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Final

KINESIOL 2C03 Final: Exam

20 Pages
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Department
Kinesiology
Course Code
KINESIOL 2C03
Professor
Audrey Hicks

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Extent of MUA (MUAmax)  Force may not be the same for ECC, similar decrease in force for CON  Speed doesn’t matter in driving MU, should have same MUA  Greater variability for MUA in ECC, declines Why is EXX MUAmax be < CON MUAmax?  Fear of maximum ECC contractions  Unfamiliarity of maximum ECC contractions – used to CON  >Reflex inhibition (GTO – golgi tendon organ – spinal reflex) in maximum ECC actions o Golgi tendon reflex:  Tendon senses force (more ECC)  Sends signal on IB afferent to spinal cord  Synapse with inhibitory interneuron  Decrease excitation (decrease recruiting and firing rate)  Decrease force on muscle  ECC: >muscle force  > stimulation of GTO  >reflex inhibition Contraction Velocity and MUA  Firing Rates and Speed Performance o As tetanus frequency increases, % force increases (force frequency relation)  Muscles differ: every muscle has a different force length relation  Plateau @ 50% @ 100 Hz, no benefits above force peak o As duration of tetanus increases, % force increases  50 Hz – reach plateau around 1 sec  No muscle reaches max instantly  Plateau is sooner with 100 Hz  Rate of force development: 100Hz>50 Hz  Even though force is the same, quicker with 100Hz  Benefits in kicking, throwing, jumping o Higher firing rate = greater rate of force development (RFD) o Increase in firing rate  increase frequency of MAPs  increase rate of Ca2+ release from SR  more rapid onset of CB cycling  increased RDF  Firing Rates and Motor Unit Types o Recruit S0 then FOG then FG  Once all recruited, increased firing rate  MU firing rate increases as force increases? o Slow ramp contractions (slow take longer, FG are short)  Progressive increase in firing rate, size principal followed o Ballistic contraction: only if trained  FG: very quick generation of force then momentum  Major force at start  MU starts with FG but rapidly decreases so progressive decrease in MU firing rate  Size principal not followed as much  SO generates less motor unit firing but decreases at same rate Neuromuscular Fatigue  Fatigue: a decrease in force and/or power (force x velocity) generating capacity, caused by exercise  Isometric: decreased force + decreased RFD + decreased RFR (relaxation)  Concentric: decreased force + decreased velocity = decreased power  Eccentric: decreased force + decreased velocity = decreased power Effect of Contraction Intensity  Sustained MVC: peak force, decline due to fatigue, contraction stopped o Start strong, as you hold get weaker  Submax to failure: force stays constant (decline in maximal force generating capacity – fatigue) o Keep going until max and then fail  Failure = fatigue Effect of Exercise Intensity on Time to Fatigue Failure  Expression of exercise intensity o Isometric % of MVC o Weight lifting: % of 1 RM o Isokinetic: maximal contractions o Aerobic exercise: % V02max  As % isometric MVC increases, endurance decreases (min) o At increased intensity, occlusion of blood flow, anaerobic, fatigue quicker o Decreased intensity (25% - oxidative)  As % 1RM increases, repetitions decrease o Exponential curve, due to blood flow  As contractions increase, % MVC or power declines slowly o Most force at beginning o Decrease as muscle tires, varies in people due to fibre distribution o FG = increased decline o SO = decreased decline  As % V02 max (% maximal aerobic power) increases, time to fatigue decreases o 100% V02 max can be held about 5 min Anaerobic Test: Windgate Test  Load set in relation to body mass  Duration is 30 sec  Velocity (RPM)/power is measured  Measure peak power, average power, % decline (fatigue) Key Points  Cannot exercise at intensities > 100% MVC or 100% 1RM o Can exercise at intensities > 100% V02 max (Anaerobic + aerobic power) Sites/Causes of Fatigue  Fatiguing Exercise  various causes/sites of fatigue  decreased CB function (decreased force)  Decreased # CBs  Decreased force decreased power  Decreased force/CB  decreased force  decreased power  Decreased CB cycling rate  decreased velocity and decreased RDF  Decreased power and isometric performance  Decreased rate of CB activation  Decreased RFD and velocity  decreased power and isometric performance  Decreased rate of CB deactivation  Decreased RFR  decreased isometric performance  As velocity increases, fatigued muscle decreases in force and power faster than unfatigued muscle  Decrease in force due to decreased # of CBs + decreased force/CB = decreased ISOmax  Decrease in velocity due to decreased rate of CB cycling = decreased Vmax  Force velocity (power) curve greater in unfatigued muscle (pg,. 173) Effect of Fatigue on Force Velocity Relation  20% difference in ECC force between fatigued and fresh muscle  50% difference in CON force between fatigued and fresh muscle  > relative (%) decrease in CON force (same as SSC b/c force is lower) Possible Sites of Fatigue  Brain (various interneurons) o Failure of volitional drive to motor cortex, decreased excitation of motoneurons (spinal cord), MU drop out and decreased MU firing rates o Decrease # of active CBs, decrease rate of CB activation  Spinal cord (motoneurons) o Influenced by brain and sensory signals o Get sense of H+ ions and stop firing to get less lactate o Decreased excitability of motoneurons (despite signal) + reflex inhibition = MU drop out and decreased MU firing rate o Decreased # active CBs, decreased rate of CB activation  NMJ (terminal, endplate) – how well AP can cross o No MAPs  Muscle fibre drop out o Decreased # of active CBs o Causes: decreased NT (Ach) release, increased threshold of endplate (ion shift)  Muscle fibre (sarcolemma, SR and CBs) o Decreased excitability of endplate  decreased MAP size + impaired T-tubule – SR function  excitation contraction coupling failure  Decreased # of active CBs, decreased rate of CB activation and deactivation o Direct influence on CB function  Decrease # of active CBs, decrease force/CB, decrease CB cycling rate, decrease rate of CB activation and deactivation Possible Causes of Fatigue  Decreased MUA o Sustained MVC  Force increases, hold, failure to hold (decrease force), told to stop o MU firing rate decreases with time (decrease summation)  FG fibre 1 drops out  FG fibre 2 continues until told to stop o Force and MUA vs. Time  Subject asked to contract as hard as possible for 1 min  Increased MU recruitment and firing rate to 100% MVC  Can’t keep firing at 100% so drops out (decrease firing rate)  Reverse drop out rate (fatigue resistance)  Neurotransmitter depletion  Decreased membrane excitability o Ion exchange (Na, K)  Fuel depletion (ATP, PCr, glycogen)  Metabolic by-products (P (ATP breakdown), H (anaerobic glycolysis), heat) Sustained MVC  MU drop out  decreased # active fibres  decreased active CBs  decreased force/power generating capacity (fatigue)  Decreased MU firing rate  decreased summation/fibre  force/fibre (decrease # of active CBs/fibre)  decreased force/power generating capacity (fatigue) Sustained Submaximal Isometric Contraction  Subject asked to sustain 50% MVC as long as possible  MUA increases, increased recruitment and firing rates to compensate for muscle fatigue = central fatigue (may not be 100% MUA)  Failure when feels like 100% force  Fatigue (decreased # of active CBs and force/CB  MU recruitment and increased MU firing rates (increased # of active CBs)  compensates for fatigue  fatigue progresses (decreased # of active CBs and force/CB)  no more MUs to be recruited + firing rates can’t increase further  can no longer maintain force (Fatigue) Possible Causes of Decreased MUA  Brain  Lack of will – uncomfortable  Decreased neurotransmitters  Increased metabolites (H+, La)  Hypoglycemia (low blood glucose)  Motoneuron o Decreased membrane excitability (ion shifts) o Reflex inhibition (increased metabolites (H+)  Increased metabolites for high intensity and short exercise  Hypoglycemia for long, low intensity exercise  Reflex inhibition in motoneuron only for short, high intensity exercise Force decreases faster as time increases for MVC. 50 Hz stimulation decreases slower (bypass spinal cord reflex?) as time increases than MVC. Voluntary force is less than stimulated force suggesting decreased MUA. Role of Arousal in Central Fatigue? Excitation Coupling Failure  Fuel Depletion o Decreased ATP  decreased sensitivity of Ca2+ channels  decreased Ca2+ release through SR release channels, cause decreased # of active CBs o Decreased glycogen  sensitivity of Ca2+ channels  decreased Ca2+ release  decreased # of active CBs  Accumulation of Metabolites o Increased Pi (inorganic phosphate)  decreased Ca2+ release  decreased # of active CBs o Increased H+  interference of Ca2+ binding to troponin  causing decreased rate of CB activation and decreased # of active CBs Direct Effect of CB Function  Decreased # of active CBs o Decreased ATP – depend process on ATP  Decreased force/CB o Increased Pi and H+  Effect of Pi on strength of actin – myosin bond  Effect of Pi and H+ on Ca2+ sensitivity Most important fuel depletion or metabolite build up depends on type and intensity of exercise. Examples on page 188. Fuel Depletion  Decreased PCr and glycogen  decreased rate of ATP resynthesis  decreased ATP (small initial store)  decreased # of active CBs Metabolite Accumulation  Pi  decreased force/CB  impaired E-C coupling  H+  decreased force/CB, impaired EC couple, sensory muscle afferents (detect pH level – pain/inhibition)  decreased # if active CBs Effect of Intensity and Duration  Glycogen depletes more in a marathon (low intensity but long) than a sprint (high intensity but short duration)  As sprint distance and time increase, muscle lactic acid increases (H+)  As running distance increases, blood lactic acid (at finish) decreases Intermittent Exercise  Ex, basketball, field hockey  1 min sprints on cycle ergometer at 150% V02max with 10 min rest periods between o glycogen decreased 63% after just 6 minutes of exercise o 10 min not enough to regenerate stores o Fatigue evident in each bout due to  Decreased ATP and PCr  Increased Pi and H+  Arm curls of 1 and 3 sets of 10 rep max (RM) with 3 min rest period o Glycogen decreased 25% after 3 sets o Fatigue evident due to increased Pi and H+ and decreased ATP and PCr Fatigue and Speed  1 sec MVC  1 min MVC  3 sec pause  1 sec MVC  Handgrip max squeeze  Fatigued muscled decreased RFD by 50% o Decreased peak force by 50% o Slower RFR (150%)  Fresh muscle relaxes quicker  Force velocity and power velocity curve o Shifts left for fatigued o Lower peak force and decreased force development o Decreased ISOmax and Vmax How Does Fatigue Decrease Speed?  FG MU drop-out, decreased MU firing rate o Decreased RFD and decreased force o Decreased speed/velocity performance  Decreased MAP conduction velocity, decreased rate of Ca2+ release, decreased rate of CB cycling o Decreased RFD and decreased Vmax o Decreased speed/velocity performance How Does Fatigue Decrease Rate of Force Relaxation?  Decreased rate of Ca2+ re-uptake from SR o Decreased Ca2+ ATPase activity Fatigue Mechanisms – Related to Speed  Decreased motoneuron excitability  decreased MU firing rate  decreased speed/velocity performance  Decreased ATP  (SR Function) decreased reuptake of Ca2+ re-uptake decreased speed/velocity performance  Increased H+  SR function + (CB cycle) decreased myosin ATPase activity  decreased rate of CB cycling  decreased speed/velocity performance Does Fatigue Induced Slowing of Muscle Contraction and Relaxation Increase the Risk of Injury?  Yes  Muscle can’t relax fast enough  forced stretching (ECC)  increased risk of strain and tear  Extensors are ~2x stronger than flexors o Don’t fatigue as fast for a given workload  Ex, sprinting o Strong CON of extensors  forced ECC of slow relaxing flexors  increased risk of strain or tear Recovery from Fatigue  Recovery – reversing/eliminating causes of fatigue  Complete vs. incomplete recover  Shorter time to fatigue failure = shorter time to complete recovery  Ex, maximal lift vs. marathon  Longest time to replenish glycogen stores  At 2 min, 140% [email protected] and 50/50 anaerobic/aerobic  Less than 2 min: more anaerobic than aerobic  Greater than 2 min: aerobic increases and anaerobic decreases  Anaerobic recovery mechanisms: PCr resynthesis, H+/Pi removal  Aerobic recovery mechanisms: muscle/liver glycogen resynthesis Time Course of Recovery  Force/Speed/Power  Neural factors o Central drive, motoneuron excitability, NMT  Excitation-contraction coupling  Metabolic factors o Fuel depletion (ATP, PCr, glycogen) o Metabolite accumulation (H+, Pi) Recovery after 60-s MVC  Neural factors completely recover in 3 min (2 min.) o EMG, MUA  Force completely recovers in 3 min  PCr completely depletes in 60 sec o Completely recovers in 3 min  ATP stays relatively constant: little depletion in exercise  Pi increases in 60 sec: fully removed in 3 min  H+ increases in 60 sec: still high after 3 min o Fatigue quicker if exercise done again o Continue to increase if not enough recovery time  Pi and PCr coupled  If only given a minute, metabolic by-products not fully removed o PCr not fully recovered o Can’t maintain reps Time Course of La (H+) Removal  Fully removed and returned to resting level after 60 minutes  Removed by oxidative metabolism o La  pyruvic acid Krebs cycle  ETC? o Occurs within exercised (trained) muscles  Can be accelerated at 30-45% V02 max exercise o Cool down, low intensity o Any less, decreased H+ removal o Any more, too intense, increased H+ o SO (type 1) fibres play major role  Increased capillarization  Benefit of mosaic o FT not recruited at low intensity  Exercise recovery o Training vs. competition  Want full recovery in competition  Training may not want full recovery – challenge system to handle lactate o Training status  Training adaptations speed recovery  Some athletes may not need as much time to recover o Decisions  Active vs. passive recovery between events  Active is you have many events and need optimal clearance rate  Passive if you have time to recover  Active vs. passive recovery in training sessions  Active used more in training  Planning competitions (time between events) Time Course of Glycogen Repletion  Resistance exercise o Depletes 40%, takes 24 hours to recover o Assume: no additional exercise to that muscle and normal CHO intake (not starved)  1 hr continuous + 6 1 min high intensity sprints o Depletes 80% o Depends on amount of exercise and muscle mass Factors Affecting Fatigability  Fibre type distribution o Resistance: SO>FOG>FG o Mito size and # o Myoglobin concentration – stores 02 o Muscle fibre diameter o Capillarization o With increasing % of type 1 fibres, increasing time to fatigue failure o Decreased torque with increased type II fibres  Increased peak torque though with increased type II fibres  Decreased torque with greater type II fibres  % type II fibres differences between muscles o As % II increases, % decline increases  Can be predicted with slope equation (y=mx+b)  Can have same % II but different % decline  Prediction error: biopsy error and test error o Type I fibres have > metabolic power  > mechanical power, > susceptibility to fatigue  >ATP, PCr and glycogen decrease  proportion of whole muscle mass in males  >Capillary “density” ? – no good evidence  >elastic tissue (SSC)  Absorbs more E and recoils  Take advantage of in certain exercises such as repetitive lifts  >%type I fibres  >fat metabolism (glycogen sparing)  Until needed at a higher intensity  Advantage is greatest at lower exercise intensities where:  Blood flow is greater (less occlusion)  Oxidative metabolism is more important – aerobic  Ex, greater endurance time (for women) with decreased relative force (%MVC)  Ex, increased time to exhaustion (for women) with decreased V02 max (lower intensity) o Why Males May Have Greater Absolute Endurance  Given load/intensity is < % of maximum  Fewer (FOG and FG) MUs recruited  SO MUs take the load  < occlusion of blood flow (longer period of time to occlusion)  See graph on page 218  Males’ advantage in absolute endurance is greatest when load/intensity is a high % of females’ maximum strength, power, etc.  See page 219 Effect of Endurance Training o
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