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KIN 2C03 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

motor unit:
1. comp
2. number and type of fibres

A
  1. motor neuron (split into collateral branch of each muscle fibre at perimysium, axon terminals form MMJ) and all muscle fibres (one type only) it innervates
  2. gross movement use MU with many fibres for high F; fine/complex movements use MU with few fibres for higher control
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2
Q

motor unit territory

A

fibres of different MU spread out over large area and overlap w/ other MU w/o mixing signals allowing for:
1. even distribution of F over large area for smooth contraction and equal F on tendon
2. delay fatigue by sharing metabolites and capillaries b/w active and inactive fibres

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3
Q

Type I muscle fibres:
1. names
2. morphological characters
3. oxidation ability

A
  1. slow twitch, slow/high oxidative
  2. smallest soma, axon diameter, number/neuron. fibre CSA
  3. oxidative metabolism, more mitochondria, slow ATPase, high blood supply, fatigue resistant
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4
Q

myosin heavy chains and fibre-type:
1. overview
2. distribution
3. changing fibre type

A
  1. each fibre type has corresponding myosin heavy chain; eg. type IIa muscle fibre has type IIa MHC
  2. mosaic/checkboard distribution throughout muscle
  3. training/disease can transform type IIa to type IIx and vice versa but cannot b/w type II and I
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5
Q

Type IIa muscle fibres:
1. names
2. morphological characters
3. oxidation ability

A
  1. fast twitch, low oxidative, fast oxidative-glycolytic
  2. med soma, size, number/neuron, and axon diameter (largest size in humans)
  3. fast ATP breakdown, uses both oxidative and glycolytic sys, less blood supply, mitochondria, and aerobic capacity than type I, less glycolytic ability than type IIx, more fatigable than type I
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6
Q

Type IIx muscle fibres:
1. overview
2. morphological characters
3. oxidation ability

A
  1. type IIb in animals, non-oxidative, fast glycolytic
  2. largest soma, diameter, number/neuron, and fibre size (med size in humans)
  3. fast ATPase, least mitochondria, blood supply, aerobic capacity, fatigueable (bc depends on carbs and make metabolic by-products that decrease ATP production)
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7
Q

6 functional characteristics of MU types

A

contraction F/strength, contraction speed/velocity, speed of activation, metabolic power, fatigue resistance/endurance, recruitment threshold

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8
Q

MU contraction F/strength
1. absolute F
2. specific/relative F

A
  1. more type II and larger CSA = much greater F, in N
  2. fast twitch MHC in type II allow for greater F/CB with more CBs attached so type II has higher F/unit CSA in N/cm^2 but since type II has similar myofilament/myofibrillar density as type I, diff is small
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9
Q

MU contraction speed/velocity
1. overview
2. myosin ATPase
3. CB power stroke speed
4. Ca2+ release/reuptake

A
  1. type IIx reach peak F fastest but also shorter time to complete contraction, highest Vmax, followed by type IIa and I
  2. myosin ATPase activity determines CBC speed, IIx myosin ATPase has high-speed CBC, increases the likelihood of CB formation bc more binding
  3. gliding V during power stroke higher in type II MHC
  4. type II has bigger SR, greater SA for rapid release and reuptake of Ca2+ for faster contraction and relaxation
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10
Q

MU contraction power
1. fundamental principle
2. Wingate test

A
  1. P=Fv, greater amount of type II = greater P bc higher F allows for higher V, measured during Wingate test
  2. pedal as fast as possible on a stationary bike at set F
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11
Q

MU F-V relation
1. CON
2. ECC

A
  1. diff b/w type I and II increase with V since the breakdown of ATP is faster in type II
  2. diff b/w type I and II decreases as V increases bc not reliant on ATP breakdown
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12
Q
  1. speed of activation in muscle fibres
  2. why no myelination for faster flow in muscles?
  3. speed of activation in neurons
A
  1. larger diameter axons have less resistance to flow for faster conduction V
  2. need slower flow for cohesive activation of muscle fibre for smooth contraction
  3. fast, myelin sheath insulates axon leaving concentrated areas of Na+ channels at nodes of Ranvier for saltatory conduction
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13
Q

metabolic power by fibre type
1. metabolic v mechanical power
2. type II
3. type I
4. context for fiber type specificity

A
  1. mechanical power (FV), metabolic power is activation and fuel for mech power (enzymes and substrates)
  2. ATP stored for contraction lasts 1-2s, E replenished via PCr by CK (lasts 10s), ATP enter glycolysis to form fuel pyruvate by glycolytic enzymes (1 min) and produce lactate (metabolic by-product)
  3. pyruvate enters oxidative phosphorylation which produces the most ATP at slower rate, used indefinitely, can convert fat and PRO into an oxidative phosphorylation intermediary
  4. more myosin ATPase activity, storage of PCr, CK activity, glycogen storage, and glycolytic enzyme activity in type II
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14
Q

4 factors of fatigue resistance

A
  1. increased mitochondrial size and density in type I allow more enzymes and enzyme activity, use more O2 to produce more ATP via O2 phosphorylation to resist fatigue
  2. more red myoglobin to store O2 and facilitate diffusion in type I fibres; type I red, type II white
  3. smaller fibres in type I have shorter diffusion distance, less time spent transporting O2
  4. Increase in MU activity increase # capillaries around fibre to support proper mitochondria func
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15
Q

recruitment threshold:
1. def
2. Henneman size priniciple recruitment
3. central wisdom

A
  1. % of max F at which MU is recruited, low threshold = low % max F
  2. MU recruited based on size of soma, larger soma has higher threshold bc req more input from CNS (voluntary activation) to gen AP
  3. CNS match MU recruitment with demands of task, low excitation/effort (endurance) preferentially recruit small motorneurons innervating type I, high excitation/effort (strength/speed) additionally recruit large motorneurons innervating type II fibres
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16
Q
  1. Motor unit activation
  2. EMG overview
  3. types of EMG
A
  1. number of MU activated and/or firing rate, 100% MUA all MU recruited and firing at max
  2. measures MU AP > more AP more MUA
  3. surface EMG on skin is non-invasive, able to capture big and complex motions, captures all muscles in area for less accurate signal; indwelling EMG req tungsten needle in muscle thus is invasive but able to get v. accurate EMG reading from deep muscles but needle limits motion
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17
Q

EMG:
1. func
2. quantification
3. processing

A
  1. collects summed response of MU AP of active MU, does not directly measure force; increase in intensity or amp of EMG wave does not equal increased F
  2. summation of MAP, increased number of MU recruited (active fibres), MU AP/fibre (firing rate), and size of fiber increase amp of EMG
  3. have to be processed into a single wave line for quantification
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18
Q

MUA and exercise intensity
1. brief maximal
2. submax
3. progressive incremental

A
  1. 1RM, MVC jump/throw, sprints; recruit all MU (type I/IIa/IIx) firing at max
  2. jogging, cycling, walking, running; can recruit all MU (type I/IIa/IIx) depending on exercise intensity but not firing at max
  3. VO2max, progressions during rowing, recruit in order of type I/IIa/IIx but increase firing rate before recruiting next type of MU
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19
Q

MUA and contraction type
1. abs v. relative force
2. contraction type
3. why is MVCON EMG greater than MVECC EMG?

A
  1. abs F (N) compared to relative F (% of max strength); EMG shows relative MU bc only measures active MU signal
  2. ECC has higher abs force than CON at same relative force bc passive elements that contribute to ECC, same EMG signal but ECC decrease at high V bc more efficient; for same absolute F, CON>ISO>ECC signal bc of increased active MU (relative F) in CON
  3. not used to/fear of maxECC and neural and GTO inhibition during voluntary contraction; during stimulation no effect bc doesn’t req neural input
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20
Q

MUA and rate of F dev

A

high firing rate, more freq MAP, more Ca2+ release, faster onset of CB, greater rate of F dev

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21
Q

MU firing rates
1. MU type
2. F-freq relation
3. coordinating recruitment and firing rate

A
  1. type IIx>IIa>I max firing rate bc of higher conduction rate (larger fibres have better Ca2+ uptake therefore req higher firing rate to maintain Ca2+ levels for summation, have faster twitches); refractory in ST (small diameter) higher than FT (large diameter) therefore have lower max firing rates
  2. higher firing rate in FT to achieve same relative force as SO bc harder to summate, thus generate higher absolute force
  3. recruitment is predom mechanism during low F production since small ST MU can’t fire v. high, firing rate is predom mechanism during high F production since almost all fibres have have been recruited
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22
Q

onion skin model
1. concept
2. research

A
  1. follows Heneman size principle, recruit small ST first with high firing rate, then recruit large FT later with lower firing rates, bc FT maintain lower firing rates, have reserve for supramaximal contraction when electrically stim (CNS)
  2. voluntary sustained isometric contraction in humans
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23
Q

after polarization model
1. concept
2. research
3. questions

A
  1. follows Heneman size principle, recruit small MU first, increase stimulation, increase MU firing rate and number of MUs, increase F; large fibres derecruited first, small last
  2. tested in decerebrate cats, no motor signal from brain, isolated stim (involuntary)
  3. cannot explain how ST able to maintain higher firing rates than FT during constant F contractions in humans
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24
Q

comp AHP and onion skin model

A
  1. both follow size prinicple
  2. AHP firing rate increases with recruitment threshold so last MU firing at max immediately after high threshold recruitment, max contraction at max firing and recruitment, jerky motion
  3. onion skin firing rate inversely proportional to recruitment threshold so ST exert more F at low threshold than FT at low threshold, max contraction with total recruitment but not total firing rate smooth motion and save E by leaving reserve
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25
Q
  1. factors impacting magnitude of EMG
  2. reasons to detect functioning MUs
  3. detecting functioning MUs using sEMG or iEMG
A
  1. increase number of MUs recruited, increase firing rate, size of fibre, increase amplitude (AP summation) all increase mag of EMG
  2. study health and estimate number of motor fibres
  3. surface EMG only detects 30% of MVC since signal is affected by muscle activation (noise) and contractile force since muscles activate synergistically, intramuscular EMG has higher signal to noise ratio; integrating both gives more insight
26
Q

high density surface electromyography
1. technique
2. pros
3. cons

A
  1. high density grids of EMG electrodes, decompose to extract MUPs
  2. non-invasive, exact estimation of conduction velocity, high detection area
  3. some cross-talk, some discharge rate of estimation, poor estimation of MU recruitment thresholds, req some technique
27
Q

training interventions on MU recruitment

A
  1. dorsiflexor ISO vol contraction training; overall decrease in relative recruitment threshold (easier to recruit) after training at high F
  2. relative recruitment threshold F individual MU decreased; more specificity
  3. increase in discharge rate (firing capability), able to produce F faster
28
Q

aging on MU

A
  1. MU number decreases with age, increased surface MUP suggests more noise, muscle atrophy; decreased neuromuscular function
  2. decrease in NeuN, PRO ID of spinal cord alpha-neurons suggest decrease in alpha motor neuron, compensate by increasing in size until it affects health and dies
29
Q

fatigue
1. def
2. Effects of fatgue on contraction type
3. submax v. max fatigue

A
  1. decrease in force/power generating capacity (F starts to drop); not point of task failure
  2. ISO fatigue reduce F, RFDev, and RFrelax; CON fatigue reduce F, V, and power; ECC fatigue reduce F, V, and power, ECC more likely to cause ultrastruc dmg bc dictated by ext load cannot ctrl
  3. max decline in F, submac decline in max F gen capacity
30
Q

exercise intensity and fatigue
1. isometric
2. weightlifting
3. isokinetic
4. aerobic
5. anerobic

A
  1. measured by % of MVC, occlusion of BF at high intensity increase rate of fatigue, F is decreasing exponential curve since less occlusion in type I and less reliance on type II for low F production
  2. measured by % 1RM, slight decreasing exponential curve since work thru whole ROM by switching b/w ECC>ISO>CON allow for BF opportunity
  3. % max F/P at set v, F decrease with contractions
  4. % VO2max measure max O2 consumption, stepwise pattern with exercise intensity up to 100% VO2max where it plateaus (req use of anerobic)
  5. power gen from glycolytic sys from wingate test by setting load relative to body mass and pedal as hard and fast as possible for 30 sec to gen peak power; measure % decline from use of glycogen and PCR stores
31
Q
  1. central concept of fatigue
  2. fatigue on F-V and P-V relations
A
  1. fatigue causes decreased CB function
  2. reduced ISOmax from decreased number of CB and Vmax form reduced rate of CBC, CON more affected than ECC bc higher use of active processes; thus FPV relations decrease with fatigue, P decrease more than F therefore power athletes need more rest to maintain power
32
Q

sites of fatigue: central

A
  1. brain and sp cd
  2. brain decreased activation of MU due to lack of will results in drop out and decrease in firing rate
  3. sp cd decrease activation of MU by decreasing excitability of motor neurons > reflex inhibition results find drop out and decrease in firing
33
Q

sites of fatigue: peripheral

A
  1. motorneurons, NMJ, muscle fibres
  2. motorneuron error with signal transduction
  3. MNJ failure by running out of neurotransmitters due to neurotoxins or disease at causes MU drop out, ECCoupling failure from decreased membrane excitability at endplate, decrease MAP size or impaired t-tubule SR func
  4. muscle fibre failure due to acidity, Ca2+ release/reuptake, myosin and actin interaction have direct effect on CB func
34
Q

possible causes of fatigue: central

A
  1. decreased MU activation due to insufficent central drive to motorneuron at brain from pain/discomfort, decrease neurotransmitters, increased metabolites, hypoglycemia
  2. inhibition of motorneuron at sp cd due to membrane excitability (ions) or GTO inhibition (increase in metabolites) or change to motorneuron intrinsic properties to prevent repetitive action
35
Q

possible causes of fatigue: peripheral

A

neurotransmiter depletion, reduced memebrane exicitatbilty (ion conc), fuel depletion (ATP, PCr, glycogen), metabolic by-products (Pi, H+, heat produced affect enzyme function)

36
Q

fatigue at MU activation:
1. sustained MVC
2. sustained submax contraction

A
  1. MU dropout and decrease in firing rate result in less active fibre and summation for less active CBs
  2. at point of fatigue increase MU recruitment and firing to offset decreased F from fatigue, when no more MU recruited and firing at max, failure occurs
37
Q
  1. detecting central fatigue
  2. overcoming central fatigue
A
  1. F decreases during vol repetitive contractions but when electrically stimulated via interpolated twitch, F increases (evidence of central fatigue) but still below baseline (evidence of peripheral fatigue)
  2. motivation increases central drive for optimal performance
38
Q
  1. fatigue on RFD
  2. fatigue on RFR
  3. fatigue induced risk of injury
A
  1. lower rate of F dev due to type IIx MU drop out and decreased firing rate (central drive)
  2. slower rate of force relaxation, decreased rate of Ca2+ release/reuptake due to decrease Ca2+ ATPase activity by SERCA from metabolite accumulation
  3. during fatigue, decreased relaxation and GTO inhibition through training leads to forced stretching during ECC, increasing risk of strain/tear
39
Q

recovery from fatigue:
1. def
2. sites and causes of fatigue

A
  1. reversing effects of fatigue, rate of fatigue is proportional to rate of recovery
  2. fatigue caused by decreased MUA, NMJ failure, ECcoupling failure, decreased ATP, decreased PCr, increased Pi (power/MVC, short events, mid length events); H+ buildup, can have glycogen depletion if repeated (short events, mid events); glycogen depletion, hyperthermia, hypoglycemia (long events)
40
Q
  1. recovery of metabolites
  2. recovery of glycogen
  3. incomplete recovery
A
  1. ATP decreases slightly but quickly recovers (most defended), Pi increases greatly and cleared quick with PCr, main cause of peripheral fatigue, PCr (3 min sys) follows opposite trend to Pi, H+ increases greatly but decreases slowly (60 min process) bc can travel to other muscles, diffusing local effect
  2. higher amount of exercise and muscle mass used depletes more glycogen, takes several hours of rest, sleep, and feed hours to fully recover with negative acceleration; mostly recovered by 20-80 hours, full up to 2 days
  3. when the substance has not returned to baseline
41
Q

fibre type distribution in fatigue
1. Type II fibre distribution
2. PCr and fibre type during high intensity exercise
3. glycogen, fibre type, and intensity

A
  1. CON during cybex fatigue test show greater fatigue (decrease in peak force with greater type II fibres distribution since type II does not use oxidative phosphorylation, produce metabolic by-products facilitating peripheral fatigue
  2. more PCr storage in type II for high ATP usage bc greater size of myofibres, larger relative decrease and slower recovery of PCr/ATP than type I, req ATP to recover PCr
  3. faster use of glycogen in type II bc greater metabolic power at high intensity; lower intensity greater type I glycogen depletion bc preferentially active type I
42
Q

sex based diff in fatigue
1. absolute v. relative endurance def
2. sex and abs v. relative endurance
3. relative fatigue and intensity

A
  1. time/reps to failure at given value intensity; time rep to failure at relative % of maximal intensity
  2. males have higher abs endurance bc higher strength (able to use type I for longer, lower type II activation, less occlusion); males have greater advantage at high intensities, females have high occlusion at high MVC
  3. females have greater relative endurance at low intensities bc type II fibres closer in diameter to type I allowing more density of capillaries (BF) and elastic tissue, high type I distribution, greater fat metabolism for glycogen-sparing
43
Q

Endurance training on fatigue

A
  1. training increase cardio output, muscle oxidative capacity, mitochondria density, myoglobin, and capillarization, thus increase aerobic capacity (VO2max) to increase both abs and relative endurance
44
Q

role of intensity in fatigue
1. high intensity
2. low intensity
3. muscle mass relationship

A
  1. short duration, high fatigue, peripheral due to impaired AP gen, decreased Ca2+ release/reuptake, decreased F gen capacity, increased metabolite accumulation
  2. long duration, low fatigue, peripheral due to central fatigue and glycogen depletion
  3. more muscle mass work at lower relative intensity bc able to upreg oxidative phosphorylation for lower peripheral fatigue
45
Q

differentiating fatigue
1. peripheral def
2. central def
3. determining central fatigue

A
  1. loss of max F bc muscle cannot gen same F as at rest
  2. loss of complete voluntary activation of muscle
  3. if truly maximal contraction then interpolated twitch decrease F due to interruption of signal; if not max then increase F bc increase activation
46
Q

how central fatigue occurs (neuro)
1. supra spinal
2. spinal

A
  1. above sp cd, local excitatory and inhibitory neurons and motor cortex (central drive)
  2. afferents send signal from muscle to brain; nociceptors (pain), mechanoreceptors (II, III), muscle spindles (Ia, II), GTO (Ib), metabotropic (metabolism, most assoc with central fatigue bc is signal of peripheral fatigue; III, unmyelinated IV)
47
Q

factors affecting central fatigability
1. muscle afferent feedback
2. psychobiological failure
3. sensory tolerance limit

A
  1. group III (thin myelin)/IV (no myelin) afferents are small diameter neurons sensitive to mech and metabolic changes signaling Pfatigue that send signals to brain decreasing central drive as braking mechanism to prevent muscle dmg and maintain Pfatigue; if not reg, higher rate of metabolites and Pfatigue, decreasing P
  2. pace reg by perception of effort (main), potential motivation (max effort to satisfy motive), knowledge distance/time remaining, prev experience of perceived exertion; higher cognitive load psychologically fatigues brain, decreasing central drive and increases perception of effort
  3. sum of all neural feedback from active/remote muscles, pain, and corollary discharge (efferent signal for perception of movement, increase cog fatigue) is processed in CNS, regulates intensity to allow tolerable continuation of exercise
48
Q

Strength training
1. Muscular strength
2. NMP of skill
3. Specificity

A

1.the force generating capacity of muscle/groups and skill of producing high abs F, measured as 1 rm, training using 5-6 rm, not used much in clinical or sports setting bc can be dangerous, measure using 10 rm instead
2. High muscular capacity and central drive
3. Guiding principle of strength = specific adaptations to imposed demands you get better at what you train

49
Q

overview of factors affecting strength performance through trainning

A
  1. at the beginning, high neuro adaptation increases strength dramatically (rookie gains) before plateauing, secondary phase hypertrophy increases strength until plateau, then req steroids to increase strength
  2. combo is synergistic, greater than sum of individual contributions
  3. Decrease as fast as it increase, neuro adaptation decrease dramatically after training stops, hypertrophy slow; if at max hypertrophy, to retain strength require training less but just enough to stimulate neuro
50
Q

muscle CSA and comp and strength trainning

A

each muscle has diff fibres thus has diff change in CSA with training but a group of muscles will follow same overall pattern; myofibrils comp 80-85% of muscle fibre vol change with training but non contractile elements such as SR, t-tube, mitochondria, lipid storage, CT

51
Q

training on hypertrophy

A
  1. increase cytoplasmic vol, increased glycogen and water increase abs CT
  2. increase PRO synth (increase myofibre size due to increased number myofibrils, no change in size of myofilament); myofibrils reach critical size and split
  3. increase mitochondria in type I endurance training due to increased use of oxidative metabolism, increase SR and TT with resistance training to increase Ca2+ release and reuptake for powerful contraction
52
Q

resistance training
1. hyperplasia
2. hypertrophy on strength
3. strength changes and sex differences

A
  1. no increase in myofibres, therefore strength increase is due to hypertrophy
  2. diminishing returns bc hypertrophic ceiling for fibre size and cannot increase number of fibres
  3. similar relative strength increase but males have greater absolute increase bc high number of hypertrophic type II fibres
53
Q
  1. Fibre-type distribution and training
  2. inactivity of muscle and training
  3. fibre type transition in sports performance
A
  1. interconversion b/w type IIa and IIx depends on training; moderate power training for type IIa; explosive for IIx; conversion b/w type I and II possible after HIIT training but takes a lot of time bc needs to increase satellite cells to convert MCHII to MCHI, creating hybrid fibres
  2. active person has equal type I and type II, sedentary has greater type II, spinal cord patients have very high type II bc muscle atrophy decreases fibres size, increase type I to compensate and lack of central drive to type I
  3. in power athletes increase IIa by shifting more I to IIa; decrease in IIx but muscle stronger as a whole
54
Q
  1. tendon adaptation to training
  2. capillarization and training type
A
  1. muscle hypertrophy increases tendon elastic E storage efficiency, tendon size, and tendon stiffness to match muscle for greater F
  2. endurance increase capillaries, fibres do not change much in size, capillary/CSA density increase; resistance with high load/low vol does not increase capillaries, fibres size increase thus density decrease; resistance with mod load/high vol increase capillaries and fibre size thus density constant
55
Q

neural adaptations to training:
1. overview
2. descending drive
3. agonist activation
4. synchronicity
5. activation v. coactivation

A
  1. increase MUA increases F
  2. increase central drive, increase central sensitivity to electric signal from brain, increase descending drive for increased vol activation
  3. decrease sensitivity of MU, higher initial firing and recruit all MU at lower threshold for all training, more consistently recruit high threshold type IIx MU for increased F with strength training
  4. neuromuscular synchronicity by increased conduction V for higher rate of F dev in elite athletes
  5. coactivation of antagonist help stabilize joint, aid in coordination, and prevent injury by decreasing F; training decrease coactivation, and increase force in agonist
56
Q

cross training/spooky gains

A
  1. when training contralateral strength, increase unilateral strength in one limb, contralateral untrained limb increased by 7-8% (25% of improvement of trained limb), indicating central command involved in activating untrained limb
  2. if hurt or immobilized unilaterally, can train other side to decrease atrophy by increasing activation
57
Q

aging as detraining
1. changes to muscle
2. compensation
3. use it or lose it

A
  1. decrease in motorneurons, MU, overall muscle fibres, and type II fibre size, increase non-contractile tissue to replace contractile tissue
  2. when young <30 intermingling of MU (mosaic), start to compensate for decrease in MU due to loss of peripheral branch by reinnervating MU by adding fibres to remaining MU to prevent fibres from dying, lose mosaic, decrease type II size, increase type II number, by 90 axonal degen kills motorneuron, severe atrophy
  3. if MU is constantly activated, decrease loss of the peripheral branch and motorneuron degen
58
Q

expressing strength measures

A
  1. in performance and research: abs strength, abs/kg body mass
  2. in research only: harder to measure, req specific technique/equipement, per kg FFM, per unit CSA
59
Q

physical components of abs strength

A
  1. greater CSA (may vary due to fibre type distribution) as basis for other factors like body size, age, sex increase abs strength
  2. larger body mass = larger muscle, more abs strength, can deviate a bit based on body comp
60
Q

strength-to-weight ratio

A

relative strength, greatest in people with small body mass bc of square cube law as area (strength, CSA) = h^2, vol (mass) = h^3 therefore greater height = even greater increase in mass than strength

61
Q
  1. influence of training status on absolute and relative strength
  2. implications of body size on sports
  3. fibre type distribution and sport
A
  1. regardless of training and sex, positive correlation b/w abs F and mass and negative correlation b/w weight and relative F
  2. sport req high abs strength dom by large people, sports req high strength/mass ratio; some sports req compromise b/w two; some sports permit size range based on role, in sports with weight class cut weight is massive advantage bc higher abs strength due to muscle size but drop water weight to lower weight class for higher strength/mass ratio
  3. endurance have higher type I, power have higher type I, mixed sports b/w but also subject to nature v. nurture
62
Q
  1. sarcomere gain/loss in series
  2. sarcomere gain/loss in parallel
A
  1. squeeze more sarcomeres while keeping muscle length is constant for more optimal length at rest after training by increasing fibre shortening velocity with constant sarcomere shortening velocity bc shortens a greater distance since more contractile units; increase Vmax, increase PP; when losing replace sarcomere with non-contractile tissue
  2. hypertrophy increase in parallel fore greater CSA, increase F for greater PP

KIN 2C03 (3 decks)

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