HS23 Exercise Physiology I PDF

1. Research Methods Epidemiology vs. Field or Laboratory Tes ng  Epidemiology: > Inves gates the factors that determine the presence or absence of a disease or disorder. Gives informa on about how many people have a disease (prevalence), if the numbers are changing (incidence) and what the eﬀects on society and economy are. It’s totally observa onal (no interven ons!). > Pros: large number of par cipants, rela vely easy to implement (ques onnaire). > Cons: Only ques ons and no measurements, less objec ve.  Field or Laboratory Tes ng: > Pros: more objec vity, be er comparability, conclusions about cause and eﬀect are possible. > Cons: smaller number of par cipants, more work, more expensive. Cross-sec onal Studies vs. Longitudinal Studies  Cross-sec onal Studies: > Collec on of data from many diﬀerent individuals at a single point in me. No interven ons. > Pros: Easy to implement, basic comparison and formula on of a hypothesis possible. > Cons: conclusions about cause and eﬀect not possible (hypothesis CAN’T be validated).  Longitudinal Studies: > The same individuals are examined several mes over a period of me to detect possible changes. No interven ons. > Pros: Cause and eﬀect can be determined (changes over me). > Cons: Takes a long me, is expensive, par cipants might drop out. Field Tests vs. Laboratory Tests  Field Tests: > Outdoor, ac vity is performed as it usually is (e.g. running in the woods, cycling uphill). > Pros: Group tes ng possible (more eﬃcient BUT presence of other people can be a confounder). > Cons: No standardisa on, especially when you measure on two diﬀerent days (weather changes etc.)  Laboratory Tests: > Indoor, ac vity is measured in the lab (e.g. running on a treadmill). > Pros: standardisa on of more factors (temperature, humidity etc.) and measure physiology more accurately. > Cons: less eﬃcient, more expensive, outdoor ac vi es have to be simulated (simulate wind, incline etc. when running on the treadmill). Measurement Devices  Choose the right measurement device for measuring VO2,max: if a pa ent has problems with balance or their joints or is overweight  bicycle. If a pa ent doesn’t know how to bicycle or is more used to running  treadmill. 1 Confounders  Physiological confounders: humidity, temperature, sleep and me of day, food, noise.  Psychological confounders: mo va on, how many people are watching and what they are saying, gender of the person conduc ng the experiment. Choose the Right Study Design  Randomised Controlled Trial (RCT): Randomize most things but balance some things (e.g. 50% male, 50% female).  Single- or double-blind study.  Cross-over study: one group does interven on, one placebo, then they switch.  Control, sham, and placebo.   siehe HST Intro I für Beispiele zu Studiendesign. 2 2. Bioenerge cs and Metabolism  See slides 3-13 and clicker ques ons for video about crea ne. Energy Systems  Factors determining which energy system is used: intensity and dura on of exercise, availability of fuel, addi onal factors like availability of substances like O2.  Energy systems to generate ATP: anaerobic metabolism (phosphocrea ne, anaerobic glycolysis) and aerobic metabolism (aerobic glycolysis, fat oxida on).  ATP-PCr System:  Glycolysis itself is always anaerobic. If there is oxygen available, glucose is completely metabolised to H2O and CO2 which creates a total of 32 ATP and is called aerobic glycolysis (= glycolysis + citric acid cycle + oxida ve phosphoryla on). If there is no oxygen, glucose is metabolized to lactate which creates 2 ATP and is called anaerobic glycolysis.  Fat metabolism is always oxida ve. Lipids are cleaved into fa y acids and triglycerides, which are inserted into the citric acid cycle and create a total of 129 ATP (palmi c acid).  Respiratory quo ent (RQ) = VCO2 / VO2 at cellular level, respiratory exchange ra o (RER) = VCO2 / VO2 measured at the mouth. In steady state, RQ = RER and amount of carbohydrate and fat used for energy produc on is 1:1, during hypo- or hyperven la on RQ != RER.  Protein isn’t a very important energy fuel during exercise (fat and carbohydrate have much higher contribu ons).  Endurance training enhances glycogen storage capacity in muscles.  Type of training doesn’t inﬂuence where fat is lost. Visceral (= in the region of the intes nes) fat is usually the one that’s used ﬁrst for energy genera on, independent of the type of exercise one does (legs or abs exercise).  Energy systems are s mulated by the presence of ADP and inhibited by ATP.  Immediate vs. intermediate vs. long-term energy system: 3 Measurement of Fuel Contribu on  PCr breakdown: single leg extensions (20 min at lower intensity or to exhaus on at higher intensity) in MR-scanner, isomeric muscle contrac on in MR-scanner.  Measure anaerobic capacity in cycling (Wingate Test): cycle 30s at max capacity  power drops rapidly. Sprint athletes have a higher peak power than endurance athletes. Sprint and endurance athletes reach hypoxia at about the same me, but it doesn’t have a great eﬀect during the Wingate Test because 30s is too short for aerobic metabolism to start genera ng energy, therefore oxygen availability is not limi ng.  Increasing dura on of an all-out test leads to decreasing average power and to increasing contribu ons of glycoly c and aerobic energy systems.  Low pH is (was?) believed to be major limit to performance in all-out exercises.  Measure energy eﬃciency with calorimetry: > 40% of substrate energy creates ATP, 60% is lost in heat produc on. > Direct calorimetry: accurate for longer dura ons and res ng metabolic measurements, but expensive, not prac cal for exercise, sweat creates errors. > Indirect calorimetry: es mates total body energy expenditure based on O2 used and CO2 produced, older methods accurate but slow, newer methods fast but expensive.  Factors aﬀec ng eﬃciency of energy expenditure during exercise: body weight, movement technique (stride length and frequency), type of muscle contrac on (eccentric during downhill walking vs. concentric during uphill walking), temperature (even more so in water), humidity.  Slide 55 4 3. Muscle Adapta on  Muscle ac ons: concentric (muscle shortens), eccentric (muscle lengthens), isometric (muscle generates force but cannot overcome external resistance).  Velocity vs. force of contrac on: at maximal velocity, power is (near) zero. At maximal power, velocity is (near) zero.  Some muscles are adapted to generate high velocity (hamstring, muscle ﬁbres parallel to direc on of contrac on), others to generate high force (quadriceps, muscle ﬁbres diagonal to direc on of contrac on).  Human muscle ﬁbre types: Power  predominantly type II ﬁbres. Endurance  need to have a mixture of everything, marathon athletes are s ll very fast even in short distance running compared to normal people.  Recruitment of motor units: type I ﬁbres are always recruited ﬁrst, then type IIa, then type IIx (the higher the intensity, the more motor units are recruited).  Fibre switching: > In animal models, ﬁbres can switch from I  II and II  I. > In humans, type I  IIx possible under extreme condi ons (e.g. spinal cord injury). > In humans, type IIx  IIa through heavy resistance training. > In humans, type IIa  mixed isoforms IIa and I (is a type IIa ﬁbre but contains enzymes and mitochondria typical for type I) thorugh endurance training. > BUT! Fibre switching only happens under extreme condi ons (e.g. swim 80 km per week, recrea onal swimming is about 4 km per week).  Type of gym equipment should be adjusted to the type of sport an athlete does. E.g. swimmers train with elas c bands because it mimics the resistance of water. Range of mo on is speciﬁc for the type of sport: a runner’s muscle is lengthened when it needs to contract (upright posture), a cyclist’s muscle is shortened when it needs to contract (bent forwards). Anaerobic Training  Goal is to enhance the anaerobic system (ATP-PCr energy transfer capacity and lactate- genera ng capacity) to enable genera on of much force in a short me (‘explosive’).  Anaerobic training is muscle-speciﬁc! Only the muscle groups that are trained will acquire enhances aerobic func on and not the body as a whole. E.g. a sprinter will train their leg muscles with brief, all-out exercises combined with short recoveries for anaerobic condi oning.  Improve energy transfer capacity of the lac c acid system through overload-training: 1 min maximal exercise makes blood lactate rise to near-peak, repeat exercise a er 3 min break  ‘lactate-stacking’ produces higher blood lactate level than just one all-out eﬀort.  Metabolic adapta ons due to anaerobic training: increase in anaerobic enzymes, glycogen content, PCr and ATP, glycoly c capacity. 5 Aerobic Training  Goals: (1) enhance capacity of central circula on to deliver oxygen, (2) enhance capacity of ac ve musculature to process the oxygen.  Training of anaerobic system boosts aerobic system (but not the other way around).  Metabolic adapta ons due to aerobic training: muscle ﬁbres contain more and larger mitochondria (old mitochondria get cleared faster so the ones that are there are younger and more eﬀec ve).  Fibre adapta on due to aerobic training: poten al switch from type IIa  isoform IIa & I and from type IIx  IIa. Increased capillarity (VEGF) leads to be er perfusion and lower distance between vessel and mitochondria.  Angiogenesis: exercise-induced ac va on of transcrip on factors in myoﬁbers induces angiogenesis. ERRγ determines baseline muscle vascularisa on (not exercise-induces), PGC1α and HIF1α (exercise- induced) enhance vascularisa on. They all bind to the VEGF-promoter on the DNA.  Beneﬁt of more mitochondria: oxygen uptake is enhanced, less accumulated substances (e.g. ADP) are necessary for same amount of VO2. No beneﬁt anymore once steady state is reached.  Aerobic training increases the body’s fa y acid oxida on: greater blood ﬂow within trained muscles, more fat-metabolising enzymes, enhanced mitochondrial respiratory capacity in muscles, decreased catecholamine release for same power output (catecholamines lead to oxida on of carbohydrate, not fat (ﬁght or ﬂight). Less catecholamines for same power means more fat oxida on).  Absolute intensity of training does not inﬂuence how much fat you burn long-term (intensity only inﬂuences amount of fat burned DURING exercise).  RER (respiratory exchange ra o) = VCO2/VO2, RER = 1 only carbohydrates burned, RER = 0.7 only fat burned.  Eﬀects on carbohydrate metabolism: reduced use of carbohydrates as fuel in submaximal exercise due to decreased muscle glycogen use, reduced glucose produc on and reduced use of plasma glucose. Enhanced capacity to oxidate carbohydrates during maximal exercise due to increased GLUT4 on membrane and increased insulin sensi vity.  Aerobic training leads to metabolic adapta ons and maximisa on of aerobic poten al in all muscle ﬁbre types. Endurance athletes have larger slow ﬁbres than slow ﬁbres in same muscle because slow ﬁbres have larger capacity for aerobic ATP genera on due to high myoglobin (O2 storage in muscles).  Changes in muscle due to aerobic training: increase in aerobic enzymes, oxida ve poten al of fast ﬁbres, higher glycogen content, be er vascularisa on, higher VO2max. Strength Training  To train strength, muscle needs to be trained near its current maximum force genera on (near exhaus on). Intensity of overload controls strength improvement.  Recovery between sets: ATP stores need to be reﬁlled because strength training depends on anaerobic energy system.  To improve strength, absolute load doesn’t ma er as long as exercise is performed to exhaus on. So managing 10 reps with a high weight has same eﬀect as managing 30 reps with a lower weight. Beneﬁcial for people who have a higher risk of hur ng themselves (e.g. elderly people, person who’s had an injury). 6  A er one month at the gym, strength will already have improved compared to day one. BUT this isn’t due to structural changes within the muscle but due to neural factors.  Neural factors: enhanced eﬃciency in neural recruitment, increased motor neuron excitability, improved motor unit synchronisa on and increased ﬁring rates, lowered neural inhibitory reﬂexes, and inhibi on of Golgi in tendons (Golgi inhibits contracted muscle through ac va on of antagonist to protect from high strain).  Strength training is speciﬁc for a certain muscle and for a certain movement!  Image on the right: neural adapta on happens fast, muscular adapta on takes longer. Both contribute to increased strength.  Increased strength comes with hypertrophy (bigger cells): reason cells become bigger is not more water in the cell but more parallel sarcomeres  more contrac on force. Muscle growth is s mulated by increase in muscular tension. Remodelling of muscle architecture (angle of sarcomere in rela on to direc on of contrac on inﬂuences velocity and force) precedes gain in muscle cross sec on.  Hyperplasia (more cells): in animals, new ﬁbres develop from satellite cells or by longitudinal spli ng. In humans, hypertrophy of exis ng ﬁbres is the main contributor to increased muscle size.  Molecular basis of muscle adapta on: > Exercise (= stress) leads to protein synthesis (basically a protec on mechanism). > Eﬀec veness of an exercise can be quan ﬁed by measuring the amount of mRNA for a speciﬁc protein present in cytosol a er exercise. > Mechanical s muli like membrane stress lead to hypertrophy, regulated by mTOR (mechanis c target of rapamycin). Resistance training leads to ac va on of mTOR (directly or via inhibi ng its inhibitor), mTOR starts protein synthesis. > Calcium, free radicals and phosphate are also involved in muscle adapta on.  Essen als of strength training: > Rest 3 min between sets, training 2 to 3 mes per week. > Doing several sets increases strength only slightly compared to doing only 1 set. > Single-set programs produce almost the same health and ﬁtness beneﬁts as mul -set programs and you can train more muscles if you do only 1 set per muscle group.  Weight training: external weight should be ﬁxed at greatest load that allows complete ROM (range of mo on) for the desired number of repe ons.  Plyometric training: to mobilize the stretch-recoil characteris cs of skeletal muscle and control the stretch reﬂex  involves rapid stretching followed by muscle-shortening (jumping in place).  Concurrent training: > Energy demands of aerobic training limits a muscle’s growth and inhibits signalling to the muscle’s protein synthesis machinery. > Combining diﬀerent modes of exercise (e.g. aerobic + resistance training) may induce antagonis c intracellular signalling mechanisms that have a nega ve impact on muscle’s responsiveness to resistance training (resistance: mTOR  protein synthesis. aerobic: AMPK  AMPK inhibits mTOR). > If both are done back-to-back, aerobic training should come ﬁrst. 7  Delayed onset muscle soreness (DOMS): mechanical damage to ﬁbres  damage to membranes  calcium leak  protease ac va on and degrada on of proteins  membrane damage + protein breakdown = inﬂamma on  nociceptors in muscle ac vated.  Eccentric contrac on (break a movement, e.g. jump down from a step, go down in a push-up) leads to more DOMS than concentric contrac on (accelerate a movement, e.g. jump up, go up in a push-up).  Repeated bout eﬀect: ini al bout of exercise results in muscle injury, which leads to physiological adapta ons (neural, connec ve ssue, cellular)  protec on of muscle during second bout of exercise (less DOMS). 8 4. Acid-Base Balance and Lactate Balance  Physiological pH of blood is 7.4, accumula on of acid or loss of bases leads to acidosis. Some athletes but their body into alkalosis before compe on (hyperven late, take sodiumbicarbonate).  Sources of acids during exercise: CO2 from aerobic metabolism, lactate from anaerobic glycolysis, H+ from ATP breakdown.  Buﬀer system: > Intracellular: his dine-dipep des (carnosine), MCT (monocarboxylate transporters, H+ and lactate out). > Type II ﬁbres have be er intracellular buﬀer system than type I. > Extracellular (blood): haemoglobin, bicarbonate.  Exercise: pH sinks (more so in muscle than in blood), increase in lactate and decrease in bicarbonate in blood.  Blood lactate increases due to higher appearance or lower disappearance: > Lactate is always produced if there is enough pyruvate and not only if there is no O2. > Lactate in blood isn’t a measurement of how much lactate is produced but of how much is le (produced but not removed again).  The lactate threshold: > Lactate concentra on in blood starts to increase (more is produced than broken down). > There are two thresholds: ﬁrst is increase from steady state (= lactate threshold in the graphic), second is when curve becomes steeper (= OBLA in graphic). > There are many diﬀerent deﬁni ons of when lactate threshold is reached.  At low intensi es, blood lactate stays in steady state. At higher intensi es, blood lactate increases but is s ll below VO2max  intensity can be upheld. At max intensity, blood lactate passes VO2max  intensity cannot be upheld for more than couple minutes.  Causes of fa gue (see graphic on next page): > Central fa gue (above neuromuscular transmission) or peripheral fa gue (below “ “). > Increased H+: reduced force per cross-bridge, inhibi on of Ca-release from SR. 9  Lactate is NOT the sole originator of fa gue. There have been studies in mice that show that K+ induces fa gue and that acids ﬁght this eﬀect, hence the force lost due to K+ is regained when lac c acid is added.  Par cipants of one study reported pain when given solu ons containing lactate: increased lactate during exercise might cause pain, which reduces mo va on to keep going  central fa gue (so NOT the molecular eﬀects of lactate are the cause of fa gue but how the eﬀects of lactate act on the brain).  Lactate shu ling: lactate is a form of sugar (broken down from pyruvate) and can leave the muscle (glucose can’t!) as a way to redistribute energy. Injec on of lactate improves performance because it can be used as fuel (basically same eﬀect as if you injected glucose).  Performance limita ons:  With long exercise dura on, at some point fat will become major source of energy.  Muscle glycogen drops dras cally for short but high intensity exercises, and less dras cally for longer but less intense exercises because then more fat is used and less glycogen.  At constant intensity, exercise will start to feel more exhaus ng over me because glycogen stores become empty.  Graphic to the right (plasma levels during 3h cycling): > Glucose increases at ﬁrst because several hormones cause its release into bloodstream before it’s taken up into the cells where it’s needed. > Insulin decreases despite constant exercise load. This is due to heightened insulin sensi vity in muscle during exercise, so less insulin will s ll lead to the same eﬀect. Advantage because insulin inhibits glucose release from liver.  Hormones released during exercise: > Adrenalin, noradrenalin, glucagon increase glycogenolysis (more catecholamine release for higher intensi es). > Cor sol increases protein catabolism (?) for gluconeogenesis in liver. 10  Eﬀects of fuel availably on metabolism: if carbohydrates (CHO) are available, body will use them as fuel ﬁrst. When no CHO are available, body will use fat as fuel, but exercise will feel more exhaus ng. At normal levels of exercise and diet, proteins aren’t used as fuel.  Hormones that increase fat metabolism when carbohydrates become depleted: epinephrine and norepinephrine, cor sol, growth hormone. Decrease in insulin increase fat metabolism.  Eﬀects of training on lactate threshold: increased mitochondria number decreases lactate and H+ forma on, it takes longer for lactate levels in blood to rise (threshold becomes ‘higher’). 11 5, 6. Cardio-Respiratory Adap ons to Exercise Graph on the right:  Tidal Volume = amount of air per breath.  Breathing when at rest: at ‘lower end’ of lung (lung isn't ﬁlled with much air).  When exercising: ﬁrst increase in size of breathing (take deeper breaths), last resort is increase in frequency.  A trained person breathes at a higher lung volume (inspirate more air): Regula on of blood gases:  Normal oxygen satura on of blood is 98-99%. Increased respira on during exercise is NOT primarily induced by lowered oxygen satura on but by other mechanisms that partly start before exercising itself even begins.  Respiratory centre in the medulla receives input from peripheral chemoreceptors, proprioceptors in joints and muscles, core temperature, and chemical state of blood, as well as from motor cortex. The respiratory centre then induces ac va on of ven latory muscles.  Increased respira on regulates blood gases: ﬁrst goal is to take up more oxygen, at some point blood cannot take up more oxygen but body s ll needs increased respira on to reduce acidosis through release of CO2.  Trained women are at risk of arterial desatura on of blood oxygen because while they can train their heart to move blood very fast (good for systemic circula on), they cannot increase the size of their lungs (women are on average smaller than men and therefore have smaller lungs). Blood ﬂow in pulmonary circula on can become too fast for proper gas exchange. Ven latory threshold (VT):  = the point where more oxygen is inspirated than can be taken up by the blood.  = the point where VE (= pulmonary respira on) increases dispropor onately to VO2 during graded exercise (dispropor onate increase in VE/VO2).  Diﬀerent ways of measuring / detec ng the ven latory threshold (see slide 11).  Ven latory and lactate threshold are not the same and can change independently. Pa ents incapable of lactate produc on s ll have a detectable ven latory threshold. Increased respira on a er maximal oxygen satura on is reached therefore cannot only be a product of accumula ng lactate in the blood. (See graph on next side). 12  Ven latory responses to constant load exercise: > Up to VT: gradual increase in respira on un l steady state is reached. > Slightly above VT: increase, steady state with dri s to maximal respira on. > Above cri cal power: increase to maximal respira on, no steady state.  Energe c costs of increased pulmonary respira on: up to 15% of VO2 goes to respiratory muscles, respiratory muscle metaboreﬂex (body priori ses respira on and takes restricts blood ﬂow to exercising limbs to send more blood to respiratory muscles). Respiratory adapta ons to training:  No changes in lung structure through training, but improvement in lung func on parameters possible (train respiratory muscles).  Decrease in VE for a given VO2  right shi of the ven latory threshold, towards higher VO2 (steady state can be held at a higher level of power, high power is s ll perceived as moderate).  Reduce fa gue of respiratory muscles: through training of respiratory muscles, their O2 demand can be reduced, which in turn reduces the compe on for blood ﬂow with exercising muscles. Cardiovascular responses to acute exercise:  Goal is to increase blood ﬂow to working muscles.  Adap ons include changes in heart rate, stroke volume, cardiac output, blood pressure, blood ﬂow, blood composi on.  Regula on of heart rate: Heart rate (HR) during exercise:  Heart rate itself isn’t a parameter that tells something about a person’s ﬁtness level or that changes in a speciﬁc manner with training. It’s rather the ‘tool’ with which other parameters can be regulated (e.g. blood pressure). Heart rate shouldn’t be used as a measurement for intensity of an exercise.  Regula on of HR: intrinsic (sinoatrial node self-depolarises) or extrinsic (sympathe c & parasympathe c, arterial baro-reﬂex, central command, cardiopulmonary receptors measure ventricle strain).  Feed-forward ou low (central command / CNS): starts before you actually start running, sympathe c ac vity (epinephrine, norepinephrine) increases HR and contrac lity of myocardium, parasympathe c ac vity (acetylcholine) slows down HR.  Normal HR is 60 to 80 bpm, athletes have HR of 30 to 40 bpm (too slow HR can be dangerous because blood can start clo ng). Maximal HR decreases with age, but there are no general value of maximal HR that determine a person’s ﬁtness level.  Steady-state HR is the op mal HR for mee ng circulatory demands (at submaximal intensity), adjustment of steady-state HR to increased or decreased intensity takes 2 to 3 minutes (less in a trained person). Steady-state HR can be used for exercise test to es mate aerobic ﬁtness level. 13  HR stressors: anxiety, stress, sleep depriva on, dehydra on, thermic stress. Stroke volume (SV) during exercise:  SV increases with increasing exercise intensity up to 40-60% of VO2max, beyond this SV plateaus to exhaus on.  SV during maximal exercise is about double standing SV but only slightly higher than supine (‘auf Rücken liegend’) SV.  Factors aﬀec ng SV: > ↑ Preload (= end-diastolic ventricular stretch) means ↑ end-diastolic volume (EDV), leads to ↑ contrac on strength (Frank Sterling mechanism) and therefore to ↑ SV. > ↑ HR leads to ↓ SV because of reduced ﬁlling me and ↓ EDV. > ↑ Contrac lity is mediated through ↑ epinephrine and norepinephrine (independent of EDV) and leads to ↑ SV. > ↓ A erload (= pressure in aorta that has to be overcome so blood can leave ventricle) due to vasodila on leads to ↑ SV because.  Cardiac output (CO) = HR * SV [V/min]. Blood ﬂow and exercise:  Higher energy demand during exercise required adjustments in blood ﬂow for oxygen and substrate supply and removal of metabolites.  Arteries in ac ve muscles dilate while vessels in non-fundamental ssue constrict.  Vasodila on in capillaries: increased blood ﬂow, increased surface area for gas and nutrient exchange.  At rest, muscles get 20% of blood ﬂow, during exercise it goes up to 80%. Blood pressure and exercise:  Increased blood ﬂow leads to increased systolic blood pressure (SBP), less steep increase during steady-state (as soon as ↑vasodila on).  DBP largely unchanged (no increase in pressure due to vasodila on).  Re-se ng of feedback mechanism (heart rate usually regulates blood pressure, in ‘exercise-mode’ re-se ng of what body considers as normal heartrate rela ve to level of exercise).  HR, SV, and blood ﬂow during upper body exercise: higher HR, VE, BP, but SV and CO don’t increase. Generally whole body response diﬀers from response to upper body exercise.  Heart recovery (how fast HR slows down a er stop of exercise) a er training: speed of recovery increases with training, Tradi onal periodisa on: uses cycles from mul -years to micro-cycles that last a few days, best from athletes focusing on one compe on (e.g. Olympic games, not ideal for team sport athletes who have 2 games per week). > Block periodisa on: 3-4 blocks that last 2-4 weeks, focus on a few skills per block.  Does training make an athlete be er? Yes.  Does a training session make an athlete be er? No, the res ng a er the session is what leads to supercompensa on, recovery period is when gains arise.  In case of op mal increase in training load, ↑ in intensity and/or volume will lead to ↑ in performance. But excessive training can lead to ↓ in strength and sprint performance (damage to muscle cannot fully be repaired anymore) without any beneﬁts compared to op mal training.  Training volume: sport-speciﬁc, value of high-volume training ques onable, less volume may ↓ risk of injury, high volume + low intensity inappropriate for sprint-type performance. 17  ↑ volume + ↓ intensity OR ↑ intensity + ↓ volume: diﬀerent emphasis with diﬀerent ﬁtness result (applies to aerobic, anaerobic, resistance training).  ↑ volume + ↑ intensity: possibly nega ve eﬀects.  Overtraining: unexplained ↓ in performance despite →/↑ of volume and/or intensity, cannot be remedied by short-term ↓ of training or more rest, accompanied by physiological and psychological changes and symptoms.  Symptoms of overtraining: > Poor performance and high fa gue. > Prolonged recovery from usual training sessions necessary. > Increased sense of eﬀort during exercise. > Disturbed mood states with fa gue, irritability, restlessness, loss of mo va on and compe ve drive (assessed with POMS, RESTQ). > Loss of appe te and/or body weight. > Increased suscep bility to infec on. > Sleep disturbances. > Overuse injuries.  Not every ↓ in performance is caused by overtraining! Check for other diseases to exclude overtraining syndrome: anaemia, crea nine and liver enzyme concentra ons in blood, infec ous disease, diabetes, ea ng disorder, cardiological symptoms, asthma, muscle injury (high CK).  Training errors that might lead to overtraining: substan al ↑ in training volume and/or intensity, training monotony, high number of compe ons.  Other contribu ng factors: environmental stressors (al tude, temperature), me zone travel, social factors (rela onships, work, coach, team).  Diagnosis of overtraining through comparison of present exercise test values to earlier results: > Maximal performance. > Heart rate, anaerobic threshold, hormonal levels, and blood lactate at rest, submaximal, and maximal levels.  Treatment of overtraining syndrome: rest or heavily reduced training load and psychological stress counselling.  Preven on: periodisa on of training, adequate calorie (carbs!) intake and recovery me. 18  External load: wa s, speed, volume etc. that is given. Internal load: how body receives it.  TRIMP (training impulse) for es ma on of internal load: takes heart rate, percep on of eﬀort, and me into considera on.  Tapering = reduc on of training volume and/or intensity prior to a compe on: > No decondi on at up to 60% reduc on of training, VO2max can be maintained. > Results in ↑ muscular strength due to more muscle repair and replenished glycogen stores. > Eﬀects unknown for team sports, might not be ideal because games are too frequent.  Op mal tapering strategy: 2 weeks dura on, decrease training volume by 40-60%, no change in training intensity and frequency.  Detraining: ‘easy’ adap ons, such as plasma volume, glycogen content, mitochondria, disappear quickly (days, weeks), ‘hard’ adapta ons like ventricular mass take longer (weeks, months).  Reducing training to 1 session per week can maintain VO2max but endurance performance suﬀers.  Avoid detraining: determine a key session (endurance, strength, power to determine where athlete is at), reduce training frequency/volume/intensity to the least interval/load needed to maintain performance.  What to consider when making a training plan: > Where is person right now (training level + how they train)? > What is the end goal, over which me period should it be achieved  realis c? > How long do we have to achieve end goal? > Performance gain is not linear, in the beginning 50% increase (run 1h  run 1.5h, li 30kg  li 45kg) will be easier, over me it will become harder to achieve the same rela ve increase. > How much me can person spare for training? 19 8. Exercise across Lifespan Children and Adolescents  Growth (increase in size) and development (func onal changes) of bones, nerves, muscles determine physiological and performance capaci es.  Maturity (fully func onal) deﬁned by chronical age or biological age (skeletal age or stage of sexual matura on).  Highest speed of growth at age 14 in males / 12 in females.  Challenges of chronical age vs stage of development: separa on based on chronical age (school classes, talent selec on in sports)  early developers favoured in ball or strength sports, late developers favoured in aesthe c sports like gymnas cs and ballet.  “Gymnasts develop later because they train so hard”  untrue, more likely that the selec on prefers late developers.  Assess skeletal age: either comparison with images from standard bone age atlas (Greulich and Pyle) or assessment and scoring of each bone and based on that, es ma on of age, then compare with actual age of child? (Tanner-Whitehouse).  Epiphyseal plate = growth plate (Wachstumsfuge) between bone segments disappears once matura on is ﬁnished.  Assessment of matura on based on sexual matura on: stages depend on appearance of pubic hair, genitals (males) and breasts (females).  Development of bones: > Ossiﬁca on is completed with growth plate closure, which is s mulated by oestrogen (mid-teens in females, early twen es in males). > Bone mineral density reaches its peak around age 30 before decreasing again, high impact exercise (like jumping) in childhood and adolescence can increase BMD.  Development of muscle and fat mass: > Muscle mass increases with growth, 30-35% in young females (oestrogen) and 40-45% in young males (testosterone). > Body fat percentage 25% in females and 15% in males at physical maturity.  Development of the nervous system: > Neurological development in childhood leads to improved balance, agility, and coordina on. > Mechanism: ongoing myelina on.  Strength increases with increasing muscle mass and requires neural maturity, peaks at 20 in females and 20-30 in males.  Lung func on and metabolic func ons increase with age.  Children compared to adults have lower stroke volume and lower cardiac output but higher heart rate (to ‘compensate’ for low SV).  Oxygen delivery to muscles is limited in children, which limits max. performance.  Res ng and submaximal blood pressure in children is lower than in adults.  Maximal oxygen consump on (VO2max) increases with age.  Movement economy improves through neural matura on, improved skills, and stride length. This increases endurance running pace with age independently of VO2max.  Metabolism of children compared to adults: larger exercise-induced surge in growth hormone and IGF, higher stress response to exercise, higher fat oxida on.  Anaerobic performance: children have similar ATP-PCr stores as adults, but lower glycoly c capacity (↓ glycogen stores and enzyme ac vity)  limited anaerobic capacity. 20  Strength/Resistance training in children: > Was historically controversial. > Resistance training is safe and beneﬁcial with low risk of injury, should be supervised, emphasis on proper technique. > Mechanisms of strength gains: mainly neural in prepubertal children, neural + hypertrophy in adolescents.  Anaerobic training for children leads to increase in PCr, ATP, glycogen, and max. blood lactate. Programs for adults can be used but risk of overtraining and injury should be reduced, use high variety in ac vi es.  Aerobic training leads to performance gains due to improved running economy in children and due to change in VO2max (↑ heart size  ↑ SV) in adolescents.  Overweight children tend to avoid normally enjoyable physical ac vi es due to social s gma, lack of physical ac vity will decrease ﬁtness and motor skills cannot be fully developed, which then discourages par cipa on further. Elderly  Frailty syndrome: mul component syndrome, when mobility and independence start to be impaired. Clinical frailty stage from 1 (very ﬁt) to 9 (terminally ill). High frailty scores have high risk for need of ins tu onal care and earlier death.  Func onal geriatric assessments:  Aging associated with compression of intervertebral disk, osteopenia (loss of bone mass and density), changes in localisa on of body fat (more central).  Muscular performance decreases with age for males and females, but gap between them becomes smaller  a er menopause, oestrogen levels drop, which means testosterone eﬀects become more signiﬁcant, that’s why drop in muscular performance in females is less dras c than in males. However, protec ve eﬀects of oestrogen on bones and blood vessels are also lost.  With age, muscle cross-sec onal area and ﬁbres decrease. Time needed to generate a given force increases with age (↑ contrac on me, ↓ motoneuron ﬁring rate), which is why old people have high risk of falling (too slow to catch the fall).  Maximal force and rate of force development (RFD) decrease with age, independent of training status.  Strength training in the elderly increases muscle ﬁbre CSA in both ﬁbre types, muscle force and RFD. Improvements despite reduced poten al of aging nervous system to process informa on.  Aging decreases muscle mass (CSA and number of ﬁbres), maximal force, and RFD. Strength training can keep or increase muscle CSA, maximal force, and RFD. 21  Hormonal changes with age:  Similar decrease in cardiorespiratory performance with age in three groups with diﬀerent ﬁtness level (sedentary, ac ve, and endurance-trained people)  performance will decrease with age, no ma er your training state.  Maximal heart rate decreases with age due to morphological and electro-physiological changes in heart muscle and downregula on of β1-adrenergic receptors (reduced response to catecholamines).  Stroke volume decreases with age due to reduced response to catecholamines (reduced contrac lity) and le -ventricular s ﬀening.  VO2max decreases with age due to reduc on in HR and SV, not due to reduced peripheral blood ﬂow.  Decrease in ﬁtness with age aﬀects everyone. HOWEVER, sedentary persons reach frailty threshold sooner.  Idea of prehabilita on: train a person BEFORE surgery to reduce the span of me a er surgery during which they will be below minimum level of func oning. 22 9. Hyperbaric and Hypobaric Condi ons in Exercise Diving (Hyperbaric Condi ons) Eﬀects of (cold) water:  Par al water immersion: ↑ in venous return, SV, cardiac output, respiratory muscle work, and ↓ in heart rate.  The Cold Shock (response to sudden par al cold water immersion): ini al deep inspira on, then substan al hyperven la on, increase in func onal residual capacity (FRC).  The Diving Reﬂex (response to full cold water immersion): apnoea, bradycardia, and peripheral vasoconstric on when cold water in contact with face and eyes, aims to reduce VO2 and therefore extend underwater survival me.  Thermoregula on: heat loss in water is 4x faster than in air (water conducts heat be er).  Muscle func on in cold water: ↓ in contrac on velocity and ﬁbre recruitment (neuromuscular coordina on), ↑ in development of fa gue.  Risk of arrythmia due to reduced heart rate and decrease in func oning of muscle ﬁbres.  Metabolism in cold water: ↑↑ in epinephrine and norepinephrine, ↑ in lipolysis and therefore FFA in blood, ↑ in use of muscle glycogen (anaerobic glycolysis). Eﬀects of hyperbaric condi ons:  The higher the ambient pressure, the smaller air-ﬁlled cavi es (lung, middle ear, paranasal sinuses) become.  Barotrauma: can aﬀect any air-ﬁlled cavity inside the body and is caused by changing ambient pressure, which induces a change in volume in said cavi es that damages the ssue.  Types of barotraumas: air emboli (air bubble blocks a blood vessel), medias nal and subcutaneous emphysema (air bubbles accumulate under skin), pneumothorax, rupture of alveoli, blockage of sinus openings or eustachian tube (failure to equalise pressure, results in ruptures of small vessels in sinuses and middle-ear or rupture of ear drum), face mask squeeze (failure to equalise pressure, results in rupture of blood vessels in eyes  face mask must include nose!). Free diving (apnoea diving):  Limi ng factors of apnoea: ↑ PaCO2 > ↓ PaO2, respiratory drive, mo va on.  Breathing pure oxygen before performing apnoea helps because par al pressure of oxygen in lung will increase, which makes it easier for oxygen to diﬀuse to blood.  Hyperven la on can prolong apnoea because CO2 in blood will decrease (↓ respiratory drive), risk is that unconsciousness due to lack of O2 will set in before s mulus to breathe.  Movement of chest (imita ng breathing mo ons) can also decrease respiratory drive.  Eﬀects of diving depth on lung volume: 6L air volume at sea level, ½ air volume at 10m depth, 1/10 air volume at 90m depth.  Max diving depth depends on rela ve residual volume (= TLC:RV), the lower rela ve RV the deeper one can dive. RV becomes higher with age. Female with smaller lung but same rela ve RV as a male can dive to same depth.  Snorkel length < 35cm (otherwise force of lung too small to inspire because hydrosta c pressure too high). SCUBA diving:  How long a 10L bo le air with 200 bar lasts depends on diving depth: volume of air at sea level is 2000L, res ng ven la on is 10L/min  it will last 200min. BUT at 10m depth, ambient pressure is 2 bar and volume of air will be compressed to 1000L, so it will last only 100min at same respira on rate. That’s why SCUBA divers are trained to breathe a lot more shallowly and slowly. 23  Oxygen poisoning: high O2 pressure (> 10m depth) leads to visual distor on, rapid and shallow breathing, and seizures because the removal of O2 from haemoglobin and ssue into blood is decreased and high O2 pressure causes vasoconstric on of brain vessels.  Nitrogen narcosis: nitrogen becomes solute in blood at high pressures, impaired judgement >30m depth because nitrogen acts like an anaesthe c gas.  Lung injury: expira on is crucial during ascent to avoid rupture of lung ssue because air expands with decreasing ambient pressure, leak of air due to lung ssue rupture leads to pneumothorax.  Decompression sickness: forma on of nitrogen bubbles that accumulate in ssue and cause pain or form emboli and close vessels. Due to too fast ascent, because nitrogen dissolved in blood becomes gaseous again (reduced ambient pressure) and has not enough me to travel to lung.  3x increased risk for nitrogen emboli traveling to brain in persons with open foramen ovale.  Preven on for decompression sickness: stop several mes during ascent to let body adjust.  Treatment for decompression sickness: provide hyperoxia (pure oxygen), recompression chamber (stop / slow forma on of bubbles). Air transport of pa ents is a problem (pressure up in air even lower). Al tude (Hypobaric Condi ons)  Adapta ons to al tude: acute (hours to days) and chronic (weeks to moths, = acclima sa on).  Acclima sa on (normalisa on of physiological changes) up to 2500 m above sea level.  Types of mountain sickness (> 2500m): acute mountain sickness (AMS), high-al tude pulmonary oedema (HAPE), high-al tude cerebral oedema (HACE). 24  Change in diﬀusion gradients: drive for oxygen diﬀusion from lung to blood is reduced at high al tudes due to reduced O2 pressure, which results from decreased ambient pressure.  Ven latory changes: hyperven la on leads to ↓ in PaCO2 and ↑ in pH  respiratory alkalosis shi s oxygen binding curve to the le (harder to release O2 in periphery). Increase in 2,3 BPG- concentra on when alkalosis is sensed, which then shi s binding curve to the right.  At moderate al tudes (up to 2500m) slight right shi due to metabolic compensa on of respiratory alkalosis via kidneys / 2,3 BPG.  At higher al tudes le shi (increase in oxygen aﬃnity, is easily taken up in lung but cannot be easily released in periphery) because alkalosis cannot be compensated anymore.  ‘Res ng breathing’ at high al tudes is hyperven la on  without that, PaO2 would be at -7 mmHg (cri cal value is 35 mmHg, below that brain func ons are impaired). When breathing pure oxygen, cri cal value can be reached at 14’000 m with hyperven la on (survival of loss of cabin pressure in airplanes with oxygen masks).  Hypoxia-induced diuresis (= more urine) leads to increase in haemoconcentra on, which works against hypoxia because O2 transport capacity per litre blood is higher. Also increase in blood viscosity, could become a problem.  Hypoxia induces sympathe c ac va on.  Cardiac output is increased at high al tudes because oxygen satura on in blood is decreased, therefore more blood needs to be pumped to provide organs with enough oxygen.  Under hypobaric hypoxic condi ons, metabolism becomes more anaerobic.  Decrease in VO2max will increase again slightly with acclima sa on (bellow 4000 m a.s.l.), increase in heart rate will decrease again with acclima sa on.  Decrease in stroke volume because of less venous return (hypoxia-induced diuresis leads to loss of plasma volume), slight increase with acclima sa on (plasma volume gained back).  Al tude mainly limits long las ng, aerobic performance (e.g. endurance running), while it may even beneﬁt short, anaerobic performance, such as cycling (faster because less air resistance at high al tudes).  Adap ons to al tude summary: ↓ plasma volume (normalises with good hydra on over me), ↑ haematocrit and Ecs per litre blood as well as absolute Ecs number, ↓ muscle CSA and mass, ↑ capillary density (rela ve and mainly due to muscle loss), ↓ metabolic poten al of muscle.  Two strategies for compe ons at high al tudes: either compete asap a er arrival (no nega ve eﬀects yet but also no acclima sa on) or train >= 2 weeks prior to compe on (most nega ve eﬀects passed, acclima sa on has started, BUT aerobic training not as eﬀec ve). Al tude-associated health problems:  Sleep disturbances: switching between hyperven la on and apnoea during sleep  wake up.  Acute mountain sickness (AMS): > Severe headache, nausea, fa gue, sleep disturbance. > Risk factors: rapid ascent, exercise or alcohol before adjustment to al tude. > Preven on: ascend slowly, take drugs that increase respiratory drive (Acetazolamid). > Treatment: increase oxygen availability (descend asap, O2 from bo le), volita onal hyperven la on or respiratory drive increasing drugs, no respiratory depressive drugs (alcohol, sleep medica on).  High-al tude pulmonary oedema (HAPE): > Vasoconstric on (unknown why) of vessels in lung  high pulmonary capillary pressure, ﬂuid leaks into lung. Symptoms are breathlessness even at rest and coughing. > Risk factors same as AMS, plus reduced NO produc on (vasodilator) or elevated endothelin-1 produc on (vasoconstrictor). 25 > Preven on: slow ascent, low physical exer on un l adjusted to new al tude. > Treatment: descend asap, oxygen from bo le, mobile pressure chamber, nifedipine (vasodila on).  High-al tude cerebral oedema (HACE): > Extreme headache resistant to pain medica on, nausea, vision distor on, neurological problems, coma. > Same treatment as AMS and upper body elevated by 30°, rapid descent to medical clinic.  Low al tude (500-2000 m asl): no eﬀects on well-being, decrease in performance can be restored by acclima sa on.  Moderate to high al tudes (2000-5500 m asl): nega ve eﬀects on well-being before acclima sa on, AMS / HAPE / HACE possible above 3000 m asl, decrease in performance and aerobic capacity cannot be restored above 4000 m asl. 26 10. Sex-Speciﬁc Aspects  Testosterone promotes bone forma on, protein synthesis, and erythropoie n secre on, oestrogen promotes fat deposi on at hips and thighs and increases body fat percentage.  Physiological sex diﬀerences: females are 25-30% weaker in lower body (only 5-15% if rela ve to body weight) and 40-60% weaker in upper body.  Fibre type distribu on does not diﬀer between females and males, but CSA of ﬁbres in females is smaller (for all ﬁbre types), hence they have less muscle mass.  Female muscles aren’t weaker, they generate a similar force per unit of muscle. Overall force is smaller in females because of smaller CSA.  Training leads to the same rela ve increase in CSA and strength in males and females.  Sex diﬀerences in changes with training were only determined in upper body strength, no diﬀerences for hypertrophy and lower body strength.  Females are more fa gue resistant because males have impaired blood ﬂow to muscle while contrac ng said muscle because their contrac on force is greater. Further possible causes are diﬀerences in substrate u lisa on, ﬁbre type ac va on, and neuromuscular ac va on.  Cardiorespiratory func ons: at same absolute intensity, males and females have the same cardiac output, at same rela ve intensity, same heart rate. Males have a higher maximal ven la on (bigger lungs) and a bigger maximal oxygen consump on (VO2max, due to smaller muscle mass, cardiac output, and plasma volume).  No sex-diﬀerences in following cardiorespiratory adap ons to aerobic training: ↑ in cardiac output due to ↑ SV, ↑ capillary density in muscles, ↑ maximal ven la on, ↓ heart rate. Focus areas for female athletes:  Menstrual cycle: there are no deﬁnite conclusions about exercise performance during diﬀerent menstrual phases. Maximal force greatest during menstrua on and follicular phase, increased risk for injury during ovula on, pre-menstrual syndrome and ↓ performance in luteal phase. 27  Menstrual dysfunc on in female athletes: eumenorrhea (= normal cycle)  oligomenorrhea (irregular cycle / less frequent mens)  amenorrhea (absent mens), most frequent in lean athletes. Possible causes are stress, low body weight or low body fat %, hormonal altera ons, energy deﬁcit.  RED-S (rela ve energy deﬁcit in sports): develops due to too low energy intake (not enough calories) and too high energy usage (intense training). Many athletes have disordered ea ng behaviour, e.g. anorexia nervosa (eat very li le, distorted body image) or bulimia nervosa (binge ea ng with purging behaviour like vomi ng or laxa ves).  Osteoporosis due to RED-S, oestrogen deﬁciency ( amenorrhea), inadequate calcium intake.  Exercise during pregnancy: concerns are foetal hypoxia (due to reduced blood ﬂow during muscle contrac on) or foetal hyperthermia (rising maternal core temperature), ↓ CHO availability to foetus (because ↑ maternal usage), pressure on foetus (muscle contrac on), injury. Recs are non-weight bearing exercise without risk of falling and no supine exercise. 28 11. Ergogenic Aids to Performance  Ergogenic aids = substances, methods, or treatments that improve exercise performance directly or via removal of restraints on performance.  Exercise mime cs = pharmacological compounds that produce beneﬁts of ﬁtness (so you have eﬀects of exercise without exercising), mostly banned by WADA.  Possible eﬀects: s mula on of CNS or PNS, increase of availability of a limi ng substrate, supplemental fuel source, reduce performance-inhibi ng metabolic byproducts, facilitate recovery.  Overview of ergogenic aids: > Mechanical: running shoes, equipment innova ons, nasal breathing strip. > Pharmacological: erythropoie n, beta-blockers. > Physiological: blood doping, saline (‘Salz’) infusion, warm-up. > Psychological: hypnosis, psychotherapy. > Nutri onal: metabolic fuels (CHO, protein, …), limi ng cellular components (crea ne), anabolic substances (protein, caﬀeine), an -catabolic (an -oxidants).  Performance limi ng factor depends on dura on of exercise, therefore ﬁ ng ergogenic aid does as well: > Ultra short events ( Short events (10-180s): anaerobic glycolysis, muscle and blood pH  acid buﬀers (Na- bicarbonate). > Moderate dura on events (3-20min): aerobic glycolysis, VO2max  ?. > Long events (21-60min): heat load, dehydra on  cooling at neck, cold drinks. > Very long events (1-4h): dehydra on, glycogen stores (heat not that important anymore because metabolic rate is too low for such long dura ons)  addi onal fuel.  Exercise mime cs: AMPK ac vators (increase glucose and FFA uptake by muscles), resveratrol (present in red wine, AMPK ac vator, an oxidant, an -inﬂamma on).  An ergogenic aid that is an an oxidant and an -inﬂammatory can be helpful short-term (because it aids quick recovery) but will inhibit improvements long-term (because oxida ve stress is necessary for performance enhancement).  Classiﬁca on of supplements into 4 groups: A) evidence supported, B) not enough evidence, C) not useful, D) illegal or risk of contamina on with illegal substances.  Supplementa on of vitamins and minerals has no beneﬁts if there is no deﬁciency present.  Buﬀering solu ons: goal is to prevent ↓ in pH, has a posi ve eﬀect for 1-2min maximum eﬀort performance or high intensity endurance performance, no eﬀect for heavy resistance training, abdominal cramps and diarrhoea possible side eﬀects.  Caﬀeine: facilitates fat use while sparing carbohydrates (direct eﬀect on adipose ssue or s mula on of epinephrine), reduces percep on of eﬀort (analgesic eﬀect), blocks adenosine receptors in CNS (enhances motoneuron excitability), no eﬀects on maximal force but increased endurance.  Ergogenic aids for thermal stress (endurance sports): > Pre-cooling: ice vests, ice bath (contra that it slows nerve conduc ng), ice slushies. > Neck cooling: only gives feeling of cool, but core temperature is actually s ll rising. > Hydra on.  Amino-acids: belief but no evidence that exogenous AAs facilitate muscle protein synthesis and boost testosterone, GH, insulin produc on. However, ming of intake of nutrients in pre- and 29 postexercise periods can aﬀect responsiveness to resistance training (e.g. CHO-protein-crea ne supplement pre-exercise or during recovery augments hormonal response to resistance training). Therefore, ming of intake of AAs is much more important than amount.  Crea ne: increase phosphocrea ne stores for more energy availability, improves muscular strength and increases performance for short, high-intensity exercises, allows greater overloads, low risk, shouldn’t be used for persons with kidney problems.  Carbohydrates: carbo-loading (increased CHO-intake) before intense aerobic exercise (>60min) beneﬁts performance and lowers perceived extor on by ﬁlling up glycogen stores. Exercise intensity determines how much CHO is used, carbo-loading doesn’t make sense if the addi onal CHOs aren’t used.  Beetroot juice (nitrate supplementa on): > Improved mitochondrial eﬃciency (increased P/O ra o, which means you get more ATP for same amount of oxygen). Can be measured in a cycling test (for same power, VO2max should be lower a er nitrate supplementa on). > Improved blood ﬂow in fast-twitch ﬁbres (vasodilator NO can be made from nitrate). > Swiss Sports Nutri on Society classiﬁed it as B, Australian Ins tute of Sport as A. > Concerns about nitrate: can cause gut discomfort, too few studies on female athletes, how much you beneﬁt depends on your aerobic ﬁtness level, use of nitrite is toxic (use natural nitrate sources like vegetables), no long-term studies. WADA banned substances at all mes:  Substances not approved for humans (veterinary drugs).  Anabolic androgenic steroids (testosterone, DHEA): more muscle mass and bone mineralisa on (anabolic eﬀects), growth of penis and prostate (only pre-puberty in females) and deeper voice (androgenic eﬀects), risks are liver damage, high LDL and low HDL (atherosclerosis), cardiovascular problems, acne, depression and aggression, infer lity.  Pep de hormones and their releasing factors, growth factors, mime cs: > Erythropoie n (EPO) and hypoxia-inducible factor (HIF): higher produc on of erythrocytes and angiogenesis, increases oxygen-carrying capacity and plasma volume (be er endurance) but also haematocrit and blood viscosity (risk for circulatory problems, thrombosis, stroke). > Cor cotropins (ACTH) and growth factors: more protein turnover and muscle synthesis lead to greater muscle mass, faster ssue-repairing eﬀects, can lead to muscle and joint pain, hypertension, and abnormal growth of organs.  Beta-2-antagonists (vasodilators, asthma medica on).  Hormone modulators (block oestrogen).  Diure cs (promote urine) and masking agents (mask other banned substances).  Manipula on of blood and blood components (take blood and re-infuse it at a later me). Wada banned at compe ons:  S mulants, narco cs, cannabinoids, glucocor coids, beta-blockers (only for sports that require calm aim like archery or shoo ng).  WADA monitoring program: substances not yet banned but under observa on.  Therapeu c use excep on (TUE): medical condi on that requires a par cular medica on (like asthma). 30 12. Wearables in Sport Sciences  Reasons to monitor physiological func ons: safety (limit, risks, medical a en on needed?), health improvement (are you doing enough? How can you do be er?), performance improvement (decisions about loading and res ng, compe on-relevant informa on).  Diﬀerence between medical device and sports device is that only medical device needs prove that it works.  Validity/agreement of device: actual measurement vs. device measurement, how much does what device measured agree with what the actual measurement is. Device can s ll be useful if validity isn’t good, but repeatability is. Things that wearables measure:  Temperature: core temperature can be measured with thermo pills or rectal probe, skin temperature isn’t relevant for performance or safety and doesn’t correlate with core temp.  Sweat: measure amount, electrolytes, lactate, glucose. Lactate in sweat is produced in sweat glands, lactate and electrolytes in sweat both don’t correlate with concentra ons in blood.  Glucose: relevant for diabe cs, not relevant for healthy popula on, could be relevant for athletes.  O2 satura on: measured with NIRS (= near-infrared spectroscopy), isn’t useful because all it shows is whether muscle is ac ve or not.  Indirect O2 consump on: Apple Watch es mates VO2max by measuring user’s heart rate response to exercise. Other devices calculate VO2max based on an equa on that doesn’t work very well.  Heart rate: measured with PPG (photoplethysmography, light-based sensor at wrist) gives massive error but with high correla on, measured with chest straps (electric ac vity of heart) more accurate. Recommenda on to run only for a few minutes at maximum heart rate makes no sense, it’s not more dangerous if you run at 100% heart rate compared to 80%. Calculated performance indexes:  Performance condi on on My Garmin Fitness Device: assesses your ability to perform compared to your average ﬁtness level, during ﬁrst 10 minutes of ac vity device will tell you “what kind of day you are having”.  Heart rate variability: ﬂuctua on in RR intervals of EEG, high variability seen as good (strong parasympathe c ac va on).  TRIMP (training impulse): describe training load as a single number, based on integra on of me and intensity of exercise.  Training load key: number from 1-5, reveals whether a session improved, maintained, or had no eﬀect on performance capaci es, very high scores indicate overreaching exercise, which may require a prolonged recovery.  Health score: number between 1-1000 represen ng overall health, normalised by age and sex. But s ll, how can you possible calculate such a thing? 31 13. Physical Ac vity for Health and Preven on  Health WHO deﬁni on: state of physical, mental, and social well-being, not solely absence of disease.  People with higher educa on tend to be healthier.  Reasons for physical inac vity: not enough me, too ring, ﬁnancial barriers.  Risk of acute myocardial infarc on is heightened during exercise, but the baseline risk is lower for people who exercise regularly.  Medical clearance for star ng with exercise: iden fy individuals with elevated risk for exercise- related sudden cardiac death or acute myocardial infarc on, assess baseline values to generate appropriate exercise plan and track improvements (for mo va on). Evalua on of healthy people has not shown to reduce exercise-associated medical risks (so age alone is not a reason).  Signs sugges ve of cardiopulmonary disease: pain in chest, neck, arms (heart ischemia, angina pectoris, infarc on), shortness of breath (reduced pumping of the heart or lung disease), dizziness (insuﬃcient brain perfusion), ankle oedema (impaired venous return due to heart insuﬃciency).  Exercise ECG: exercise on treadmill or bicycle with progressing intensity up to maximal intensity, monitoring for indicators of coronary artery disease and arrythmias. Gadgets like smartwatches cannot perform an exercise ECG, they only work at rest.  Physical ac vity prevents chronic inﬂamma on. Insulin resistance, type 2 diabetes, atherosclerosis, neurodegenera ve diseases, cancer are all associated with inﬂamma on.  IL-6 is a pro-inﬂammatory cytokine. However, when released during long exercise it shows an - inﬂammatory mechanisms and increases glucose uptake and fat oxida on.  Brain-derived neurotropic factor (BNDF): a biomarker for mortality, circula ng BNDF levels decreased in obesity, type 2 diabetes, cardiovascular disease, depression, demen a.  Hyperglycaemia impairs BDNF release in brain. Exercise (4h) increases BDNF plasma levels, BDNF leads to more fat oxida on.  Exercise improves oxida ve capacity, ROS produced by exercise promote healthy muscle phenotype and increase an oxidant enzymes.  Exercise promotes autophagy and regenera on (release of stem cells).  Exercise relieves chronic pain due to an -inﬂammatory eﬀects.  Exercise promotes sleep, unless it is high-intensity and performed 70, frailty, chronic illness (diabetes, hypertension), physical inac vity.  Assessment of func onal capacity: gait speed, me to complete 5 chair sit-to-stand repe ons, handgrip strength, quadriceps femoris thickness.  Limited evidence and inconsistent study results about prehab. Rehabilita on  Rehabilita on = set of interven ons to op mise func oning and reduce disability.  Currently, need for rehabilita on largely unmet.  Examples: speech therapy a er brain injury, modifying an older person’s home environment to improve safety, exercise training and educa on for heart disease, psychotherapy for depression. Rehabilita on for overweight and obesity:  Decrease chronic inﬂamma on, stabilise joints, and decrease weight through endurance and resistance exercise.  Nutri onal interven on to reduce calory intake and change composi on of diet.  Same measures for people with type 2 diabetes and overweight. If type 2 diabetes without overweight, exercise s ll important to reduce hyperglycaemia (GLUT4 transloca on). Rehabilita on a er cancer treatment:  Endurance and strength training to recondi on pa ent (o en muscle loss due to disease), rehabilita on reduces remission rate for some cancers. Rehabilita on for cardiovascular disease:  Hypertension: isometric resistance training lowered systolic blood pressure same as medica on.  Blood vessels: HIIT (high-intensity interval training) and MICT (moderate-intensity con nuous training) both lower pulse-wave velocity (fast PWV means s ﬀ vessels).  Blood pressure: HIIT showed be er results in reduc on of blood pressure.  Heart a ack and heart failure (‘Herzinsuﬃzienz’): changes in lifestyle, medica on (lower LDL levels), endurance and strength training (start slow, check with a professional what’s possible).  Peripheral arterial disease (PAD / ‘Schaufensterkrankheit’ because pa ents have pain in legs and need to stop o en when walking): changes in lifestyle, medica on, exercise and walking training, dila on (stent) or bypass surgery as last resort (long-term training more successful).  Stroke: neuro-motor training to ‘rewire’ the brain, then endurance and strength training. 33 Rehabilita on for COPD:  Pathophysiology: cigare e smoke leads to (1) TGFβ produc on in lung epithelial cells  ﬁbrosis, and (2) ac va on of macrophages and neutrophils  proteases  alveolar wall destruc on (emphysema), mucus hypersecre on in airways.  Symptoms: chronic bronchi s (cough and expectora on in the morning) and dyspnoea.  Dis nguish asthma: starts early, symptoms vary day-to-day but don’t worsen progressively.  FEV1 (‘Einsekundenkapazität’) and FVC (forced expiratory vital capacity) reduced with COPD.  Therapy: smoking cessa on, medica on (bronchodila on such as beta-2-antagonists, an - inﬂamma on such as cor sone), oxygen supplementa on, rehabilita on (exercise), surgery.  Respiratory muscle training: inspiratory resistance or threshold training, in- and expiratory endurance training. People with moderate to severe COPD proﬁt more from exercise if it is combined with respiratory muscle training. General notes: - See clicker ques ons!!!!! 34

HS23 Exercise Physiology I PDF

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