5: Muscle Adaptations to Anaerobic Exercise*** - Anaerobic training intensities are ones done above VO2max and fuelled primarily by the ATP-PC and glycolysis systems. Adaptations from this system are different to that of endurance training. - 10-30 second effort, recruits both type 1 and 2 fibres, exercise lasting less than 10 seconds is fuelled by the ATP-PC system - Exercise that\'s 20-30 seconds, 80% of energy is needed anaerobically and the remaining 20% is aerobic. - Adaptations include: better buffering capacity, hypertrophy of type 2 fibres, elevates enzymes involved in both the ATP-PC system and glycolysis. - HIIT training greater than 30 seconds, promotes mitochondrial biogenesis. - 4 - 10 weeks of anaerobic training can increase the peak anaerobic capacity by 3-25% across individuals.     ***5.6: Training - Muscle and Systemic Physiology*** - Biochemical adaptations to training influence physical responses. Eg: changes to epinephrine/norepinephrine has an impact on HR and ventilation - Peripheral feedback from skeletal muscle to then go to the CNS: training leads to improved muscle homeostasis during exercise and reduced feedback from the muscle chemoreceptors to the CV control centre. Less feedback from the group 3 and 4 fibres of the CV centre means less work is required from the CNS = lower HR, ventilation, etc. - Central control of the physiological response to exercise: endurance exercise training reduces the feed forward output from the higher brain centres to the CV control centre during sub maximal exercise. When exercise adaptations occur there are improvements in muscle fibre oxidative capacity and reduced central command outflow during submax exercise **MODULE 6: TRAINING CONSIDERATIONS** ***6.0: Intro*** - We need to optimise athlete training, as they spend more time training than they do competing. - Training considerations are important as they encompass numerous areas of training and help to avoid common errors when prescribing a training program.   ***6.1: Warm up*** There\'s 2 purposes to a warm up: 1. Increase CO and blood flow to skeletal muscles to be used during training 2. Increase muscle temperature to elevate enzyme activity   [Video Notes ] - Warm ups are done prior to exercise. They aim to increase muscle temp, arousal and level of focus on the event/task at hand. - In a warm up we need activities that are identical to the performance, general warm up or activities directly related to performance. Warm up recommendations 1. Short term: (\10s, \5min): 60-70% VO2max, max 5-10 minutes. Too much may deplete muscle glycogen stores or increase thermal strain. Want to keep warm up at the lower end of suggested ranges, especially in a warm environment. In a cold environment, upper end of the ranges may be of benefit. Stretching - Increases flexibility - Increases muscle tendon compliance. - Evidence suggests that high stretch shorting cycle activities reap benefits of stretching. - There is mixed evidence on stretching and reduced injury risk.   ***6.2: Concurrent Training - Adaptations and Performance*** - The combination of endurance and resistance training in exercise - There is mixed evidence surrounding this concept. Growing studies concluded that concurrent training on the same day results in impaired strength training when compared when strength training alone.   Mechanisms theorised to explain the impairment of strength gains: 1. Neural: concurrent training may impair neural adaptations to RT and impair MUR. Limited evidence on this concept. 2. Overtraining: could contribute to an inability to obtain optimal strength gains, but there is no direct evidence for this. 3. Depressed protein synthesis: good deal of evidence for this. Endurance training cell signalling can interfere with protein synthesis. Inhibition of mTOR by activation of AMPK   ***6.3: Nutritional Influence on Adaptations*** - Low muscle glycogen is a positive influence on endurance training induced skeletal muscle adaptations. Entering sessions with low glycogen promotes adaptations = increased protein synthesis and mitochondria formation due to higher activation of PGC-1a (master regulator of mitochondrial biogenesis), due to greater stimulation of both AMP kinase and p38 which serves to upstream promoters of PGC1a activation. - To induce a low muscle glycogen level, you can either: restrict dietary carbs or train twice per day every other day which means entering the second training session with lower muscle glycogen. However restricting dietary intake can lead to chronic fatigue and training impairments. Training twice every other day is a more appropriate approach. - Protein availability and MPS: commonly thought of as only being relevant for power/strength, but is also very important for endurance. Ingesting protein increases MPS, can be consumed pre or post session (amount and timing is in another module). Can increase gains in anaerobic power.   Supplementation with mega doses of antioxidants - Exercise promotes formation of free radicals that may damage cells and contribute to fatigue. - Antioxidants may help prevent/limit damage and fatigue - High doses of antioxidants may block training adaptations. - We need a certain amount of free radicals in response to exercise to activate certain signalling pathways. Hence, too many antioxidants will inhibit adaptations.     ***6.4: Common Training Mistakes*** Overtraining - Workouts that are too long or strenuous - Inadequate recovery - May result in injury and impair immune function - Psychological staleness = lack of enthusiasm. - Considered a syndrome. - Is a greater problem than undertraining - Symptoms: higher HR and blood lactate levels at lower working intensities, loss in BW, chronic fatigue, psych staleness, colds and decreases in performance.   Undertraining - Not adequately stimulating the physiological responses in the body   Performing non specific exercises - Won\'t enhance energy capacities used in the sport - Won\'t adequately prepare the athlete due to not replicating the demands of the sport   Lack of long term training plain - Misuse of training time - Won\'t see ongoing adaptations   Failure to taper before a performance - If we don\'t taper, athletes won\'t have their optimal levels of performance - May have residual fatigue. - When tapering is appropriately done, it allows muscles to resynthesise glycogen and help from training induced damage = improved performance in both strength and endurance events.   **MODULE 7: PERORMING IN HEAT AND COLD** ***7.0: Performing in the heat and cold*** - Weather will always pose an unknown variable, so regardless of how well trained the athlete is, it can still effect them. - Severe weather changes has led to extreme health repercussions and even death.   ***7.1: Exercise in a hot environment*** - Poses challenges to being able to maintain a normal body temperature and fluid balance. - Hot temperatures alters our ability to lose heat through radiation/convection and evaporation. Eg: if it\'s a super humid day, our sweat will just sit on our skin instead of evaporating and letting us cool down. This results in an increase in core temperature and a higher sweat rate, which in turns increases the risk of hyperthermia and heat injury. - When we have a high sweat rate, we can sweat as much as 4-5L/hour. This also then increases our risk of dehydration.   [General Guidelines to help prevent heat injuries ] (should aimed to be adhered to as much as possible) - Exercise in the coolest part of the day - Minimise intensity on hot days - Expose as much skin as possible - Have frequent cool down breaks in the shade - Avoid dehydration - Measure BW at the start and end of training to help calculate fluid replacement requirements.   Preventing Dehydration - Dehydration can result in a 1-2% loss in BW, impairing performance. - Hydrate prior to exercise, both the day of and in the days leading up to - Having 400-800ml of fluid within 3hrs prior to the end and have 150-300ml every 15-20 minutes during exercise (this would adjusted due to conditions) - Ensure that the athlete rehydrates appropriately following exercise. Have 150% of the weight loss. 1kg = 1.5L replacement. - Sports drinks in this instance are better than water to help refill electrolyte stores. Check urine colour.   ***7.2: Heat and performance*** In hot and humid environments, exercise is impaired due to: - Accelerated muscle fatigue: increased radial production, increases acidosis, muscle glycogen depleting faster. - Cardiovascular dysfunction: reduce SV, decreased CO during high intensity exercise and decreased muscle blood flow. - CNS dysfunction: decreased motivation and reduced voluntary activation of motor units These factors, whilst have been proposed to be independent, can interact together and the severity depends on the exercise being performed and the intensity.   Heat - Hyperthermia: elevated body temp - Health related problems: heat cramps and syncope - Heat exhaustion: may need medical attention, heat stroke or medical emergency - Treatment: cold water immersion   **Illness** **Signs and Symptoms** **Immediate Care** -------------------------------------------------------------------------------------------------------------------------- ------------------------------------------------------------------------------ ------------------------------------------------------------------------------------------------------------------------------- *Exercise induced muscle cramps*: sudden involuntary muscle contractions during or after exercise Visible cramping Rest, passive stretching, icing, massage and rehydrating *Heat syncope*: orthostatic dizziness attributed to dehydration, hypotension and venous pooling Brief fainting episode accompanied by dizziness and tunnel vision Move to a shaded area, elevate legs above heart, cool skin and rehydrate *Heat exhaustion*: inability to effectively exercise in the heat due to CV insufficiency, hypotension or central fatigue Excessive fatigue, fainting, confusion and disorientation Move to a shaded area, remove excess clothing, elevate legs leg, cool with towels and fans, rehydrate and seek medical help *Exertional heat stroke:* characterised by neuropsychiatric impairment and high body temp \> medical emergency Disorientation, confusion, hysteria, rectal temp \>40.5C and hot sweaty skin Remove excess clothing, lower core temp to \