Gregory Gordon, MA
By far, the most commonly asked question we get from our clients here at E-I HQ is “What do you think about stretching?” This is totally understandable. Over the past ten years, there has been a steady, if temperate, increase in media reports questioning stretchings efficacy. Usually followed by an article demonstrating the ten best stretches to do at your desk. In the same periodical. Combine that with the fact that most of us have been told that we need to stretch for general health daily since toddlerhood, it is not surprising that confusion abounds. As an education company we felt that it would be helpful to put out a position statement for our clients and colleagues to clarify where we currently stand, based on our current understanding of the multiple elements involved to help provide a Northstar to those who might be looking for one. This four part position statement will cover Background, Stretching Taxonomy, Areas of Controversy/Concern and finally our general recommendations.
When discussing anything related to stretching, first, it must be understood that there are at least 4 recognized categories of stretching; ballistic, dynamic, static, and contract/relax (PNF). These categories also each have subtypes which include different application nuances. So, to bring any reasonable degree of specificity to the conversation as to stretchings potential risks or benefits, the stretching domain first needs to be identified.
Then it should be clarified as to why someone is stretching; what problem are they attempting to solve? Prevent injury? Reduce pain? Most commonly, our clients tell us they stretch to increase a perceived lack of joint range of motion. Understanding the intended goal is critical towards determining whether an individual is making appropriate choices to achieve it.
Broadly, all categories of stretching can be beneficial for increasing blood flow to an area (Hotta et. al 2016, Kruse et al., 2016), reducing acidic ph of muscle (Butler, 2000) temporarily increasing range of joint motion (behm et al., 2016) with static stretching also demonstrating decreases in joint stiffness (Nakamura, 2012) and increases in muscle tissue length (Blazevich et al. 2014).
Historically there have been two major schools of thought as to how stretching actually works to increase joint range of motion; Stretch Tolerance and/or neurological gating mechanisms.
1-Stretch Tolerance- Stretch tolerance is the phenomena which happens when an individual is actually able to increase the joint range of motion (ROM) without a concomitant reduction in joint stiffness. Stiffness is the amount of resistance the joint offers or the amount of force necessary to move a joint. Magnusson et. al, performed several studies where individuals were able to achieve greater degrees of joint ROM without a reduction in the torque necessary to achieve the position. The term to describe this is “stretch tolerance”. Stretch Tolerance suggests that the increase is due to an individual’s cognitive ability to better cope with the discomfort that accompanies the tissue tension at the end range of motion. As we know through pain science, pain is based on context, pain affects every region of the brain, is not linear in its response, and many different variables can contribute to an individual’s ability to tolerate it (Butler and Mosely, 2016).
Thixotropic influence- Muscles are composed of long strands of proteins, bundled together and enveloped in concentric rings of connective tissue eventually called fascicles. A bundle of fascicles is what eventually creates a muscle. When a muscle contracts certain proteins form crossbridges, sort of like velcro, across each other which helps give the muscle some rigidity.
Muscles have a high fluid content (70-75%) composed of water and other solutions that give it a viscous nature. Viscosity is the friction produced by the concentration of fluids, think of coconut oil; becomes thick in colder temperatures (high viscosity) and liquid in heat (low viscosity).
The current viscosity of a muscle is dependent on its previous action. If it has been recently active through an applied stretch, the viscosity will decrease partially due to reductions in crossbridge formation (Hagbarth et al., 1987, Proske et al., 2014). Other fluid dynamics, such as an increase in blood flow to the working muscle can also help explain viscosity reductions in muscle after stretching (Kruse et al., 2016).
2-Neurological Mechanisms-Inside muscle, joint, skin and connective tissues are receptors that tell the Central Nervous System (CNS) about a wide range of stimuli; pressure, stretch, chemicals and vibration. There are also certain types of receptors; nociceptors, that relay any danger to the tissue they are embedded in. These receptors work via pumps which need to reach a certain threshold in order to fire off a “danger” signal to the CNS. These pumps have properties which can bring them closer or further away from firing via networks with other receptors that can excite or dampen their firing ability. When the CNS is in protection mode, it can lower the firing threshold of the danger receptors, causing them to fire off more easily. When the CNS is in safe mode, the danger receptor thresholds return to their normal state (Butler & Mosely, 2016). During “stretch tolerance” the individual may be dampening the ability of the danger receptor to fire because, due to the context, they enjoy the pain from the stretch because they believe it is doing them good, potentially increasing the threshold of danger receptors above normal levels to fire, reducing the pain perception as well.
Also, there are receptors in muscles and that communicate the current length of a muscle and the rate at which that length may be changing in a muscle as you move. These specialized receptors; muscle spindles (static and dynamic), will cause a simple muscle contraction when stimulated, like what happens when the doctor bangs his mallet on your knee. However, when a limb is held in the same position for an extended period of time (over 60 seconds), muscle spindle activity declines (for both types), and muscle relaxation occurs. In addition to receptors inside the muscle, there are receptors located in the tendon portion of muscle, golgi tendons (GTO) that relay tension being placed on the tissue. The excitation level of muscle spindles and GTO's are variable, and through repeated applications of a stimulus the CNS can cause responses can to become dulled and habituated or more easily excited by the forces being placed on muscle tissues. By manipulating the intensity, duration and frequency of a specific type of stretch intervention, a certain type of response can be facilitated.
And, now, for some new stuff...
3-Fascicle lengthening-Ok, this is where it starts to get interesting. Credit needs to go to the esteemed Greg Lehman (Greglehman.ca) for introducing this paper to me. Blazevich et. al (2014) was the first group to demonstrate that muscle length actually did increase after a three week, 2x a day stretching protocol. Interestingly enough, tendon length did NOT change. This is significant because the force the muscle generates gets transferred to the tendon, and then to the bone. If a tendon where to increase in length and lose some of its stiffness, it’s ability to transmit force to the bone would decrease. This study demonstrated that the muscle-tendon unit’s (MTU) ability to produce maximal force and maximal rate of force development was un-altered after the stretch treatment. This data, in addition to ultrasound imaging, demonstrated an almost 20% increase in muscle length. It is speculated by authors that different muscles may react differently to stretch based on composition, location, fiber arrangement & tendon length, but, nonetheless, these are very interesting & promising findings.
1)Blazevich, A D. Cannavan,2 C. M. Waugh,3 S. C. Miller,3,4 J. B. Thorlund,5 P. Aagaard,5 and A. D. Kay6 (2014) Range of motion, neuromechanical, and architectural adaptations to plantar flexor stretch training in humans. Journal of App Phys, 117: 452-462
2)Butler, D. (2000) The sensitive nervous system. Pain Mechanisms and Peripheral Sensitivity pg 46-68
3)Butler, D, Mosely, L (2016) Explain Pain Supercharged. Supercharge your pain biology pg 37-77
4)Behm, D, Blazevich, A, Kay A, McHugh, M (2014) Acute effects of muscle stretching on physical performance, range of motion, and injury incidence in healthy active individuals: a systematic review. J Strength Cond Res
5)Kruse, N, Sillet, CR, Scheuerman, B (2016) Influence of passive stretch on muscle blood flow, oxygenation and central cardiovascular responses in healthy young males. Am J Physiol Heart Circ Physiol. 310(9):H1210-21
6)Nakamura, M, Ikezeo, T, Takeno Y, Ichihashi, N (2012) Effects of a 4-week static stretch training program on passive stiffness of human gastrocnemius muscle-tendon unit in vivo. European J of App Phys. Jul;112(7):2749-55.
7)HagbarthJ. V. HägglundM. NordinE. U. Wallin (1988) Clinical Aspects of Sensory Motor Integration. Advances in Applied Neuroscience (vol 4) pg 91-97
8)Proske, U (2014) Muscle thixotropy as a tool in the study of proprioception. Experimental Brain Research. Volume 232, Issue 11, pp 3397–3412