Is an EMG signal present when the muscle shortens using only pre-stretch?

Discussion in 'Tennis Tips/Instruction' started by Chas Tennis, Sep 24, 2012.

  1. Chas Tennis

    Chas Tennis Hall of Fame

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    Trying to understand some basic biomechanics related to racket head speed and the stretch-shortening cycle -

    When muscles are consciously activated to shorten, electrical signals can be measured.
    http://en.wikipedia.org/wiki/Electromyography

    Example of EMG measurements of the tennis serve.
    http://coutinhocci.net/pdf/5.pdf

    When muscles are prestretched and allowed to shorten rapidly, as in the Hill Muscle Model, what is going on with the EMG signal, is it still present?

    An EMG signal seems to imply that the muscle is active and important for the motion? But if the prestretch component does not produce an EMG signal and is also faster then.....???.......

    I believe that it's understood in biomechanics that prestretched muscles can produce more force (than unstretched muscles) at high shortening velocities. To research this issue in biomechanics measurements of force as a function of muscle shortening velocity are made. 'Force-velocity' curves are used for display. This prestretch supplied force probably drops to zero when the muscle is shortened to less than its resting length, that is, when the muscle has no stretch.

    From another thread -

    An interesting question is - when the body is using pre-stretch to shorten muscles, how does it feel? Is there a lack of feeling when using pre-stretch - the 'relaxed arm' 'free energy' that one of the Bryan twins described? Does it feel as if you are not doing that much when using prestretch?
     
    Last edited: Dec 27, 2012
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  2. charliefedererer

    charliefedererer Legend

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    The stretch shortening cycle has been well studied.
    [​IMG]


    But the stretch shortening cycle has not been well studied in tennis players.

    It's role in the "modern forehand" - or any stroke - is purely conjectural.

    It may have a role, or the observed stroke may depend on set up, timing and movements of the muscles through time and space.


    Consider:

    Stretched muscle fibers have a longer length to contract and hence develop more force through active contraction.

    Maintenance of a muscle fiber in a stretched state without immediate contraction would require that muscle to expend ATP [if not being acted on by an outside force], so the subsequent maximum force will always be less than after an immediate contraction.




    I doubt that passive muscle shortening has as much as a 1% contribution to the power encountered in a stroke.




    Prestretch can occur from one of two mechanisms:

    1. Using gravity, or some outside force, to load muscles. (Eg. "Bending your knees quickly before going up for a jump shot in basketball.)
    2. Using movements from one muscle group to cause lengthening of another muscle group. (Eg. Rapid hip and shoulder rotation during uncoiling can cause lengthening of the arm muscles, as the arm is left behind as the body swings around forward.)



    I don't know about you, but I am concentrating on hitting that ball so much, I'm not really aware my legs are pushing off violently and my whole body is spinning rapidly about my center axis as I uncoil.

    I certainly don't notice "free energy" or "prestrech".

    As above, I wouldn't consider it "free" in any event. I earned that prestretch by rapidly coiling and uncoiling in the first place, as well as timing my "knee bend" and leg push off.
     
    Last edited: Sep 24, 2012
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  3. tricky

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    Sort of like a mild cramp. Many weightlifters will try to trigger the prestretch reflex by loosening their grip or going "free-fall" with the bar at the point of full stretch (i.e. bottom of ROM.)

    It's not as feasible in tennis, due to racquets not being especially heavy and difficult of tracking a fast moving ball.
     
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  4. boramiNYC

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    Any whip like motion involves the SSC. A preceding segment pulls on the next segment inducing stretch. SSC gives a spring like quality and the stronger the elasticity the wave will travel faster.
     
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  5. Chas Tennis

    Chas Tennis Hall of Fame

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  6. charliefedererer

    charliefedererer Legend

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    While Elliot implicates stretch shortening in his research, he doesn't do any EEG or other physiological analysis to prove his points in his review article "Biomechanics and tennis". http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577481/

    He uses data from studies of others, and uses it as analogy to phenomena he sees in tennis players.

    "In a stretch‐shorten cycle, elastic energy stored during the eccentric phase of the action (the stretch) is partially recovered, such that the concentric phase (shorten) is enhanced. This is also supported by the fact that the concentric action begins with the appropriate muscles under higher tension than would be created if they were to contract purely concentrically from a resting state. Research has shown that the benefit to performance from these two factors, particularly the muscle pre‐tension, is critical to success in sports such as tennis.6 Examples from selected strokes are:

    Service: A subtle coaching point in maximising power in the serve is the timing of the “leg drive” with the racquet preparation for the drive to the ball. The eccentric stretch and pre‐tensing of the anterior shoulder muscles (particularly the internal rotators) is maximised by a vigorous leg drive which positions the racquet “down behind and away from the lower back” in preparation for the drive to the ball.
    Groundstrokes: Rotation of the shoulders greater than the hips (creating a separation angle) and the positioning of the upper limb relative to the trunk during the backswing phase of these strokes, place appropriate muscles on stretch. This is why in the backhand a separation angle (one handed ∼30°; two handed ∼20°) is created in the backswing in preparation for the swing to the ball.7
    Volley/service return: The split step, an integral part of preparation for a volley, service return, or groundstroke, places the quadriceps muscle (extensor at the knee joint) on stretch, permitting storage and subsequent release of energy to enhance quick movement in preparation for the subsequent stroke."
    - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577481/

    The 6 reference applies to a study done in weightlifters doing a squat. http://www.ncbi.nlm.nih.gov/pubmed/9451623

    The 7 reference to Elliot's studies only showed that all the college players studied did not have a pause from their backswing to forward swing. http://www.ncbi.nlm.nih.gov/pubmed/14658135
    There really is no study of the stretch shortening cycle.



    "Elliott et al9 showed that speed of internal rotation of the upper arm was increased by about 20% for a no‐pause compared with a 1.5 second pause condition. In tennis it is therefore essential that only a short pause occurs between the backswing and forwardswing phases of stroke production or at maximum knee flexion during the serve."
    - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577481/

    The 9 reference is to 9. Elliott B, Baxter K, Besier T. Internal rotation of the upper arm segment during a stretch‐shorten cycle movement. J Appl Biomech 1999. 15381–395.395.
    I don't have access to this article. But while it might be considered a proof of pre-stretch to observe an increase in power, it is hard to disprove that maintaining a stretch is not just the loss of muscle power as the muscle expends ATP to maintain that stretch. But perhaps the greater loss in power would be the interruption in a tennis player's smoothly coordinated movements by adding a hitch into his swing. I just am not sure how to measure a player and ask them to change just one component, and not be sure it is not changing other components of their swing. (Perhaps this is an analogy of the Heisenberg Principle that bedevils physics.)



    Checking the ITF publication site, they list three volumes of Tennis and Technology from the years 2000, 2003 and 2007. Reviewing all of the topics at their meetings, I don't see a single reference to the stretch shortening cycle.


    Doing a PubMed search for "stretch shortening cycle tennis" reveals only three references, and none really deal with this subject, except tangentially.


    Therefore I still am not sure the stretch shortening cycle has really been well studied in tennis players.

    I would welcome more information if you have it.



    I don't have an answer to your question Is an EMG signal present when the muscle shortens using only pre-stretch?

    I have to admit I have a bias about the way muscle fibers work from the study of Starling Curves in the heart. Basically, the more the heart muscles are "stretched" by quickly infusing more intravenous fluid into a subject, the higher the subsequent heart contraction, as measured by stroke volume or cardiac output.

    [​IMG]

    I believe it is pretty well accepted that this increase in cardiac muscle contraction is all due to the muscle actually contracting harder, and none is due to a passive elastic spring back by the heart.


    Thus my belief is that an EMG would be showing active muscle contraction in skeletal muscle during the stretch shortening cycle in tennis players, just as it had been shown during athletes doing squats:
    "To isolate any difference muscular contraction history may have on concentric work output, 40 trained male subjects performed three separate isokinetic concentric squats that involved differing contraction histories, 1) a concentric-only (CO) squat, 2) a concentric squat preceded by an isometric preload (IS), and 3) a stretch-shorten cycle (SSC) squat. Over the first 300 ms of the concentric movement, work output for both the SSC and IS conditions was significantly greater (154.8 +/- 39.8 and 147.9 +/- 34.7 J, respectively; P < 0.001) compared with the CO squat (129.7 +/- 34.4 J). In addition, work output after the SSC test over the first 300 ms was also significantly larger than that for the corresponding period after the IS protocol (P < 0.05). There was no difference in normalized, integrated electromyogram among any of the conditions. It was concluded that concentric performance enhancement derived from a preceding stretch of the muscle-tendon complex was largely due to the attainment of a higher active muscle state before the start of the concentric movement. However, it was also hypothesized that contractile element potentiation was a significant contributor to stretch-induced muscular performance under these conditions."
    - http://www.ncbi.nlm.nih.gov/pubmed/9451623
     
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  7. julian

    julian Hall of Fame

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    #7
  8. julian

    julian Hall of Fame

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    Please see my post #7 above

    Please see my post #7 above
     
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  9. Chas Tennis

    Chas Tennis Hall of Fame

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    I looked at your links then. As I recall I spent some time and found the links related to the subject but did not notice new information that I was after.

    (So that the readers don't have to figure things out or look for things, I suggest that you identify your point clearly and also find and spell out exactly where things are in the links that you give.)
     
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  10. Chas Tennis

    Chas Tennis Hall of Fame

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    While I am reading your reply please consider one thing -

    What if the passive stretch component can supply muscle shortening force and the active component can't for high racket head speeds. See the Hill Muscle Model & Force vs Velocity results for muscle shortening.
     
    Last edited: Sep 25, 2012
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  11. charliefedererer

    charliefedererer Legend

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    You have to remember that Hill developed his model before there was any knowledge of the actin/myosin contracture mechanism (never mind feedback from the muscle-spindle afferents and the existence of the golgi tendon organs), and that the model was really only developed from the study of a few muscle fibers in a lab:

    "In 1922, A. V. Hill (see Hill, 1970) first noted that activated muscles produce more force when held isometrically (i.e., at a length fixed) than when they shorten. When muscles shorten, they appear to waste some of their active force in overcoming an inherent resistance. This resistance could not result from the series elastic element because it resists lengthening not shortening. So Hill thought of this resistance as another kind of passive force in the muscle. He found that the faster a muscle shortens, the less total force it produces. Assuming a constant active force, Hill concluded that the faster shortening leads to a larger resistive force."
    - http://www.shadmehrlab.org/book/musclemodel.pdf

    His equations are only valid for isolated muscle fibers after tetany, and on re-stretching muscle fibers:

    "The gastrocnemius is the calf muscle, and somehow the frog’s gastrocnemius became a prototype for skeletal muscles in the early days of motor physiology. Other muscles may differ in certain details, but the basic principles of striated muscle are highly conserved in evolution. In the
    experiment described here, the muscle was stimulated electrically. As Figure 3A shows, the first excitatory input caused an initial isometric twitch. Later, during maximal activation, tetanus occurred, which represents the maximal sustained output that the muscle can produce. During maximal activation, the muscle was stretched (Figure 3B) and held in a fixed, stretched state for about one second, then released. Shortly after release, the stimulation stopped.
    Immediately after the stretch, the muscle’s force level increased rapidly. According to the model, the series elastic element must have caused this increase because the active component had reached its maximal output prior to the stretch—recall that the muscle was in tetany.
    After the stretch, the force in the muscle slowly declined to a steady-state value."
    - http://www.shadmehrlab.org/book/musclemodel.pdf


    I think you are trying to use his equations as proof of a large passive spring loaded force present in muscles.


    But if you read from the above source, there is another neuromuscular mechanism built into muscle to account for the curves seen in Hill's early experiments:

    " The contractile element of the spindle lies at the pole region, which receives synaptic inputs from γ-motor neurons and sensory innervation from a secondary (Group II) muscle-spindle afferents. The central region—
    called the nuclear bag region—lacks contractile properties and receives sensory innervation from primary (Group Ia) muscle-spindle afferents. Forces that stretch the muscle spindle result in length changes in the nuclear bag and pole regions, and the muscle-spindle afferents transduce this length change into firing rate...

    Consider what the spindle afferents in the model should do if you suddenly stretch the muscle-spindle and maintain it at a given increased length. Remember that the parallel elastic element cannot change length immediately, due to its viscous component, but the series elastic element can. Accordingly, you should see a large initial increase in the discharge of the primary muscle-spindle afferent. Gradually, as the parallel elastic element overcomes the effect of its viscosity, it will increase in length. Because the sum of the lengths of the parallel and series spring-like elements equals the total length of the muscle spindle, and the spindle length remains constant after the stretch, length of the series elastic element should gradually decrease after the stretching stops. As a result of this relaxation in the polar region of the muscle-spindle, the nuclear-bad regions should gradually shortening, which should result in a reduction in the discharge of the primary muscle-spindle afferents. In fact, this predicted pattern of activity—a rapid increase followed by a gradual decrease—resembles the discharge dynamics of primary muscle-spindle afferents during a sudden stretch (Figure 7). "

    "Now consider how the velocity of stretch might affect the activity of the spindle afferents. Assume that you stretch a spindle 0.5 cm but at a very slow rate, 5 mm/s. In this case, the effect of the viscosity will be small and, accordingly, the parallel elastic element will lengthen almost as quickly as the series elastic element. In contrast, when you stretch the spindle rapidly, for example at a rate of 30 mm/s, the viscosity greatly resists stretch of the parallel elastic element and more of the total stretch in the spindle will be taken up by the series elastic element, at least at first. Therefore, during a rapid stretch, the primary muscle-spindle afferent will fire much more than during a slow stretch. These properties create the appearance of a velocity signal, as illustrated both in the model and in recordings from a cat soleus muscle in Figure 10."

    "Role of the γ-motor neuron
    As the model in Figure 7 suggests, activity of the γ-motor neuron contracts the spindle and affects the lengths of the series and parallel elastic elements. This contraction, in turn, affects the discharge of the muscle-spindle afferents.
    If your muscle spindles did not have γ-motor neurons, their length changes would simply reflect the length changes in the extrafusal muscle. What benefit does the nervous system gain by having a muscle-spindle system in which length depends not only on the extrafusal muscles—and therefore the angle of joints—but also on the activity of γ-motor neurons? As you see in this section, activation of γ-motor neurons allows the CNS to bias the sensitivity of the primary spindle afferents and turns them into a sensor that measures movement errors."

    "Figure 13 schematically summarizes the functions of the muscle-spindle and golgi-tendon-organ afferents in terms of a feedback control system. Inputs to α-motor neurons cause muscles to produce force that acts on tendons, shortens muscles, and changes joint angles. Muscle-spindle afferents sense changes in muscle-length, as biased by activity in the γ-motor neurons. The golgi tendon organs sense force changes, with their signal to inhibitory interneurons modulated by the descending inputs.
    The feedback control system rejects perturbations and helps ensure that the limb follows the desired trajectory. Two locations in the model adjust outputs: one modulates the level of γ-motor-neuron activation, the
    other does so for the interneurons that golgi tendon organs act on. Consider a situation in which the load exceeds expectations. For example, you see a milk carton you assume to be empty, so you decide to dispose of it. When you begin to lift the carton after grasping it, its weight—the load on your muscles—is more than expected. The primemover muscles will shorten, but because of the increased load, they will not shorten as much as expected for an empty milk carton. You saw earlier that the γ-motor neuron activity is set based on the expected length change in the muscle. When the muscle shortens less than expected, afferent signals further activate the α-motor neuron, producing more force, and countering the effect of the load, at least to some extent. The force feedback system,
    mediated by the golgi tendon organ, works similarly. As depicted in Figure 13, inputs signaling force from the golgi tendon organs inhibit activity in motor neurons via a spinal interneuron. This influence would have the effect of a negative feedback loop in which high levels of force result in decreasing the motor command and therefore moderating the force. By inhibiting the interneuron that the golgi tendon organ acts upon (unfilled arrow in Figure 13), descending inputs can modulate how effectively force feedback inhibits the α-motor neurons. Strong inhibition from the descending inputs imposes a high threshold for the force feedback pathway. Only if the force exceeds this threshold will the feedback pathway inhibit the α-motor neuron."
    - http://www.shadmehrlab.org/book/musclemodel.pdf


    I fear the complexity of function for large motor tasks is so complicated by the local and spinal feedback loops that trying to decipher what aspects are from passive recoil are not possible.
     
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  12. Chas Tennis

    Chas Tennis Hall of Fame

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    References

    I believe that Elliott, Knudson and other tennis biomechanic researchers assume that the stretch-shortening cycle is an important part of tennis strokes. Elliott's book discusses the stretch-shortening cycle for tennis strokes. I have Knudson's book and first became interested in the velocity of muscle contractions & stretch-shortening being fast because Knudson discussed it.

    References for Tennis -

    Technique Development in Tennis Stroke Production (2009), Elliott, Red, & Crespo

    Biomechanical Principles of Tennis Stroke Technique (2006), D. Knudson

    There is a problem with applying squat results to this issue. While squats might use stretch at the bottom, the muscle shortening velocities are always limited because of the mass of the body. If the muscle shortens slowly then the active components of the contraction can keep up. This issue is discussed in the reference below.

    Reference for Velocity & Training -

    I read that squats are good strengthening for the motion of shot-putters but not as effective for the motion of throwing lighter objects such as Javelins (p. 31).

    Science and Practice of Strength Training, 2nd ed., (2006), V. Zatsiorsky, W. Kraemer

    The book has an interesting finger-snap demonstration (p. 27). Take your index finger and bend it. Straighten it as fast as possible. Now take your index finger and hold it back with your thumb. Apply as much force as you can and let the index finger snap forward. Doing it against a piece of paper would make the velocity difference stand out.
     
    Last edited: Sep 26, 2012
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  13. Chas Tennis

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    Research paper on the microscopic active & passive components.

    With reference to the Hill Muscle Model -

    I don't understand this 2002 research paper very well. It deals with research on the microscopic level into the active and passive muscle cell components and their velocity of shortening. Acton & mycosin, in sacomeres, are the source of the active muscle shortening component. Titin, a large protein molecule, is recently believed to be the source of the passive (elastic) forces.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290211/

    The 2002 research paper is a study of the issue of the shortening velocity vs force of the active actin-myosin sarcomere in comparison to the passive Titin molecule. Probably more recent research has closed in on this important velocity of shortening issue.

    For tennis, does this mean that above a certain muscle shortening velocity the force from the active component falls off and for the highest velocities - racket head speeds - the passive component force takes over?


    Actin-myosin illustrations-
    https://www.google.com/search?q=act...UJLDW0gGYpIGgBg&ved=0CDQQsAQ&biw=1334&bih=692
     
    Last edited: Mar 21, 2015
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  14. charliefedererer

    charliefedererer Legend

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    From the source you cite http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290211/:

    Opening line: "The shortening velocity of skeletal muscle fibres is determined principally by actomyosin cross-bridges."


    Discussion: "Although the spring-like behaviour of titin implies that the protein is somehow involved in determining the shortening characteristics of stretched muscle, we know of no attempt aimed at quantifying the titin-based contribution to shortening velocity."


    "The present study was initiated to measure this contribution in the single myofibril preparation, in which passive elastic recoil should essentially reflect the properties of no other structures than the titin filaments."
    That is, this study was done one incredibly thin (microscopic) strand of muscle.

    "Results also suggest that the passive recoil of elastic structures is significantly slowed down by the contractile elements. However, the retractive force of stretched titin filaments, which underlies the elastic recoil, may be important in that it acts as an additional driving force on the contractile system at short release steps and during shortening from longer physiological SLs."
    The most the authors can say is that the the retractive force of titin filaments "may be important".



    You may be interested in reading this 2011 review:
    "Structure and Function of the Skeletal Muscle Extracellular Matrix"
    Allison R. Gillies, B.S1 and Richard L. Lieber, Ph.D1,2
    - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177172/

    Here is the first line from the conclusion:
    "The role of ECM in muscle mechanics and pathology is not well understood, but it is becoming more evident that changes in ECM are clinically significant. Further studies are required to define the detailed structure and composition of ECM, characterize its mechanical properties, and determine the way in which these relationships change in diseased states."

    And specifially regarding biomechanical properties of ECM:
    "As mentioned above, to date, measurement of ECM biomechanical properties has consisted of studying epimysial sheets that are easily dissected and tested or isolation studies that remove all components from muscle with the exception of endomysium, perimysium, and epimysium collagen fibrils. However, biaxial testing of ECM sheets or isolated collagen fibrils may not represent the in vivo loading or structural environment of ECM, and new methods are needed to accurately measure the in vivo mechanical properties of the composite ECM."

    So it appears we are really only n the infancy of understanding the role of titin and other contractile elements in actual muscle function at a macroscopic physiological level.
     
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  15. Chas Tennis

    Chas Tennis Hall of Fame

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    A biomechanical researcher has answered my question. He said that the passive (stretch) component of muscle shortening is not accompanied by an EMG signal.

    When reading publications that discuss EMG measurements in association with muscle shortening keep in mind that passive shortening might contribute force without EMG signals.

    I'd like to learn more about EMG signals and Titin with a good reference. Need a recent up-to-date reference that discusses the Hill Muscle Model and includes the passive Titin structure (stretch/passive contributor, the 'spring'). Does anyone have a suggestion?
     
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  16. Chas Tennis

    Chas Tennis Hall of Fame

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    Stretch Shortening Cycle

    This is probably Biomechanics 101 (?) -

    The most important characteristic of the Stretch Shortening Cycle for athletics is that it provides muscle shortening force (from Titin) at higher velocities of muscle shortening than the active forces from myosin-actin sliding filaments.

    See Force vs Velocity Curves for active and passive components and the Hill Muscle Model.

    For hitting a tennis ball high velocities of muscles shortening are used. The use of the SSC may also be more reproducible leading to consistency. (?)

    The skilled use of the SSC is probably the most important thing that distinguishes high performance in athletics.

    This also seems reasonable if you visualize the Actin-Myosin as it moves to shorten the muscle. Videos are on the internet. Titin, a giant protein molecule in each muscle cell, is the rubber band, it was only recently discovered, and Titin is in each muscle cell. The view that the tendon stretches for the SSC in recent texts is probably completely wrong.

    I'm not certain of this picture and hope that some college students taking Biomechanics 101 can help out, or better yet a biomechanical researcher can set things straight. (posting is anonymous)

    If you don't agree please provide some references to research to back up your views.

    http://tt.tennis-warehouse.com/showpost.php?p=7103826&postcount=5
     
    Last edited: Jun 3, 2014
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  17. Curiosity

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    Charliefederer: Thanks for the patient thorough review.
     
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  18. dominikk1985

    dominikk1985 Legend

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    there are two things that are caused by the stretch:

    1. the elastic element (which is often confused with the SSC):
    this is elastic energy stored in the tendons (muscles don't really store elastic energy) which then snap back. this is entirely passive and re-uses some of the energy like a rubber band.

    2. the actual stretch shortening cycle:
    this is not a passive process. the SSC means that receptors are stimulated during the pre stretch which causes a nerve signal to the spine telling the muscle fibres to fire harder. this also happens involuntary but it still is an active contraction of the muscle.
    https://www.youtube.com/watch?v=F871bBWS4oY

    generally the rubber band theory is rather flawed. some of the energy is re-used but most of the stretch in the muscle is dissipated into heat. most of the work is still active contraction.

    that doesn't mean that the SSC is not important however. the stretching (I would not call it pre stretch since it is nothing that can be held for a longer period like a rubber band) does increase the firing power of the muscle (I think up to like 25% or so).
     
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  19. Chas Tennis

    Chas Tennis Hall of Fame

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    Dominikk1985

    I don't understand the complex detail of how the sarcomeres work. In 2012, what I found indicated that this area of research, related to Titin, was new and very active, mainly with understanding the role of Titin in passive muscle shortening. I thought that tendon stretch was not important for SSC because of very basic research involving studies of isolated muscle cells. The muscle cells themselves were producing enough stretch force to account for the observed forces without tendon forces. I am shaky now on remembering the information for that conclusion. The paper is probably in my threads.

    I can't argue details of how Titin works. Titin is in the muscle cell (sarcomere) itself. There are some references and videos in my last post. Please read and look at the videos. My interpretation of the material that I read, including several papers, basic Hill Muscle Model descriptions and especially Force vs Velocity curves is that Titin is the source of SSC for force at higher velocities of muscle shortening.

    There are some complications that I knew about in 2012 but decided that they were not important. For example, the Golgi tendon organs (senses force) are located, I believe, in tendons and they function especially to alert the body that the joint may be approaching the end of its range of motion. And that the body should automatically activate counter forces to stop the motion and protect the joint. Maybe this activation is used in squatting to get more lifting force at the bottom. (?) Squatting is a very slow form of muscle shortening because of the mass of the body. I also consider this Golgi response an active EMG muscle action. Muscle Tendon Unit proprioceptors (spindle sensors) also provide information by sensing muscle length. But I have a poor understanding of this complex phenomenology and don't want to spend time debating this subject because I don't know it. We need a biomechanical researcher to set us straight.

    Also, a very interesting point, that I believe, is that Titin can do stretch shortening cycle at any muscle length not just near the end of the muscle's range of motion. I believe a demo is simple. Take a small mass, a can of soup, in your hand. Flex and extend the elbow very rapidly over a comfortable range, say, 10", around elbow flexion angle of 90°. The oscillation will have a natural oscillation frequency that is more comfortable. I believe that the very rapid oscillation is the stretch shortening cycle with forces from elastic Titin.

    Speculation- Another issue is - if you stretch a muscle and then continue to apply stretch force - as in the service motion - does that increase, or somehow maintain the stretch? In which case, more energy would be available available than with stretch, wait a time with no force, then use the stretched muscle. Little or no energy dissipation for, say, the 300-400 millisecond delays for the serve. ?

    My view is speculative since I don't understand this subject very well. Maybe the views are in agreement with the current biomechanical view. Even with Biomechanics 101. ?? I'm not a biomechanical researcher publishing something, so take it or leave it. But do look at my references in this thread and the others with the reply on Titin, the muscles cell videos and other references and comments. Research Titin and the Force vs Velocity curves on your own.

    Pictures Titin.
    https://www.google.com/search?site=....1ac.1.45.img..0.5.504.Whq_4y5H7ZI&gws_rd=ssl
     
    Last edited: Mar 21, 2015
    #19
  20. dominikk1985

    dominikk1985 Legend

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    thanks for that reference. The titin in an interesting molecule.

    however I still think that you should not overlook the actual Stretch shortening cycle which is not an elastic component but a neuronal Signal after stretching that Triggers an active contraction.

    the elastic component is probably important too though.
     
    #20
  21. Chas Tennis

    Chas Tennis Hall of Fame

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    There may be different usage of the term Stretch Shortening Cycle and what it includes and does not.

    From Fundamental of Biomechanics, 2007, D. Knudson.

    "There are four potential sources of greater force in the concentric phase of an SSC:

    1) contractile potentiation
    2) relfex potentiation
    3) storage and reutilization of elastic energy
    4) and the time available for force development"

    I interpret #3 to be associated with Titin. #1 & 2 probably the Actin Myosin cross bridges of the sliding filament model. Probably reflex #2 use the Muscle Tendon Unit(MTU) spindles that sense muscle length and/or Gogli sensors for muscle force. #1 & #2 are going to be slower. #3 is going to be faster.

    A text book printed in 2007 very likely will not mention Titin. I am not that well informed on the latest Titin research but would say that this field is being changed now and the view that the tendons supply considerable elastic energy is loosing out to Titin. Read some of the recent research and judge for yourself.

    What seems important to me is in Hill Muscle Model - stretched muscles can supply force at higher velocities of muscle shortening than #1 and #2 above.

    Another very important point that I realized yesterday from reading Knudson's book. The tennis strokes by using multiple muscle groups, as body rotation, are first getting the arm and racket up to a speed before the last muscles shorten to work on the arm. That may relate to #4 above. Therefore, although the arm and racket are already moving form the body turn, the joint with the last stretched muscle has not started shortening yet. This is one reason why "arming" the ball is going to be slower than getting the arm and racket up to speed with body turn and then letting other pre-streched muscles shorten to take over. Research what the force vs velocity curves mean for each type of microscopic muscle cell shorteners, for the Titin (fast) and for the Actin-Myosin parts (slow) of each muscle cell.

    Force vs Velocity Curves
    https://www.google.com/search?q=for...WJYKRyAS7-4HACA&ved=0CCEQsAQ&biw=1113&bih=688
     
    Last edited: Jun 6, 2014
    #21
  22. boramiNYC

    boramiNYC Hall of Fame

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    An excellent summary of significance of fascia:

    http://breakingmuscle.com/mobility-recovery/the-top-5-ways-fascia-matters-to-athletes

    What's most interesting is how much nerve endings are in fascia. Seems very likely most of the muscle control occurs via fascia. Including the SSC type movements since it is the main sensor for tension as well. IMO Titin is much more minor component inside muscle itself that gives passive elastic characteristic to the muscles. A SSC that spans multiple muscles should involve facsial system not titin.
     
    #22
  23. dominikk1985

    dominikk1985 Legend

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    chas, the golgi reflex is not the SSC. the golgi tendon reflex actually does the opposite and actually releases tension.

    the SSC is a nerve signal that causes the muscle to contract (see the video I posted).

    the elastic component (actually called "series elastic component") again is another thing.

    at lot of different mechanisms:).

    here is an article explaining the difference in easy words:
    http://www.sport-fitness-advisor.com/plyometrics.html
     
    Last edited: Jun 5, 2014
    #23
  24. dominikk1985

    dominikk1985 Legend

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    Last edited: Jun 5, 2014
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  25. GuyClinch

    GuyClinch Hall of Fame

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    Long story short - this means active use of the forearm muscles in forehands and serves no? :p If we are saying that SSC is just a way to amplify contractions - doesn't that imply active use of those muscles? And it will show up in EMG if it is active?

    So whats the EMG of a serve and forehand? That would seemingly solve this debate..
     
    #25
  26. Chas Tennis

    Chas Tennis Hall of Fame

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    All motions are likely to be a mixture of active and passive muscle contractions. The terms "active" and "passive" have the defined meaning as used in the Hill Muscle Model. Search: Hill Muscle Model

    The issue for this thread was -

    If you read a research paper where EMG signals are measured for certain muscles during a tennis stroke does that mean that the shortening of those particular muscles is the most important thing for the stroke?

    Answer: No, EMG signals do not occur when using passive pre-stretched components. I believe that those forces are dominated by Titin because of the references linked in this thread.

    (I had seen research papers where EMG signals were measured and wanted to understand if the important stuff goes on without EMG signals. Research papers - http://scholar.google.com/scholar?hl=en&q=emg+signal+tennis+stroke&btnG=&as_sdt=1,21&as_sdtp=)
     
    Last edited: Jun 6, 2014
    #26
  27. dominikk1985

    dominikk1985 Legend

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    I don't have the data. There most likely is an EMG Signal and active contraction but active still doesn't mean it isn't involuntary. the SSC Signal goes directly over the spinal cord bypassing the brain so that you don't have to voluntarily contract those muscles.
     
    #27
  28. Chas Tennis

    Chas Tennis Hall of Fame

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    How do you interpret this quote for each numbered item?

    From Fundamentals of Biomechanics, 2007, D. Knudson.

    "There are four potential sources of greater force in the concentric phase of an SSC:

    1) contractile potentiation
    2) relfex potentiation
    3) storage and reutilization of elastic energy
    4) and the time available for force development"
     
    Last edited: Jun 6, 2014
    #28

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