Kinetic chain dysfunction
What's the difference between bodybuilders and strength athletes like powerlifters, Olympic weightlifters, and strongman/woman competitors? Seriously--that's not a rhetorical question. These two groups of individuals definitely have different training goals--and there may even exist within-group differences when looking at the strength athletes--not to mention that the latter group could perform the deadlift, clean and jerk, and farmer's walk with the former group as weight implements! However, when you look at the true general objective of training, you see that the bodybuilders, train muscles and muscle groups, while the strength athletes train movements. Bodybuilders often incorporate powerlifting and even weightlifting movements into their routines, but the inclusion of these exercises is still to improve the size of select muscles. Whether they realize it or not, strength athletes see the big picture. They see that the body is designed to function as a chain--in movements and movement patterns--not as individual muscles or muscle groups. Disrespecting the body as a chain can lead to minor or major dysfunction. The purpose of this article series is to help you gain a greater understanding and respect for the body as the kinetic chain; however, it is not in any way intended to serve as an impromptu PT session. Part I establishes the general framework by discussing the kinetic chain and kinetic chain dysfunction. Part II of the series will discuss some common muscular, neuromuscular, and arthrokinematic considerations associated with dysfunction of the kinetic chain. Again, it is important to reiterate that the purpose of these articles is not necessarily to diagnose individual dysfunction but rather to illustrate rather interesting concepts related to performance and function. The body is an amazing machine that moves in all three planes of motion (frontal, sagittal, and transverse) and has the ability to accelerate, decelerate, and maintain stability. Essentially, that is the function of the body and is the premise behind functional training: to train movements in all three planes of motion employing a spectrum of muscle and neuromuscular actions (concentric, eccentric, isometric). The scope of this article does not encompass the analysis or promotion of functional training. However, it is important to note that many of the advocates of functional training have an outstanding understanding of the body, and the principles of such training integrate several training components that are often missing but necessary ingredients in bodybuilders' and strength athletes' training programs. In general, both populations of trainees could not only get bigger, faster, and stronger by incorporating these ideas, but they would also be better prepared to prevent and rehabilitate injuries--an oft overlooked part of training. The kinetic chain is composed of all of the body's soft tissue (muscle, ligaments, tendons, etc.), the nervous system, and articular system (i.e., bones and joints) (Clark, 2001). These different systems work synergistically to allow for proper alignment of the musculoskeletal system (structural efficiency) and for the neuromuscular system to perform functional tasks most efficiently (i.e., with the least amount of energy) while creating the least amount of stress on the entire kinetic chain (functional efficiency) (Clark, 2000). Therefore, if any one of these systems or even a single component of one of these systems is not operating efficiently, the other systems will be forced to compensate and adjust. The resulting compensations and adjustments include tissue overload, decrements in performance, and forcastable patterns of injury known as serial distortion patterns (Clark, 2001).
As Eric Cressey pointed out in a previous Scientific Answers column, there exists an optimum length of the muscle fibers from which the muscle is able to generate maximal tension (length-tension relationship) (Siff, 1997). Muscles at the optimum length can develop maximum tension because the optimum number of crossbridges can be formed by the proteins myosin and actin (the contractile proteins). If the muscles are lengthened or shortened beyond this optimum length, the amount of tension that the muscle is able to develop diminishes. The central nervous system has the responsibility of selecting the appropriate combination of muscles to produce movement. Muscles act as force couples to generate force, dynamically stabilize, and decrease force efficiently. Joint arthrokinematics represent the actions that occur between two articulations; normal movement patterns produce predictable patterns of joint arthrokinematics (Clark, 2000). Reciprocal inhibition, a fundamental principle of kinesiology, refers to the decreased neural drive (i.e. relaxation) to the functional antagonist while the agonist contracts. Essentially, it is a built-in, automatic neurological function, designed to provide for optimum joint function and longevity. However, Clark (2000) defines reciprocal inhibition as "the process whereby a tight muscle causes decreased neural drive to its functional antagonist," thereby expanding the definition to the current discussion of dysfunction. Consider the iliopsoas and the gluteus maximus, which are functional antagonists, for example. A tight iliopsoas will result in decreased neural drive to the gluteus maximus, which will alter the normal force-couple relationships. Because the activation and force of the prime mover--in this case, the gluteus maximus--are decreased, compensation and adaptation are forced upon the kinetic chain. As a result, the synergists (i.e., hamstrings) and stabilizers (i.e., erector spinae, which also serve as synergists) are required to compensate and substitute for the prime movers (gluteus maximus). This latter phenomenon is referred to as synergistic dominance. In this particular example, the reciprocal inhibition of the glutes--and subsequent synergistic dominance of the hamstrings--may easily result in a hamstring injury because of the excessive burden placed on the hamstrings. As such, Clark (2000) defines synergistic dominance as "the process whereby a synergist compensates for a prime mover to maintain force production." This continuous process (i.e., reciprocal inhibition and synergistic dominance) alters ordinary joint arrangement and, in turn, the normal length-tension relationships around the joint. Muscle tightness and weakness, joint dysfunction, and decreased neuromuscular efficiency all have the tendency to instigate this dysfunctional pattern. Arthrokinetic inhibition is another neuromuscular phenomenon that is the result of a joint dysfunction that inhibits those muscles that surround the dysfunctional joint (Clark, 2000).
By this point, you should begin to be able to see that rarely is any kinetic chain dysfunction an isolated event. That is, a dysfunction within the kinetic chain is typically the result of a chain reaction involving the development of several compensations and adaptations. Remember that all muscles are designed to function in all three planes of motion, as well as throughout an entire spectrum of muscle actions. Therefore, if a muscle is very strong in one plane of motion concentrically but is relatively weak in another plane of motion eccentrically or isometrically, it is likely that compensations will occur that result in kinetic chain dysfunction. Functional strength then can be defined as the ability of the neuromuscular system to perform muscle actions concentrically, isometrically, and eccentrically in all three planes of motion (Clark, 2001). Muscle imbalances are the product of poor posture, pattern overload (i.e., repetitively performing the same exercise in the same plane of motion, with the same weight, at the same speed, through the same range of motion), injury, lack of core stability, and lack of neuromuscular efficiency. Likewise, there are specific causes of kinetic chain imbalances: postural stress, muscle imbalances, joint dysfunction, decreased neuromuscular control, decreased functional strength, decreased core strength and neuromuscular control, and lack of multi-planar eccentric neuromuscular control (Clark, 2000). Vladimir Janda (1983) has developed two functional classifications for muscles: a movement group and a stabilization group. The movement group is prone to developing tightness, is readily activated during most dynamic movements, and is overactive during new movement patterns or in fatigue situations (i.e. synergistic dominance). The stabilization group is prone to weakness or inhibition, is less active during most dynamic movements, and fatigues easily during dynamic activities. A common illustration of this latter point is seen during the front squat, during which the rhomboids and mid- and lower traps serve as stabilizers. It is not uncommon for these stabilizers to fatigue prior to the movement group. Additionally, if the movement group is prone to developing tightness and overuse, then those muscles can trigger reciprocal inhibition in their functional antagonists. This occurrence results in reduced neuromuscular efficiency and kinetic chain dysfunction. Likewise, the stabilization group is prone to weakness and inhibition; these muscles can permit synergistic dominance, which leads to kinetic chain dysfunction, reduced neuromuscular efficiency, and further reciprocal inhibition. The following table provides Janda?s functional muscle division (note: the movement and stabilization groups are not placed in any particular order).
So, what's all this kinetic chain jargon really mean? Well, as mentioned, maintaining the integrity of the kinetic chain is important to uphold optimal length-tension relationships, force-couple relationships, arthrokinematics, sensorimotor integration (i.e., proprioception, mechanoreceptors), neuromuscular efficiency, and tissue recovery. Additionally, kinetic chain dysfunction leads to serial distortion patterns and leads to compensations and adaptations--better termed maladaptations--in other parts of the chain. At this point, you're probably thinking one of two things: 1) that this is some really cool stuff and you can readily see how this information applies to yourself or someone you train; or 2) I'm speaking some foreign language. If the former is the case, great! In the latter instance, don't worry; this takes some time to grasp. In the next installment, I will provide some specific examples of common kinetic chain dysfunctions, citing articular, muscular, and neuromuscular considerations. A very special thanks to my main man Eric Cressey. The resident anatomy guru humbled me once again with his outstanding knowledge and understanding of kinetic and functional anatomy!
References 1. Clark, MA. ( 2000) A Scientific Approach to Understanding Kinetic Chain Dysfunction. California: National Academy of Sports Medicine. 2. Clark, MA. (2001). Integrated Training for the New Millennium. California: National Academy of Sports Medicine. 3. Cressey, EC. (2003). Unpublished. 4. Janda, V. (1983). Muscle Function Testing. London: Butterworths. 5. Siff, MC. & Verkhoshansky, YV. (1997). Supertraining: Special Strength Training for Sporting Excellence. Ohio: Strength Coach, Inc. |
