PNF Stretching: What does current research say about its mechanism
PNF or proprioceptive neuromuscular facilitation stretching is a popular technique used in conjunction with manual therapy. PNF can be regarded as a set of stretching techniques to enhance the range of motion. PNF uses the body’s proprioceptive system to facilitate or inhibit muscle contraction. To increase the ROM of target muscles, PNF involves a shortening contraction of the target or opposing muscle. The techniques were credited to physiologist Charles Sherrington, who in the mid-1900s, defined the concept of neuromuscular facilitation and inhibition. Following on, Herman Kabat, a neurophysiologist, developed clinical PNF stretching techniques in the 1950s.
There are various forms of PNF stretches, mainly Contract Relax or CR, Agonist Contract or AC and Contract Relax Agonist Contract or CRAC. In CR the target muscle(s) is placed into a position of stretch, then a static contraction of the target muscle. This is followed by a gentle stretching, where the muscle is moved into a greater position of stretch. In AC (which is the basis of Active Isolated Stretching) the target muscle is placed into a position of stretch to its end-range, then concentrically contracts the opposing (antagonist) muscle, followed by moving the joint to a new position in the range of motion. CRAC stretching is similar to CR except that following the contraction of the target muscle, a shortening contraction of the opposite muscle is used to place the target muscle into a new stretch position.
PNF stretching has been well-proven to improve and provide a greater range of motion (ROM) as compared to the static or other types of stretching (Sharman et al., 2006). Despite its success, controversies remain on the mechanism of actions. Neurological reflex muscle relaxation following isometric muscle contraction is the main basis of mechanism suggested for PNF stretches. However such mechanisms are not substantiated by research. Eyal Lederman in his book Therapeutic Stretching said that Post Isometric Relaxation is an erroneous premise. Ian Shrier in Evidence Based Sports Medicine wrote that Reciprocal Inhibition is a myth that continues to be promoted in textbooks and the medical literature. Let’s look at the two common mechanisms proposed for PNF stretching and examine what the antagonists said.
Autogenic Inhibition
The common explanation of the basis of CR stretching is autogenic inhibition or “reduction in excitability of a contracting or stretched muscle” due to the Golgi tendon organ (GTO) reflex. As part of the body’s self-regulatory mechanisms, GTOs protect muscle and tendon from overstretching. If the muscle belly contracts too forcefully, the GTO sends a signal to the nervous system that triggers the GTO reflex to inhibit the muscle from contracting. In other words, muscles relaxed after voluntary muscle contraction. It is also referred to as post-isometric relaxation (PIR) (Hindle et al., 2012).
Lederman in his book wrote: “Under normal circumstances, when a person is fully relaxed there is no motor tone in the muscles, i.e. there is no demonstrable activity on the EMG trace. Similarly, when a person is stretched passively the muscle is motorically silent. If muscle activity is observed, it is usually when the stretching reaches the end of ROM at the onset of discomfort and pain. This increase in motor activity is likely to be an evasive response to pain. It means that during the early phase of stretching, the muscle is relaxed and therefore, further inhibition is not possible – cannot relax a relaxed muscle, whereas, at the end-ranges, motor activity is likely to increase; an outcome which would defeat the purpose (muscle relaxation).”
Studies showed that following the contraction of a stretched muscle, inhibition of the stretch reflex response is transient and only lasts less than a second. Researchers questioned whether such short period of inhibition can result in a clinically meaningful muscle relaxation (Chalmers, 2004). In addition, the hypothesis is that muscle activity should be minimum, but studies using electromyography (EMG) have shown that muscle activity is actually increasing after PNF (not relaxed) (Wilkinson, 1992).
Chalmers wrote: “Studies examined suggested that decreases in the response amplitude of the Hoffmann and muscle stretch reflexes following a contraction of a stretched muscle are not due to the activation of Golgi tendon organs, as commonly purported, but instead may be due to presynaptic inhibition of the muscle spindle sensory signal.”
Reciprocal Inhibition
AC techniques were based upon the basis that stretching of the antagonist muscle creates reciprocal inhibition of the agonist muscle. As explained by Susan Salvo (2007) in Massage Therapy: Principles & Practices:
“ When the central nervous system sends a message to the agonist muscle (muscle causing movement) to contract, the tension in the antagonist muscle (muscle opposing movement) is inhibited by impulses from motor neurons, and thus, must simultaneously relax. This neural phenomenon is called reciprocal inhibition.”
However, when the initial hypothesis was proposed, muscle activity was not measured. When EMG was recorded in the late 1970s, the reciprocal inhibition theory was mostly disproved. As described in the previous section, data from laboratory do not support the theory that contraction of a stretched muscle prior to further stretch, or contraction of opposing muscles during muscle stretch, produces relaxation of the stretched muscle. Muscles are electrically silent during normal stretches until near the end ROM. PNF stretch actually increases the electrical activity of the muscle during the stretch (during antagonist contraction, the muscle supposed to be relax), even though the range of motion is increased (Chalmers, 2004). While the effect of RI can be observed, it is brief and mostly happening under normal voluntary contractions.
Studies also showed that PNF has a ‘cross-over’ effect, during a unilateral leg PNF stretching, the ROM in the unstretched leg also increases. The electrical activity in the unstretched leg was also active when the stretched leg was contracting against resistance. ROM gain following a CR stretch is the same whether the target stretching muscle is contracted, or an uninvolved muscle is contracted (Markos, 1979).
Summary
Various mechanisms other than the spinal processing of proprioceptive information have been proposed. The contemporary view proposes that PNF stretching influences stretch perception or toleration (Magnusson et al, 1996), however, the mechanisms behind these changes are yet to be discovered, although pain modulation has been suggested. Other possible mechanisms have been speculated:
- Distraction that increased stretch tolerance
- Analgesia following sustained isometric contraction thus increased stretch tolerance
- Changes in viscoelasticity of the muscles induced by PNF
A study by Konrad et al. (2014) from Austria evaluated a six-week stretching program (including static, ballistic, or PNF stretching) on the various parameters of the gastrocnemius muscle and the achilles tendon. Several functional (Range of Motion, maximum voluntary contraction, etc.) and structural (fascicle length, tendon and muscle stiffness, etc.) parameters were evaluated. They showed that PNF increases ROM and decreases tendon stiffness. All stretching intervention increased ROM. However only in PNF stretching, structural changes (decrease of tendon stiffness) were observed. However, the decrease in tendon stiffness could not solely explain the change in ROM. Thus, Konrad and Tipp (2014) concluded that the increased ROM due to stretching was most likely due to increased stretch tolerance possibly due to adaptations of nociceptive nerve endings.
Although there are still controversies behind the mechanisms underlying PNF, there is no doubt on its efficacy. Sharman et al. (2006) recommended the following:
“PNF techniques that are more effective utilise a shortening contraction of the opposing muscle to place the target muscle on stretch, followed by a static contraction of the target muscle. The inclusion of a shortening contraction of the opposing muscle appears to have the greatest impact on enhancing ROM. When including a static contraction of the target muscle, this needs to be held for approximately 3 seconds at no more than 20% of a maximum voluntary contraction. The greatest changes in ROM generally occur after the first repetition and in order to achieve more lasting changes in ROM, PNF stretching needs to be performed once or twice per week.”
References
Chalmers, G. “Strength training: Re‐examination of the possible role of golgi tendon organ and muscle spindle reflexes in proprioceptive neuromuscular facilitation muscle stretching.” Sports Biomechanics 3.1 (2004): 159-183.
Hindle, K., et al. “Proprioceptive neuromuscular facilitation (PNF): Its mechanisms and effects on range of motion and muscular function.” Journal of human kinetics 31 (2012): 105-113.
Konrad, A., M. Gad, and M. Tilp. “Effect of PNF stretching training on the properties of human muscle and tendon structures.” Scandinavian journal of medicine & science in sports (2014).
Konrad, A, and Markus T. “Increased range of motion after static stretching is not due to changes in muscle and tendon structures.” Clinical Biomechanics (2014).
Lederman, E. Therapeutic Stretching in Physical Therapy: Towards a Functional Approach. Elsevier Health Sciences, 2013.
Magnusson, S. P., et al. “Mechanical and physiological responses to stretching with and without preisometric contraction in human skeletal muscle.” Archives of physical medicine and rehabilitation 77.4 (1996): 373-378.
Markos, P. D. “Ipsilateral and contralateral effects of proprioceptive neuromuscular facilitation techniques on hip motion and electromyographic activity.” Physical therapy 59.11 (1979): 1366-1373.
Osternig, L.R., et al. “Muscle activation during proprioceptive neuromuscular facilitation (PNF) stretching techniques.” American Journal of Physical Medicine & Rehabilitation 66.5 (1987): 298-307.
Sharman, M., et al. “Proprioceptive neuromuscular facilitation stretching.” Sports medicine 36.11 (2006): 929-939.
Shrier I. “Does stretching help prevent injuries?” In: MacAuley D, Best T, editors. Evidence-based sports medicine. London: BMJ Publishing Group, 2007.
Wilkinson, Andrew. “Stretching the truth. A review of the literature on muscle stretching.” Australian Journal of Physiotherapy 38.4 (1992): 283-287.