In the previous article, we examined some of the current conceptions and misconceptions of flexibility training. This included a general appraisal of the available literature, suggesting that current techniques are in danger of losing sight of any real support, and concluded with information regarding the most accepted techniques. The purpose of this article is to venture deeper into the anatomy of stretching.
Why might this be important? There are two reasons; the first is that it is useful to know what we are really doing to a muscle, to ensure that what we are doing is as effective as possible. This will give support to our recommendations and make it easier to explain to others what we are trying to achieve and how. Secondly, if there is a risk of developing an injury, then we need to know how any microtrauma might be exacerbated by flexibility training. The primary purpose of this article is to examine anatomy for the purpose of the first reason. The next article will investigate the relationships between flexibility and injury risk.
When we prescribe a resistance training programme, or a resistance training component of a more holistic training programme, we can probably all impart varying depths of bewildering information to our clients regarding what actually occurs in the muscles. We might start by explaining that there are different types of muscle fibres, consisting of various exciting proteins, which we overload during the workout with the goal of instigating some degree of overcompensation. We might refer to recovery and overtraining, the need for proteins and energy, and the importance of a balanced exercise programme. But what do we bore our clients with when we are stretching them? Do we describe the fascinating and sexy world of Golgi tendon organs (GTOs), for example? I hope not, because we would probably be very wrong indeed, and the purpose of this article is to highlight just what is going on.
The Anatomy of Muscle Tissue
The muscle spindle is a mechanoreceptor, which responds to mechanical events within the muscle, and signals this information to the central nervous system. The spindles send messages to the Central Nervous System (CNS) regarding the absolute length and the velocity of stretch of the skeletal muscles. Once the nerve impulse travels to the CNS, the CNS sends a signal to the corresponding muscle, stimulating a contraction. This muscular contraction, known as the stretch- (or myotatic-) reflex, then inhibits the muscle from lengthening further. Although the muscle spindle is often thought of as a control system, it is more accurate to think of it in terms of a communication system, which signals information but does not in itself lead to a set reaction.
When a muscle is held in a stretched position for a prolonged period of time, the muscle spindles become desensitised, leading to reduced signalling to the CNS. This leads to the ability to elicit a greater lengthening of the muscle as the stretch progresses in duration.
The desensitisation of the muscle spindles permits a greater range in the muscle before the protective stretch-reflex inhibits further lengthening. This could be beneficial for martial artists, or other athletes, that require ballistic muscle lengthening during activity. For martial artists in particular, prolonged static stretching may then permit greater range on motion during ballistic stretching. The problem is that the stretch reflex is beneficial for preventing muscular injuries. Combined with proprioception, if a runner moves their ankle into excessive inversion for example, as their foot moves over an angled surface (or if a rock or something similar moves away underfoot), it is partly the stretch reflex which initialises the response in the muscles required to bring the ankle back into a safe position. If the muscles have been desensitised during prolonged stretching, then there is an increased risk of injury occurring during any following activity. This example is transferable to all sports or activities, so questions have to be raised as to how, when and why to stretch prior to specific physical activities.
Golgi Tendon Organs
The Golgi Tendon Organ (GTO) is located within the tendon, close to the musculotendinous junction. The GTO is hypothesised to act as a feedback monitor which sends signals to the CNS in response to tension. In contrast to the muscle spindles, the signal sent by the GTO to the CNS is suggested to result in an inhibition of the associated muscles.
Specifically, following six seconds of stretch, the GTOs are believed to send sensory impulses to the CNS which lead to an inhibition of the corresponding muscles. This inhibition, or reflex relaxation, allows the agonist muscle(s) to be stretched further, reducing the risk of damage. This demonstrates the possibility that stretching for a short duration, specifically maintaining a static stretch for less than six seconds at a time, is of little use. This is due to the inability of the GTOs to respond to the changes in length and tension.
This author should maybe apologise for the vagueness of the previous two paragraphs. But he is not going to. The reason for the lack of conviction is because we do not actually know to what extent the GTO is involved in normal human movement. Introductory exercise physiology and biomechanics textbooks generally suggest that GTOs inhibit muscle contractions when excessively high forces are detected. This is hypothesised to prevent any injury occurring in the muscle as it is subjected to very high forces. Several research studies also demonstrate a GTO-mediated reflex inhibition of an active muscle.
Although limited, data show that an all-encompassing role of GTOs (i.e., that activation of GTOs through muscle contraction results in inhibition of muscle activity), is not possible. There are no specific studies of GTO activation in humans, and the sweeping statements found in textbooks are mainly from studies of cat or rodent hindlimbs, often assessing GTOs via the direct stimulation of isolated sensory nerves. So, not only are the studies not on human subjects, but they are assessing nerve function in isolated muscles and nerves, through an artificial sensory stimulation. Thus, it may be some time before we can say for sure precisely what it is that the GTO does, and what other sensory apparatus are involved.
In summary, the current consensus is that GTO reflexes are not a simple predictable pathway that can be encompassed into a single statement, such as “GTO activation inhibits muscle contraction” (Chalmers 2002). The GTO may have a number of effects depending upon a number of variables (such as the task, the muscle activated, and input from other neural systems). Studies have only examined animal muscle and nerve function in isolation via an artificial sensory stimulation. No experimental studies in humans have examined the true roles of the GTO during natural movement.
One hypothesis regarding chronic lengthening of skeletal muscle tissue refers to the viscoelastic properties of the musculotendinous junctions. When a substance is exposed to a stretching force, then depending upon that particular material's properties, that substance will deform. When a relatively low stretching force is applied over a sustained period of time, then the deformation will tend to occur in a time-dependent manner. This behaviour is referred to as "creep" and is a result of the material's viscoelastic properties. When the force is no longer applied, then the material will return to its original length, also in a time-dependent manner.
Ultimately, skeletal muscle tissue has properties which can be described as viscous (i.e., where deformation is rate dependent) and elastic (i.e., where deformation is load dependent). In order to stretch a muscle effectively, a stretch needs to be maintained for an extended period, and then the stretch repeated for a number of sets. As the stretch progresses with time, the amount of progression from one set to the next decreases, as the muscle’s stiffness is overcome and total available length is approached. Once the muscle has been stretched in this way, it will then return to its normal length within one hour.
The increased range of motion observed following effective static stretching is the result of the viscoelastic properties of the corresponding muscles. This therefore presents a biomechanical rationale for the short-term changes in muscle length observed following a stretch. Any permanent increase in muscle length is the result not just of biomechanical but also biochemical and structural changes within the muscle, as might be associated with an increase in the number of sarcomeres in series. Thus, the temporary increase in muscle length following static stretching, when repeated a few times a week over several weeks, signals an alternative response which leads to a more permanent increase in muscle length. This response, however, is not related to the muscle’s viscoelastic properties, but to the physical apparatus of the muscle fibre itself.
Muscle fibres are dynamic structures capable of changing with stress. The number of sarcomeres in series determines the distance through which the muscle can shorten during normal limb movement. It is then the job of the tendon to determine when the individual sarcomeres are lengthened to an extent that enables them to exert their maximal tension. Deliberately stretching a muscle pulls the sarcomeres to a length whereby there is insufficient overlap of myofilaments for maximum tension to be developed. Therefore, chronic stretching of muscles can theoretically lead to an increase in the total number of sarcomeres. By increasing the number of sarcomeres, the muscle will be longer with sufficient overlap of myofilaments, and thereby be able to exert maximal tension at an increased length. Not only that, but the total distance that the muscle can be stretched to will also be greater, so absolute joint range of motion (ROM) will also be improved (it is worth pointing out that ROM is affected by both muscle length and joint integrity, but we are interested only in ROM due to muscle length in this article).
In order to increase the length of a muscle fibre and therefore the number of sarcomeres, a process known as myofibrillogenesis, and a number of other processes have to take place. Passive stretching of the connective tissue (endomysium and perimysium, specifically) has to be sufficient to induce signal sensing and signal transduction within the associated muscle fibres. This then leads to gene transcription. Once this has occurred, it is then possible for new sarcomeres to be assembled from available proteins. In other, nicer words, there are a number of biochemical changes that need to be induced by stretching for muscle lengthening to result. What is key to understand is that although in the studies reviewed, the process pointed to this exact process having taken place, the problem was that the studies examined animal subjects rather than humans. It is therefore down to the reader to decide whether this scenario is compelling enough to take as read, but further research is definitely required to show that this process occurs in a similar manner in human muscle tissue.
The studies also examined the muscle length following prolonged stretching over and above what would occur in human studies. What human studies have shown us, however, is that muscle length can be chronically increased following several sets of static stretching, of appropriate duration (30 seconds per set seems to be the common recommendation), over a few days a week, for a period of four or more weeks. It seems likely that the chronic lengthening seen in the human studies, and the chronic lengthening seen in the animal studies, are both due to the same thing: an increase in the number of sarcomeres in series along the stretched muscle(s).
When discussing flexibility, it is necessary to understand the anatomy and physiology of stretching, something that very few fitness professionals really understand. We should not be concerned with describing what we do not really know, such as to the degree of involvement in human movement of the Golgi Tendon Organ, but rather we should concentrate on what we do know. We know that muscle tissue has viscoelastic properties. This tells us that when we stretch a muscle effectively, the muscle will eventually return to its normal length, and we know that this will happen within about an hour. We know that muscle spindles can become desensitised, and we should therefore be conscious about prescribing stretching to athletes prior to competition or arduous training. We also know that holding a stretch for a while (such as 30 seconds), for a few sets (somewhere in the region of three to five), and repeating this three times a week for four or so weeks, leads to a permanent lengthening of the muscle fibres. It is likely that this lengthening is due to the increase in sarcomere numbers in series along the fibre, but we are not too sure, so we won’t shout about that too loudly just yet.
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