I’ve googled for SPS and Progressive Stretch relaxation. Pretty much all I come up with is that there is too little research to say that Dynamic Splinting is superior to SPS (or the other way around). Sunshinekid gets to correct me if need be, but I understand that progressive stretch is used a lot in manual therapy, and is considered good. It is the use of mechanical devices that is not researched (random trials etc) enough.
Here is an excerpt from AETNA http://www.aetna.com/cpb/data/CPBA0405.html
Published reports of the effectiveness of JAS splints are limited to case reports and small uncontrolled case series. There are no prospective randomized studies demonstrating that the addition of the use of JAS devices to the physical therapy management of patients with joint injury or surgery significantly improves patient’s clinical outcomes. Thus, JAS splints are considered experimental and investigational.
I can’t find anything on whether or not any of the stretch methods means that the tendons grow in length or if they are stretched (except for claims made by JAS, who sell SPS stretchers and their competitor Flexionator). I did find a note about growth of muscle however - and that the muscle growth likely took place in the narrowing section close to the tendons.
Here http://www.ptjournal.org/PTJournal/…1/v81n2p819.cfm they claim that (this is a long article and there is a lot I didn’t quite understand):
Some examples of stretch-induced myofibrillogenesis come from an orthopedic procedure in which the muscle is indirectly lengthened (distraction osteogenesis).32-34 If the extensor digitorum lateralis muscle is lengthened 3 mm (by distraction in rabbits), laser diffraction studies show an increase in sarcomere length from 3.1 to 3.5 µm.35 When that stretch is maintained for several days, the sarcomere length returns to a value of 3.1 µm, suggesting the addition of sarcomeres. Similar observations were made in muscle when the joint was immobilized in different positions.36-38 The investigators who documented these observations also noted that when muscles are immobilized in a stretched position, they initially undergo less atrophy than when muscles are immobilized in a shortened position. These observations have led to a stretch-induced hypertrophy hypothesis. This hypothesis states that, if stretched, a muscle responds by adding more sarcomeres.32,39,40
Some researchers36-38,41 have suggested that stretch-induced hypertrophy occurs at the fiber ends (toward the insertion into the tendon) of the muscle. This adaptation of muscle (ie, making more sarcomeres in series, thus creating a longer muscle by myofibrillogenesis) provides the theoretical basis for a new treatment for strabismus.42 A surgical technique entails the shortening of the rectus lateralis muscle, leading to a lengthened rectus medialis muscle. Both muscles, in theory, adapt to the new length, and, ultimately, similar sarcomere lengths and contractile properties are found in both muscles.42 To summarize, there are a number of experiments that support the concept that sustained passive stretch leads to the generation of a longer and functionally intact muscle, albeit by unknown mechanisms.
Growth factors and their cognate receptors. Another possibility of how muscle may adapt to passive stretch is based on the autocrine (ie, the muscle fiber itself) or paracrine (ie, the fibroblasts or other cells contiguous with the muscle fiber) regulation of muscle growth. Growth factors are molecules, secreted by cells, and have a potent biological activity.69-72 In addition to specific effects, growth factors, in general, stimulate cell proliferation.69-72 Several growth factors are involved in muscle development and have been identified. Insulin-like growth factor 1 (IGF-1),69,70 platelet-derived growth factor (PDGF),71 and fibroblastic growth factor (FGF)72 have been documented to stimulate either myoblast proliferation or, to a certain extent, muscle maturation.
The release of an IGF-1-like molecule from muscle fibers during passive stretch was described by Goldspink and colleagues,70 and these findings provide support for the theory that a similar mechanism might occur during the passive stretching of a muscle. Whether IGF-1 is directly involved in stretch-induced hypertrophy needs to be verified, and the molecular mechanisms of a stretch-sensitive increase in IGF-1 or other molecules during stretch-based rehabilitation protocols is not known. Insulin-like growth factor 1 (secreted with passive stretch)69 and PDGF (there are relatively more PDGF receptors at the myotendinous junction than at the nonjunctional membrane)71 are the likeliest candidates to regulate satellite cell proliferation during stretch-based rehabilitation. These growth factors could stimulate cell division of the myosatellite cells. The addition of more sarcomeres (ie, myofibrillogenesis) could be the result of the proliferating myosatellite cells, which have fused with preexisting muscle fiber cells. The proliferation of myosatellite cells is proposed to explain overload-induced muscle enlargement,73-75 and perhaps they could also be stimulated by passive stretch as it is applied therapeutically to function in a manner similar to how they behave during limb lengthening (growth).33 Such adaptation seems to occur preferentially at the distal portion of the muscle.34
Taped onto the dashboard of a car at a junkyard, I once found the following: "Good judgement comes from experience. Experience comes from bad judgement." The car was crashed.
Primary goal: To have an EQ above average (i.e. streetsmart, compassionate about life and happy) Secondary goal: to make an anagram of my signature denoting how I feel about my gains