There are a wide variety stretching procedures and it can be confusing to figure out which is the most effective. Some  practitioners advocate a short duration stretch (about 2-3 seconds) as used in the Mattes method of Active Isolated Stretching (AIS). Others advocate a long duration of static stretching (15-20 seconds or more), as in practices such as yoga.

The research literature has studied stretching extensively but there is no conclusive evidence for a best stretching method yet. It appears that certain stretching methods work better in one situation while others work better in another. As I was doing some research on stretching recently it occurred to me that there are some additional factors in stretching that we may want to investigate.

In any stretching procedure there are two primary components that need to be addressed to effectively encourage muscle elongation. The first is a neurological component that governs the muscle’s resistance to stretch. It is here that the proprioceptors play a major role in stretching techniques. Techniques such as PNF or other facilitated stretching methods have been developed to focus on the neurological components of stretching.

Another factor in stretching is the mechanical elasticity of connective tissue (fascia) that surrounds muscles and bundles of muscle fibers. This connective tissue has a resistance to tensile (stretching) forces when those forces are rapidly applied. As you hold tensile force on this connective tissue, its resistance to stretching decreases. The decreasing resistance to stretch tension in connective tissue is a property called creep. Maximizing the effectiveness of connective tissue creep is an argument for a longer held stretch.

Recent research into the physiological properties of fascia have shown that it contains contractile cells. It has also been determined that a prolonged tensile force on connective tissue, such as that used in myofascial release or other fascial techniques, can cause a reduction in contractile activity in these fascial cells.

We now know that connective tissue elongation is enhanced by manual therapy methods of stretching fascia. We also know that connective tissue stretch (resistance to creep) is a limiting factor in stretching methods.  What if we were to combine the two and encourage use of these myofascial techniques on muscles as they were in their fully stretched position? I’m sure some practitioners must be doing this already, so it would be interesting to see some comparative studies performed on this method.

One of the great things about keeping up with current research is that it often causes us to change course and reconsider ways that we may have been treating various pathologies. While it is certainly frustrating to have to reverse something you have been teaching for years, it is actually refreshing to develop a better understanding of how the body functions. A colleague recently sent me a link to this article on the anatomy of the iliotibial band and it is one of those things that is a radical shift from our previous understanding.

Most of us who have been immersed in the field of orthopedics, sports medicine, and biomechanics have been talking for years about iliotibial Band (ITB) friction syndrome as a repetitive overuse disorder caused by excess friction between the distal ITB and the lateral epicondyle of the femur. However, now it turns out that this concept may be mistaken.

One of the common misconceptions of the ITB is that it is a single discrete band of connective tissue running down the lateral side of the thigh. Actually it is a thickened part of a fascial sleeve that surrounds the entire thigh (the fascia lata). The authors of this study investigated a number of cadaver specimens and live individuals with MRI and found some interesting new discoveries. Apparently the ITB is firmly anchored to the distal femur and does not rub back and forth across the lateral epicondyle of the femur as most of us have been describing it. In addition, they state that there actually isn’t a bursa under the ITB, as it is often described.

When the knee moves into flexion, there is a simultaneous internal rotation of the tibia. This internal tibial rotation puts increased tensile loads on the ITB. The authors suggest that the increased tensile load on the ITB further compresses it against underlying tissue. There is a layer of fatty tissue under the distal ITB that is richly innervated with Pacinian corpuscles. They suggest it is this increased compression against the fatty tissue that is the cause of the pain and not a bursitis or friction of the ITB against the femoral epicondyle.

So, now that we know this, how should we change treatment strategies? One would think that if the primary problem in this condition were additional compression of the ITB against underlying tissues, then further direct compression in this area would not be a good idea. The authors suggest that the primary problem originates with improper function of the hip musculature (which tensions the band). As a result, the primary treatment should focus much more on correct hip muscle function and not on treating the knee region. The article and abstract are located under this citation:

Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band during flexion and extension of the knee: implications for understanding iliotibial band syndrome. J Anat. Mar 2006;208(3):309-316.