Is Bob Wylie of the Cleveland Browns right about stretching? (If you don’t get the reference, watch this before proceeding) It’s known that prolonged static stretching reduces maximal force output in skeletal muscle, but why does this phenomenon occur? Here is a link to the study which may support our new favorite linemen’s coach’s strong opinion on stretching.
We often see static stretching performed by competitors prior to an event. “It is purported that stretching exercises could increase range of motion and decrease injury incidence, especially in high-intensity stretch-shortening cycle activities, by increasing the compliance of the muscle-tendon unit.” It is common place for coaches to recommend stretching prior to practice or competition, but is this a warranted suggestion?
“For example, static muscle stretching performed with total (i.e. accumulated) duration of 60 s or longer was found to elicit an average force reduction of 7.5% when testing was performed within a few minutes of the stretching, and longer-duration stretching has been shown to reduce force for up to 1 h or more.”
What is the mechanism behind this loss of force production?
It could be said that static stretching may influence the musculotendinous unit itself. This is hypothesized to decrease whole muscle-tendon unit passive stiffness decreases after static stretching- a spring that is not tightly coiled cannot reproduce force rapidly. Static stretching may “… affect the excitation-contraction (E-C) coupling process, reducing contractile force capability.” A study using rodent subjects saw an increase in myofibrillar calcium concentration, which was then associated with diminished contractile force. Again, this was seen in a study with rodents, but is yet to be proven in humans.
There may be a reduced efferent signal from the descending pathways (poor neural drive), which results in diminished voluntary contraction force. Previously, efferent neural drive has been recorded by measuring pre- and post-intervention EMG activity. “Nonetheless, it is critical to note that the reduction in electromyogram (EMG) amplitude may more broadly indicate either (or both) a decrease in efferent neural drive to the muscle or changes in post-synaptic potentials within the muscle, which typically result in a reduced force production.” This information does not give a precise location of where the neural drive activity is dampened- supraspinal, spinal, and/or neuromuscular synapses. EMG amplitudes are generally lessened after a static stretch, but studies have shown mixed magnitudes of decrement which could reduce the reliability of the mechanism of this hypothesis.
Supraspinal centers and decreased force production:
“From an exercise-related perspective, reductions in muscular force during and after continued activation of a muscle (i.e. muscle fatigue) have been shown to result from an inability of the descending supra-spinal drive to maximally activate the muscle’s motor neuron pool.” This has been observed after repeated and sustained-effort training/events which create high levels of fatigue. “For instance, an 18% decrease in maximal voluntary force was reported after running a marathon”. “The mechanisms underpinning this sub-optimal input from the motor cortex to the motor neuron are still unclear and need further investigation.”
Stretch-related mechanisms acting on the motor cortex:
“In 1953, Gellhorn and Hyde demonstrated that changes in muscle length could affect the extent of the cortical area from which a specific muscle could be activated via surface electrical stimulation. Moreover, evidence from animal and human experiments provides convincing evidence that stretch-sensitive afferent fibres project to the cerebral cortex.” It has been shown that certain muscle spindle fibers stem from the cortical areas which may shed a bit of light that on the relationship of muscle stretch and cortical activity (motor cortex / somato-sensory cortex). Also, skin and joint receptors project to the motor cortex via the thalamus, which may also affect cortical outflow. From this information, it is very reasonable to think that stretching may influence cortical activity, which can therefore alter subsequent force development.
Inhibition at the spinal level:
“For instance, structures such as muscle spindles, Golgi tendon organs and free nerve endings have been suggested as the most likely candidates to mediate the neural, and thus force, inhibition caused by passive stretching.”
Muscle spindles can sense both static and dynamic changes in muscle length. “Hence, it is possible that stretch-mediated reductions in the efficiency of the Ia afferent pathway to elicit excitatory postsynaptical potentials might arise from desensitisation of muscle spindles rather than pre-synaptic inhibition of Ia terminals and could impair the ability to develop PICs in spinal motor neurones and ultimately reduce the ability to produce maximal force.” Here, we have the concept of motor neuronal disfacilitation. Again, it is not clear where exactly this is happening (pre- or post-synaptic neurons), but we do know that it is happening.
A GTO is sensitive to active changes in force production sensed at the musculotendinous junction. It was proposed that a GTO may play a role in this stretch-force debate via autogenic inhibition, decreasing neural excitability, but there is currently a lack of evidence that this mechanism could result from a passive stretch (as opposed to active stretch).
Free Nerve Endings:
“Another interesting possibility is the involvement of free nerve endings, located at the muscle or connective tissue, in the process of muscle tension control. For instance, it has been shown that free nerve endings innervated largely by group II and III afferent fibres are sensitive to stretch. Moreover, it is thought that these free nerve endings are responsible for the clasp-knife reflex, which is a typical response in humans with spasticity, which promotes a fast reduction in the muscle’s passive tension in response to stretch . Interestingly, this inhibition lasts beyond the termination of stretch . It is therefore reasonable to speculate the involvement of free nerve endings in the force inhibition caused by passive muscle stretching; however, this assumption has not been verified…”
The existing literature points to a variety or neural mechanisms that are likely to contribute to the loss of force produced after a static stretch (of a minute or greater). Neural drive has been extensively reported, yet it is not clear where these reductions are stemming from (motor cortex, spine, efferent, etc.).
So, is the juice worth the squeeze? I think it is if you require a large range of motion that may be currently lacking. In (most) situations where this is not the case, I vote skip the static stuff and stay dynamic.
Consume more content by subscribing and sharing with peers.