NASM Chapter 7 Concepts and Program Designs

Dynamic Stretch

The active extension of a muscle, using force production and momentum, to move the joint through the full available range of motion Mechanism of Action -Reciprocal Inhibition Acute Variables -1 to 2 sets, 10 to 15 repetitions, 3 to 10 exercises Prisoner Squats Multiplanar lungers Single-leg squat touchdowns Tube walking Medicine ball lift and chop

Static Stretching

The process of passively taking muscle to the point of tension and holding the stretch for a minimum of 30 seconds Mechanism of Action -Autogenic inhibition or reciprocal inhibition Acute Variables - 1 to 3 sets, hold each stretch for 30 seconds

Active-Isolated Stretching

The process of using agonists and synergists to dynamically move the joint into a range of motion Mechanism of Action -Reciprocal inhibition Acute Variables -1 to 2 sets, hold each stretch 1 to 2 seconds for 5 to 10 repetitions

Davis's Law

soft tissue models along the lines of stress. Soft tissue is remodeled (or rebuilt) with an inelastic collagen matrix that forms in a random fashion. It usually does not run in the same direction as the muscle fiber. They create road blocks, preventing the muscle fibers from moving properly which creates alterations in normal tissue extensibility and causes relative flexibility. If a muscle is in a constant shortened state, it will demonstrate poor neuromuscular patterns. An inelastic collagen matrix will form along the same lines of stress created by the altered muscle movements. Because the muscle is consistently short and moves in a pattern different from its intended function, the newly formed inelastic connective tissue forms along this altered pattern, reducing the ability of the muscle to extend and move in its proper manner.

Active Flexibility

-Self Myofascial release -Active Isolating techniques Improves extensibility of soft tissue and increases neuromuscular efficiency by using reciprocal inhibition. It allows for agonist and synergist muscles to move a lib through a full range of motion while functional antagonist is being stretched. ex. Supine straight leg raise. Phase 2/3/4 of the OPT model

Functional Flexibility

-Self myofascial release -Dynamic Stretching Requires integrated, multiplayer soft tissue extensibility, with optimal neuromuscular control, through the full range of motion, or essentially movement without compensations. Phase 5 of the OPT Model or before athletic competition.

Three causes of muscular Imbalances

Altered Reciprocal Inhibition, synergistic dominance, arthrokinetic dysfunction.

Arthrokinetic Dysfunction

Altered joint motion can be caused by altered length-tension relationships and force-couple relationships, which affect the joint and cause poor movement efficiency.

Benefits of flexibility training

Correcting muscle imbalances, increasing joint range of motion, decreasing the excessive tension of muscles, relieving joint stress, improving the extensibility of the musculotendinous junction, maintaining the normal functional length of all muscles, improving neuromuscular efficiency, improving function.

3 phases of flexibility training with the OPT model

Corrective, active, and functional.

Corrective Flexibility

Increases joint ROM, improve muscle imbalances, and correct altered joint motion. -Self myofascial release Uses principle of autogenic inhibition to cause muscle relaxation -Static Stretching Uses either autogenic inhibition or reciprocal inhibition to increase muscle length depending on how the stretch is performed. Phase 1 of the OPT Model Stabilization level.

Controversial Stretches

Inverted hurdler's stretch, plow, shoulder stand, straight-leg toe touch, arching quadriceps

Golgi Tendon

Located in the musculotendinous junction (muscle and tendons meet), they are sensitive to changes in muscular tension and the rate of tension change. It causes muscles to relax. Autogenic inhibition occurs when neural impulses that sense tension are greater than the impulses causing muscle contraction.

Cumulative Injury Cycle

Poor posture and repetitive movements create dysfunction within the connective tissue of the body and the body will treat dysfunctions as injury. -Tissue trauma -Inflammation -Muscle spasm -Adhesions Adhesions form a weak, inelastic matrix (inability to stretch) that decreases normal elasticity of the soft tissue, resulting in altered length-tension relationships (leading to altered reciprocal inhibition), altered force-couple relationships (leading to synergistic dominance), and arthrokinetic dysfunction (leading to altered joint motion). Left untreated, these adhesions can begin to form permanent structural changes in the soft tissue. -Altered neuromuscular control -Muscle imbalance -Repeat

Muscle Imbalance can be caused by a variety of mechanisms

Postural stress, emotional duress, repetitive movement, cumulative trauma, poor training technique, lack of core strength, lack of neuromuscular efficiency.

Synergistic Dominance Example

Psoas is tight, it leads to altered reciprocal inhibition of the gluteus maximus, which in turn results in increased force output of the synergists for hip extension (hamstring complex, adductor magnus) to compensate for the weakened gluteus maximus. This leads to to faulty movement patterns, leading to arthrokinetic dysfunction and eventual injury (hamstring strain).

Muscle Spindles

They are sensitive to change in muscle length and rate of length change. They prevent muscles from stretching too far or too fast. However, when a muscle on one side of a joint is lengthened (because of a short muscle on the opposite side), the spindles of the lengthened muscles are stretched. This information is transmitted to the brain and spinal cord, exciting the muscle spindle and causing the muscle fibers of the lengthened muscle to contract. This results in micro muscle spams or feeling of tightness.

Muscle Spasms

When a lengthened muscle is stretched, it increases the excitement of the muscle spindles and further creates a contraction (spasm) response.