Why should exercises be pain-free? Part 1 – pain & kinematics

This blog is an amended version of some text from my recent PhD that looked at the assessment and management of patellofemoral pain. As such, my work is a product of supervision and collaboration.  So I would like to start by acknowledging and thanking my supervisors Pip Logan and Paul Hendrick, and collaborators Marcus Bateman, Sinead Holden, Chris Littlewood, Fiona Moffatt, Michael Rathleff, James Selfe and Toby Smith.

Introduction

The blog aims to take a look at exercise prescription for MSK pain. Why do we prescribe exercises the way we do? What does the evidence tell us? Does exercise work the way we think it does?

Let’s start by thinking about what pain is and why might we think exercise is helpful for it.

What is pain?

The International Association for the Study of Pain (IASP) defines pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage’ [1]. The traditional view of pain further summarises: 1) pain is viewed as a symptom and warning sign, the function of which is to avert the person from harm; 2) it provides a pivotal role in identifying underlying pathology; 3) ethically, medical and rehabilitation practice should aim to avoid or alleviate pain as much as possible [1,2].

grayscale photo of man

In short – the traditional view of pain is that it is a direct sign of tissue damage that should be avoided.

No wonder cross-sectional online questionnaire surveys of practice that examined this aspect of exercise prescription have demonstrated that many physiotherapists suggest avoiding pain when prescribing exercises [3,4]. Many physiotherapists in these studies also recommend limiting all forms of physical activity in the presence of pain.

This biomedical model of pain typically attributes the sensing of harmful stimuli to nociception*. It fails to distinguish between sensation and the perception of pain. Pain was thought to be conveyed to the brain directly from nociceptors [5].

*Nociceptors are specialised primary sensory neurons situated in various body tissues, such as skin, muscles and tendons, which are involved in the transduction and transmission of information from the periphery to the central nervous system [6,7].

Found this blog useful? Want to learn a contemporary, evidenced-based approach to the assessment and management of patellofemoral pain? Have a look at available course dates and course information. tile

Why exercise?

It is often assumed that the primary mechanism by which exercise improves pain and disability in musculoskeletal pain is biomechanical, i.e. changes to the load distribution of the musculoskeletal system [8]. Improvements in joint range of movement, muscle strength and endurance and postural control after exercise programmes are thought to contribute to changes in loading at the painful site, thus reducing the painful stimuli. With a corresponding decrease in nociception and pain perception [9].

Does the evidence support this? Perhaps not…..[8,10]. Improvements in pain and function after exercise programmes often occur in the absence of any changes to joint position and movement in knees, shoulders and backs.

side view photo of woman doing lunges against black background

For example:

  1. Rathleff’s 2014 systematic review looked at hip strength and patellofemoral pain. They included 27 articles and 1,971 participants [11]. The review demonstrated that while hip-strengthening exercises appear to improve pain and symptoms for people with patellofemoral pain, these improvements in pain they do not to change any kinematics and alignment dysfunction at the knee or patella [11].

     

  2. A 2012 systematic review assessing changes in pain and, joint position and movement with exercise interventions for low back pain included 16 articles and 1,476 participants. They demonstrated that people with LBP gain some improvements with exercises, but that pain reductions were not attributable to changes in joint position or movement [9].

     

  3. Similarly, a 12-week strengthening programme for patients with knee osteoarthritis (OA) improved pain and symptoms, without any changes in joint load [12]. In an RCT (n = 89), Bennell (2010) compared a therapist-supervised exercise program to no intervention in people with medial compartment tibiofemoral OA and varus malalignment [12]. It was hypothesised that strength improvements would reduce joint load (as measured by knee adduction moment) and improve pain and function, as cross-sectional research shows increased varus malalignment and higher peak knee adduction moment in patients with knee OA [13,14].  The study demonstrated a discrepancy between prospective and cross-sectional research findings, with improved symptoms and function occurring without altering medial compartment loading.

     

  4. Finally Drew et al. (2014) conducted a systematic review to evaluate the relationship between observable structural change and clinical outcomes following therapeutic exercise [15]. They included trials that measured the structure of a tendon (US, MRI or CT) before and after a course of therapeutic exercises. They included 20 studies with 625 participants and concluded that on average patients improve over time in terms of pain and function; observable structural pathology did not change [15].

It is likely that changes in biomechanics, with subsequent changes in load distribution of the musculoskeletal system, do not fully explain the improvements in pain and symptoms seen with exercise interventions. The inconsistency demonstrated indicates how more complex and unexplored this topic is but does challenge the idea that exercises need to reduce tissue loading at painful body sites.

man wearing black and white stripe shirt looking at white printer papers on the wall

The second part of this blog will discuss the philosophy of pain and how that influences exercise prescription.

References

[1]         Merskey H. Pain terms: a list with definitions and notes on usage. Recommended by the IASP Subcommittee on Taxonomy. Pain 1979;6:249–52.

[2]         Duncan G. Mind-body dualism and the biopsychosocial model of pain: What did Descartes really say? J. Med. Philos. A Forum Bioeth. Philos. Med., vol. 25, Journal of Medicine and Philosophy Inc.; 2000, p. 485–513.

[3]         Littlewood C, Lowe A, Moore J. Rotator cuff disorders: a survey of current UK physiotherapy practice. Shoulder Elb 2012;4:64–71. doi:10.1111/j.1758-5740.2011.00164.x.

[4]         Smith BE, Hendrick P, Bateman M, Moffatt F, Rathleff MS, Selfe J, et al. Current Management Strategies for Patellofemoral Pain: An online survey of 99 practising UK physiotherapists. BMC Musculoskelet Disord 2017;18. doi:10.1186/s12891-017-1539-8.

[5]         Gatchel RJ. Clinical essentials of pain management. American Psychological Association; 2005.

[6]         Carlton SM. Nociceptive primary afferents: they have a mind of their own. J Physiol 2014;592:3403–11.

[7]         Gold MS. Molecular biology of sensory transduction. Wall Melzack’s Textb Pain Philadelphia, Pennsylvania, USA Saunders 2013:31–48.

[8]         Booth J, Moseley GL, Schiltenwolf M, Cashin A, Davies M, Hübscher M. Exercise for chronic musculoskeletal pain: a biopsychosocial approach. Musculoskeletal Care 2017.

[9]         Steiger F, Wirth B, De Bruin ED, Mannion AF. Is a positive clinical outcome after exercise therapy for chronic non-specific low back pain contingent upon a corresponding improvement in the targeted aspect (s) of performance? A systematic review. Eur Spine J 2012;21:575–98.

[10]      Smith BE, Hendrick P, Smith TO, Bateman M, Moffatt F, Rathleff MS, et al. Should exercises be painful in the management of chronic musculoskeletal pain? A systematic review and meta-analysis. Br J Sports Med 2017;51:1679–87. doi:10.1136/bjsports-2016-097383.

[11]      Rathleff MS, Rathleff CR, Crossley KM, Barton CJ. Is hip strength a risk factor for patellofemoral pain? A systematic review and meta-analysis. Br J Sports Med 2014;48:1088. doi:10.1136/bjsports-2013-093305.

[12]      Bennell KL, Hunt MA, Wrigley T V, Hunter DJ, McManus FJ, Hodges PW, et al. Hip strengthening reduces symptoms but not knee load in people with medial knee osteoarthritis and varus malalignment: a randomised controlled trial. Osteoarthr Cartil 2010;18:621–8.

[13]      Hurwitz DE, Ryals AB, Case JP, Block JA, Andriacchi TP. The knee adduction moment during gait in subjects with knee osteoarthritis is more closely correlated with static alignment than radiographic disease severity, toe out angle and pain. J Orthop Res 2002;20:101–7.

[14]      Baliunas AJ, Hurwitz DE, Ryals AB, Karrar A, Case JP, Block JA, et al. Increased knee joint loads during walking are present in subjects with knee osteoarthritis. Osteoarthr Cartil 2002;10:573–9.

[15]      Drew BT, Smith TO, Littlewood C, Sturrock B. Do structural changes (eg, collagen/matrix) explain the response to therapeutic exercises in tendinopathy: a systematic review. Br J Sport Med 2012:bjsports-2012.