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What changes when you are lifting a specificweight with blood flow restriction compared to normal flow?
With blood flow occluded training, you use a low mechanical load, but BF restricted get a decrease in blood velocity, decrease in venous return, decrease in SV, increased HR, no change in Q, Increase SBP & DBP, increased HR + SBP = inc. RPP. This leads to increase metabolic stress, which increases muscle CSA + strength. Phosphorylation of proteins in mTOR, and MAPK signaling pathways enhanced & muscle protein synthesis increased.
What stays the same when you are lifting a specific weight with blood flow restriction compared to normal flow?
- Increased SNS activation, increased HR, increased intramuscular pressure, blood trapped in periphery, decreased circulation, decreased venous return, increased temperature, No strength gains observed in subjects who trained at low intensity without occlusion or who had occlusion applied
- without training.
With regard to the things that change, how are
they affected and why? (blood flow restricted training)
- Low Intensity + Occlusion → ↑ knee-extensor strength at all velocities tested, ↑ cross-sectional
- area of knee extensors and ↑ plasma [GH] 15 minutes post exercise. Metabolic Stress: Strong blood [lactate], growth hormone, epinephrine and norepinephrine
momentary muscular failure
- MMF achieved despite voluntary effort can longer move the load. Neuromuscular
- fatigue has two components:
- central fatigue – an activity-induced
- inability to fully activate a motor unit voluntarily;
- peripheral fatigue – reduced capacity for
- a muscle to develop tension upon activation (disruption at or distal to NMJ).
- Catastrophe Theory – exercise terminates when physiological and biochemical limits of the
- body are exceeded causing a catastrophic failure of intracellular homeostasis.
- perceived sensations about position & velocity of movement & muscular forces generated to perform task. (ex. [muscle spindles detect
- changes in length , resist stretch = stretch reflex], Tendon organs detect force generated/tension , tnendon reflex inhibition of agonist “relaxation”, activation of antagonist] , joint receptors detect info on control of movement position, change in position, velocity/acceleration.
Type I (SO) fibers
- generate ATP predominantly through oxidative means, contains high mitochondria density, low
- myosin ATPase activity, low speed of contraction (twitch last 100-200ms), slow
- calcium handling, less developed glycolytic capacity, highly resistant to fatigue
Type IIa (FOG) fibers
- generate powerful contractions, few mitochondria, resyntehsize ATP by oxidative & some by anaerobic glycolysis, moderate resistance to fatigue, speed of contraction
- faster compared to Type I ( < 100ms)
Type II x/b (FG) fibers
- generate most powerful contractions, few mitochondria, resynthesize ATP mainly by glycolysis, contract strongly & quickly, but fatigue rapidly, activated for intense anaerboic
- movements short duration
chronic adaptations to resistance training
- increased CSA, caused by hormonal (GH), norepinephrine, insulin and testosterone metabolic factors (metabolite
- build up) & mechanical stimuli (stretch, contractile tension development)
chronic adaptations to resistance training
activation maximality , decreased coactivation of antagonist muscle, change in spinal cord connection, coordination of muscle involved in task (M.U. coordinated)
chronic adaptations to resistance training
force x CSA, possible inc. caused by, inc. density myofilaments, efficacy of force transmission from sarcomeres to skeleton (titin & nebulin) -> holds actin- myosin together, pulling translates to bone
Interpolated twitch and what it tells you about
- ITT : electrically stimulating a motor neuron w/ 1-4 supramaximal shocks while a subj. is
- performing an MVC, if ITT elicits no increase force, than = MVC.
acute adaptations to exercise (i.e., fatigue);
Most people can voluntarily recruit muscles maximally, can tell us about the source of fatigue; Central Fatigue; if tiwtch force on MVC increases progressively, Central Fatigue Factors; influences of the brain (central drive) influences to the brain (afferent input),
if amplitude of twitch from muscle still decline after sustained MVC (Peripheral Fatigue Factors; impairment of neuromuscular propagation, failure of activation, myofibrillar fatigue, metabolic factors, impaired blood flow),
relative contribution of central
- & peripheral mechanisms to fatigue is task dependent
chronic adaptations to exercise (i.e.,
Training could cause an increase in neural drive (supraspinal center) that would result in more maximal activation of agonist (interneuron -> motor neuron) , ITT could allow for maximal activation, inc. EMG during MVC, beginners EMG inc. after training, viable neural adaptation
Bilateral deficit: What it is?
- Concurrent activation of
- both limbs, dec. force during MVC
Bilateral deficit: Why does it exist?
Neural limitation that doesn’t allow in signals to both ways (L/R) don’t have as much signal to go around at same time
Bilateral deficit: How does it change as a chronic adaptation to bilateral strength training?
- Neural adaptations that overcome limitations, weightlifters show bilateral facilitation, bilateral
- training allows for one to get more neural signal at bilateral vs. unilateral exercise. Thus weightlifter exhibit greater maximal isometric force during bilateral
Agonists vs. antagonists
- Agonist: causes movement (prime mover) provides accelration towards target
- Antagonist: actions opposite those agonist.
- Only time antagonist acts is when you whip something down faster than speed of
- gravity, or during antagonist coactivation
concentric muscle action/eccentric muscle action
Conc. Action = contractile elements develop tension and ends are drawn together i.e. muscle shortens, internal > ext. torque (H- & I- bands reduce) thus muscle shortens.
Ecc. Action = Contractile elements develop tension, but ends of muscle are drawn apart, Int < Ext. Torque (H- & I- bands widen) muscle lengthens
- Relaxation = Stretch reflex ; reciprocal innervation results in generation of IPSP in motor neurons of the antagonist of the
- stretched muscle, which causes it to relax (reciprocal inhibition).
- Coactivation = tendon reflex, reciprocal
- innervation results in activation of motor neurons that innervate the antagonist of the ‘over-tensed’ muscle, which causes it to develop tension.
Isokinetic strength testing comparison with free weight testing
Isokinetic testing = independent variable is velocity, dependent variable is torque
Free Weight testing = independent variable is force, dependent variable is velocity. Max Strength at a specific velocity w/out taking ROM into account, similar to 1RM testing w/ free weights
Isokinetic strength testing; Torque = Force x Moment Arm
Isokinetic testing can reveal peak torque at a specific velocity, w/o taking ROM into account. Rotational work reveals strength throughout ROM, torque may be modified by changing either the force or the moment arm. Peak torque, throughout the ROM torque builds, comes down as reach full extension, ability to push at different capacities due to strength curve inside body, changes with speed, at faster velocity, peak torque occurs at a lower joint angle. KNOW DIFFERENCE BETWEEN NTERNAL AND EXTERNAL FORCE
Strength curves: What factors inside your
body are responsible for them (Note: things that happen outside your body do not affect your strength curve, but they can be manipulated to provide a loading pattern that is optimal in relation to it; e.g., see lab 1.)
Momen Arm: When a joint angle varies, the moment arm of a muscle spanning the joint also changes.
- Inside the body: muscle length increases/ decreases (sarcomere), length tension relationship: The tension that myofilaments can generate (i.e., contractile force) varies with the amount of overlap between actin and myosin Active - cross-bridge cycling, force developed maximal at intermediate length & decreases at shorter & longer lengths,
- Passive forces - connective tissue & cytoskeleton exert an elastic force that augments the force exerted by a
Antagonist Coactivation: protects ligaments from excessive strain at end range and provides for homogenous distribution of compression forces over the articular surfaces of the joint.
Outside the body - loading pattern optimal in relation, match resistive load to strength curve, muscle taxed all joint angle not just the sticking point.
With respect to the parenthetical addendum in
the preceding bullet point, how can you manipulate the two specific aspects of
the resistive load in order to achieve this objective?
- RJM “Torque”, modified when either force and/or external MA change as motion occurs. Vary Force as motion occurs= partner assisted forced reps, manual resistance, chains/bands ,
- isokinetic loading. Vary Ext. MA = Variable resistance machines, free weights, the machines work w/ cams that vary length of MA through which force is transmitted as movement occurs, using free weight via cable/pulley system.
Force-velocity curve and how its configuration
dictates peak power. How can force-velocity configuration (e.g., concavity) be changed to shift power peak horizontally?
F-v curve is configured on the relationship between Fmax & Vmax. Peak Power occurs somewhere in between i.e. 30% of Fmax/Vmax. since P= F x V. At Vmax have dec. F due to inc. displacement (series) & dec. parallel (dec. F), at Fmax (dec. displacement) (series) (dec. V) & Inc. parallel (Inc. F). How to Shift Curve? Training dynamic at high V and/or isometric w/ ballistic intent shift curve, also if have more Type IIx Peak Power occurs at higher (V & F) max torque (F) w/ inc. V at a lesser joint angle
50 consecutive repetitions to predict muscle
fiber type proportionality via fatigue index: Why do the discrete fiber types perform differently when faced with such a challenge (see Lab 2)?
- Type I fibers are resistant to fatigue thus perform different will see a relatively consistent
- performance throughout the 50 reps , they can sustain prolonged contractions for many hours, due to high mitochondria content, reliance on oxidative metabolism
- Type II fibers are more fatiguing, thus will see a large drop in rep performance after the initial few reps, rapid energy generation during quick muscle action, high myosin ATPase , larger CSA, hypertrophy more, thus present in bodybuilders
Strength vs. power: Which is important in
Strength is important when demonstrating strength in competition i.e. powerlifter. Strength is important for ADL; decrease relative intensity, for example angina occurs at a RPP, stronger muscles lessen BP and HR response since activity is not as stressful
- Most sports are power related only one that isn’t is powerlifting. Power can be important
- during daily life i.e. recovering from a fall, how quickly tension can be generated determined by how much power can be generated by muscle e.g. powerful everters are able to grab on quicker, while less powerful ones despite being strong don’t grab on time.
How to maximize power during resistance training?
- Explosive resistance training, load at or sligtly above P.P. (30% MVC), velocity specificity ->
- ballistic muscle action, motor units discharge in transient burst which precedes the actual force production, high intial frequency, can operate under dynamic & isometric conditions
Ducheateau and Hainut (1984) vs. Behm and Sale (1993)
- Hainut; both types training inc. F, contractile speed (tension dev.), Inc. F > w/ isometric,
- Inc. tension development > w/ dynamic training. State a velocity-training specific response, Isometric : Increased speed vs. heavy Loads, Dynamic: Increase speed movement vs. light loads.
- However Sale (1993) : Intent rather than actual movement velocity, determines velocity-specific training response, neural pattern of activation
- affecting isometric trained limb, & concentric limb, equally with intention of ballistic vs. ramp action.
Pennate muscle fiber architecture
Fibers lie at an angle relative to longitudinalaxis & run obliquely into tendons. Advantage allow more fibers to be packed into a given CSA, overall F capacity is summation of all shortening fibers, Thus physiological CSA is > Anatomical CSA , i.e. > # fibers compared to longitudinal, more sarcomeres in parallel (increased Force)
Angle of pennation: Potential for change and
implications regarding such
Resistance training -> increased pennation angle, study heavy RT + sprint/jump training leads to increase pennation angle, with no change in fasicle length, Sprint/Jump only leads to decrease in pennation angle, and inc. in length. Training effect can’t have excessive hypertrophy since the body doesn’t need it to survive, otherwise reach a point where angle is equal to 90 degrees and wouldn’t be able to move.
Right Link, Wrong Link
- Ex. Leg Press w/ BF occuluded is right link. Why? Degree of Effort still 100%, motor unit
- recruited, metabolic stress is what matters, and achieving appropriate overload for the target muscle being trained, i.e. hard for the right reasons.
Stretch shortening cycle and plyometrics
SSC = Inc. Performance, high speed motor tasks are performed w/ movement patterns that allow muscle-tendon units to be stretched immediately before shortening, Inc. Performance, due to: recovery potential energy from stretched cross-bridges, cytoskeleton and tendon (series elastic), eccentric phase = Inc. time for muscle activation, & stretch reflex (Ia and II afferents, muscle spindles).
Plyometric: Quick powerful concentric movement, preceded by a counter-movement that activates the SSC. Req’ immediate use of enhanced force production, precipitated by the stretch. “amortization phase” . ROM & time during stretch also important facts that affect performance.
Cardiovascular training stimulus and heart rate
Resistance training has dec. venous return, dec. blood circulation, due to blood trapped in periphery i.e. inc. TPR., inc. HR due to Sympathetic response
- Stimulus that drives cardiovascular conditioning => Inc. blood circulation, Inc. venous return,
- Inc. venous filling, eccentric LV hypertrophy, Inc. SV. HR is elevated by a SNS response or a
- baroreceptor reflex, HR can be elevated without a cardiovascular training effect.