Adaptations to Anaerobic and Aerobic Training PDF

CHAPTER 12 PART 1 Adaptations to anaerobic and aerobic training Introduction Focus: - prolonged exercise (aerobic) lasting minutes-hours - high intensity (anaerobic) – speed, agility and power training With weight and strength training there is...

CHAPTER 12 PART 1 Adaptations to anaerobic and aerobic training Introduction Focus: - prolonged exercise (aerobic) lasting minutes-hours - high intensity (anaerobic) – speed, agility and power training With weight and strength training there is more of an emphasis on how the muscles will change structurally to generate more force and how the nervous system also has to make a lot of adaptations - why: skeletal muscles are voluntary and will only respond if get message from the brain In muscle cells adaptations must be made in response to training When thinking about continuous prolonged training (run/swim) – the most important thing is that you must try to get enough oxygen to the muscles - because enough oxygen allows muscles to use aerobic energy system o Aerobic energy system: the energy system that can work for long periods of time provided the muscles get oxygen - we measure oxygen in VO2 (volume of oxygen) = which determines how long you can continue your exercise Low vs high intensity exercise Low intensity: don’t need lots of oxygen delivered to muscles at a fast rate High intensity exercise: there is still lots of oxygen going to the muscles at a faster rate compared to low intensity - However, you are still breathing therefore still oxygen present Muscles need a certain amount of oxygen and at a sufficient rate so that the muscles can do the work - limitation: oxygen does reach the muscles but sometimes can’t keep up with the rate at which it is needed Difference between athletes who are very good at endurance and someone who is a strength trainer = the rate of oxygen delivery - Strength training athlete uses anaerobic systems o purpose of strength athlete = get stronger and larger muscles  o Why do they use anaerobic: in the process by training the muscles they use anaerobic systems and therefore they are not dependent on muscles get oxygen rate delivery Adaptations to Aerobic Training Cardiorespiratory endurance Have the ability to sustain prolonged, dynamic exercise Improvements are achieved through MULTIsystem adaptations - Cardiovascular - Respiratory - Muscle - Metabolic The lungs and heart must ensure oxygenated blood gets to muscles Max cardiorespiratory endurance capacity= vo2 max - VO2 max = Measures the capacity of the cardiovascular system to deliver O2 to the muscles The harder you work the higher your oxygen consumption – until you reach vo2max - Graph with plateu when reach vo2max “Elite endurance athletes are born, not made” - True statement - Have to be born with right genes o Gene that determines skeletal muscle fibre type (type 1) ▪ You can change muscle fibre type but only can change a small percentage of the muscle fibre o Body build is also genetically determined o Cardiorespiratory system is also genetically determined ▪ Larger heart to circulate more blood ▪ 2/3 of cardiorespiratory capacity is explained via genes Endurance training  Maximal endurance capacity =  V O2max  Submaximal endurance capacity Lower HR and VO2 at same submaximal exercise intensity More related to competitive endurance performance Resting and submaximal VO2 Resting VO2 is UNCHANGED with training Submaximal VO2 is UNCHANGED OR DECREASES slightly with training - Decreases if athlete has improved their exercise economy VO2 max AKA: Maximal aerobic capacity Best indicator of cardiorespiratory fitness Increases substantially to training (15-20%) Increases due to increased cardiac output and muscle oxygen extraction As exercise intensity increases, oxygen consumption eventually plateaus/decreases, even with further increases in workload = indicates true VO2max How to measure it: Direct measure: in a laboratory with an ERGOMETER and METABOLIC SYSTEM VO2 (l/min) The VO2 equation: Fick equation: VO2 = CO x (a-v)O2 difference Cardiac output (CO): the ability of the heart and lungs to deliver enough oxygen to the muscles (a-v)O2 difference: the ability of the muscles to extract enough oxygen from the blood VO2max is determined by: 1. Age 2. Sex 3. Training status (aerobic fitness) 4. Genetic composition  Age Vo2 max decreases as you get older Reasons: 1. organs don’t work as perfectly as they did when younger 2. as you age – type 11x convert to type 1 (therefore cant compete at high intensity) lose muscle mass 3. Don’t exercise as much (not as physically active) - Life long physical activity minimises the decline of vo2max as you age - Vo2 max starts to decline around age 30 Sex Women have lower VO2max than men Reasons: 1. Women lower haemoglobin levels than men 2. Smaller skeletal muscle mass / higher % of body mass = they have a higher metabolic rate There are smaller difference in VO2max between elite men and women athletes 4,0 Maximal oxygen 3,5 uptake, l/min Male 3,0 Female 2,5 2,0 1,5 1,0 10 20 30 40 50 60 Age, years 6 Maximal oxygen uptake, Active male 4 Sedentary male l/min 2 0 20 30 40 50 60 70 Age, years Training status (aerobic fitness) Potential to increase vo2max depends on your training status Only determiner that can be changed If start at high level of vo2max then smaller increase Training to increase VO2max - Large muscle groups with dynamic activity - Duration: 20-60 min, 3-5 times a week with50-85% VO2max Expected increases in VO2max - 15% increase is the average increase - 40% increase – strenuous or prolonged training and starting from a sedentary state - Greater increase in highly deconditioned or diseased subject o Why: rapid early adaptations and low baseline levels Change in Vo2max following 12 months of endurance training: Adult athletes reach their highest VO2max within 8-18 months of intensive, endurance training Genetic composition Influence of genetics on VO2max: Identical twins = are closer to line of identity compared to non twin bothers - If one had a low vo2max the twin would also - Why: identical twins share 95-99% of genes, therefore vo2max is similar Non identical twins= explains why vo2max may differ slightly Nontwin brothers = greater difference between vo2max Genetic composition is responsible for 25-50% VO2max Genetic factors determine the boundaries for the athlete, however with endurance training it can push the VO2max to the upper limit of the boundaries Factors that influence the change in VO2max 1. Initial fitness level (training status) - Relative improvement depends on fitness - The more sedentary the individual = the greater the increase - The more fit the individual = the smaller the increase 2. Specificity of training - Active skeletal muscle mass determines the ranking of vo2max o Use legs = higher vo2max than rowers who use arms - Skiers have higher vo2max cuz live in a higher altitude 3. High responders vs low-responders (genetics)  - Finite VO2max range is determined by genetics - Training alters VO2max within that range - Identical twins vo2max is more similar than fraternal - Genetically determined variation in VO2max for same training stimulus and compliance - Accounts for variation in training outcomes for given training conditions Variations in the % increase in VO2max for identical twin following the same 20-week training program Long-term improvement Highest possible VO2 max achieved = after 12-18 months Performance continues to increase after VO2max plateaus - Why: lactate threshold continues to increase with training Individual responses is dictated by: 1. Training status and pretraining VO2max 2. Heredity  CHAPTER 12 PART 2: CV and Circulation Cardiovascular system revision Circulation through the heart Inferior and superior vena cava →Right atrium (RA) → right ventricle (RV) → Left and Right Pulmonary arteries → Lungs → Left and Right pulmonary veins → left atrium (LA) → left ventricle (LV) → aorta → system Definitions End-diastolic volume (EDV) (preload): Volume of blood in the ventricles at the end of diastole - Increased in: hypervolemia, regurgitation of cardiac valves, heart failure Contractility: the relative ability of the heart to eject a stroke volume at a given prevailing afterload and preload Afterload: resistance LEFT VENTRICLE must overcome to circulate blood - Increased in: hypertension, vasoconstriction 3 - Increased afterload= increased cardiac workload Total peripheral resistance: the amount of force exerted on circulating blood by the vasculature of the body Heart size: measured in relation to the total thoracic width - the Cardio-Thoracic Ratio (CTR) Stroke volume (SV): the volume of blood pumped out of the heart's left ventricle during each systolic cardiac contraction (ml) Heart rate (HR): the speed at which the heart beats. - Average: 72 bpm Cardiac output (CO): the quantity of blood pumped by the heart in a given period of time (l/m) Blood pressure (BP): the pressure of circulating blood against the walls of blood vessels Blood volume: the volume of blood in the circulatory system of any individual Oxygen consumption (VO2): the amount of oxygen taken in and used by the body per minute (l/m) End systolic volume: the volume in the ventricle at the end of systolic phase (contracts just before it relaxes) Measuring the heart Echocardiograph and Echocardiogram - Assessment of size of heart chambers, thickness of walls and action of heart valves Increase in chamber size can be measured with a sona – clinical test Structural changes to the HEART due to aerobic training Training = heart mass (cardiac hypertrophy) and left ventricular volume increase which leads to increased stroke volume The left ventricle does most of the work and undergoes greatest adaptation in response to endurance training The type of adaptation depends on the type of exercise training performed Endurance training increases diameter through which blood can flow Endurance training mainly leads to: ( Plasma volume) →  LV volume →  end-diastolic volume (EDV) →  SV Endurance training has a VOLUME LOADING effect on the heart To get more blood into circulated = more blood must accumulate in LV so that there is more volume Increased plasma volume If compare resting cardio output in trained vs untrained = trained will have a higher blood volume – make more plasma - Not necessarily red blood cells - Increased in plasma = increased in LV = increases end diastolic volume = increased stroke volume Increased left ventricle Cardiac hypertrophy = when heart size increases Heart muscle is like skeletal muscle fibres (type 1) therefore if you train, you train your heart muscle The hypertrophy will increase the volume of the left ventricle  - Why: the left ventricle needs to work a lot harder especially during exercise because the left ventricle needs to create enough pressure to pump blood into the aorta and then to rest of the body – needs to create a high pressure High pressure can only be achieved if you have a strong muscle (contraction force must increase) The right ventricle will also make some small changes but not as much as the left ventricle - Why: The right side of the heart receives deoxygenated blood and that blood only needs to be distributed to lungs - Right ventricle does not have to generate so much pressure as lungs and heart are on same physiological plane Cardiac hypertrophy from endurance vs resistance training Endurance: increased preload (volume overload) - LV chamber size increases = allows for increased LV filling = increased SV - Increase size is due to training induced plasma volume = increased left ventricle EDV - Heart rate decreases at rest and submax exercise intensity = LONGER DIASTOLIC FILLING TIME - Increased plasma volume + diastolic filling time = increased LV chamber size o At end of diastole Resistance: increased afterload (pressure overload) - With resistance/strength training = far more hypertrophy - LV must contract against increased afterload from systemic circulation o Extremely high BP during resistance training = high resistance that must be overcome by LV - Develop a much thicker cardio wall = push of blood is much stronger than endurance - Increases LV wall = increase contractility - Little change in ventricular volume Things that can change in aorta that can limit amount of blood - High blood pressure = pressure in aorta is very high which means that LV must work extremely hard to push the blood into the aorta (negative consequence for having hypertension) - Afterload = If afterload is very high then the volume of blood expelled - Want afterload to be as low as possible Increase the size/diameter of the heart chamber o Happens with endurance training o Bigger chamber = more room for blood to drain into lv o More blood in LV = more blood in aorta o Volume of blood is called preload/ end diastolic volume - Can make volume bigger by increasing the total amount of blood circulating the body (plasma volume) Heart hypertrophy from exercise and from disease Cardio hypertrophy is not always a good sign If someone suffers from hypertension for long periods of time - LV constantly has to work very hard to pump the blood out - Almost like strength training for heart = develop thick walls - That hypertrophy developed from hypertension = bad - Hypertrophy can negatively affects the heart How do you distinguish if you have an athletes heart or if you have a failing heart Athletes heart (exercise training) = see hypertrophy but all other cardio functions are normal - diameters and volumes of chambers are normal - it is reversible In a failing heart: see hypertrophy but there is reduced cardio functions and there are volumes and diameters in chambers that are less than what its meant to be , - irreversible - heart cells can die due to lack of o2, related to higher risk of dying from cardiovascular disease - Reason why prolonged hypertension is bad as its irreversible - Cell death and fibrosis - Increased mortality Why would cyclists have a higher left ventricular mass compared to runner Runners have a greater active muscle mass Body position: cyclists are in hunched position , heart has to work harder to pump blood out More pressure: because of hunched position, respiratory muscles have to work harder and heart has to pump harder LVID: left ventricular internal diameter MWT: mean wall thickness LVM: left ventricular mass If stroke volume increases at rest what does that say about heart rate Better trained = resting heart rate drops Why: because the stroke volume increases, heart can pump out more blood and therefore doesn’t have to pump that quickly to get oxygenated blood to muscles Why is it an advantage if heart doesn’t have to contract so quickly: - each contraction needs ATP, therefore if it has to contract and relax less, then the heart is able to do less work (less ATP) = more efficient Difference between untrained and trained in terms of max stroke volume = a lot Why don’t you train when you are ill When you are ill, there is more load on your heart Can cause inflammation in heart Makes heart have to work harder, and will make hypertrophy but will move into the hypertrophy that is associated with heart failure Cardiovascular changes 1. Stroke volume 2. Heart rate 3. Cardiac output 4. Blood pressure 5. Circulation (blood flow and blood volume) 6. Blood Stroke volume Stroke volume adaptions = positive and negative Def: The amount of blood that comes per heart beat (ml/beat) that comes form lv into the aorta Stroke volume increases after training - Plasma volume increases with training = increased EDV o Frank-starling mechanism:  EDV →  stretch of the ventricle walls →  force of contraction - Resting and submaximal HR decreases with training o This increases filling time = increased EDV - Increased LV mass with training = increased force of contraction and decreased ESV  - Increased TPR with training = decreased after load SV adaptations to training decrease with age Changes in SV with endurance training Factors that determine stroke volume 1. Preload – if it increases = increase in SV - Why: when you get better trained, make more blood and plasma volume increases. Greater filling time of the ventricles. Hypertrophy 2. Afterload – AKA total peripheral resistance (TPR) - Is determined by blood pressure in the aorta - If have normal bp (120/80 mlHg) then have a relatively low afterload = high sv - If hypertensive (200/140) then heart has to work extremely hard to pump the blood to against the high pressure - All blood vessels have a certain amount of resistance against blood flow (capillaries / smaller arteries = more resistance against blood flow) - Will increase if: hypertensive or if you have obstructions in smaller arteries/ veins 3. Contractility – why does it increase: cuz of hypertrophy Low stroke volume can be compensated by increasing HR - Bad cuz: Higher HR = more ATP SV contributes up to 50% Factors increasing stoke volume Heart Rate If you increase your cardiovascular fitness, then your resting heart rate DECREASES - The same happens at any of the submax exercise - Indicates that the efficiency of the heart rate is increasing Resting HR Decrease markedly Mechanism: increased parasympathetic activity, decreased sympathetic activity in heart Submaximal HR Decrease HR for same given absolute intensity More noticeable at higher submaximal intensities Maximal HR Def: highest HR achieved in all-out effort to volitional fatigue No significant change with endurance training Decreases with age  Aerobic training has a major impact on HR at rest, during submaximal exercise, and during the recovery. However, maximal HR very seldom changes with training HRmax = 220 - age Measuring HR HRmax = 220 – age In general if your heart rate is above 220 then the filling time is negatively affected We don’t want our heart rates above 220 With age: - HRmax = 208 – (0.7 x age in years) - HRmax = 211 – (0.64 x age in years) Why does resting and submax heart rate decrease as you get aerobically fitter: 1. Either something to do with parasympathetics nerves (inhibit pacemaker cells) - Greater filling time = increase SV 2. Or sympathetic nerves Low heart rate Advantage of low heart rate: lowers the work load of the heart - Doesn’t need to contract and relax as often The direct effect of low heart rate = the increase in filling time - What does this mean: the blood coming back from rest of the body drains in the RA - Filling time: how much time the ventricles have to fill up - The longer the valve stays open = the more time the blood has to fill ventricles = more blood being able to be pumped If heart rate is very high = your heart contacts/relax at high rate - Not a lot of filling time - The ventricles don’t fill completely with blood = less blood goes to lungs to get oxygenated = less blood to rest of body - Why it bad: more ATP needed to pump blood at high rate and less filling time If you get aerobically fitter = it doesn’t lead to higher HR at exhaustion Why during the VO2max test your HR max doesn’t reach 200 1. You stopped the test prematurely 2. You had to stop prematurely – reason could be due to the heart or legs couldn’t keep up Maximum HR can increase/decrease by 10 There are 2 reasons why heart rate can adapt with aerobic exercise Has to do with autonomic nervous system – parasympathetic nerves 1. Parasympathetic nerves - If lots of impulses goes to SA node = it inhibits the sa node and decreases HR - Less action potentials per minute - What happens when you get aerobically fitter o Stronger than sympathetic nervous system 2. Sympathetic nerves - When get a fright = HR increases cuz nerves are stimulated - When get a fever = stimulates sympathetic nerves In sport science, we like to look at during recovery If you observe a faster recovery with training, the HR comes down very rapidly during recovery = increase in cardio fitness Do a standardised test and then rest for a couple of minutes and then calculate the recovery What does this mean if heart rate recovery improves – physiological mechanisms 1. Theres a decrease in sympathetic activity to the heart 2. If aerobically fitter – smaller increase in body temp, adrenalin and noradrenalin, less sympathetic stimulation - Less hormones = less sympathetic activation  3. Less metabolic waste product - Not lactate – used as an energy source - H+ = if they accumulate, it affects pH so therefore it’s a metabolic waste product o If aerobically fitter = less h+ ions o Will contribute to faster recovery rate - If have lot of metabolic waste products = need higher HR t flush them out of your circulation Summary HR x SV = Cardiac output Lungs = part of circulation Heart = LV and RV Muscles and other tissue = need oxygen RV is connected to the lungs so that blood can be oxygenated by the lungs 1. Oxygenated blood comes back to left side of the heart to the LA Aorta = atrial blood vessel 2. Takes oxygenated blood to the muscles and tissue in the body Blood vessels going back to RA – which takes deoxygenated blood back to the heart The heart makes structural changes: (1) Hypertrophy of the left ventricle o Make sure can explain why its more on left than right (2) And if you endurance athlete – diameter of aorta Cardiac Output Symbol: CO or Q CO = Heart rate x stroke volume Increases with increased intensity Plateaus near VO2max Normal values Resting Q ~5 L/min Untrained Q max ~20 L/min Trained Q max 40 L/min COmax = a function of body size and aerobic fitness Analysing the graph CO matches the O2 consumption required for any given intensity of effort Training creates little to no changes at rest or submaximal exercise Maximal CO increases considerably – 5x with training - CO increases due to increase SV Changes in CO with endurance training during walking, then jogging and finally running on a treadmill as velocity increases Pre-training: - CO starts 5 L/min at 5kph - Increases linearly to 20 L/min at 16kph - Plateaus at this value despite further increases in treadmill speed Post-training - CO starts at 5 l/min at 5kph - Increases to 28 l/min at treadmill speed of 20kph - Plateaus at value despite further increases in treadmill speed Blood Pressure BP = Q × TPR (Q , TPR  slightly) If we do exercise then the blood pressure needs to increase even more to get blood quickly to where it needs to go , also because of the other changes that occur that affect blood pressure Blood pressure is determined by CO: - CO increases with exercise - Therefore, BP also increase - Reflected by the top value (systolic value) - As you increase your exercise intensity = CO increases = systolic bp also increases o Direct relationship - Systolic is related to cardiac output Why do you need a blood pressure of (120/80): The left ventricle must pump the blood against the resistance and spread to your whole body Without blood pressure, the blood wouldn’t get to whole body Intensity levels: BP at rest and any given submax intensity = DECREASE Maximal intensity = INCREASE systolic and DECREASE diastolic - Systolic BP increases linearly with workload o Higher workload = higher SBP o Increase due to larger CO with higher workload o If work with very heavy weight = systolic bp gets up to 300/400 mlHG - Diastolic bp decreases slightly at max workload o Why: widespread vasodilation in the body which decreases TPR o Not much change to diastolic bp As we increase workload, and diastolic bp increases after ever increment = we conclude that widespread vasoconstriction or vasodilation in the skeletal muscles doesn’t occur - what we see when diastolic bp doesn’t stay level Systolic bp should increase with exercise = if doesn’t then person can’t increase CO TPR is determined by 2 things that can change in blood vessels - Vasodilation: Blood vessels can widen (specifically the blood vessels that have smooth muscle in them) = allows for more blood flow - Vasoconstriction: blood vessels narrow = limits amount of blood flow to the muscles What is the effect of training on bp Healthy individuals = very little change Hypertensive patients = will see a decrease in bp - both systolic and diastolic - if they exercise regularly it can help improve bp Blood flow and blood volume Increased blood flow to active muscles - why: deliver sufficient amount of O2 (vasodilation) Changes in heart contribute to increased blood flow Additional changes include: 1. Increased capillarization - Increased capillary: fiber ratio - Increased total cross-sectional area for capillary exchange 2. Increased Capillary recruitment - increase in capillaries around active muscles - allows the blood to be nicely distrusted all over the muscle o advantage: diffusion of oxygen will occur at a quicker rate from blood to muscle cells - Fewer muscle fibres, but larger in size - More capillaries per fibre - Decreased blood flow to inactive regions o Vasoconstrictions in arterioles 3. Increased total blood volume - Prevents any decrease in venous return as a result of more blood in capillaries - contributes to increase in cardiac output  4. Increased recruitment of existing capillarisation Redistribution of blood flow during exercise Increased blood flow to working skeletal muscle - At rest: 15-20% of CO to muscle - Maximal exercise: 80-85% o When we exercise, the blood vessels going to skeletal muscles undergo vasodilatation so more of CO can go to active skeletal muscles Decreased blood flow to less active organs - Liver, kidneys , GI tract Brain cant get less CO, so there isn’t blood distributed away from brain and heart The resistance against blood flow = TPR - influences diastolic bp - Vasodilation and vasoconstriction = level each other out o therefore overall TPR doesn’t change - widespread overall vasodilation = small decrease in TPR Increased Blood flow to skeletal muscle during exercise: mechanisms 1. Skeletal muscle vasodilation - Metabolic demand of tissue - When exercise the leg muscles need more oxygen = increased metabolic demand - Autoregulation o Blood flow increases to meet metabolic demands of tissue o Due to changes in PO2, PCO2, nitric oxide, potassium, adenosine and pH o Automatic response - Changes in po2 pco2 o if you have lots of oxygen in arterial blood coming to muscles, then po2 will also be high o if there is lots of oxygen or oxygenated blood going into the capillary bed = high po2 o if po2 decreases during exercise because muscle takes lots of oxygen o the same time , the muscles are using oxygen and producing co2 = increase in pco2  o if po2 decreases and pco2 = it’s a stimulus for vasodilatation – the message comes from skeletal muscle and allows more blood to muscles o if you have lots of oxygen in arterial blood coming to muscles, then po2 effect of exercise training on angiogenesis: very NB training adaptation for aerobic training - what are the advantages of having more capillary: more oxygen going into muscles and more co2 being taken out - pH decreases due to all the hydrogen ions o when decreases it also stimulates vasodilation - If demand increases leads automatically to vasodilation 2. Vasoconstriction to visceral organs and inactive tissues - Sympathetic nervous system vasoconstriction How do we get vasodilation The smooth muscle in blood vessels can respond to different stimuli - can either relax to certain stimuli o if relax: allow more blood to entering the small arteries and entering capillary bed (vasodilation) - or can contract o if contract = limits amount of blood going to capillary bed Precapillary sphincters = similar to smooth muscle = can either constrict or relax and will do so to the same stimuli that the smooth muscle Blood volume increase Total volume increases rapidly (within 2 weeks) Main mechanisms: 1. Increased in plasma volume - Via increased plasma proteins (albumin) - This increases oncotic pressure which results in reabsorption of fluid from the interstitial space into the blood vessels o Oncotic pressure: pressure exerted by the concentration of proteins in a solution, drawing water from regions with lower oncotic pressure 2. Increase in the release of antidiuretic hormone and aldosterone - This causes increase in water and sodium ion retention in kidneys - This increases blood volume Secondary mechanism: Increase in red blood cell volume - Haematocrit may decrease - More diluted in greater volume of blood - Therefore, decreases plasma viscosity - Reason for 2nd: very little increase in RBC with exercise training o Why: through exercise we destroy a lot of red blood cells – especially weight bearing blood cells o Why do we damage red blood cells = weight bearing (running/ contact sport) – falling on ground can destroy red blood cells o Therefore only makes small contribution How to change red blood cell count: 1. train in a room or tent where you can decrease o2 pressure or go to high altitude (hypoxic enviro) - Low po2 values that you are exposed to: stimulates bone marrow to produce more red blood cells - Improves oxygen capacity of the blood 2. use hormone that is active in bone marrow that produces red blood cells - Illegal - Erythropoietin - Stimulates production of red blood cells Difference between plasma and concentration of red blood cells (haematocrit)  - You can increase RBC count which should show high haematocrit but very often its not Red blood cells Highly trained athletes: both total amount of HB and the total number of RBC are elevated - Ensures the blood has more than adequate O2 carrying capacity Turnover rate of RBC may be higher with intense training Decreased plasma volume = hemoconcentration - Fluid percentage of blood decreases, cell percentage of blood increases - Hematocrit increase up to 50% (or beyond) Net effects Red blood cell concentration increases Hemoglobin concentration increases O2-carrying capacity increases Structure No nucleus, cannot reproduce Replaced regularly by hematopoiesis Life span = 4 months Produced and destroyed at equal rates Hemoglobin Oxygen-transporting protein in RBC (4 O2/hemoglobin) Heme (pigment, iron, O2) + globin (protein) 250 million hemoglobin/RBC Oxygen-carrying capacity: 20ml O2/100ml blood Blood viscosity Thickness of blood (due to RBC) Twice as viscous as water Plasma volume must increase as RBC increases - Occurs in athletes after training , accumulation - Hematocrit and viscosity remain stable - Otherwise, blood flow or O2 transport may suffer  CHAPTER 12 PART 3: RESPIRATORY SYSTEM AND MUSCLES (a-v)O2 diff = O2 uptake (peripheral factors) 1. Structural changes to muscles 2. Pulmonary changes 3. Oxidative capacity of muscles 4. Metabolic (LT, RER, Subma Vo2, pH) Pulmonary changes Introduction Most NB part of the lungs are the alveoli - Why: place where gas exchange takes place - Reason why the walls are thin and has large surface area Oxygen needs to bind to specific protein = hemoglobin - NB as hemoglobin has 4 binding sites that can bind to oxygen - If you have low hemoglobin values (anemia) = going to affect the oxygen levels in the atrial blood - Reason why feels faint when you anemic Oxygen must move over lots of layers - What could go wrong: o Buildup of fluid in spaces – occurs during lung diseases (lifelong smokers – emphysema) ▪ Lungs can’t get rid of excess fluid and then the fluid accumulates in spaces ▪ The distance that the gas molecules need to travel to get from into the arterial blood gets longer o When get flu: fluid can build up in alveoli and the fluids can get infected ▪ Increases distances that oxygen needs to travel to get into arterial blood and makes it more difficult Pulmonary changes: There are 3 things that need to happen in the lungs during exercise 1. Pulmonary ventilation: - VE = VT x fB - Def: the process of air flowing into the lungs during inspiration (inhalation) and out of the lungs during expiration (exhalation) - Must increase the volume of air that you ventilate per minute - Measured: l/min - Dependent on tidal volume (the volume of air that you take into your lungs with each breath, +- 500ml per breath) and respiratory frequency (amount of breaths that you take per minute) o Increase in these 2 factors = increase in maximal pulmonary ventilation - Lactic acid changes pH, pH has a huge effect on breathing o Lower pH = higher breathing frequency - When breathing muscles don’t have to work hard = less co is needed to go to lungs - Rest: no changes - Decreases at give submaximal intensity. WHY? o Improved oxygen extraction by alveoli o May be due to lower blood lactic acid levels o Less sensory feedback to stimulate breathing - Increases at max intensity o Why: due to increased lung perfusion If better trained – GRAPH 1 IS LOWER - You can manage at the submaximal intensity - Hyperventilation will occur later AT – anaerobic threshold (AKA Lactate threshold) As you work harder – HR will increase - Ventilation increases non-linearly OBLA – Onset of blood lactate accumulation Most important adaptation to lung = pulmonary ventilation There are changes in pH as a result of changes in lactic acid level - Drop in pH = increase breathing rate Lactate concentration stays constant up till a certain pint and then suddenly increase until point of exhaustion Change in blood lactate concentration can explain changes in pulmonary - Lots of lactate produced during exercise - lactic acid gives off h ions, - h ions accumulate due to lack of buffer system - then h ions decrease pH, and low pH stimulates ventilation 2. Pulmonary diffusion: - Def: how much of the gases diffuse into the atrial blood - CO2 needs to get back into alveoli - O2 needs to get into atrial blood - Only increases during max intensity – due to increased lung perfusion - Diffusion can increase due to better blood circulation through the lungs, not because your breathing more 3. Oxygen extraction: (a-v)O2 diff - how much of the air that we breathe in , how much oxygen can we extract into the atrial blood - large amount of oxygen in muscle cells = able to use aerobic metabolism - muscles cant extract all oxygen - when training: adapt muscles to extract more oxygen from arterial blood o trained individuals have made adaptions in and around the muscles to extract more oxygen from arterial blood  o less oxygen in venous blood system - What improves oxygen extraction = o increase in capillaries as the more you have the better the spread of ▪ Training adaptation aswell o Adaptation with exercise training - mitochondria become bigger ▪ More mito = make more enzymes in mito that is responsible for aerobic ▪ Improves oxygen extraction If we increase our pulmonary ventilation (increase tidal volume and increase frequency of our breathing) , will that lead to more oxygen in the atrial blood. If we want to get more oxygen to our muscles, is one of the adaptations to increasing our pulmonary ventilation. To an extent: If you breathe in more air and the pressure gradient is large, then more oxygen can get into atrial blood Each hemoglobin molecule can bind 4 oxygen molecules to itself If all the hemoglobin bind with 4 molecules of oxygen, then we say the blood is fully saturated with oxygen - Can measure with oximeter: measures what percentage of your haemoglobin is fully saturated o Saturation of atrial blood with oxygen (SaO2) resting value: 98-99% o 1% is in solution (in the plasma) If you increase our pulmonary ventilation – it wont increase the amount of oxygen in the atrial blood as the all of the haemoglobin is fully saturated so it doesn’t matter  - If at high intensity exercise the SAO2 is the same Can increase the amount of oxygen in solution only by a little bit – but cuz its in solution and not carried by a molecule = disappears very quickly Only way to increase SaO2 is to increase amount of haemoglobin molecules - Can achieve this with altitude training o Training in hypoxic enviro o Issue at high altitude: the diffusion is limited due to change in gradient - Or can achieve by injecting yourself with hormone EPO o Works in bone marrow Arterial-venous O2 difference Increases due to increased oxygen extraction and active muscle blood flow Increased oxygen extraction due to increased oxidative capacity Factors: 1. ↑ mitochondrial size and numbers 2. ↑ oxidative enzymes in mitochondria 3. ↑ [myoglobin] in muscle cells 4. ↑ capillary density and recruitment 5. ↑ diffusion of O2 from capillaries to sarcoplasm 6. ↑ distribution of CO to active muscles CaO2 - CvO2 Structural changes to muscles What are the factors that change in the muscle that improves oxygen extraction 1. Mitochondrial function improves - Increase in size and number of mitochondria o Magnitude of change depends on training volume - more mitochondria = place where aerobic metabolism occurs and improve it o aerobic metabolism = less lactic acid produced - lactate levels stay low = pulmonary ventilation stays low - PGC-1a: regulator protein involved in mitochondrial biogenesis - Mitochondrial health associated with ageing Endurance exercise training effects quality of muscle mitochondria - Increase production of new, healthy mitochondria (biogenesis) o PGC-1 alpha - Decreasing the degradation of mitochondria o PGC-1 alpha - Clearing away damaged mitochondria (mitophagy) 2. Oxidative enzymes (SDH, citrate synthase) - Increased activity with training - more mitochondria = make more enzymes that are involved in aerobic metabolism - activity and amount of oxidative enzymes increase with aerobic training - Continues to increase even after VO2max plateaus - Enhanced glycogen sparing 3. Myoglobin - Oxygen carrier within the cells - Once the oxygen diffuses from a blood into the muscle cell – that oxygen must bind to myoglobin molecule which takes the oxygen into the mitochondria - Lack of myoglobin = oxygen that was diffused will disintegrate in fluid as don’t have carrier - Increased myoglobin content by 75-80% - Supports increase oxidative capacity in muscles 4. Capillary supply - More capillaries = spread blood over muscle fibers = decrease diffusion distance - Angiogenesis - Key factor in increase VO2max Muscle capillarisation - With aerobic training, there’s an increase in the number and size of capillaries supplying blood to the muscle - Greater surface area exposed for O2 and CO2 exchange o Decreases diffusion distance - Strength training = NO difference o Light weight training may also increase capillary bed 5. O2 diffusion - Cuz increasing number of capillaries = more SA for diffusion and smaller distance to travel - Also a cardiovascular system adaptation 6. Distribution of CO at active muscles - Redistribution - Larger proportion of CO is redirected to the active muscles Improves function of breathing muscles Mainly occurs in skeletal muscles Metabolic changes (1) Lactate threshold info Lactate threshold: point at which the blood lactate accumulation increases markedly - Lactate production rate is less than lactate clearance rate - Interaction of aerobic and anaerobic systems - Good indicator of potential for endurance exercise Usually expressed as percentage of VO2max - Best determinants of an athletes pace in endurance events - Eg: LT at 80% VO2max suggests greater exercise tolerance than a LT at 60% VO2max 2 ppl with identical VO2max values – person with highest LT exhibits the best performance The ability to exercise at high intensity WITHOUT accumulating lactate = beneficial DISADVANTAGE TO EXERCISE ABOVE LT: - Increased blood and muscle lactate - Increase in acidosis - Other markers of muscle fatigue Important facts Measurement: mmol/l 2 different kinds of thresholds 1. LT: sudden rise in lactate above resting values 2. OBLA: 2mmol/l or 4mmol/l fixed (lactate) REST: average around 1mmol/l - More than 2mmol = indicates insufficient recovery AVERAGE LT: +- 60% VO2max  - Endurance athletes: more than 70% VO2max Very high [La] at max exercise intensity = greater proportion of fast muscle muscles When measuring the lactate conc in the blood (finger prick or prick of earlobe) - Venous blood - Capillary blood Not lactic acid conc in the muscles - Lactic acid is produced by cells in the body and almost immediately dissociates and becomes lactate LT – response to training Increase to higher % of VO2max Decrease lactate production, Increase lactate clearance Increase oxidative capacity of muscles, which leads to Increase aerobic metabolism Allows higher intensity without lactate accumulation If we start with low lactate value - First couple of values = not a huge change in lactate value - Normally stays below 2 or just above 2 (not more than 3) The athlete will then reach exercise intensity and the lactate level will increase until exhaustion = point is called lactate threshold LT is an indicator of your potential for endurance exercise How well can u do with a prolonged exercise Good indicator of your aerobic fitness - reason why as aerobic fitness: at low work loads up til LT, you will mainly use aerobic metabolism (oxidative phosphorylation) - exercise intensity is lower enough to mobilise the fatty acids and enough time to make ATP - also phase where you can maintain the low values and can extend the time till you reach LT if you have made the 6 adaptations o therefore you have ability to extract lots of oxygen - The better trained = less lactate produced and better the removal mechanisms What happens systematically when reach LT The intensity of the exercise becomes too much for the aerobic systems to generate enough ATP , point where fat metabolism is too slow to keep up with amount of ATP needed Drawback for anaerobic glycolysis = produce lots of lactate Changes in energy systems Graph tells that in beginning we burning fats and carbs under aerobic conditions What about anaerobic glycolysis = completely inactive? - Lactate value will show: very low readings (from other tissues in body) Always lactate in body = anaerobic glycolysis is always active You reach an exercise intensity (=-60% of vo2max) where you need ATP at a greater rate - Start using type 2 muscle fibres o Type 2 muscle fibres produce more lactic acid compared to type 1 ▪ Why: use type 2 muscle fibres at higher intensity Lets look at the graph: Changes in LT with training expressed as % of VO2max Untrained individual: Blood lactate starts at 2mmol/l and remains steady at this value as VO2max increases Then sharply increases when VO2max is about 55% Trained individual: Blood lactate starts at 2mmol/l and remains steady at this value as VO2max increases Then sharply increases when VO2max is about 80% Shift in the graph from untrained to trained: Can see rightward shift = means athlete can run for much longer predominantly using aerobic metabolism - Blue LT = 80% The max values: - Even at exhaustion blue will produce less lactate LT can shift to the right (gets closer to vo2max) Scenarios 1. If we compare 2 athletes where one is 60% and 80% - Athlete with 80% has better aerobic fitness and will most likely win and their average pace that can maintained will be higher 2. If we get 2 individuals with exactly same vo2max values but one has higher lactate value = will chose one with higher LT o Person has better aerobic fitness , and can contain a higher pace throughout the race o Vo2max is a nice to know and tells you what your potential is as an endurance athlete o Athletes might reach vo2max plato , one thing that can still change is lt and can move it closer to vo2max Max value on graph depends on the individual 1. The muscle fibre ratio of individual - If you have a typical endurance athlete = athlete will have more type 1 fibres  o Persons max value will always be lower than a 100m athlete who has more type 2 fibres - Athlete with value of 10 and other athlete with value of 20 o Reason for difference: the athlete with value of 20 has more type 2 muscle fibres than the other o Athletes with more type 2 muscle fibers should have value higher than 20 What does lactate threshold tell us: - How much lactate is produced and how much lactate is removed from the blood - Why is lactate not considered a waste product o Lactate can be used as another energy source The graph describes the 2 distinct phases Through training adaptations , less lactic acid will be reduced and removal mechanisms will be better (used for glucose) Phase 1: before LT Lactate removal is quicker than lactate production Lactate production is less than lactate remove ATP comes predominantly from aerobic metabolism Phase 2: after LT Produce more lactate than can be removed Therefore get accumulation of lactate Lactate production is more than lactate removal In terms of energy system: ATP comes mainly from anaerobic metabolism - Don’t switch off aerobic metabolism but majority ATP comes from anaerobic If we know at what speed or HR the LT occurs = then we can tell athlete that its there ideal race pace (can look on graph) Lets look at graph: Change in LT with training expressed as an increase in speed on treadmill Untrained individual: Blood lactate starts at 2mmol/l and remains steady at this value as treadmill speed increases Then sharply increases when treadmill speed is 9 km/h Trained individual: Blood lactate starts at 2mmol/l and remains steady at this value as treadmill speed increases Then sharply increases when treadmill speed is 12km/h Best pace = 12km/h If lactate threshold goes up during event = must ensure comes back down - Otherwise will run into trouble: if exercise for long in phase 2 = fatigue earlier Relationship between LT and race pace (average intensity you can maintain for long periods of time) Change in race pace with continued training after maximal oxygen uptake stops increasing beyond 71 ml/kg/min Practical applications of LT 1. Indicator of aerobic fitness 2. Indicator of race pace 3. Measure of training programme - Looking for physiological markers that still change with training - Because can measure lactate with simple blood ample, we can determine LT very accurately - If there’s change in training adaptations can see easily 4. Training zones - Can use response graph and can divide graph into 3-5 training zones - If you want to do recovery training then need to exercise at less than 50% of vo2max - Can relate to heart rate (your recovery runs must be at a rate of less than ___) - Simplest = 3 training zones - As get better trained = training zones change  5. Effects of training interventions - What if we pout the athlete on a high intensity interval training program (heat programme ) and compare with moderate training - What effect on LT: if one of the training programmes improved LT then use that programme 6. Drugs and nutritional supp - Some supp that may help switch later to anaerobic metabolism - Increase aerobic capacity - Can test effectiveness of supp - If athlete was on training programme and redo test after 8 weeks and LT didn’t change or get worse = then need to look for reason o Did follow programme? o Slow responder - Shift to left = indicator of over training (2) RER Respiratory exchange ratio: VCO2 / VO2 (DON’T HAVE TO REMEMBER EQUATIONS) Function: 1. Determines how much o2 or how much ATP comes from carbs and how much comes from fat 2. Predicts substrate use, kilocalories/ O2 efficiency If you want to emphasis or make adaptations to the body to increase fat oxidation directly, then useful to look at RESPRIATORY EXCHANGE RATIO (RER) - Ration between oxygen production and oxygen consumption Understanding RER How it works: RER or 1 molecule of glucose = 1.0 - To metabolise 1 molecules of glucose you need 6 molecules of oxygen - Produced 6 co2 values - Ratio = 1 If RER stays above 1 = mostly metabolising carbs If burn primarily carbs = RER value will be 1 or higher If you burn primarily fats = RER value will be +- 0.7 - lots of fatty acids that could be burned what is the RER value at 8km per hour: 0.7 Longer can contain value of 0.7 = more fats burned What will value be at end: 1.15 -1.2 (max value) What will value be at 14km/h: 1._ (above 1) - wont be above 1.15 or 1.2 as they are expected at max What will value be at LT : 1 Only carbs can be metabolised without oxygen The person is on the other side of LT and the person is burning mostly carbohydrates LT in diabetic = very low - insulin inhibits fat metabolism - will reach LT very early What will happen to LT if had good breakfast of oats and 2 glasses of OJ and 2 slices of jam on oats - will decrease as body likes to burn carbs - if have high carb before exercise = body will want to burn before fats o fats take more effort to metabolise - the sugar is available easily Relationship between LT and RER values When carbs is 100 and fats is 0 = LT is 1 - switch from fats to carbs RER at different training intensities Decreases at absolute and relative submaximal intensities Increases dependent on fat Decreases dependent on glucose  PRE POST (3) Resting and submaximal VO2 Resting and submaximal V O2 - Resting V O2 unchanged with training - Submaximal V O2 unchanged or  slightly with training (in case of the latter, it shows that the athlete also improved his/her exercise economy) Maximal V O2 (V O2max) - Best indicator of cardiorespiratory fitness -  Substantially with training (15-20%) -  Due to  cardiac output and muscle oxygen extraction (4) pH Anaerobic metabolism: Increased lactate and increased H+ Endurance training: increased aerobic metabolism What occurs during exercise: Lactic acid is produced by the muscles and immediately gives off an H+ (dissociates) and then we get a lactate which is in the blood - that H+ molecule can change pH of blood and fluid enviro within cells Effects of pH 1. Enzymes work optimally within a narrow pH range 2. Generation of ATP may be delayed - if your pH drops (with high intensity) effects capacity of enzymes to do their jobs, slowing down steps where enzymes are involved, ATP generation will be slowed - this leads to muscle fatigue Lactate graph analysis and pH Before LT (aerobic phase) = little change - the lactic acid dissociates and h ions are made - body has buffer bicarbonate - bicarbonate mops up the h ions – binds to h ions and it therefore maintains pH Resting Ph LEVEL = 7.4 When reach LT – the lactic acid increases - lots of H+ coming of lactic acid molecules - there is not enough buffers available to clear H+ - H+ that don’t bind to buffer cause pH to drop What major effects of excess H+ : 1. Enzymes then get effected 2. When have lots of free H+ in muscle cells, some H+ bind to troponin c - Affects cross bridge cycle as it can only form when a calcium binds troponin c - When cant form cross bridges = contraction decreases Advantage of being better trained = can keep pH level constant for a longer period of time When the pH starts to drop is related to LT The lactate can be used to make glucose - Therefore cant be reason for muscles soreness and fatigue - It’s the H+ - The higher lactate conc = the more h ions that need to be buffered Can you change your buffer capacity: Yes can consume extra sodium bicarbonate Can extend point where pH starts to drop What are the reasons for the delayed drop in pH 1. Greater oxidative capacity 2. Less lactate is produced and more is cleared 3. LDH enzymes coverts pyruvate into lactate - H form of LDH is found in type 1 skeletal muscle fiber o Favours the conversion of lactate into pyruvate o Explains why type 1 muscle fibres produce less lactate than type 2 o If you are better trained , you make more H form of LDH which will help the removal of lactate by converting it to pyruvate 4. Greater buffer capacity  - As you get better trained, you develop a better buffer capacity - Without taking additional buffers, already have a better bc 5. Redistribution of blood - Greater portion of CO goes to skeletal muscle which takes out lactate of muscle cells - The different MTC transporters take lactate into blood stream which is then converted into glucose pH changes with training Drop in pH = metabolic acidosis Why: - More mitochondria - Less lactate is produced and lactate is cleared at a faster rate - Change in LDH iso-enzyme* o Changes to the LDH iso-form that is mostly found in Type I muscle fibers; this iso-enzyme converts La easily into pyruvate acid. o The LDH iso-enzyme in fast fibers favours the conversion of pyruvate acid into Lactate - Greater buffer capacity (bicarbonate) - Increased blood flow to clear lactate Biochemical Adaptations and Blood pH Fig. 12.14: Adaptations to chronic endurance exercise Adaptations to aerobic training: fatigue across sports Endurance training critical for endurance-based events Endurance training important for non-endurance-based sports too All athletes benefit from maximizing cardiorespiratory endurance Factors that affect aerobic training responses 1. Initial level of aerobic fitness 2. Training intensity 3. Training frequency 4. Training duration Is strenuous training more effective? 70% HRmax, 20 – 30 min: stimulates a training effect 90% HRmax: upper limit for aerobic training Generally, the higher the intensity, the greater the training improvement in VO2max. Is there an optimal training duration? No threshold duration per workout for optimal aerobic improvement More time devoted to workouts does not necessarily translate to greater improvements, particularly among active individuals Does training frequency matter? Not sure, but 1 day a week does not result in meaningful changes More frequent training produces beneficial effects when training occurs at a lower intensity. Normally: 3 days per week Effects the same with or without rest days The stimulus for aerobic training links to exercise intensity and total work done. Does training mode matter? Mode does not matter if intensity, duration and frequency is comparable Must involve large muscle groups Autoregulation extra notes Autoregulation The manifestation of local blood flow regulation Def: the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure Myogenic autoregulation Myogenic mechanisms are intrinsic to smooth muscle blood vessels - Small arteries and arterioles If the PRESSURE within a vessel is suddenly increased – vessel responses by constricting which leads to contraction - Vascular smooth muscle cells depolarize when stretched Diminishing pressure within the vessel causes relaxation and vasodilation The myogenic mechanism plays a role in autoregulation of blood flow and in reactive hyperemia Metabolic autoregulation Blood flow is closely coupled to tissue metabolic activity in most organs of the body. The metabolic theory of blood flow regulation For example, an increase in tissue metabolism, leads to an increase in blood flow (active hyperemia). Actively metabolizing cells surrounding arterioles release vasoactive substances that cause vasodilation - Reason for tissue metabolism: occurs during muscle contraction or during changes in neuronal activity in the brain Increases/decreases in metabolism lead to increase/decrease in the release of these vasodilator substances Metabolic mechanisms ensures: 1. that the tissue is adequately supplied by oxygen 2. Products of metabolism (CO2, H+, Lactate) are removed Hypoxia, Adenosine, CO2, H+, La-, K+, Inorganic phosphate Endothelium mediated autoregulation What are endothelial cells and their function: Def: Endothelial cells line the inside of every blood vessel in the body. Function: They form a one-cell-thick layer called the endothelium, which is also found on the inner walls of the heart chambers and lymphatic vessels, which carry excess blood plasma around the body. The endothelium produces several vasoactive factors that are involved in the regulation of blood flow, e.g. nitric oxide Vascular actions of nitric oxide (NO):  Direct vasodilation Indirect vasodilation by inhibiting vasoconstrictor influences (e.g., inhibits angiotensin II and sympathetic vasoconstriction) Anti-thrombotic effect - inhibits platelet adhesion to the vascular endothelium  CHAPTER 12 PART 4 – ADAPTATIONS TO ANAEROBIC TRAINING Introduction Beyond LT = anaerobic Anaerobic exercise – any exercise that is less than 30 seconds - Any more than 30 sec will use aerobic system to greater extent If want to test anaerobic system need a test that is up to 30 seconds Another test for 10 seconds – major energy pathway used to ATP-PC system Only standardised anaerobic test = called Wingate anaerobic test - Wingate – refers to an institution in Israel Anaerobic capacity is important for all types of activity Some sports = far more important than for others All athletes need a certain amount of anaerobic capacity Changes in: 1. Heart 2. Muscles 3. Energy systems 4. Buffering capacity Heart Changes in the structure of the heart in response to aerobic = volume overload Anaerobic structure changes cause a pressure overload - CO doesn’t increase as much o With anaerobic exercise both ATP-PCr and glycolytic system does not need oxygen to make ATP o Therefore don’t need lots of oxygenated blood to provide muscles with oxygen as can generate ATP without oxygen Anaerobic excise has more pressure changes OUTSIDE and inside the heart - Athletes very often during this type of exercise will hold their breath (100m sprint) - Blood pressure – with aerobic exercise our blood pressure increases to 180/200 but with anaerobic can increases to more 200/300  o That is the pressure overload Structural adaptations - different patterns of hypertrophy 1. Thickened septum = more significant hypertrophy - Not only on outside walls 2. Thickening of posterior wall - Septum (wall in between the atria and ventricles) will thicken 3. Concentric hypertrophy - Increased left ventricular mass with no change in left ventricular EDV Athletes hearts and individuals with chronic hypertensions hearts look similar Adaptations in muscle Shift in muscle fiber type: - Increase in type 2a, 2x cross-sectional area - Increase in type 1 cross-sectional area (lesser extent) Decrease % of type 1 fibers Increase % of type 2 fibers Adaptations in energy systems Two systems: 1. ATP-PCr system 2. Glycolytic system ATP-PCr system Little enzymatic change (CK) with training  - Evidence of changes after strength training and HIT Increases in intramuscular ATP and CP concentrations ATP-PCr system-specific training leads to increase in strength Short sprint-type anaerobic training DOESN’T enhance anaerobic endurance Phosphocreatine stored in cells = reason why we use this system in short exercise - ATP is already in cells and PC can make more ATP Enzymes: Most NB enzyme – creatine kinase - Only enzyme that is involved in breaking down PC Strength training and high intensity training = 2 types of training methods that will increase production of creatine kinase How the enzymes change with very short bouts of exercise (6s vs 30s) - In both: the 30 s sprints resulted in better adaptations - If you want to optimally train the ATP-PC system = 30 sec bouts of exercise are far better than short sprint Changes in enzymes in response to maximal sprints CK: Creatine kinase MK: Myokinase What does happen with all types of anaerobic exercise = the muscles develop the capacity to store more ATP and PC - Storage capacity increases o Reason why it increases: undergo muscle hypertrophy , therefore more space to store o More substrate to use in energy system To improve this energy system – need to do specific types of exercise (high intensity exercise training increases the energy system the most) Glycolytic system Evidence of increases in glycogen content of muscles with long sprint bouts (more than 10 seconds) Increase in key glycolytic enzyme activity with training - Enzymes: glycogen phosphorylase, PFK, LDH, hexokinase o PFK: the major rate-limiting enzyme of glycolysis - More improvements with 30s exercise bouts compared to 6s bouts Performance gains from increase in strength - the fact that muscles become stronger and muscle hypertrophy, not so much because of change in enzyme activity or fact you have more substate to make ATP Changes in PO after maximal sprints - Power output and rate of fatigue (i.e. decrease in power production) the same for 6s and 30s bouts, suggesting no change in anaerobic yield of ATP Optimize the glycolytic system = you can only breakdown carbs - Doesn’t break down fats - Very dependent on the among of glycogen that is stored in the muscles - The storage capacity for glycogen can be increase o Longer sprint bouts of more than 10 secs - Can be used for training program design if this is energy system you want to target o Use longer sprint bouts but less than 30sec - Increase in glycolytic enzyme activity o PFK, KDH, hexokinase, glycogen phosphorylase o LDH = most nb Buffer capacity If H+ produced during glycolysis are buffered = intramuscular acidity (pH) stays constant This is important for: 1. The optimal function of enzymes - Enzymes work optimally within a narrow pH range 2. Maintaining muscle force and power during exercise - If have free floating H+, they bind to troponin C rather than calcium binding - This leads to less crossbridge forming = cant generate tension Types of buffer systems 1. Bicarbonate 2. Phosphate 3. Protein Both endurance and sprint-type training shows increase in buffering capacities Buffering systems: take care of h ions Most NB: bicarbonate buffer system Haemoglobin acts as a buffer If we have a well developed buffering system then we can take care of free h ions and can maintain pH for longer during exercise Can also boost buffer capacity by supplementing Bicarbonate loading: Benefits: - increased blood pH and buffering capacity - Delayed onset of anaerobic fatigue Effects: - 300 mg/kg leads to increased all-out performance for 1-7min - Enhanced H+ removal from muscle fibers Risks: - GI discomfort (bloating and cramping) - Sodium citrate = similar results without risks Adaptations to High-Intensity Interval Training HIIT Def: time-efficient way to induce many adaptations normally associated with endurance training Types: 1. Short HIIT - 30-40 x 15 second intervals at 100% VO2max - 15 second passive recovery 2. Long HIIT - 4-6 x 4min intervals at 90% VO2max (90-95% HRmax) - 2-3min passive/active rest o Active: 50-70% HRmax - Greater increases in VO2max with long HIIT o Why: have to stimulate aerobic system 3. 5 x 2min running at more than 95% HRmax, 1min rest What is an indicator to start HIIT: If gets to a point where reach plato in performance and vo2 measure doesn’t change - Time to do interval training Effects of HIIT in highly training athletes: 1. Increases PPO 2. Increases VO2max 3. Increases skeletal muscle buffering capacity 4. Increases myoglobin (?) 5. Increases both glycolytic and oxidative enzyme activity 6. Increases Type I muscle fibers 7. Increases capillarization of Type I fibers HIIT vs MICT Mitochondrial enzyme cytochrome oxidase (COX)  same after HIT versus traditional moderate-intensity endurance training Similar changes in COX and cycling performance with HIIT and MICT Specificity of training and cross-training Specificity of training VO2max substantially higher in athlete’s sport-specific activity Likely due to individual muscle group adaptations Cross-training Training different fitness components at once OR training for more than one sport at once Strength benefits BLUNTED by endurance training Endurance benefits NOT BLUNTED by strength training Sport-specific training The VO2max of the athletes during their sport-specific activity was as high, or higher than the values during treadmill running Concurrent training: Strength and endurance trained simultaneously Results 1. Excess fatigue 2. A greater catabolic state 3. Differences in motor unit recruitment pattern 4. Possible shift in fiber type Endurance capacity is enhanced by simultaneous strength training When strength training is done with endurance = less games in strength - Interference phenomenon Interference effect: Occurs when targeting 2/+ conditioning components in the same microcycle of a phase that leads to a lower gain in any one component than would have been expected if had trained separately  CHAPTER 17 – INTRO TO CHO LIFESTYLE Energy Balance Model (AKA CICO model, Calories in and Calories out) - Believes causes of weight gain exclusively is behavioural - Balance between food and exercise = weight maintenance Two simple solutions to obesity problem: 1. Exercise more 2. Eat less - Aka gluttony and sloth causes obesity These solutions are based on the Energy Balance Model Cause of overeating / underactivity is BEHAVIOURAL Exercise more If you exercise more = lose the weight/ maintain the weight ‘’Experts’’ routinely claim thar exercise is the key to weight loss NOT TRUE - Exercising more on its own does not help you to lose weight Example: no significant change in body composition was observed when observing sedentary individuals who completed an 18 month program Why is exercise alone not an answer Exercise stimulates your hunger - Worse in women than men - The higher your physical activity level = the higher your energy intake (according to the graph) o Not talking about athletes, talking about general population Eg: If 1kg muscle burns – 12calroies per day during rest and 1 kg fat burns – 4 calories per day during rest - If you convert 10 kg of fat to muscle – a major achievement – then you can eat an extra 80 cal per day. Anything extra and you will gain weight o 80 cal = boiled egg or 5 t sugar or slice of bread What most ppl believe: the most powerful determinant of your dietary intake is your energy expenditure Reality: 1. If you’re more physically active, you’re going to get hungry and eat more 2. In general, the more a person engages in daily exercise, the more inactive they are during the rest of the day - Notably amongst children Eat less Experts claim that you should - Cut calories - Follow the next magic diet - Burn fat by taking supplements/pills and potions Nothing magical about ANY diet. The question is rather whether the diet is sustainable, and most are not, nor is cutting calories After period of being on a diet – people pick up more weight than what they lost in the diet CICO adherents believe you take in, subtract calories out and whatever is left over is dumped into fat stores like a potato into a sack. - believe that fat stories are essentially unregulated There are 2 compartments where calories an go: 1. Expended as energy “calories out’’ 2. Stored as fat However: EATING LESS WILL NOT MAKE YOU WEIGH LESS The body is in balance: 2000 cal in = 2000 cal out - Calories go out as basal metabolism (vital for organs, heat production etc) and exercise Diet: cut 500 calories, you expend the same amount of calories - Why: immediately when cut calories, your body responds by slowing down metabolism - The major mechanism is that the body shuts down/slows down all the metabolic processes in the body - STILL not addressing fat stores  1500 calories 1500 No calories change Fat storage = dependent on the hormone insulin - Cutting calories does not affect function of insulin - Therefore cant see change in fat storage - Fats from adipose tissue is NOT mobilized through eating less - If insulin levels are high – cant mobilize the fat stores o You have to do something to mobilize the fats If you eat carbs before gym, the body will metabolize the carbs as its easier Criticism on model Too simple Far more factors involved in daily energy balance that are not accounted for in the model To exercise more and/or eat less is NOT recipe for weight loss Factors influencing energy intake: - Appetite - Environment - Psychology Factors influencing energy outtake: - Basal metabolic rate - Exercise activity - Non-exercise activity - Thermic effect of food Low carb diet Type of calories you consume has an important role in whether you gain or maintain weight - Most problematic calories = from refined carbohydrates - Why problematic: cause the greatest insulin response Hormonal Theory of Obesity Low carb diet - the link between carbs and hormone insulin If you have consistently high insulin levels = lead to weight gain Obesity causes these 2 behavioural aspects: 1. Eat too much 2. Exercise too little Insulin is a fat storing hormone - Fats are under hormonal control - Intake and expenditure of calories under hormonal control o Hunger/ basal metabolic rate - Intake and expenditure of calories are linked to each other Calories are primarily pushed into storage leaving inadequate amounts for energy expenditure - Either increase caloric intake or decrease energy expenditure Patients with type 2 diabetes - Dependent on insulin injections - Mostly overweight as get older - Glucose levels are too high – insulin helps take it up by cells We do not get fat because we overeat We overeat because we get fat! Glucose stimulates insulin release by the pancreas How glucose enters the cell Glucose cant enter into cells on its own Glucose enters via the glucose receptor protein embedded in cell membrane - GLUT-4 in skeletal muscle, adipocytes, brain and heart Insulin binds to and opens the receptors to let glucose into the cell Insulin glucose +Receptor cell Purpose of glucose in skeletal muscle cells: 1. Need glucose to make ATP 2. Insulin allows for glucose to enter in cell How quickly and how much insulin released, depends on type of carb you consume - Carbs are all sugars GI -glycaemic index High GI: - If you consume carbs that have high GI = the glucose will be released quicky in blood and cause a high strike in glucose in blood o Sweets - More insulin: The faster the glucose release into bloodstream = more insulin necessary to open up receptors - Fats storage activated and breakdown inhibited: If receptors are not open, cant be taken up into cell and then glucose is converted to fats and stored Low gi index - slower released of sugar into blood stream = less insulin is needed Glucose causes a release of insulin and causes a spike in glucose levels in blood Major function of insulin: 1. To counter the concerted action of hyperglycemia-generating hormones 2. To maintain low blood glucose levels What is effect of insulin on fat metabolism 1. Stimulates fatty acid synthesis in liver = NON ACHOLIC FATTY LIVER DISEASE 2. Inhibits the breakdown of fats in adipose tissue - Cannot mobilize triglycerides into free fatty acids - Only way to mobilize adipose tissue = consistently having low insulin levels, means that you must have low glucose levels Insulin leads to ACTIVATION of fatty acid synthase and glycogen synthase - Fatty acid synthase: makes fat - Glycogen synthase: makes glycogen for short-term storage of energy Insulin leads to INACTIVATION of hormone-sensitive lipase and glycogen phosphorylase - Hormone-sensitive lipase: breaks down fat - Glycogen phosphorylase: breaks down glycogen Insulin also leads to PRODUCTION of cholesterol - Activates HMG-CoA reductase Whether fat is stored or used as energy depends on INSULIN in blood Aetiology of obesity Problem with obesity is insulin which is driven by carbohydrates Individuals differ in terms of sensitivity for carbohydrates - Some can eat lots of carbs (low GI) and don’t gain weight - Others are very sensitive (doesn’t matter type of carb) meaning they have high insulin responses to carbs (impact on fat storage and mobilization) Carbohydrate-Insulin Hypotheses Healthy response with changes in insulin with meals: Decrease of insulin between meals and fasting Insulin resistance: if insulin stays high, with/without eating Fasting – you get reduced levels of insulin - Will see same effect who are fasting throughout the day - Fast will help keep low insulin level Better to have 5 or 7 smaller meals per day rather than 3 meals a day - Don’t drop below baseline levels - Depends on o type of carbohydrate o If its combined with fats Every time insulin levels drop – goes below baseline - Higher spike = lower the drop - Hypoglycaemic - Issue with having more meals a day = increase risk of having more hypoglycaemic responses Carb sensitive = insulin resistance - Even if eat little carb = massive insulin response = will experience hypoglycaemia Insulin burst will cause high level of insulin in blood stream all the time Fasting period and then eat at lunch time = still in a fasting state - Will burn mostly fat - Why you practice intermitted fasting will burn fat - Force your body to burn fat when glycogen levels are low Blood insulin levels are affected by: 1. Type and amount of CHO (glycaemic index and glycaemic load) - High GI and GL: greater insulin response 2. CHO plus fat: lower insulin response 3. CHO plus protein: Higher insulin response 2 things for lower insulin levels - Fasting – more acute effect (drop in insulin levels are far more) - Restrict carbs - Combo = best results Slow puree – low GI carb - Lower insulin response than high Fast puree – high GI carb Carbs + fat = low insulin response Carbs + protein = slightly higher insulin response Problem is that if insulin levels are low = will it have effect on protein synthesis s - No - What we actually need is a lot less - Because we have fat stores we can mobilize - Should try keep glucose blood levels as consistent as possible - Liver can convert lactate and proteins into glucose - Don’t forget about lactate during exercise that can be converted - Ketos can be converted to glucose - Don’t need massive amount of carb to sustain exercise as have other sources of energy Different individual responses to insulin Individuals have different glucose and insulin responses to same meal – even if healthy Insulin response is not age dependent - However, does worsen with advancing age If person responds with HIGH glucose and insulin levels to carbs = risk of/already have developed INSULIN RESISTANCE - Must be careful with CHO intake - Will have difficulty losing weight – unless limit CHO Insulin resistance The sensitivity of insulin receptors is blunted Large amounts of insulin needs to be secreted to activate the receptors to allow glucose uptake Greater effect on fat storage Insulin resistance = high insulin levels The new science of diabesity Insulin resistance requires 1. High hormonal levels 2. Constant stimulus Refer to low carb diet as low carb, high fat diet Reason for high fat: 1. Fat can provide you with lots of ATP – must just teach body to access 2. Fats with comb of carbs = lower insulin response Some combo protein and carbs - Will give higher insulin response If purpose of diet to lose weight = low carb, high fat If weight isn’t problem and worried about muscle building = low carb, high protein When wont body store fat: 1. If your muscles are significantly glycogen depleted. This is achieved by strenuous exercise (sprinting, resistance training, interval training) 2. If blood glucose levels, and thus insulin levels are low. Fats are broken down for fuel and excess glucose is not stored as fatty acids. How to store fat: Keep CHO intake low - + 50 g per day are recommended  CHAPTER 17: CHO RESTRICTION AND SPORT PERFORMANCE Definitions Define these kinds of diets according to amount of carbs in diet - Lower value = greater advantages - Plans to loose weight = stick closer to 50g Paleo diet - Original diet - Restrictive - Comes from long ago - Mainly ate meat and fish and veg and fruit - Excluded dairy and processed food The LCHF diet - AKA banting diet - Based on whole foods - Low carb diet - Similar to paleo - Includes dairy and minimal fruit - 50-120g CHO per day o Recommended for all healthy people - The younger you are and more active = the higher the intake - Most serious athletes need max 120g of CHO Diet in low CH - Don’t aim to consume specific number of calories Basic principles 1. Not about number of calories, you will eat when you are hungry - Will eat til you are full o More healthier kind of diet - Better than saying: I must eat 2000 calories and drink so much water - Athletes would train very hard = more hungry than general population o Idea must be to get away from aiming to get certain amount of calories o Body’s metabolism is very different amongst ppl ▪ One recipe isn’t suitable for everyone 2. eat until you are satisfied 3. eat real food Ketogenic - More restrictive - 25g of CHO o Less than 10% of total calorie intake - Consists mainly of fat (80%) - 15% of proteins - Where carbs are VERY LIMITED - Sometimes people find it very difficult to eat 80% of calroies from fat o Solution: increase protein intake The Ketogenic diet (KD) 80% calories from fat 15% calories from protein 5% calories from CHO Processes 1. Ketogenesis - Acetyl CoA → Ketone bodies, via beta-oxidation in the liver Ketogenic = production of ketones which are used as energy source, can also be converted to glucose - system takes a lot of time - body has to adapt - adaptation period: 2-4 weeks - we find that most of the individuals can develop ketosis in 2-4weeks 2. Ketolysis: - Ketone bodies → Acetyl CoA, via succinyl CoA Ketosis can be achieved via: 1. Short-term fasting 2. Exercise 3. Low CHO diet Cannot fast for 1 day or exercise in fasted state and think you are in ketosis Best eg of athletes that burn mostly exclusively fat and improve performance : Alberian husky - nature of dogs: minimal carbs - consists mainly of fat - successful dogs have vo2max that is twice the Tour de Frans cyclists - Dogs and cats get diabetes = shows metabolism isn’t too different KD and Sport performance With endurance exercise: most studies show no change in performance - No change in performance - Athletes who follow ketogenic diet don’t perform worse - Negative finding or no finding in difference on running on fats or carbs - But shows performance is not impaired - While athletes are training: they are training as mot little carbs o Use small amount of CHO during events and competition - Diet of high performance athletes High performance athletes need a little more CHO - Reason why top up CHO during competition - Takes a couple of days to get back into ketosis With strength and power: no change in performance - No change in performance o Will perform equally well with or without CHO - Blunted hypertrophy: muscle hypertrophy response, protein synthesis is impaired o If purpose of training = wont have optimal responses High performance athlete = little different Inconclusive results in sport studies: 1. Too few studies - Only may use small sample of participants 2. Too short KD adaptations periods - Keto-adaptations takes 2-4 weeks 3. Studies are a mix of untrained and trained - Untrained vs trained responses Less muscle hypertrophy with KD? One argument 1. KD can inhibit the protein signalling pathways through mTOR or satellite cells - Contradictory results: signalling pathways are effective - Jury is still out 2. The function of insulin and insulin-like growth factor may not be optimized - Research is inconclusive - That the functions are also impaired when restrict CHO intake - Not much support for this argument KD generates very high concentrations of beta-hydroxybutyrate (ketone bodies), which leads to a reduction in leucine oxidation and this will favor the preservation of muscle mass. - If reduce leucine oxidation (breakdown of leucine) = preserve muscle mass Second argument Too much glucose and/or insulin interfere with training adaption All the signalling pathway must function optimally and genes must be activated in the right manner to make training adaptions (muscle hypertrophy ) If lots of CHO available (before, during or after) there might be decrease activation of signalling pathway - Means that their functions will be inhibited - Outcome: wont function optimally - Decreased activation of cell signalling pathways - Decrease in fat oxidation - Decrease in mitochondrial enzyme activity - Decrease in mitochondrial content Sport performance = little or no change - Lots or little CHO wont affect performance Concerning that u training too hard but too much CHO in the blood = will inhibit genes that are responsible for training adaptions Another study: The glycogen content of skeletal muscle determines the regulation of transcriptional activation of many genes - How the genes are activated and how much activated to do job - Genes function better in low glucose/cho diet - Athletes training adaptions during recovery = NB o Training in fasted state How long to activate genes = 1-4hrs post exercise - Returns to resting (pre-exercise) values within 16-24hrs - Reason why recovery = NB - Training adaptions are made during this time o Why: signalling pathway are activated and reach a peak - But the dietitians also say that 4hr post exercise is critically period o Consume enough CHO to fill glycogen store o Consume enough protein - Physiologists: compromising signalling pathways - Mustn’t eat all CHO after training so that it can prolong period of signalling pathways CHO eaten before exercise (not in fasted state) Training in fasted state = most important Critical what you do after exercise In recovery: need to make sure that you eat within first 2 hours following exercise Training adaptions occur post training (1-4 hours post) How to prolong the transient increases in mRNA transcription: Starting exercise with low muscle glycogen stores and/or withholding CHO during recovery from strenuous endurance Results in: greater or more sustained signal Keto adaptation Metabolic benefits 1. Brain fuel = ketones provide lots more brain fuel compared to glucose - Concentration is better (ketones fuel brain) - Lots of energy 2. Decreased ROS – molecules that break down 3. Improved insulin sensitivity 4. Protein sparing 5. Decreased central fatigue 6. Less lactate 7. Decreased ventilatory drive 8. Improved body composition 9. Better recovery Summary Far too much emphasis on CHO - No function in the body that only uses or needs CHO - There are a lists of functions for proteins and fats - Can go without CHO - If you are Olympic athlete = not 100% true - True in general population Idea that CHO are ideal for sport performance and health = remember negative effects - Specifically effect on fat metabolism and insulin Sport performance will not be impaired if properly fat adapted and follow low carb - May not perform better but not worse