Factors contributing towards stiffness
The definition of flexibility is the ability to move the limbs and trunk through a full range of motion with resistance. One of the main passive/non-contractile factors that influences the flexibility/stiffness of the body is the health and function of the connective tissues within and around muscle tissue (epimysium, perimysium and endomysium), tendons and fascial sheaths (deep and superficial fascia). Collagen is the primary structural component of living tissue and collagen fibres are the main constituents of ligaments and tendons. Increasing stiffness with age may be experienced because physical and biochemical changes take place as collagen ages, namely:
- Reduction in extensibility
- Increased rigidity
- Decreased lubrication due to loss of water in the tissues (from 85% in babies to 70% in adults).
Therefore movement will be increasingly limited as collagen ages.
Collagen is the main constituent of ligaments and tendons, which contribute 4% and 47% to total resistant to movement in a joint respectively. A key term used to describe the way collagen behaves is viscoelasticity. Viscoelastic tissues are made up of viscous and elastic properties; a viscous tissue will deform and stay deformed permanently whereas an elastic tissue will return to its original length when the force is removed.
The second most important factor in determining stiffness is the fascial connective tissue, which allows muscles to change length. The sum of the muscles fascia accounts for 41% of total resistance to movement.
When joints are immobilised for any length of time the connective tissue of the capsules, ligaments, tendons, muscles and fascia lose their extensibility due to a change in chemical structure, specifically a 40% decrease in hyaluronic acid and water. This is evident after immobilisation of a muscle for 4 weeks or longer. The fascia may thicken, shorten, calcify and erode and come in closer contact and eventually stick, encouraging the formation of cross-linking and loss of extensibility and increased tissue stiffness. Excessive training also causes more cross-linking to occur between collagen fibres.
Other passive restraints include the alignment of joint surfaces and other joint constraints e.g. capsules and ligaments. Furthermore, an increase in intramuscular fluid (fluid in the muscle cell) can increase stiffness due to a splinting effect.
The nerves passing through the limbs can also limit flexibility i.e. reflex responses that cause the muscle to increase resistance to a stretch. Certain neuromuscular mechanisms acting on the muscles influence ‘tension’ and have important implications for the value of stretching. These mechanisms include the stretch reflex, autogenic inhibition and reciprocal inhibition.
- The stretch reflex is governed by a long thin receptor in muscles called a ‘muscle spindle’. The spindle’s role is to let our feedback systems know about muscle length and the rate of muscle lengthening. When a muscle is rapidly stretched, the spindle (via a loop of nerves) triggers a reflex contraction of the muscle undergoing stretch. A high-speed stretch will therefore trigger the spindle and a reflex contraction of the muscle will limit its ability to stretch. Excessive repeated muscle contractions cause high volumes or neural discharge and a muscle can remain in a state of high resting tone following training sessions.
- The spindle is also responsible for the phenomenon known as reciprocal inhibition. What happens here is that if a muscle contracts, the opposite or antagonistic muscle will relax to allow the movement to occur without resistance. For example, if the quadriceps are contracted, the hamstrings should relax to allow the knee to straighten
- The Golgi tendon organ (GTO) is the important receptor to consider in ‘autogenic inhibition’. The role of the GTO is to provide information on tension increases in muscles. This tension can come from contraction or stretch. The GTO connects with a small nerve cell in the spinal cord that inhibits or relaxes the muscle where the GTO is found. The GTO will trigger if a stretch is sustained (for longer than six seconds) or if the muscle contracts forcefully.
These 3 mechanisms are the major factors involved in proprioceptive neuromuscular facilitation (PNF).
Methods for improving flexibility
We should be wary of increasing flexibility by trying to free up bony stops or loosening up cartilaginous restraints, joint capsules, tendons and ligaments. What we can do is lengthen nerves and the bellies of muscles, the two kind of extendible anatomical structures that run lengthwise through limbs and across joints. It is not enough to increase the length of muscle fibres alone; expansion of the connective tissue within and around the muscle is also needed. A program of stretching should be focussed towards elongating the fascia, the connective tissue that surrounds packets of muscle fibres and the wrapping of individual fibres. This stretching is most effective when stretching using a low force for long duration at higher temperatures as the connective tissue gradually follows the lead of the muscle fibres so the muscle as a whole gets longer and flexibility is improved.
The nervous system also plays a pivotal role in causing muscles to either relax or tighten up and this either permits stretch or limits it. Proprioceptive Neuromuscular Facilitation (PNF) is the optimal stretching method if the aim is to increase the range of motion. PNF uses the concept that muscle relaxation is fundamental to elongation of muscle tissue. In theory, it is performed in a way that used the proprioceptive abilities of the GTO and muscle spindle to relax or inhibit the muscle in order to gain a more effective stretch. It does so using autogenic inhibition and reciprocal inhibition.
PNF stretching exists in a number of different forms, including contract relax (CR), hold-relax (HR) and contract relax and antagonist contraction (CRAC) methods to name a few.
- Contract relax (CR) The contract-relax technique uses the development of tension in a muscle by isotonic contraction (i.e. where muscle tendons pull against bone to cause joint movement) to facilitate the relaxation and therefore stretch a muscle. By facilitating the relaxation of muscles we can improve circulation and improve extensibility of myofascial tissues. To accomplish this the muscle is placed in a maximally stretched position and resistance is applied to a muscle contraction of the muscle that is being stretched (direct contraction) or that muscles antagonist (reciprocal relaxation). Movement occurs during this contraction. Following this contraction the limb is relaxed and upon relaxation is actively or passively stretched further.
- Direct Contraction – For example, when stretching the hamstring, the hip is placed in 90 degrees with the person lying on his back. The knee is flexed against moving resistance isotonically and then relaxed. The hip held at 90 degrees, the knee is moved into its fully extended position so as to apply a stretch to the hamstring.
- Reciprocal Relaxation – For example, when stretching the hamstring, the hip is placed in 90 degrees with the person lying on his back. The knee is then extended against resistance, contracting the quadricep. The activity in the quadricep causes reciprocal inhibition of the hamstrings allowing for a greater stretch.
- Hold relax (HR) Very similar to contract relax as above, but the contraction type is static/isometric; Isometric exercises are static, meaning no joint movement is involved. The muscle to be stretched is passively taken to end of range. Maximum contraction of the muscle to be stretched is performed against resistance (usually another person). With this form of contraction, the muscle does not shorten during its isometric contraction. This is continued for at least six seconds (allowing autogenic inhibition to occur). The muscle is then relaxed and taken to a new range and held for about 20 seconds. This can be repeated 3-4 times
- Contract relax antagonist contraction (CRAC) The first part of this stretch is similar to the CR method above; however, when the muscle to be stretched is relaxed after its six second contraction, the opposite or antagonist muscle is contracted for at least six seconds (allowing reciprocal inhibition to occur). The antagonist is then relaxed and the stretched muscle is taken to a new range.
Essentially PNF can be utilised to achieve a deeper stretch and involved a shortening contraction of the opposing muscle to place the target muscle on stretch.
Increasing flexibility in a yoga class
A number of factors can facilitate Hatha yoga in order to improve flexibility and reduce stiffness:
Heat: Increase in temperature causes a decrease in muscle stiffness. When connective tissue is heated it becomes more viscous and adhesions between collagen layers are reduced, removing one of the major constraints of flexibility. This can be environmental temperature (e.g. heated room in Bikram yoga) or temperature increases induced by friction of muscle contraction e.g. dynamic ashtanga yoga practice.
Pace: Slow controlled stretching prevents over-lengthening ligaments and de-stabilising joints. Static stretching allows time for the relaxation response to establish and long slow stretching prevents the stretch reflex (causing the muscle to contract) being initiated too quickly ensuring the muscle can be stretched further. Greater peak tensions and more energy are absorbed the faster the rate of stretch. This means that a tissue will generate greater tension if the rate of stretch is faster and therefore not achieve the same length as a tissue undergoing a slow stretch.
Duration: It takes 12-18 seconds to reach stress relaxation so a stretch held between 20 and 30 seconds will be effective. It is important to note that there is an optimum window for achieving the most effective stretch; whilst a longer duration of stretch is directly proportional to being more effective, this is only applicable to up to approximately 30 seconds i.e. a 60 second stretch gave no greater gains in terms of improved flexibility compared to a 30 second stretch meaning that there is no evidence of an advantage in holding a static stretch for longer times.
Repetition: Evidence from studies on the cyclic loading of tissues suggest that the most deformation of collagen occurs in the first stretch and has shown that repetition of the stretch up to 4 times leads to increased flexibility compared to holding just once, however repetition of the stretch more than 4 times showed no further gain in flexibility as there is little change in ultimate length. Once elongated, length changes are not rapidly reversible due to the viscous nature of the tissue. However, deformations are not permanent because the elastic properties will eventually bring the tissue back to its original length. Lasting changes come from adaptive remodelling of the connective tissues, not mechanical deformation. One study in South Africa showed that stretching every four hours was the most effective way to achieve elongation in a muscle. This may suggest that the temporary change in length following a stretch may start to regress after four hours.