The positive effect of static passive stretching on flexibility is undeniable, with studies reporting improvements in joint range of motion (ROM) following all types of stretching appearing ubiquitously throughout the scientific literature (Behm et al., 2016; Behm et al., 2021; Duong et al., 2001). In addition, researchers have posited various mechanisms underlying changes in flexibility in response to stretching over the years, which are discussed briefly in this post.
Stretch (Pain) Tolerance
For decades, structural changes in muscle fibre length were believed to be the primary mechanism for stretch-induced changes in flexibility. However, the lack of modifications in muscle stiffness following stretching in several studies led to the rise of an opposing theory, namely that increased ROM after stretching was primarily caused by alterations in stretch tolerance (Magnusson et al., 1996).
A stretch is initially uncomfortable because the central nervous system (CNS) interprets the signals transduced via mechanoreceptive cells in the tissues being stretched as a danger to the structural integrity of those tissues. Subsequently, the brain creates an output of brain that is associated with the amount of tissue deformation. Put differently, the greater the stretch, the more the CNS interprets tissue length as potentially risking injury to the health of the affected tissues.
When the same stretch is repeated over time - and the tissues are exposed to the same amount of deformation or change in length - the CNS realises that the health of the tissues is not at risk, so it lowers the threat value of the stretch. The result is decreased perceived pain, and a trainee can stretch further (Folpp et al., 2006; Ben & Harvey, 2010; Chan et al., 2002).
Human skeletal muscles display viscoelastic behaviour in response to tensile loads imparted by stretching, which is not influenced by reflex activity of the neural apparatus embedded within the muscle-tendon unit (Taylor et al., 1990; Ryan et al., 2012). Creep is a viscoelastic characteristic in which tissues continuously lengthen with time when a load (stress) is applied and held constant.
It is a rheological property (i.e., stress-strain relationships) and a key feature of living cells that enables them to adapt to external stresses and varying mechanical properties of their environment. Researchers measure creep using a technique called rheometry, which involves stretching a single living cell between two glass microplates - one rigid and the other flexible - and the stiffness of the flexible plate is calibrated such that the researchers can calculate the force applied to the cell by how much it causes deflection (bending) of the plate.
Zitnay and colleagues (2020) theorised that damage to collagen molecules is the principal mechanism for creep in tendons. When tissues display creep, they stretch further but will usually return to their original length some time after the tensile load is removed. Therefore, acute increases in ROM caused by tissue viscoelasticity are temporary, which helps to explain why flexibility tends to return to baseline levels after a single stretching application.
Stretch Reflex Inhibition
Stretching can influence afferent (sensory) inputs to the nervous system, which can change excitability in the brain and spine (Matthews, 1981). It is common to see authors claiming that static passive stretching always has an inhibitory effect on neuromuscular activity. However, reports of the effect of stretching on muscle activation as measured by surface electromyography (sEMG) are often contradictory.
For example, reductions in sEMG activity have been reported immediately after static passive stretching (Babault et al., 2010; Marchetti, 2022) and even up to 1 hour afterwards (Avela et al., 1999). However, other studies demonstrated no significant sEMG reductions after static passive stretching, even when stretches were held for significant durations of 2 minutes (Kay and Blazevich, 2009) or even 5 (Mizuno et al., 2014), 9 (Herda et al., 2008), or 10 minutes (Barbosa et al., 2019). The contribution of reflex modifications to increased flexibility in long-term stretch training is probably smaller than is often reported in the literature.
The increase in number of studies reporting no changes in muscle-tendon unit stiffness led to a concomitant growth of claims by health and fitness professionals that static passive stretching does not alter structural or morphological properties of musculoskeletal tissues.
However, it is worth considering that authors of many of the studies that reported no changes in muscle stiffness following static passive stretching failed to do two critical things: 1) they did not evaluate fascicle length with ultrasound imaging, and 2) they measured stiffness at short muscle lengths (changes in the length-tension relationship, and therefore stiffness, will be observable at long muscle lengths).
Several studies have reported observable changes in fascicle length, likely caused by longitudinal hypertrophy of muscle cells (Freitas and Mil-Homens, 2015; Simpson et al., 2017; Panidi et al., 2021). However, keep in mind that stretching adaptations are mostly neural in the first eight weeks of training, and thus architectural changes are presumably a chronic response to flexibility training.
There is no doubt that static passive stretching increases flexibility, but the underlying mechanisms are somewhat more contentious. Current evidence points to four primary ways in which stretching causes positive changes in ROM: 1) alterations in pain tolerance, 2) viscoelastic characteristics of skeletal tissues, 3) inhibition of neural reflex processes, and 4) muscle fibre longitudinal hypertrophy. Increased flexibility in the first 3 to 8 weeks is likely caused mainly by improved tolerance to the discomfort of stretching, with structural changes occurring much later.
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Barbosa, G. M., Dantas, G. A., Pinheiro, S. M., et al. (2019.) 'Acute Effects of Stretching and/or Warm-Up on Neuromuscular Performance of Volleyball Athletes: A Randomised Crossover Clinical Trial.' Sports Sciences for Health volume 16, number 1, pages 85-92.
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