Body Tempering (BT) is a soft tissue treatment technique developed by Donnie Thompson in 2014 (1,2) that involves deep and heavy pressure to muscles using weighted steel cylinders that are held statically on or moved slowly along the length of a muscle (1,2). BT has been shown clinically to be beneficial for athletes, as it provides an alternative to traditional stretching, foam rolling, and deep tissue mobilization to facilitate repair of muscle strains, improve soft tissue extensibility, and reduce pain (1-5). BT has also been shown to improve soft tissue elasticity for load absorption, thus reducing the risk of soft tissue injury (1,3,6). BT may also help reduce overloading of “Cinderella fibers” (7) by improving the load tolerance/absorption6 of neighboring fibers, thereby reducing muscle fatigue and spasm (7). Furthermore, after comparing BT, foam rolling, and TheraGun for muscle recovery, only athletes that received BT improved their vertical jump performance post-treatment (5). Moreover, athletes that received BT reported feeling more relaxed, as they experienced less soreness than the two comparison groups (5).
BT appears to help prepare soft tissue for activity and improve muscle recovery, with longer-lasting results than static stretching, massage, or other soft tissue interventions (1,2,4-6,8). BT has become increasingly popular, particularly among athletes, (1-4) and it was recently credited with reducing soft tissue injuries in professional football (i.e. NFL) players by 30% during the 2017-2018 season (1,3). Notably, while improvements in pain, soft tissue extensibility/relaxation, circulation, hydration, recovery/tissue repair, and enhanced proprioception are all considered goals of BT,(1,2,4) the physiologic mechanisms associated with the improvements following the use of BT remain to be elucidated.
Body tempering attempts to rapidly apply intense loading of soft tissue structures, both statically and dynamically, in order to achieve active and passive elongation (1-4). Based on the local and systemic effects of BT, there are likely several physiological processes at work (1,2,4,5).
Although not yet specifically investigated, BT may initiate descending supraspinal mediating effects so as to ultimately improve psychological aspects of pain, such as fear-avoidance (9). Additionally, the intensive nature of BT likely stimulates the periaqueductal gray similar to manual therapy, thereby initiating Diffuse Noxious Inhibitory Controls (DNIC) to reduce pain and sympathetic activity along with temporal summation in the dorsal horn of the spinal cord (9). As such, and like other forms of instrument-assisted manual therapy, BT may lead to changes in motor neuron pool activity, afferent discharge, and muscle activity changes (9). Manual therapy has also been shown to cause a reduction in blood-serum cytokines, as well as an increase in anandamide, endogenous cannabinoids, N-palmitoylethanolamide, Beta-endorphins, and serotonin (10,11). Soft tissue manual therapy has also led to a reduction in substance P, thereby reducing inflammatory processes related to exercises (12,13). Given that BT and manual therapy likely target similar tissues (albeit one uses heavy steel instruments and the other uses the hands directly), it is possible that both techniques function through the same neurophysiologic pathways (5).
BT may be used to target and release painful myofascial trigger points (MTrPs) and fascial perforation, points where there is compression of nerves and vascular structures (14). As a result, enkephalins are released, which counteract substance P and other pain-associated neuropeptides (9), which can be instrumental in combating chronic pain (8,15). Therapeutic loading of soft tissues causes an immediate effect on neurobiologic receptors and promotes long-term fibroblastic synthesis of proteoglycans and collagen.16 The mechanical loading of soft tissue structures also likely improves the motion of collagen fibers, thereby reducing the likelihood of developing irregular cross-links between fibers and other macromolecular aspects of the extracellular matrix (16). Nevertheless, both efficacy and mechanism trials are needed to test these hypotheses in individuals with chronic myofascial pain syndromes following the application of BT.
The mechanical loading and stress applied using BT may cause a cellular response and structural change to the soft tissues via mechanotransduction (17,18). Mechanocoupling occurs when the weighted tempering rod causes a direct physical perturbation of cells in musculoskeletal tissue via shearing and tensile loading (17). The demand placed on the soft tissue leads to the release of signaling proteins (such as inositol triphosphate and calcium) across gap junctions to neighboring cells, allowing for a cascade of cell-to-cell communication and new signal registration distally (17,18). An ensuing effector cell response likely occurs in two ways. The integrin proteins stimulate the cell’s cytoskeleton, which is in direct physical communication with the nucleus (18), and activate biochemical signals that influence gene expression in the nucleus (18). As a result, transcribed mRNA is sent to the endoplasmic reticulum to stimulate protein synthesis. The new proteins are then incorporated into the extracellular matrix, leading to tissue remodeling (18,19). The adaptation and addition of collagen fibers leads to a stronger musculoskeletal system relative to the amount of load (weight of the tempering rods) applied (6,8). Furthermore, mechanical overload leads to upregulation of insulin-like growth factor, mechanogrowth factor, chondrocytes, and osteocytes in local and distal muscle (20,21), bone (22), tendon (23-29), and articular cartilage (30). Even while immobilized due to a fracture, mechanotransduction can be initiated via vasopneumatic compression and has been shown to improve strength and ROM by up to 26% and 14%, respectively, for up to 10 weeks (18,22).
Dynamic BT also likely causes thixotropy, a reaction in which ground substance transitions from a viscous to fluid state via kinetic energy (8,31,32). This results in improved hyaluronic acid lubrication, vascular endothelial function, decreased smooth muscle tension, release of nitric oxide concentration, and rehydration (restoring interstitial fluid content) (8,25). BT also likely stimulates piezoelectricity, an increase in electric charge in response to mechanical loading that reduces viscosity and increases the rate of a fibroblast’s collagen fiber production (8). Furthermore, BT may provide extrication of adhesions/fibrocartilage blocks and stimulate sympathetic and parasympathetic activity, which leads to vasodilation (6,34,35).
Techniques such as stretching and massage are unlikely to cause forces that surpass the elastic limits of connective tissue (i.e. the top region of stress/strain curve) (6). As a result, the tissues will gradually return to their initial resting length once the load is removed (6). This could explain the apparent transient therapeutic benefits of techniques such as foam rolling (36). Importantly a low level of connective tissue damage (i.e. microfailure) is necessary for plastic deformation and permanent changes in length (6,8). Permanent tissue elongation is initiated at the end of the linear phase of the stress-strain curve (3% strain) but at less than 8% (macrofailure) (37). At about 224 to 1136 N (i.e. 53 to 253 pounds), connective tissue experiences microfailure, as broken fibers will not recoil (6). As a result, a new, balanced relationship is established between the elastic recoil of intact collagen, resistance of glycosaminoglycans, and intrinsic tissue water (6). Notably, fibroblastic proliferation requires extreme pressure (1.5 N/mm2 or 210 PSI) via Graston techniques (38). Body tempering is capable of producing both tensile and shear stresses up to or greater than the weight of the cylinder applied, which ranges from 20 to 200 pounds (1), suggesting that BT may induce consistent tissue lengthening at an appropriate intensity (6,8,37). Similarly, the concept of force relaxation occurs when a tissue is stretched at a rapid rate until peak strain is achieved, at which point the tissue assumes a new resting length (8). The more rapid the rate of stretch, the larger the peak force, deformation length, and resulting relaxation of the soft tissue (37). This may explain the immediate changes in soft tissue extensibility and analgesia via BT, which are likely more robust than stretching (1).
Ischemic Compression-Induced Release
BT may be thought of as a progression from passive NDT/Bobath inhibitory pressure techniques (39-41) to ischemic compression-induced myofascial trigger point release (42-45) PNF hold/relax, and Active Release Techniques (46). Tempering rods are used as a tool to provide deep/heavy inhibitory pressures described by NDT (39-41) to reduce hypertonicity (47), and acts on the Golgi tendon organ, tactile receptors, and muscle spindles to reduce Type Ia/II afferents (8). Pressure via a weight over a tendon or muscle belly causes a dampening effect (8) to reduce abnormal tone that interferes with movement and restores normal alignment in the trunk and extremities by lengthening shortened muscles (48). The deep pressure of the weight also likely improves kinesthetic awareness via cortical homuncular re-education (neuroplasticity), muscle proprioceptors, and tactile receptors (9,14,39). Additionally, the consistent contact of the rod likely acts on the parasympathetic nervous system via slowly adapting tactile receptors, providing a calming effect and desensitization of the skin and underlying structures (9,14).
In short, static body tempering provides a form of ischemic compression or myofascial trigger point release (49,50). Ischemic compression is a sustained deep pressure with skin blanching to the trigger point of a muscle until it is no longer tender; furthermore, it has been shown to improve pressure pain thresholds, pain intensity, range of motion, and stretch perception (49,50). Therefore, BT is hypothesized to perpendicularly compress contracted sarcomeres, causing longitudinal lengthening of the sarcomere (44,51). Tempering pressures could elicit inhibition of both active and latent myofascial trigger points (44,51). Release normally occurs within 90 seconds, and the heavier the pressure (within limits of course!), the faster the release seems to occur (44,51). This may explain the rapid pain relief that has anecdotally been reported by many clinicians following the application of BT in individuals with a variety of chronic myofascial pain syndromes (1,2,4).
BT may also incorporate principles similar to Active Release Technique (52), whereby trigger or tender points are compressed while the involved muscle is taken through a sequence of passive and active shortening/elongation cycles (1). Like PNF (46), the movement involves isometric, concentric, and eccentric muscle contractions followed by relaxation and stretching (53). In a randomized, placebo-controlled study, treatment of myofascial trigger points with a variety of ischemic massage techniques demonstrated increased pain-pressure thresholds in the region of trigger points (53). The static use of BT over palpable, taut, ropey bands associated with trigger point formation likely therefore provides the same effect as manual compression or massage techniques but with increased reproducibility between patients and clinicians.
BT is a relatively new technique, and the full array of its physiologic mechanisms and effects on myofascial pain and athletic performance remains to be elucidated. High-quality empirical evidence is needed; nevertheless (3), randomized controlled trials are presently being conducted at the University of Texas Rio Grande Valley to investigate the effects of BT on performance of vertical jump, broad jump, and 1 repetition-max knee extension.
Dr. John Putnam, DPT, Cert. DN, Cert. SMT, Dip. Osteopractic
Owner and CEO, Back to You Osteopractic Physical Therapy & Rehabilitation
Fellow-in-Training, AAMT Fellowship in Orthopaedic Manual Physical Therapy
Royal Oak, MI
Dr. Clint Serafino, DPT, FAAOMPT, Cert. DN, Cert. SMT, Dip. Osteopractic
Senior Faculty, AAMT Fellowship in Orthopaedic Manual Physical Therapy
Dr. Raymond Butts, PhD, DPT, MSc (NeuroSci), Dip. Osteopractic
Senior Faculty, AAMT Fellowship in Orthopaedic Manual Physical Therapy
Dr. James Dunning, DPT, MSc (Manip Ther), FAAOMPT, MMACP (UK)
Director, AAMT Fellowship in Orthopaedic Manual Physical Therapy
1. Thompson D. Restorative Tissue Techniques, Body Tempering, Tissue Flossing and Strength Training. AAMT Fellowship Week 2 Intensive. August 2018.
2. Thompson D. Body Tempering. BodyTempering.com. https://bodytempering.com/body-tempering/. Published 2018. Accessed November 23, 2018.
3.Gray K. Team response to body tempering. September 2018. E-mail correspondence in regards to the Philadelphia Eagles’ response to the implementation of body tempering for warm up and recovery.
4. Duffin C. Why Body Tempering Works. elitefts. https://www.elitefts.com/education/why-body-tempering-works/. Published January 28, 2017. Accessed November 23, 2018.
5. Avalos C, Chapa C, Espinoza L, et al. Acute Effects of Recovery Methods on Delayed Onset Muscle Soreness in Males and Females. Department of Health and Human Performance, Graduate Thesis, THE UNIVERSITY OF TEXAS RIO GRANDE VALLEY, Brownsville, TX USA, May 6, 2018.
6. Threlkeld AJ. The Effects of Manual Therapy on Connective Tissue. Physical Therapy. 1992;72(12):893-902.
7. Treaster D, Marras WS, Burr D, et al. Myofascial trigger point development from visual and postural stressors during computer work. Journal of Electromyography and Kinesiology. 2006; 16(2), 115–124.
8. Schleip R. Fascial plasticity – a new neurobiological explanation: Part 1. Journal of Bodywork and Movement Therapies. 2003;7(1):11-19.
9. Bialosky JE, Bishop MD, Price DD, Robinson ME, George SZ. The mechanisms of manual therapy in the treatment of musculoskeletal pain: A comprehensive model. Manual Therapy. 2009;14(5):531-538.
10. Degenhardt BF, Darmani NA, Johnson JC, Towns LC, Rhodes DC, Trinh C, McClanahan B, DiMarzo V. Role of osteopathic manipulative treatment in altering pain biomarkers: a pilot study. J.Am.Osteopath.Assoc. 2007;107:387–400.
11. McPartland JM, Giuffrida A, King J, Skinner E, Scotter J, Musty RE. Cannabimimetic effects of osteopathic manipulative treatment. J.Am.Osteopath.Assoc. 2005;105:283–291.
12. Smith LL, Keating MN, Holbert D, Spratt DJ, McCammon MR, Smith SS, Israel RG. The effects of athletic massage on delayed onset muscle soreness, creatine kinase, and neutrophil count: a preliminary report. J.Orthop.Sports Phys.Ther. 1994;19:93–99.
13. Field T, Diego M, Cullen C, Hernandez-Reif M, Sunshine W, Douglas S. Fibromyalgia pain and substance P decrease and sleep improves after massage therapy. J.Clin.Rheumatol. 2002;8:72–76.
14. Schleip R. Fascial plasticity – a new neurobiological explanation Part 2. Journal of Bodywork and Movement Therapies. 2003;7(2):104-116.
15. Kovacs FM, Abraira V, Pozo F, et al. Local and remote sustained trigger point therapy for exacerbations of chronic low back pain: a randomized, double-blind, controlled, multicenter trial. Spine. 1997 Apr 1;22(7):786-97.
16. Lundon K. The effect of mechanical load on soft connective tissues. In Hammer W. Functional Soft-Tissue Examination and Treatment by Manual Methods, 3rd ed. Boston: Jones and Bartlett, 2007:15-30.
17. Wall ME, Banes AJ. Early responses to mechanical load in tendon: Role for calcium signaling, gap junctions and intercellular communication. J Musculoskeletal Neuronal Interact 2005;5:70–84.
18. Khan KM, Scott A. Mechanotherapy: how physical therapists’ prescription of exercise promotes tissue repair. British Journal of Sports Medicine 2009;43:247-252.
19. Alberts B, Johnson A, Lewis J, et al. Molecular biology of the cell. New York: Garland Science, 2002.
20. Goldspink G. Gene expression in muscle in response to exercise. J Muscle Res Cell Motil 2003;24:121–6.
21. Jarvinen TA, Jarvinen TL, Kaariainen M, et al. Muscle injuries: Optimising recovery. Best Pract Res Clin Rheumatol 2007;21:317–31.
22. Challis MJ, Jull GJ, Stanton WR, et al. Cyclic pneumatic soft-tissue compression enhances recovery following fracture of the distal radius: A randomised controlled trial. Aust J Physiother 2007;53:247–52.
23. Banes AJ, Tsuzaki M, Hu P, et al. PDGF-BB, IGF-I and mechanical load stimulate DNA synthesis in avian tendon fibroblasts in vitro. J Biomech 1995;28:1505–13.
24. Scott A, Cook JL, Hart DA, et al. Tenocyte responses to mechanical loading in vivo: A role for local insulin-like growth factor 1 signaling in early tendinosis in rats. Arthritis Rheum 2007;56:871–81.
25. Olesen JL, Heinemeier KM, Haddad F, et al. Expression of insulin-like growth factor I, insulin-like growth factor binding proteins, and collagen mrna in mechanically loaded plantaris tendon. J Appl Physiol 2006;101:183–8.
26. Heinemeier KM, Olesen JL, Schjerling P, et al. Short-term strength training and the expression of myostatin and igf-i isoforms in rat muscle and tendon: Differential effects of specific contraction types. J Appl Physiol 2007;102:573–81.
27. Olesen JL, Heinemeier KM, Gemmer C, et al. Exercise-dependent IGF-I, IGFBPS, and type I collagen changes in human peritendinous connective tissue determined by microdialysis. J Appl Physiol 2007;102:214–20.
28. Ohberg L, Lorentzon R, Alfredson H. Eccentric training in patients with chronic achilles tendinosis: Normalised tendon structure and decreased thickness at follow up. Br J Sports Med 2004;38:8–11; discussion 11.
29. Boyer MI, Goldfarb CA, Gelberman RH. Recent progress in flexor tendon healing. The modulation of tendon healing with rehabilitation variables. Journal of Hand Therapy. 2005;18: 80–5; quiz 86.
30. Alfredson H, Lorentzon R. Superior results with continuous passive motion compared to active motion after periosteal transplantation. A retrospective study of human patella cartilage defect treatment. Knee Surg Sports Traumatol Arthrosc 1999;7:232–8.
31. Twomey L, Taylor J. Flexion Creep Deformation and Hysteresis in the Lumbar Vertebral Column. Spine. 1982;7(2):116-122.
32. Juhan D. Job’s Body. Barrytown, NY: Station Hill Press; 1987.
33. Okamoto T, Masuhara M, Ikuta K. Acute Effects of Self-Myofascial Release Using a Foam Roller on Arterial Function. Journal of Strength and Conditioning Research. 2014;28(1):69-73.
34. Payrau MB, Quéré PN, Bois PD. Vascular Fasciatherapy Danis Bois Method: a Study on Mechanism Concerning the Supporting Point Applied on Arteries. International Journal of Therapeutic Massage & Bodywork: Research, Education, & Practice. 2011;4(4).
35. Uzer G, Manske SL, Chan ME, et al. Separating fluid shear stress from acceleration during vibrations in vitro: identification of mechanical signals modulating the cellular response. Cell Mol Bioeng. 2012;5:266–276.
36. Aboodarda S, Spence A, Button DC. Pain pressure threshold of a muscle tender spot increases following local and non-local rolling massage. BMC Musculoskeletal Disorders. 2015;16(1).
37. Butler DL, Grood ES, Noyes FR, Zernicke RF. Biomechanics of ligaments and tendons. Exerc Sport Sci Rev. 1978;6:125-81.
38. Gehlsen GM, Ganion LR, Helfst R. Fibroblast responses to variation in soft tissue mobilization pressure. Medicine & Science in Sports & Exercise. 1999;31(4):531-535.
39. Veličković T, Perat M: Basic principles of the neurodevelopmental treatment.Medicina 2005, 41: 112-120.
40. Kerem M, Livanelioglu A, Topcu M. Effects of Johnstone pressure splints combined with neurodevelopmental therapy on spasticity and cutaneous sensory inputs in spastic cerebral palsy. Developmental Medicine & Child Neurology. 2007;43(5):307-313.
41. Kramer P, Hinojosa J. Frames of Reference for Pediatric Occupational Therapy. Philadelphia: Williams & Wilkins; 1999.
42. Travel JG, Simons DG. Myofascial pain and dysfunction; the trigger point manual, vol. 1. Philadelphia: Williams and Wilkins; 1983 (19).
43. Dommerholt J. Trigger point therapy. In: Fascia: The Tensional Network of the Human Body. Churchill Livingstone; 2012:297-302.
44. Hains G, Descarreaux M, Hans F. Chronic Shoulder Pain of Myofascial Origin: A Randomized Clinical Trial Using Ischemic Compression Therapy. Journal of Manipulative and Physiological Therapeutics. 2010; 33(5), 362-369.
45. Hong CZ. Treatment of myofascial pain syndrome. Current pain and headache reports. 2006 Sep 1;10(5):345-9.
46. Sharman MJ, Cresswell AG, Riek S. Proprioceptive Neuromuscular Facilitation Stretching. Sports Medicine. 2006;36(11):929-939.
47. Park E-Y, Kim W-H. Effect of neurodevelopmental treatment-based physical therapy on the change of muscle strength, spasticity, and gross motor function in children with spastic cerebral palsy. Journal of Physical Therapy Science. 2017;29(6):966-969.
48. Jelica S, Šeper V, Davidović E, Bujišić G. Optimizing the function of upstanding activities in adult patients with acquired lesions of the central nervous system by using the Bobath concept approach–a case report. Collegium antropologicum. 2011 Jan 31;35(1):309-11.
49. Trampas, A., Kitsios, A., Sykaras, E., Symeonidis, S., & Lazarou, L. Clinical massage and modified Proprioceptive Neuromuscular Facilitation stretching in males with latent myofascial trigger points. Physical Therapy Sport. 2010; 11(3), 91-98.
50. Gemmell H, Miller P, Nordstrom H. Immediate effect of ischaemic compression and trigger point pressure release on neck pain and upper trapezius trigger points: A randomised controlled trial. Clinical Chiropractic. 2008; 11(1), 30-36.
51. Mcevoy J, Dommerholt J. Chapter 16 – Myofascial Trigger Points of the Shoulder. 5th ed. Elsevier Inc.; 2012:351-379.
52. Tak S, Lee Y, Choi W, Lee G. The effects of active release technique on the gluteus medius for pain relief in persons with chronic low back pain. Physical Therapy Rehabilitation Science. 2013 Jun 31;2(1):27-30.
53. Lewit K: Postisometric relaxation in combination with other methods of muscular facilitation and inhibition. Manual Medicine. 1986, 2:101–104.
54. Moraska A, Schmiege S, Mann J, et al. Responsiveness of myofascial trigger points to single and multiple trigger point release massages – a randomized, placebo controlled trial. Am J Phys Med Rehabil. 2017 Sep; 96(9): 639-645.