Contract-Relax Technique (CR)
Proprioceptive Neuromuscular Facilitation Technique
Applying a passive stretch after contraction at end range uses the “latency” period after the contraction to apply a greater stretch while minimizing neuromuscular impediments.
The contract-relax method originated from the proprioceptive neuromuscular facilitation school of thought.
We can divide contract-relax into two methods:
- Contract-relax technique
- Contract-relax agonist technique
Isolation Contract-relax Technique
The standard contract-relax technique includes a static-stretch (SS) phase followed by an intense isometric contraction of the muscle, followed by another SS phase1.
- Passive stretch phase:
- Contraction phase:
- Passive stretch phase:
Agonist Technique
The contract-relax agonist technique involves:
- Active stretch phase:
- Contraction phase:
- Active stretch phase:
Physiologic mechanism
There are 2 proposed theories by which CR works:
Autogenic inhibition
Autogenic inhibition is proposed to occur during the contraction phase of the CR technique1. During the contraction phase, a stretch is applied to the tendon, causing the golgi tendon organ to activate and transmit stretch signals via type Ib sensory afferents back to the spinal cord1. An inhibitory signal is created and the α-motor neurons innervating the extrafusal fibers are inhibited through hyperpolarization1.
“This output could reduce the effectiveness of homonymous Type Ia muscle afferent output during stretch, inhibiting the activation of the α-motoneuron pool, thus possibly enabling further increases in ROM (1,36). Intuitively, a reduction in α-motoneuron pool activity may enable further increases in ROM, but there is no direct evidence of a causal relationship.”1.
“However, Golgi tendon organ activity substantially decreases or ceases once the contraction has terminated, with several studies reporting increased resting EMG activity immediately following the contraction phase of CR stretching”1.
“Thus, autogenic inhibition is unlikely to be the primary underlying mechanism explaining either the increases in ROM or the superiority of CR stretching in increasing ROM above other stretching modalities”1
Read more about autogenic inhibition here
Gate control theory
Gate control theory is another inhibitory mechanism that is theorized to the mechanism of contract-relax techniques1.
During the contraction phase, there are increased signals from the Type III sensory afferents which could inhibit pain perception1.
This is possible since pressure receptors and nociceptive fibers (type IV sensory afferents) output to the same spinal interneuron in the spinal horn1. Since pressure receptors are larger myelinated neurons whereas nociceptive type IV afferents are smaller unmyelinated, the pressure signals take precedence and block the nociceptive signals from travelling up the spinal cord1. With dampened nociceptive signalling reaching the brain, this could enable one to move further into end range ROM before stopped by pain.
- Increased peak passive torque at full volitional ROM
- Increased stretch tolerance
Contract-relax examples
Other neuromuscular stretches
- PAILs & RAILs