Force Velocity relationship overview
- at zero velocity, peak tension for max F isometric contraction
- as V gets more positive, CON F decreases to zero at Vmax
- as V gets more negative (speed increasing in neg dir), ECC F increases before a plateau
concentric force-velocity relationship mechanisms
increase velocity, decrease F until Vmax, no F
1. neg braking gen opposing force to direction of motion, decreasing overall CON F
2. increased V increases slacking of the SEC, decreasing CON F
3. sliding filament effect decrease F bc decreased number of CB bound
eccentric force-velocity relationship mechanisms
V increases, increases tension, increasing ECC F until plateau when all myosin heads bound onto actin
1. increasing stretch over same binding time, greater positive braking
2. increase V, increase number of myosin heads activated to try and prevent actin from being pulled away too fast
measuring force-velocity relationship
1. method
2. results
- isokinetic dynamometer (biodex), set velocity at one joint, measure CON F to gen V-F graph with ISOmax at V=0 and Vmax at F=0
- force at constant velocity is not applicable to real-life, flip axes gen load-V graph, with Vmax with no load, 1RM with v. heavy load, and ISOmax at load that is too heavy to move
common-load velocity setup:
1. pros
2. cons
- more lifelike, uni/bilateral motion, motion at single/multi joints, more relevant to performance
- CON only, harder to measure at a certain variable V over ROM, safety issues (spotter)
velocity load performance:
1. fundemental idea
2. in sport
3. 1 repetition maximum
- F=ma, therefore, for given load, gen max F to increase V; greater load, decrease V
- baseball = small load, high V; olympic lift = large load, low V
- 1RM is max load that can be lifted without reaching ISOmax (cannot lift)
- ISO max v. V max
- individual differences in force-velocity relation
- at ISOmax, no V bc no motion, Vmax with no F
- diff people have diff F at the same V, gen diff F-V relation curves depending on their training, if two people have same relation but at diff mag, the person with smaller mag can train to the greater mag
- work
- power
- CON power velocity relationship
- ECC power velocity relationship
- Fibre type and power
- W = Fd
- P = FV = W/t
- P=0 at V=0 and at Vmax (F=0), peak power when F-V relation between ISOmax and Vmax
- increase power with increased length
- fast twitch have higher peak power than slow twitch
- Stretch shortening cycle v. isolated CON
- amortization
- use of SSC
- ECC force lengthen muscle, stretch SEC, increase tension F to potentiate (raise physi threshold) for increased CON force comp to isolated CON
- muscles contract in order of ECC/ISO/CON, during ISO, time delay b/w overcoming negative work of ECC and decrease generating force for CON
- leverage higher CON using ECC to save ATP during daily life
mechanisms of SSC potentiation
1. high initial F lvl and historical action
2. Taking up SEC
3. Storing elastic E
4. Reflex potentiation
- in isolated CON, force takes to dev due to electromagnetic delay but in SSC potentiation, F from CB already dev by ECC and NM preactivation allows for immediate CON
- increased F from SEC taken up during ECC adds to high initial F of CON
- elastic energy stored in myosin CB, cytoskeleton PRO, and tendon pre-ECC gets released (recoil) during CON increases F generated
- muscle spindle fibres detect stretch (ECC) and trigger the stretch reflex to contract muscle and prevent dmg (CON), increasing F
stretch reflex
- muscle spindle fibres detect stretch from ECC
- sensory neurons send AP to sp cd alpha motor neurons
- alpha motor neurons send signal tocontract muscle to resist stretch
- gamma motor neuron send AP from sp cd to muscle spindle to contract and maintain proper tension in spindle while muscle contracts
how ECC initates stretch reflex during reflex potentiation
- increased stimulus recruits more MU
- increase rate of firing to MU
- inhibit Golgi tendon organ near myotendinous junction (detect extreme tension in tendon at MTJ and send signal to sp cd, inhibitory interneurons send signal to alpha motor neurons to relax muscle in response to stretch reflex to prevent muscles and tendons from dmg due to high tension during CON
contributions of titin to high inital force
increased stiffness from ECC bc residual Ca2+ allows N2A to bind actin, increase tension in PEVK, increases ISO F but not CON
Effect of:
1. V on SSC potentiation
2. SSC on concentric F-V relationship
3. F of ECC
- when EEC faster, ECC F increase for greater potentiation (CON has higher start pt) for faster and stronger CON than isolated CON with same velocity
- same relationship as isolated CON but with greater overall F bc ECC priming
- Max CON F and efficiency depends on how maximal ECC F is; max ECC with submax CON greater F and less ATP than submax ECC with submax CON bc higher priming
Efficiency:
1. inhibition
2. efficiency def
3. No SSC or SCC
4. E lost as
5. E cost of walking and running
- Fear/protective mechanism by CNS and GTO to prevent muscle dmg from high CON F on muscle, can train to bypass this fear and tamp down GTO response
- E out/E in x 100%
- No SSC req work to begin bio process for CON, SCC uses NM pre-activation and physiological priming from ECC (more efficient) to potentiate stronger CON
- E only 25% efficient, rest of the E is transferred into heat
- Walking E cost low bc req little E and no SSC, 8 km/hr where spend more E than running while leveraging ECC
- how can training improve SSC potentiation?
- when is SSC inappropriate?
- Increase ECC F through increased muscle size and neural activation (recruitment and freq of AP), increase of elastic E in stiffer tendons and cytoskeleton PRO, increase reflex potentiation by reducing GTO inhibition and training past the fear
- When rules of task forbid it, increase chance of injury, and no time for ECC
Force-length relation: whole muscle
1. passive force
2. active force
3. total force
4. optimal length
5. resting length
- exponential increase in resistance of relaxed muscle to stretch from passive elements of SEC and PEC
- quadratic force-length relation with peak sarcomere at optimal length, Lo (part of active F is passive > cytoskeleton PRO)
- active + passive force (summed), cubic looking func
- sarcomeric length of greatest active F
- length of which passive F begins to dev
sacromere F-length relationship
1. optimal length
2. longer than optimal
3. shorter than optimal
4. interspecies differences in sarcomere
- all CBs bound to actin for max possible F with 0.2 micrometeres of bare zone of no myosin heads to allow actin to slightly overlap for optimal F
- incomplete overlap, less CBs bound, reduce F
- actin filaments overlap, Z disks compress myosin, starts to bulge, disrupt CB config, reduce F and increase potential dmg to PRO
- myosin little var, actin is larger in larger animals > can’t always comp species
working range of muscles
- muscles are limited by the joints they move
- due to joint limitation, muscles operate on diff parts of F-length relation
strength curve:
1. def
2. main factors affecting shape of strength curve
- graphical rep of % max (ISO/CON/ECC total) F throughout ROM joint angle
- Torque/strength = Fma; diff muscles operate on diff parts of the F-length relation throughout ROM depending on moment arm (perpendicular distance b/w line of pull and joint angle) to produce unique strength curves
small moment arms:
1. overview
2. static contraction
3. pros
4. cons
- small moment arms at larger joint angle
- upward torque = downward torque, no Fnet
- large ROM, higher speed
- decreased torque/strength since ma decrease, higher risk of injury bc req large F to overcome decreased torque for motion
other influences on strength curve:
1. training
2. sex diff
3. fatigue
4. injury
- train to increase remodelling neurological firing and strength via hypertrophy in certain ROM or across ROM
- no diff depends on training and hypertrophy; if muscle is smaller, F peak at lower angle bc less bulging = more efficient line of pull but less efficient F at higher angles bc line of pull gets stretched out too far
- overall decrease in strength curve due to decrease in ability to gen F, esp at shorter length
- can be general decrease but also exaggerated at specific part of ROM
- measuring peak isometric F
- measuring peak isokinetic F
- use strength curve to find optimal ROM since some ppl perform better at certain ranges and measure using biodex
- force across whole ROM using CON and ECC
- resistance training on strength curves
- varying resistance
- training through injury
- ideally max strength across whole ROM but hard with standard resistance training bc weight constant, resistance doesn’t match the strength curve, easy to fail at weak pts of ROM
- using cables esp. variable rad cam that changes resistance through ROM can reduce risk of injury/failure, diff machines at gym bc every muscle has diff strength curve
- use biodex to match resistance to weakened strength curve
