Antagonistic Relaxation

Antagonistic RelaxationTM
refers to minimizing, but not eliminating, the role of antagonist muscles in movement. One of the methods that P3 uses to encourage Antagonistic Relaxation (AR) is by emphasizing the speed of descent in movement. This emphasis improves elasticity, or increases the energy stored in the stretched muscle. These increased speeds also causes larger preloading, an increase in cross bridge formation prior to the concentric contraction. Another benefit from this greater speed in the eccentric portion of the movement is the alteration of myosin filaments, allowing more favorable positions to produce greater amounts of force (Bobbert, 1996).

By the definition at P3, Antagonistic Relaxation can also reduce coactivation, or simultaneous contractions, of both agonist and antagonist muscles. Even basic resistance training has been shown to decrease the interfering effect between agonist and antagonist muscles (Jaric, 1995). By preventing coactivation, a greater amount of force is produced in the desired direction, rather than the “tug of war” that may occur in less traditionally trained individuals. While a minimal level of coactivation may be required for joint stability, higher levels of simultaneous contraction may lead to injury. Most muscle strains tend to occur in these antagonist muscles that are contracting in an attempt to decelerate the movement.

Coactivation can also be caused by fatigue (Miller, 2000). Insufficient relaxation can lead to an increase in intramuscular pressure which impairs blood flow, causing reduced tissue oxygenation and earlier onset of fatigue (Folkow, 1970). The end result is decreased torque production and a decreased reaction time (Styf, 1999). An inability to achieve AR can also permanently stress the motor neurons. Because the characteristic of fast twitch fibers is high force and high fatigability, these type II neurons are depleted first. As a result, less force is produced from insufficient relaxation (Lattier, 2004).

Perhaps the most beneficial portion of AR is the reduction in inhibition from the Golgi Tendon Organs (GTOs). These receptors reside in the musculotendinous junction to regulate force, and they send afferent nerves to inhibit the motor neurons that supply agonist muscles. With proper training, these GTOs may provide less inhibition, allowing the body to produce and absorb greater amounts of force.

Muscle spindles, on the other hand, send afferent nerve impulses to excite agonist neurons and inhibit antagonist neurons, allowing more efficient, faster movement. As training modulates GTOs, it also may enhance the facilitation of these muscle spindles to improve ballistic movement. This process most likely occurs in the central nervous system as it modulates spindle sensitivity through gamma motor neurons.

Most of the flexibility improvements at P3 come from movement, especially due to this emphasis on AR that allows athletes to achieve greater ranges of motion due to the lack of resistance from antagonists. This increase in joint range of motion improves elasticity by allowing greater stretches, corrects posture through hip flexibility, and lengthens running stride.

REFERENCES

Bobbert, M.F. , Gerritsen, K.G.M., Litjens, M.C.A. and van Soest, A.J. Why is countermovment jump height greater than squat jump height? Med Sci Sport Exer 28:1402-1412, 1996.

Folkow B, Gaskell P, Waaler BA. Blood flow through limb muscles during heavy rhythmic exercise. Acta Physiol Scand. 1970 Sep;80(1):61-72.

Lattier G, Millet GY, Martin A, Martin V. Fatigue and recovery after high-intensity exercise part I: neuromuscular fatigue. Int J Sports Med. 2004 Aug;25(6):450-6.

Miller JP, Croce RV, Hutchins R. Reciprocal coactivation patterns of the medial and lateral quadriceps and hamstrings during slow, medium and high speed isokinetic movements. J Electromyogr Kinesiol. 2000 Aug;10(4):233-9.