Introduction

Muscle energy technique (MET) is a type of osteopathic manipulative medicine (OMM) developed by Fred Mitchell, Sr, D.O., in 1948, designed to improve musculoskeletal function through mobilizing joints and stretching tight muscles and fascia, to reduce pain, and to improve circulation and lymphatic flow.[1][2] These methods are unique in OMM as they are “active” techniques, requiring the patient to perform isometric contractions.[3] MET is contraindicated in individuals with poor energy, fractures, significant joint disease, or recent surgery.[4] MET is characterized by a patient-induced skeletal muscle contraction against an operator’s resistance in a controlled direction and position.[1] More specifically, isometric MET entails the following steps:

1. Isolation of the target joint and/or muscle barrier through joint positioning, generally to a pathologic barrier.
2. This is followed by active muscle contraction by the patient in a specific direction, generally away from the restriction, for a specified period against provider-applied counterforce. Conventionally, the amount of force generated by the patient should be the maximum amount comfortably tolerated by both the patient and practitioner.
3. Relaxation of the contracted muscle.
4. Passive movement of the patient’s anatomy toward a new pathologic barrier
5. Repeat steps 1 to 4 as tolerated until physiologic pain sufficiently relieved and/or the achievement of the desired range of motion.[5]

Within this framework, different protocols have been developed with varied specifics for each step, including duration and strength of contraction, duration of rest, and the number of repetitions.[1][6][7][8] For example, the Greenman method proposes a five-to-seven second relaxation step and three-to-five repetitions overall.[1]

The goal of this therapy is to induce relaxation of a muscle or muscle group, the hypertonicity of which is proposed to be the source of pain and/or loss of mobility in a body part and/or joint. The primary theories behind this phenomenon entail post-isometric relaxation – the reduction in tone of an agonist muscle following isometric contraction, and reciprocal inhibition – the reduction in tone of an antagonist muscle after its agonist has undergone isometric contraction.[1][9] Both of these phenomena are well understood on a cellular level.

Cellular Level

Post-isometric Relaxation

Golgi tendon organs (GTOs) are mechanoreceptors found in most skeletal muscles. They are sensitive to muscular contractile force, and in contrast to muscle spindles (see below), GTOs are rarely and inconsistently activated by muscle stretch. These encapsulated bundles of collagen are innervated by fast-conducting type Ib afferent fibers, and are present at muscle-tendon or muscle-aponeurosis junctions; they attach to an individual muscle fascicle tendon on one end, and the whole muscle-tendon or aponeurosis of the other. This positioning, often described as “in-series,” meaning the receptor is part of the functional unit, stands in contrast to the muscle spindle that operates adjacent to the functional unit, “in parallel.”[10][11]  GTOs are activated at high levels of force and hypothetically inhibit muscle activity, preventing musculoskeletal injury.[12]

Physiologically, increased tension to the GTO prompts the activation of the type Ib afferent fibers that project to the spine, where they provide positive input on inhibitory interneurons that, in turn, add negative or “inhibitory” input on the efferent α-motor neurons that receive input from the cortex to the homonymous muscle.[13] In effect, sufficient GTO stimulation can override the muscle-activating signal from the brain, leading to relaxation. This phenomenon is known as the “inverse stretch” or the “autogenic” reflex.[14][15]

Reciprocal Inhibition

Muscle spindles are stretch-sensitive mechanoreceptors found in skeletal muscle. A muscle spindle is a bundle of striated, “intrafusal” muscle fibers within the fascicles of force-producing, “extrafusal” muscle fibers. “Fusal,” comes from the term “fusiform,” meaning spindle-shaped. Any stretch, change in length, of the extrafusal fibers thus results in a stretch of the intrafusal fibers, which is then detected in the equatorial and polar regions of the muscle spindle. This physiology stands in contrast to GTOs that are relatively insensate to passive changes in length but respond to an increase in muscle force. The stretch sensation is measured by two types of afferents: primary (type Ia) and secondary (type II). There is a single Ia fiber and anywhere between zero-to-five II fibers per spindle.[16] The Ia fiber is comparable in size and speed of transmission to the previously mentioned Ib fibers and supplies all intrafusal fibers in the spindle at the equatorial region.[10] The exact function of type II fibers is less understood; however, these smaller fibers terminate on the polar ends of the spindle. Muscle spindles are unique among proprioceptors in that efferent fibers innervate them. These myelinated γ-motor neurons derive from the same efferents that supply the extrafusal muscle. Excitation of these γ-motor neurons does not affect overall muscle tension but appears to maintain tension on the muscle spindles to track the length of the extrafusal fibers effectively. Lastly, spindle afferents are tonically active, with an increased firing rate in response to passive stretch in a velocity-dependent manner.[16] For more, see the Monosynaptic Reflex article.[17]

Physiologically, stretch to a muscle fiber produces activation of Ia muscle spindle afferents that project to the spine and activate the efferent α-motor neurons, and subsequently, the γ-motor neurons of the homonymous muscle leading to contraction of the intra- and extrafusal fibers. Simultaneously, the Ia fibers activate inhibitory interneurons in the spine to inhibit the α-motor neurons of the antagonist muscle. This circuit is simply described as the “stretch reflex.”[18][19] This pathway is thought to prevent over-lengthening of a muscle and to be instrumental in activities such as bipedal walking and posture.[20][21][22]

Development

Before birth, the first evidence of GTOs is observable in the aponeurosis where Ib axons terminate within islets of collagen bundles and myotubules.[23] In the first postnatal week, the innervated core elongates as collagen bundles, and Schwann cells continue to proliferate. Within the capsule that is completed by day two, collagen fibrils are laid down between the Schwann cells and the terminal nerve ends. These bundles of collagen link the muscle fiber tips to the aponeurosis, thus establishing the connection between muscle tension and GTO activation. Muscular contraction thus applies force to the collagen bundles, which directly stimulate the nerve endings within the GTO.[10][11]

Muscle spindle differentiation starts around 11 weeks of gestation when the intrafusal and extrafusal fibers differentiate. The arrival of the Ia afferent axon to the spindle prompts the formation of the nuclear bag, a term given to intrafusal fibers with multiple equatorial nuclei.[24][25] Subsequently, the motor nerve supply reaches the spindle.[24][26] The spindle reaches a mature form between 24 to 31 weeks and continues to increase in length after birth.[26]

Mechanism

As mentioned in the introduction, METs take advantage of the physiologic mechanisms of post-isometric relaxation and reciprocal inhibition, primarily, to improve musculoskeletal function and to reduce pain. For a given joint, MET is performable in a “direct” or “indirect” fashion based on the indication of treatment.[1] Combining the MET method and the cellular physiology, MET may be illustrated as follows: take the example of the elbow joint with hypertonicity in the biceps muscle. 

Indirect (reciprocal inhibition)

1. The elbow is extended to the pathologic barrier - limited by the hypertonicity of the biceps. 
2. The patient is instructed to contract the triceps against the provider’s counterforce. This action stimulates muscle spindles of the triceps, which activate Ia efferents that project to the spine and activate the inhibitory interneuron that synapses onto the α-motor neurons that project to the biceps, thus producing relaxation of the intra- and extrafusal fibers.
3. The patient is instructed to relax the triceps.
4. The patient’s arm is passively extended as permitted by the biceps muscle. This action is facilitated by the reciprocal inhibition produced in step 2.
5. Repeat steps 1 through 4 until achieving the full range of motion, or the procedure is intolerable.          

Direct (post-isometric relaxation)

1. The elbow is extended to the pathologic barrier - limited by the hypertonicity of the biceps. 
2. The patient is instructed to contract the biceps against the provider’s counterforce. This action activates the GTOs of the triceps, which activate Ib efferents that project to the spine and activate the inhibitory interneuron that synapses onto the α-motor neurons that project to the biceps, thus producing relaxation.
3. The patient is instructed to relax the biceps.
4. The patient’s arm is passively extended as permitted by the biceps muscle. This action is facilitated by the post-isometric relaxation produced in step 2.
5. Repeat steps 1 through 4 until achieving the full range of motion, or the procedure is intolerable. This technique is limited by pain in the affected joint and/or muscle.

Pathophysiology

The increased muscle tone purportedly treated by muscle energy technique is comparable to that of the hypertonicity and/or spasticity that presents in upper motor neuron disease.[1][27] Increased activity of the extrafusal muscle fibers may be secondary to either increased activity of the muscle spindle or abnormal sensory processing in the spinal cord. In the former, increased activity of γ-motor neurons leads to abnormally shortened muscle spindles, thus leading to a hyperexcitable state such that movement within the physiologic range of motion produces reflexive muscular contraction. Similarly, type II fibers have been hypothesized to contribute to spasticity through direct α-motor neuron activation.[27]

Clinical Significance

As mentioned in the introduction, MET primarily serves to improve range of motion and to reduce pain.[1][2] These techniques are used by physicians, both osteopathic and allopathic, as well as physical therapists and chiropractors as primary or as adjunctive therapy.[5] In the case of the former, MET is commonly used to reduce pain secondary to hypertonicity in the back, neck, and other major joints, but may hypothetically be used to directly treat nearly any joint in the body.[28][29] As for the latter, MET, in addition to standard of care treatment, as well as other osteopathic techniques, has been demonstrated to improve outcomes in conditions such as pneumonia and fibromyalgia. In these cases, the complementary effects are attributed to fascial stretching, which is proposed to improve lymphatic and hemodynamic function.[3][30] 

A handful of metanalyses have been performed to assess the effectiveness of MET in the treatment of various conditions, particularly of low back pain. While some yielded mixed results, there is an apparent consensus on the positive effects of MET on low back pain, with insufficient and inconsistent evidence to support its use in other circumstances.[1][28][31][5]