It’s well documented that several weeks of stretching exercises result in a permanent increase in joint range of motion. However, the mechanism behind this change in flexibility achieved from stretching is not clear. Several theories have been proposed to explain this observed increase in muscle extensibility. Many of these theories suggest a change in the properties of the stretched muscle. Recently, a sensory theory has been proposed suggesting that increases in muscle extensibility are due to changes in a person’s stretch tolerance rather than any change in the muscle tissue itself.
A complete review of the different theories on stretching and a more detailed explanation of the senory theory can be found here.
There are several problems with the sensory modification theory that I haven’t seen addressed and that is the basis of this article.
The sensory theory is based on evidence from studies that showed despite increases in flexibility after regular stretching there was no change in muscle stiffness. Basically, the people that stretched were able to move into a greater range of motion after completing a stretching program, but more force was required to move them to that increased range. Consequently, there was no shift in the torque/angle curve plotted from the measurements taken.
The proponents of this theory claim that a change in muscle length would result in a right shift in the passive torque/angle curves of the muscles being tested.
Below is an example of a torque/angle graph:
A shift to the right in the torque/angle curve is often seen after a single bout of stretching. This means that after stretching the muscle will stretch farther than before, if the same amount of force is applied. This is what a right shift in the curve looks like:
A right shift in the curve after a single session of stretching is thought to be caused by temporary changes in the viscoelastic properties of muscle, and not permanent deformation of the stretched tissue.
Because this right shift is not seen after weeks of regular stretching, some investigators have taken this to mean that the increase in flexibility cannot be coming from a change in the length or other properties of the muscle tissue and therefore must be the result of increased tolerance to the sensation of stretch. This is where I believe a mistake is being made.
Problems with the Stretch Tolerance Theory
There are several problems when trying to accurately measure muscle and joint stiffness in live subjects. Torque/angle curves only represent an estimation of the elongation/load of muscles being stretched. Many of the assumptions made for testing the mechanical properties of traditional materials are not valid when testing biological soft tissue samples.
Proteins, cells, and tissues are not homogeneous and have a wide range of material structures and properties. Muscle is also biologically active tissue capable of generating and modifying passive and active resistance to tensile forces.
Unique Properties of Muscles
In addition to the passive tension arising from various components of muscle tissue and tendons, muscles also have the ability to generate active tension. As one author wrote in an article on the biomechanics of stretching:
Active and passive tension cannot be considered separate structural elements of muscle because the connective tissue matrix of muscle is quite complex (within muscle and between muscles in anatomical compartments) and actin cross-bridges have elastic properties.
A highly complex structural arrangement of cells within and around muscles and numerous molecular interactions influence the stiffness of a muscle. These properties cannot be accounted for by simply examining the tension/length graph of a muscle or joint being stretched. The contractile elements of muscle (myofibrils), other proteins housed within muscles cells (e.g. titin), and extracellular structures all have an influence on the stiffness of a muscle.
Muscle Length Changes in Past Research
The conclusion that muscles do not adapt to stretching because no change in the muscle’s stiffness is measured is a large leap, and not consistent with a lot of what is known about how muscles respond to stretch. Animal studies have extensively shown that muscles lengthen as the result of stretching by the addition of sarcomeres in series. Sarcomeres are the basic units of muscles. The addition of sarcomeres theoretically increases the length of muscles. I’ve seen claims that stretching studies done with animals can’t be generalized to people because the growth potential of animal cells is different than human cells. While this is true for some animals, this lengthening of muscle tissue has been observed in skeletally mature animals as well. Additionally, stretch-induced hypertrophy has been documented in denervated (without nerve supply) muscles–further suggesting the passive tension, not neurological input, is the driving factor for growth.
Instead of viewing the addition of sarcomeres in series as increasing length, a more accurate way of thinking of this can be that the added sarcomeres increase a muscle’s potential to generate force at longer lengths. It could be argued that our bodies have a strong incentive to limit our flexibility to the extent a muscle can stretch while still having the potential to contract. The pain that controls the limits of how far we allow a joint to stretch is a neurlogical safeguard–a warning from the nervous system that if we keep pushing bad things might happen.
Because of obvious ethical and practical concerns, the research on which the sensory theory is based did not examine the muscle tissue after stretching to look for changes. It seems more reasonable to think similar adaptations take place in human muscle tissue than to assume they don’t without looking for them. Someday I’m sure we will have the technology to better investigate tissue properties in vivo.
Currently we have a good understanding that muscles have the ability to grow in response to resistance training. In humans, the ability of muscles to adapt to stretch is the basis for a number of surgical procedures like limb lengthening and strabismus correction.
Muscle Tissue Change without Torque/Angle Curve Shift
Past studies on animals have also shown that it’s possible for sarcomeres to be added to a stretched muscle without producing a change in the passive torque/angle curve 1,2. Researchers in those studies suggested that any association between the sarcomere number changes and the passive length-tension changes is not likely a direct one. These findings directly refute the main argument for the sensory theory.
A left shift (stiffening) has been observed in muscles that were immobilized in a shortened position, indicating the muscle itself had shortened. However, this was thought to be more due to an increase in connective tissue infiltrating the muscles rather than the decrease in the number of sarcomeres.
Additionally, at least one stretching study did show a right shift in the toque/angle curve that occurred after stretching, indicating there was a change in the mechanical properties of muscle as a result of stretching.
The proponents of the sensory theory suggest this result may have been due to the vigorous stretching protocol used in that study (5 days per week for up to 20 minutes). Even if these changes were the result of aggressive stretching, in excess of what most people would perform, taken together with the other points mentioned we have to consider that the sensory modification theory is not wholly accurate.
One explanation for why no shift is seen in the torque/angle curve in some of these human studies is because, in addition to a lengthening of the muscle tissue (by the addition of sarcomeres in series), there was a concurrent increase in the cross sectional area of the muscle. Potential changes in the cross sectional area of the muscles being stretched was not accounted for but would have an impact on the calculation of passive muscle stiffness.
Also not accounted for were possible changes or remodeling of the connective tissue in and around the muscles. If a muscle is being lengthening through the addition of sarcomeres, it’s possible a related change occurs in the structural components of the muscle tissue to allow it to maintain a constant resistance to stretch.
Mechano-signal transduction has been suggested for a number of years to contribute to exercise-induced muscle growth (5). The transmission of tension across the cytoskeleton structure of the muscle has the ability to influence changes in gene expression and activation of various signaling mechanisms. Many changes can occur at the tissue level that would have an effect on the measured viscoelastic properties of a muscle being stretched.
There are also the inherent properties of muscle tissue, many of which are still not entirely understood, that allow it to resist being stretched and control extensibility. These properties are not accurately assessed by simply looking at torque and joint angle.
Stretching is complex and not entirely understood phenomenon. The increase in range of motion seen after passive stretching likely involves the contribution and interaction of biomechanical, neurological, and molecular mechanisms. The problem with the sensory theory is that it makes a faulty assumption based on the interpretation of torque/angle measurements and discounts evidence of the biomechanical and molecular influences on flexibility.
I would not go so far as to say stretch tolerance and the nervous system plays no role in altering flexibility. The sensory theory however downplays the ability of muscles to adapt to mechanical stimuli. Muscles grow in response to tensile forces happens during resistance training. It doesn’t make sense to rule out their ability to adapt in response to tensile forces applied with stretching like the sensory theory proposes.