What happens to the Human Movement System with injury, poor posture, and muscular imbalance?
Looking at this question in regards to the Human Movement System, I believe that the foundation begins with the Neuromuscular Efficiency. That is, our body operates on the ability to create the right amount of force, on the right joint, at the right time. Simply stating, our bodies do not want to work harder than they are required to. This Neuromuscular efficiency that is controlled by our Central Nervous System recruits the appropriate muscles to provide the proper amount of force at the necessary joints to create the desired movement.
Throughout life, our body adapts to movements that we perform in normal daily living (motor learning), and our CNS becomes conditioned to activate certain muscle patterns to create this desired movement. Ideal alignment is crucial throughout each movable joint and if any joint is out of alignment, the CNS will draw upon additional means of muscle movement and correction to create this desired configuration of movement (Sahrmann, 2002). These pre-programmed patterns of movement are constantly modified to react appropriately to external forces such as gravity, ground reaction forces, momentum, and external loads or force around a joint (torque) (Neumann, 2010). As life progresses, we are introduced to dysfunctions of the human movement system through injuries, muscular imbalances, and faulty posture and mechanics. These possible misalignment’s are the beginning stages of micro trauma to the joints and supporting structures (Sahrmann 2002). When this occurs, as stated by the NASM, relative flexibility through the kinetic chain, our body will always take the path of least resistance (Clark 2011). When are bodies are subjected to injuries that affect any of our optimal neuromuscular control such as arthrokinetics, dysfunctional length-tension relationships and force-couple relationships, our bodies will begin to exhibit dysfunctional movement patterns such as reciprocal inhibition, synergistic dominance or altered arthrokinimatics. These muscle dysfunctions can result from arthrokinetic inhibitions, relative flexibility, and pattern overloads (Clark and Lucett 2011)
One neuromuscular dysfunction is reciprocal inhibition, where an overactive or tightened agonist muscle can create a decrease neural drive to its antagonist muscle. Simply stating, if a primary mover is over active or tightened from over use or lack of extensibility training, that muscles’ direct antagonist will not receive the direct stimulus from the CNS and will call upon a synergistic muscle of that antagonist to help perform the desired motion. This reciprocal inhibition leads to synergistic dominance. When this occurs, it creates arthrokinetic inhibition, which in turns will eventually lead to joint or muscle injury as an unbalanced force will be created on a joint and possibly an adjoining joint. As an example, it is very common for adolescent male athletes to stretch and provide proper hip motion through the adductor complex, which become very overactive and tightened. This over-active muscle complex, decreases the neural drive when the gluteus medias is called upon to create frontal plane motion such as abduction, maybe a lateral push off that might happen in pushing off to steal second base in baseball. This decrease neural drive to the gluteus medias puts additional emphasis on the tensor fascia latae muscle and creates more tension on the IT band. Through constant repetitive motion and chronic adaptations of the tensor muscle, additional tension is applied to the lateral portion of the patellar femoral joint and results in a knee injury or chronic knee pain. This reciprocal inhibition also will affect our muscles ability to create proper force at a given joint and alter the length-tension relationship of that joint and surrounding joints. The overactive or tightened muscle will also be accompanied by a under active or loose antagonist muscle (Clark and Lucett, 2011). When called upon to create force in a specific joint, the CNS will have to call upon a synergistic muscle to balance out the force at that joint, which will in turn affect the length tension relationship that exists between the synergist that was called upon and another antagonist muscle which will most likely become the under active or loosened muscle. This arthrokinetic inhibition will develop a new neural pattern in the CNS and will eventually enter the cumulative injury cycle (Clark and Lucett 2011).
Sahrmann 2002, clearly states that “a restricted joint motion is considered the consequence rather than the cause of movement faults.” This treatment approach takes a much broader view than treating or rehabilitating the joint action that is causing musculoskeletal pain (MSP). This optimal neuromuscular functioning of the human movement system shows the vast importance on the fitness professional to create and design exercise movements that work through multiple planes of motion and do not just focus on the isolated movement of a joint. Length-tension relationships and force-couple relationships demonstrate how a single muscle can alter the kinetic chain of muscular patterns and affect multiple joints in the HMS.
Clark, Micheal, and Scott Lucett. NASM Essentials of Corrective Exercise Training. Philadelphia, PA: Lippincott Williams & Wilkins, 2010. Pr
Sahrmann, S. (2002). Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis, MO: Mosby, Inc.