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KIN 2C03 Exam Review - After Midterm.docx

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McMaster University
Audrey Hicks

KIN 2C03 – Neuromuscular Exercise Physiology Fatigue Resistance Graph: Contraction force & duration of contraction  SO > FOG > FG - SO has the highest fatigue resistance o Not as strong but can maintain contractile activity for longer o Oxidative characteristics allow to continue contracting for long periods of time o Use oxygen, fat, proteins, and glycogen that has gone through glycolysis for oxidative phosphorylation to make ATP - FG has the least fatigue resistance Determinants of Fatigue Resistance Mitochondrial Size & Number - Mitochondria use oxygen & produce CO 2 - Mitochondria also use myoglobin which uses oxygen - Lactic acid gets released from the system - SO fibres have: o More & larger mitochondria (allowing for more ox. Phosphorylation to take place)  >oxidative enzyme activity  >use of O  >2atigue resistance Myoglobin - Gives meat its red colour b/c it has red pigment related to oxidative state of iron, change in color after cooking is due to change in ox. State of iron - Stores O –2don’t rely on just diffusion - Facilitates O 2iffusion from capillaries - Predominance of fast type II fibres – white muscle - Predominance of ST muscle fibres (type 1) – red muscle fibres (b/c of myoglobin) Muscle Fibre Diameter - Type II fibres have a larger muscle diameter, type I fibres have a smaller diameter - O 2ets into muscle from capillaries that surround the fibre - Larger fibres have a larger diffusion distance - Type 1 fibres are more efficient b/c you get O in t2e middle of fibre in shorter time Capillarization - Capillaries are not anatomically part of the motor unit - MU activity affects the # of capillaries around its fibres & therefore its fatigue resistance - Capillarization is dependent upon activity of fibre, we recruit ST fibres more than FT b/c the demand is greater therefore we get an increase in capillaries around the ST fibre - Type I – more capillaries - Type 2 – less capillaries Recruitment Threshold - Relates to how NS decides which motor units to recruit - = % of max force (or effort) at which a motor unit is recruited (activated) Low vs. High Threshold MUs - Low threshold: recruited at low % of maximum force or efford - High threshold: recruited at high % of maximum force or effort Size Principle - FT unit are the biggest, therefore they have the most fibres - Motor units are recruited in order according to the size of the motoneuron’s cell body (soma) - Larger size = higher threshold - SO  FOG  FG - Emwood Henneman – identified mechanism behind size principle of motor unit recruitment - Depolarization threshold potential (V): is same for all MUs; they are categorized as high and/or low threshold based on the degree of activation needed (1 in ohm eqn) to cause them to reach threshold for firing AP Graph: Size Principle of MU Recruitment – time x force - Hand grip: increase squeeze to max holding it as long as you can - Increased force – start recruiting intermediate units - At peak – you recruit FG - SO first, then FOG, then FG - Within each MU, you can havea range of size of cell bodies in MU type – some are smaller than others Mechanism of Size Principle - Voluntary effort (from brain)  excitatory input  small: FG wont respond, SO reach threshold  large: FG 1AP, SO 2 APs - Spectrum of sizes in each sublevel: small, intermediate, large - Georg Ohm – electrophysiology - V=IR (velocity = current x resistance) (ohm’s law) - I=excitatory input - V=depol threshold - Smaller cell body has larger input resistance (R). Thus, for a given current (I) there is a greater chance for depol threshold (V) to be reached in a small cell body vs. a larger cell body - Size of cell body is related to I/R, increased size = decreased R Ohm’s Law: V = IR - If Vis the depolarization threshold needed to initiate an AP, and I is a given input current, cells with a higher input resistance (R) will reach depolarization threshold easier than those with a lower input resistance Larger cell body (soma)  more difficult to “excite”  more difficult to recruit  higher activation needed to reach threshold Graph: ‘Central Wisdom’ and the Size Principle - time x force (%) - Small soma motoneurons innervating fatigue-resistant SO (I) fibres are preferentially recruited - Low intensity (force) exercise – ex. 5 km slow run - Larger soma motoneurons innervating more fatiguable FOG (IIA) and FG (IIX) fibres are reserved for high force/speed or when SO fibres finally fatigue ‘Central Wisdom’ and the Size Principle - CNS matches MU recruitment with the demands of the task (diff MUs have different characteristics) - Low excitation (effort) levels preferentially recruit small motoneurons innervating fatigue resistant type I fibres (eg. Endurance exercise) - High excitation (effort) levels additionally recruit large mononeurons innervating the strength/speed type II fibres (eg. Max lift, jumps, sprints) Graduation of Contraction - Graduation = increase or decrease in contraction force - Two mechanisms: 1. Motor Unit Recruitment 2. Motor Unit Firing rate - Coordination of two mechanisms Graph: Motor Unit Recruitment – force x time - Increasing force SO  FOG  FG - Therefore increase excitatory input + activate larger neuron - “size principle” in effect Graph: active muscle fibres, % x exercise intensity, % VO max 2 - Depending on what % of VO max, you will recruit diff moto neurons 2 - Walking – SO - Running – SO + FOG + FG o Recruited in order @ start of exercise - As you increase the intensity of the exercise, the muscle fibres will be recruited in succession Graph: Motor Unit Recruitment – weight lifter for single repetition Motor Unit Firing Rate - Number of nerve impulses/second sent from MU soma to muscle fibres - Each nerve impulse causes one MAP in each muscle fibre (eg. 20 impulses/s = 20 MAPs) - Twitch – 1 nerve impulse therefore 1 MAP in each muscle fibre of the motor unit - Tetanus – train of nerve impulses therefore train of MAPs - MU firing rate in tetanus is higher Graph: force-frequency relation - firing rate (impulses/s) x MU force - As firing rate increases, force increases - First a twitch, then a tetanus, then plateau Graph: representative MU of each type - % max contractions x MU firing rate (impulses/s) - SO firing rate gets to 30 impulses/s at max contraction - FOG firing rate gets to 40 impulses/s at max contraction - FG firing rate gets to 60 impulses/s at max contraction Why “Faster” MUs need Higher Firing Rates - SO (I) has 1 stimulus which has 1 AP one right after the other - has a slight summation - FOG (IIB) has a quicker twitch – no summation b/c twitch is quicker therefore need to have stimuli closer together to get any summation of force - FG (IIB) – MU APs need to be closer together for summation  higher firing rate - Shorter twitch contraction times require higher firing rates for summation (i.e stimuli must be closer together) - Higher firing rate needed to achieve force plateaus in FG units - 95% of MUs recruited in first 50% of MVC Coordination of the Two Gradation Mechanisms - Both mechanisms used throughout force range - Recruitment the predominant mechanism in the low force range - Firing rate increase/decrease predominant mechanism in the high force range Motor Unit Activation (MUA) = # of units activated and their firing rates 100% (complete, maximal) MUA = all units recruited and firing at maximal rates (reached plateau) - How is MUA measured? o Electromyogram (EMG) detects a summed response “Quantifying” EMG - # of fibres conduction MAPs (# of MUs recruited per second) + # of MAPs/s per muscle fibre (MU firing rate) + size of fibre MAPs  quantity of EMG Raw EMG - Sustained MVS to fatigue o Signal will gradually decrease b/c:  MU drop-out  Decreased MU firing rates  NMJ failure  Decrease fibre AP size - Submax contraction sustained to failure (hold 50%) o Will increase over course of contraction  Increase MU recruitment to sustain force of 50%  Increase MU firing rates MUA and Exercise 1. Effect of Exercise Intensity - Brief, maximal effort exercise o Ex. Max lift, MVC, jump, throw o Recruit FG + FOG + SO (100% of muscle fibres) - Submaximal Effort Exercise o Ex. Walking, jogging, running, cycling, swimming, etc o 3 levels  Hard: running (recruited everything but not all are firing) FG, FOG, SO  Moderate: jog (can talk) FOG, SO  Easy: walking (can talk the whole time) SO  First 0-50% of max is recruitment + second 50% is increased firing rate - Progressive, incremental exercise o Eg. Aerobic power (VO m2x) tests o “step” increases in intensity o SO  FOG  FG o Increased firing rate  2. Effect of Contraction Type on MUA - Absolute vs. relative force - Extent of MUA (MUA MAX) - Raising and lowering of same absolute weight o Concentric  Moderate resistance (25 lbs) o Eccentric  Less EMG w/ECC  High resistance 35 lbs - Amount of EMG on 25 lbs is less than 35 lbs - ECC is less than CON phase but same weight b/c ECC is stronger therefore lower % of ECC max than CON Graph: EMG (MUA)(%) x (ABSOLUTE FORCE) - ABSOLUTE FORCE o CON and ECC EMG increases as absolute force increases o CON max is at 100% MU activation, it is at less force than ECC o Will take more force before you get to ECC max o CON MUA > ECC MUA for given absolute force o ECC EMG < CON EMG at given force o ECC vs CON  For same absolute force, ECC has • > force/CM  < # of CBs< # of muscle fibres # attached CBs/fibre plus added +ve braking force  than observed, how do we know? • Sometimes you don’t get expected increase in F w/velocity • If you do, then you can see the muscle wasn’t giving 100% effort Why may ECC MUA MAXbe < CON MUA MAX 1. Fear of maximum ECC actions? – natural fear, hold back, fear of muscle rip 2. Unfamiliarity of maximum ECC actions? – not used to it so only use submax, only really used to incorporate SSC but still only submax 3. > reflex inhibition (GTO [golgi tendon organ]) in max EXX actions? o GTO has sensory receptors in tendon which sense strain/force o When too much strain/force – send afferent signal back to spinal cord + synapses w/inhibitory interneuron therefore inhibits alpha neuron activation therefore decreases neuron activation which in turn decreases firing rate, which decreases force o Essentially relaxes muscle aka doesn’t generate force o In ECC: >muscle force  > stim of GTO  >reflex inhibition  neuron activation *Use of Intramuscular EMG Electrode - Inserted into muscle (fine wire electrodes) - Needle inserts + leaves fine wire electrodes in muscle - Allows you to follow specific motor units Effect of Contraction Velocity on MUA - Not interested in shape but in frequency - Calculate time interval btwn successive spike - Fast recording speed = biphasic shape - Slower still – spike occurs - Spike is same but compressed in time - Increased interspike interval  increased firing rate “Slow” vs. “Fast” isometric contractions - RFD – rate of force development - Slow o F increases gradually up to peak o Cannot hit max right away (some exceptions) o 1 second to get to max o Increased firing rate  ISI decreases as you get to max effort - Fast o Extremely high V and acceleration  Punch, kick o Generate increased force at increased velocity, rest of motion is momentum from force o Duff type of MU activation  MU starts off fast  Slows down after  Ex. Lizards sticking tongue out fast  Ballistic action Ramp vs Ballistic Contractions - Slow is like a ramp, starts off low and increases - Fast is ballistic: rapid firing and then slowing down Firing Rates and Speed Performance Graph: Functional Role of very high MU Firing rates - tetanus frequency (Hz) x force (%) - Force frequency relation - Increases to a plateau - 100 Hz – no increase in force here o No benefit at firing b/c no extra force? o Slight ben firing at freq higher than when reach plateau Graph: duration of tetanus (s) x force (%) - Force plateau at 50 hx - High firing rate = greater RFD - Increased firing rate  increased freq of MAPs  increased rate of Ca2+ release from SR  more rapid onset of CB cycling (at start of movement b/c Ca in viscinity of CB)  increased RFD - Increased APs therefore increase rate of Ca2+ release b/c it is released w/each AP Graph: firing rates + MU types: MU firing rate (Hz) x type on contraction - Slow ramp contraction: progressive increase in MU firing rate o Size principle followed o SO  FOG  FG - Ballistic contraction o Progressive decrease (rapid) in MU firing rate o Size principle not necessarily followed NEUROMUSCULAR FATIGUE Definition of Fatigue - A decrease in force and/or power (force x velocity) generating capacity, caused by exercise - Muscle fatigue – failure in force generating capacity (muscle isn’t doing what you want it to do) Fatigue: Isometric vs. Dynamic Contractions - Isometric: decreased force + decreased RFD + decreased RFR - Concentric: decreased force + decreased velocity  both lead to decreased power - Eccentric: decreased force + decreased velocity?  both lead to decreased power? Effect of Contraction Intensity Graph: time x isometric force (%) - At sustained MVC (max voluntary (iso) contraction) o Peak force then decline in force (fatigue) till contraction is stopped - Submax to failure o Decline in max force generating capacity (fatigue) to failure o When you start a 50% contraction, MVC starts declining w/fatigue and when 2 lines intersect you reach MVC and cant do it anymore Effect of Exercise Intensity on Time to Fatigue Failure How Exercise Intensity is Expressed 1. Isometric: % of MVC 2. Wt. Lifting: % of RM 3. Isokinetic: max contractions 4. Aerobic exercise: % VO ma2 Graph: Isometric contraction - %isometric MVC x endurance (min) - Exponentially shaped curve - Can only hold 100% a few seconds, 75% ~30 sec, 50% ~1min, 25% ~3-4 min - Anything beyond 50% has occlusion of blood therefore decrease in O2 to muscle and decreased ability to remove CO2 Graph: Bench Press Wt. Lifting - %1 RM x Repetitions - Closer you get to max, the less # of reps you can do Graph: Isokinetic exercise – contractions x % max force/powier - Decrease in force at set velocity - 50 max contractions at set velocity, by 50 contraction you wont gen as much force as 1 st Graph: %max aerobic power (%VO2 max) x Time to exhaustion (failure)(min) - As you increase your max aerobic power, your time to exhaustion decreases - You can go beyond 100% VO2 max - Plateau can be held for 5 min at 100% of VO2 max - You start relying on anaerobic energy stores metabolizing ATP w/o use of O2 Graph: Special Anaerobic Test: Wingate Test – power x time - Load set in relation to body mass - Duration set (30 s) - Velocity (rpm)/power measured - Theres a peak power, then average power, then % decline Key Points 1. Cannot exercise at intensities >100% MVS or 100% 1 RM 2. Can exercise at intensities > 100% VO2 max b/c you have anaerobic power as well as aerobic power Sites/Causes of Fatigue Overview - Decrease MUA - NMJ failure - EC Coupling Failure - Direct Effect on CB function Bottom Line on Fatigue - Fatiguing exercise (not gen same force anymore)  various causes/sites of fatigue  decreased CB function - Decreased # of CBs o decreased force  decreased power  decreased isometric performance - Decreased force/CB o decreased force  decreased power  decreased isometric performance - Decreased CB cycling rate (how quickly you go through CB process) o decreased velocity  decreased power o decreased RFD  decreased isometric performance - Decreased rate of CB activation o Decreased velocity  Decreased power o Decreased RFD  Decreased isometric performance - Decreased rate of CB deactivation (depends on Ca2+ getting back into SR) o Decreased RFR  Decreased isometric performance Graph: velocity x force x power - Decreased ISO max force in fatigued from unfatigued fibres due to: o Decreased # of CBs + decreased force CB - Decreased power in fatigued from unfatigued fibres due to: o Decreased rate of CB cycling Effect of Fatigue on F-V relationship - CON o >relative (%) decreases in CON force o 50% diff in force for fatigued fibre at 30% vmax - ECC o Same V of lengthening is less than 20% diff Possible Sites of Fatigue - Brain (various neurons) - Spinal cord (motoneurons) – lactic acid developed from anaerobic glycolysis o Has H+ions that affect muscle sensors afferents o H+ ions activates sensory afferents to inhibit interneurons - NMJ (where ACh released) (terminal endplate) - Muscle Fibre (sarcolemma, SR, CBs) What can happen at the possible sites of fatigue? - Brain: failure of volitional “drive” to motor cortex  decreased excitation (refers to current coming from brain to neuron) of motoneurons  MU “dropout” + decreased MU firing rates - Spinal Cord: decreased excitability (dependent on balance btwn inhibition + excitation currents) of motoneurons + reflex inhibition (b/c sense change in acidity)  MU “dropout” + decreased MU firing rates - NMJ: NMJ failure (no transmission)  muscle fibre “drop out) o Decreased excitability of endplate  decreased MAP size + impaired T-tubule SR function  excitation-contraction coupling failure o Direct effect on CB function How does this affect CB function? - Brain  decreased # of active CBs  decreased rate of CB activation - Spinal Cord  decreased # of active CBs  decreaed rate of CB activation - NMJ  decreased # of active CBs (1)(2)(3)  decreased force/CB (3)  decreased CB cycle rate (3)  decreased rate of CB activation (2)  decreased rate of CB deactivation (2)(3) Possible Causes of Fatigue - Decreased MU activation - NT depletion - Decreased membrane excitability o Ion exchange (e.g Na+, K+) - Fuel depletion o ATP, PCrr, glycogen (muscle, liver) - Metabolic by-products o Pi, H+, heat Graph: decreased MUA – time (s) x force (%MVC) - A sustained MVC o Starts to decrease b/c of fatigue + told to stop Graph: time (s) x MU firing rate (Hz) - Two sample MUs – FG 1, FG 2 - Decreased summation for both - MU firing rate decreases over time, some will drop out - Summation of force depends on firing rate so if firing rate decreases then not as much summation - Force depends on obtaining optimal summation Graph: sustained ISO MVC – force and MUA x Time (s) - Increased recruitment + firing rate to 100% MUA (100% MVC force) - Drop out – decreased firing rates - Not only cause of fatigue - Decline in signal b/c drop out of MU as they get tired or decrease firing rate - Sustained MVC  MU DROP OUT  decreased # of active fibres  decreased # of active CBs  decrease MU firing rate  decrease summation/fibre  force/fibre (decrease # of active CBs/fibre) - Both result in force/power generating capacity (FATIGUE) Graph: Sustained Submaximal isometric contraction - Cannot get 100% b/c processes that inhibit MUA + develop as fatigue increases - Asked to sustain 50% MVC as lon as possible – increased recruitment + increased firing rates - Submax sustained contraction o Fatigue w/respect to force o Decreased # of active CBs + decreased force/CP  increased MU recruitment + increased MU firing rates (increased # of active CBs)  compensates for fatigue  but fatigue progresses (decrease # of active CBs + decreased force/CB)  no more MUs to be recruited + firing rates cant increase further  can no loner maintain force (fatigue) Possible Causes of Decreased MUA - Brain o Lack of will to endure pain o Decreased NT o Increased metabolites (blood doesn’t like to be more acidic) o Hypoglycemia – brain runs out of glucose which is fuel - Motoneuron o Decreased membrane excitability + o Reflex inhibition (increased metabolites; eg. H )  Sensory afferents respond to metabolites and send signal for inhibition - Brief, high intensity exercise vs. prolonged, low intensity exercise o Ex. 400 m, and 42 km o 400 m  Brain will have lack of will, decreased NT, decreased metabolites  Motoneuron soma will have decreased membrane excitability, reflex inhibition o 43 km  Brain – lack of will, decreased NT, hypoglycemia  Motoneuron soma – decreased membrane excitability Graph: Example of ‘Central’ factors limiting force gen – time (s) x force (% MVC or Po) - MVC decreases as force held for longer - Fact that voluntary force is less than stim. Force suggests a decrease in MUA Arousal - Can sometimes overcome central fatigue mechanisms (eg. Decreased MUA due to lack of will) - NMJ “failure” o Ach depletion demonstrates fatigue o No MAPs  fibre “dropout”  decreased # of active CBs o Due to decreased NT (Ach) release o Increased threshold of endplate E-C Coupling Failure - What can happen during fatigue process that could affect E-C coupling? 1. Fuel Depletion o Decreased ATP  decreased sensitivity of Ca channels  decreased Ca 2+ release through SR release channels, causing decreased # of active CBs o Decreased glycogen  decreased sensitivity of Ca channels  decreased Ca 2+ release, causing decrease # of active CBs 2. Accumulation of metabolites o Increase Pi  decreased Ca release causing decrease # of active CBs o Increased H  interference of Ca binding to troponin, causing decreased rate of CB activation and decreased # of active CBs Fuel Depletion vs. Metabolite Accumulation Energy Metabolism During Exercise - Major Sources of Fuel Depletion o ATP – no large stores in the muscle therefore the muscle is dependent on metabolism to generate ATP  Generated from glycolysis, and oxidative phosphorylation, and ADP+Pi o Glycogen – limited, forms glucose for glycolysis o Glucose – long term you can run out of blood glucose o PCr – phosphocreatine – used for 8-10s of max, then we run out - Major Metabolites o Pi – used to form PCr when bonded with creatine o Lactic acid – H+ can affect any level of the system – produced when running out of oxygen - Fuel Depletion – ATP, PCr, glycogen - Metabolite Accumulation – Pi, H+ Examples: - Gymnastics routine o High intensity o ~30 s o Ability to gen ATP quickly is compromised therefore decreased ATP o Decreased PCr o Increase Pi o Increased H+ o Similar activities: hockey shift, windgate test, 200 m sprint run - Rowing race o High intensity o ~4-5 min o Ability to gen ATP compromised o Depletion of PCr stores o A bit of decreased glycogen o A lot of anaerobic work therefore lactic acid development o Increased Pi, increased H+ o Similar activities: 1500 m run, canoe/kayak race, figure skating - Marathon Run o Low intensity – running below anaerobic threshold o 2h+ o Muscle glycogen stores decreased to generate ATP o Hypoglycemia (liver glycogen decrease) - losing blood glucose o Hyperthermia (increased body temp) – no reactions will work properly in metabolic system o Dehydration (decreased plasma volume) – HUGE problem Fuel Depletion - Decreased PCr/decreased glycogen decreased rate of ATP synthesis (small initial store)  decreased ATP (small initial store)  decreased # of active CBs Metabolite Accumulation - Pi  direct negative effect  decreased force/CB - H+  decreased force/CB  impaired E-C coupling  calcium release+reuptake  decreased # of active CBs  muscle afferents (Sensory fibres sensitive to acidity so send msgs back to motoneuron) – pain, inhibition  decreased # of active CBs Effect of Exercise Intensity and Duration - Glycogen depletion  a little bit for sprint (high intensity short duration)  A lot of depletion for marathon (low intensity, long duration) - Muscle lactate turns into blood lactate Graph: muscle lactic acid (H+) x sprint distance and time - A lot of lactic acid by the end of the run Graph: blood lactic acid at finish x running distance - The longer the distance of the run, the less amount of blood lactic acid at the end of the run Intermittent Exercise - Basketball - Field hockey - Football - Ice hockey - “interval” training - Weight training - Etc. Graph: 1 min “sprints” on cycle ergometer at 150% VO max, 10 2in (PCr could have been restored b/c of quick recovery) rest periods between sprints – glycogen (%) x bout # - Glycogen % decreases as the # of bouts increases - Only 6 min exercise - Fatigue is evident in each bout due to: ↓ATP, ↓PCr, ↑Pi, ↑H+ Graph: Arm curl 1 or 3 sets of 10 RM (3 min rest periods) – glycogen (%) x sets - At rest – 100% glycogen - After 1 set – decrease of 13% - After 2 sets – decrease of 25% Fatigue and Speed Graph: 1 s MVC  1 min MVC  3-s pause  1 s MVC - Fatigued fibre will have a decrease in RFD and force of 50%, and an decrease in RFR of 150% - The steeper the slope, the quicker the RFD Graph: concentric force – and power-velocity relationship - Fatigued fibre will have a > ↓ in power - b/c power = F x V, then greater ↓ in power than force pb/c power also depends on velocity - this is important if doing an event where you have to gen force quick How does Fatigue Decrease Speed - FG MU drop out, ↓ MU firing rate (contributes to ↓ in EMG when sustaining max effort)  ↓ force/↓RFD  ↓ speed/velocity performance - ↓ MAP conduction velocity/↓rate of Ca++ release/↓ rate of CB cycling  ↓RFD/↓Vmax  ↓ speed/velocity performance How does Fatigue Decrease Rate of Force Relaxation? - ↓ rate of Ca++ reuptake from ST (↓ in Ca++ ATPase activity therefore slower pumping of Ca++ due to metabolic build up) What are the Fatigue Mechanisms (related to ‘speed’)? - Examples of Sites/Causes - ↓ motoneuron excitability (spinal cord)  ↓ MU firing rate  ↓speed/velocity performance - ↓ ATP  SR function: will affect enzyme activity relying on ATP ∴ ↓ rate of Ca++ reuptake  ↓speed/velocity performance - ↑H+  SR function: will affect enzyme activity relying on ATP ∴ ↓ rate of Ca++ reuptake  CB cycle: ↓ myosin ATPase activity  ↓ rate of CB cycling  Both result in ↓ in speed/velocity performance Does Fatigue-induced slowing of muscle contraction and relaxation increase risk of injury? - Yes! Especially in events that rely on synergistic activation, relaxation of agonist and antagonist Slowing and Injury - Muscle cant relax fast enough b/c CBs still attached  forced stretching (ie ECC – therefore breakage and pulling)  ↑risk of strain/tearing - Knee extensors – twice as strong as flexors o Propelling is harder for flexors than extensors o Sprinting: repetitive contractions of flexor + extensors  Timing of contraction/relaxation of flexors/extensors is key  Strong CON of extensors to keep sprint speed going  if flexor is not in relaxed mode therefore forced ECC of slow relaxing (fatigued) flexors  ↑RISK OF FLEXOR STRAIN/TEAR Summary of Sites/Causes of Fatigue P 193**** Recovery from Fatigue - Recovery = reversing/eliminating causes of fatigue - Complete vs incomplete recovery - Shorter time to fatigue failure  shorter time to complete recovery (eg. Max lift vs marathon) Graph: Max efforts for timed events - % energy contribution x minutes - <2 min – anaerobic primary - At 2 min – 50/50 in terms of aerobic + anaerobic energy contribution - >2 min – aerobic primary - Recovery Mechanisms o Anaerobic – PCr resynthesis, H+, Pi removal o Aerobic – muscle/liver glycogen resynthesis Time Course of Recovery - Force/speed/power - “neural” factors (central drive, motoneuron excitability, NMT) - E-C Coupling - Metabolic Factors o Fuel depletion (ATP, PCr, glycogen) o Metabolite accumulation (H+, Pi) Graph: Recovery after 60 s MVC – PCr, ATP, H+, Pi x minutes (MVC and recovery) - During 60s MVC o Increased H+ & Pi o Decreased ATP, and PCr o EMG decreases, force decreases - During recovery o Recovery of PCr coupled w/depletion of Pi – by 3 min o Peak force recovers, EMG recovers – by 3 min o ATP only increases a bit but recovers by 3 min o H+ depletes very slowly - peak force may recover but ability to resist fatigue takes longer to recover Graph: diff btwn 3 min rest and 1 min rest during weight training - Recovery after 1 min isn’t as strong as recovery after 3 min - starting the second set after 1 min recovery w/elevated H+ ion, lingering Pi – still fatigued and can’t do as much exercise Time Course of La (H+) removal - at brief, high intensity exercise – increased La produced at the beginning - ~ 60 min to return to resting level of H+ How is La removed during recovery? - By oxidative metabolism (occurring in exercised muscles) - La  pyruvic acid (in presence of O )2 KREBS cycle  ETC (electron transport system) (mitochondria) - PCr is recovered in 3 min - ~60 min to deplete H+ levels Can La (H+) removal be accelerated? - Yes! - 30-45% of VO ma2 is optimal intensity for cool down w/max clearance rate of La o Metabolizes La - SO (type 1) fibres play a major role - Most La generated in muscle fibre is picked up by capillaries during cool down and put through oxidative metabolism - FT(IIA & IIB) not recruited at low intensity - How long should the exercise be done? o Depends on:  Training vs. competition • Training: may not want full recovery  Training status • Training adaptations speed recovery Decisions - Active vs passive recovery btwn events - Active vs passive recovery in training sessions - Planning competitions (time btwn events) Time course of glycogen repleation - Resistance exercise – 6 sets, 10 RMs o Recovery pattern assumes: no additional exercise, normal CHO intake o Takes many hours to replete! - 1 h continuous exercise + 6 1 min high intensity sprints o Deplete almost completely o Increased amount of exercise, increased muscle mass o Almost 2 days recovery Factors Affecting Fatigability 1. Fibre Type Distribution 2. Gender 3. Training Fibre Type Distribution Graph: Fatigue resistance – contraction force x duration of contraction - SO > FOG>FG o mitochondrial size + number o myoglobin concentration o muscle fibre diameter o capillarization Graph: ti
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