Kinetic Chain Dialogue

The kinetic chain is magnificent. There is nothing simple about the kinetic chain. It’s complexity allows us to be able to do the most fascinating endeavors imaginable. Like anything, when there is a lack of understanding, neglect isn’t too far behind

The kinetic chain isn’t an indestructible system (more about this later). Most will break down the kinetic chain into nerves, joints & muscles. Is this right or wrong? Neither, more like a simple representation. Nothing wrong with breaking down the kinetic chain into a simpler version, as long as you have a complete grasp of it’s more complex version:

kinetic chain simple version: nerves, joints & muscles work together to produce, reduce & control all sport, lift & athletic movement patterns

kinetic chain complex version: the synergistic effect from each one of the independent anatomical systems** to work together interdependently to produce, reduce & control all sport, lift & athletic movement patterns

** mindset, hormonal, cardiorespiratory, nutritional, skin, connective

tissue, nerves, joints & muscles

kinetic chain principles & concepts

KC kinetic chain, NI neural input, MPO muscle power output, N[I] neural inhibition,

The kinetic chain is a suspension-based system which requires stabilization to be present before force & velocity can be generated. The kinetic chain has one primary functional mandate: protection & performance. Protection & performance are not two different components they are teammates with obligated roles that must happen simultaneously for the KC to be effective & efficient. Protection [stabilization] and performance [force & velocity]

Because the KC is a suspension system what it seeks is stability and not symmetry. This is hard for many practitioners to grasp

The kinetic chain system is a mechanism. Things that are mechanized will malfunction. This is an important concept. One of the most difficult things for a parent or athlete to grasp; how can doing something seemingly ordinary cause the kinetic chain to breakdown and produce an injury pattern with zero trauma being associated

NOTHING in the KC happens in isolation. Don’t take this statement lightly. A shift, bend, twist, pull, re-alignment, restriction, tension or translation all lead to micro & macro stabilization implications throughout the entire KC altering force & velocity during sport, lift & athletic movement patterns

The kinetic chain is only as strong as its weakest link [you are only as fast or explosive as your weakest leg]. Neural input will only allow muscle power output to the degree that the kinetic chain can maintain dynamic stabilization [adaptive enough to change but always equalizing. I believe explains exactly how motor control maps preplanned athletic movement patterns by reverse engineering]

The more mobile linkages within the kinetic chain are under 9x higher stress/strain force factors compared to less mobile linkages. The kinetic chain is prone to break down at the weakest linkage & mobile linkage, misplacing forces elsewhere throughout the kinetic chain: tissue overload, compensation, adaptation & substitution patterns

Each tissue within the kinetic chain has a different breakdown rate [referred to as the tissue stress continuum] micro-trauma failure occurs in the collagen fibers at 6-8 percent deformity rate. This will cause the NI to compensate to maintain MPO to generate force production & reduction

Forces should be transferred seamlessly across different structures within the kinetic chain. A lack of stability within the kinetic chain adds higher stress/strain factors which will decrease MPO leading to NI alterations: muscular length changes, synergists overactivation, & arthokinematic inhibition

Movement over muscles: NI select optimal movement strategies to ensure MPO is at its highest level. Translation: individual muscles need to be as strong as possible so when they are recruited to work within a force group to accomplish a specific sport, lift or athletic movement pattern they are able to produce/reduce & dynamically stabilize force at max effect

If the prime mover is weak or slow to activate, synergist muscles are recruited to maintain MPO. Problem, synergists fatigue more quickly and lack the precise MPO equal to that of the prime movers. This ultimately leads to faulty movement patterns creating tissue overload

In addition, if a specific muscle isn't strong enough during a specific moment under a specific load, again a synergist muscle will kick-in to help elevate the overall strength value to maintain performance potentiation. For instance, let’s presume while running to catch a ball then decelerate, turn and change directions require the glute med to produce 750 newtons upon GCF but the current strength value of the glute med is only capable of putting out 500N then the QL/IO will kick-in to bring up the overall strength value so that the force output requirement necessary to accomplish this movement pattern efficiently is maintained [substitutes are secondary for a reason]. We always want the prime movers to be strong enough to prevent the synergist from kicking in. This redundancy*** mechanism is a protective mechanism not a performance mechanism

*** redundancy is representative of: suboptimal and not meaning excess or not useful. Suboptimal to what? Suboptimal comparatively to the prime move which has optimal strength value and mechanical leverage, whereas synergists do not