# Stretch-induced hypoalgesia: a pilot study

Marie-Claude Larouche, Samuel Camiré Bernier, Rosalie Racine, Olivier

Collin, Mikaël Desmons, Catherine Mailloux, Hugo Massé-Alarie

► To cite this version:

Marie-Claude Larouche, Samuel Camiré Bernier, Rosalie Racine, Olivier Collin, Mikaël Desmons, et al. Stretch-induced hypoalgesia: a pilot study. Scandinavian Journal of Pain, 2020, 20 (4), pp.837-845. 10.1515/sjpain-2020-0018. hal-05149910

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## Original Experimental

Marie-Claude Larouche, Samuel Camiré Bernier, Rosalie Racine, Olivier Collin, Mikaël Desmons, Catherine Mailloux and Hugo Massé-Alarie*

# Stretch-induced hypoalgesia: a pilot study

https://doi.org/10.1515/sjpain-2020-0018

Received January 23, 2020; accepted July 10, 2020; published online
September 2, 2020

## Abstract

**Objectives:** Stretching is an intervention often used in various kinds of rehabilitation protocols and the effects on pain sensitivity has sparsely been investigated, especially when addressing potential effects on pain. The objective is to investigate the immediate effects of an axial and peripheral prolonged stretch on pressure pain sensitivity (PPT) and temporal summation (TS) on local and distal sites in healthy subjects.

**Methods:** Twenty-two healthy volunteers were recruited to participate in this pilot study. Two prolonged stretching protocols were performed: low back and wrist extensors stretches. PPT and pinprick TS were measured pre- and post-intervention at local and remote sites. Repeated measures analysis of variance (ANOVA) was used to examine the effects and significance of the interventions.

**Results:** The low back stretch induced an increase in PPT for both local and remote sites, and the wrist stretch produced a PPT increase only at the local site. TS did not change.

**Conclusions:** Low back stretching induced an increase in PPT at both local and remote sites whereas the wrist stretch only increased PPT locally, suggesting hypoalgesia at these sites. Further studies are needed to confirm the effect and mechanisms using randomised, controlled and parallel study design. Considering that pain sensitivity is different than clinical pain, results are difficult to extrapolate to clinical practice. Future studies testing clinical

pain are needed to better understand the clinical implication of these results.

**Keywords:** exercise-induced hypoalgesia; pain sensitivity; stretching; pressure pain threshold; temporal summation.

## Introduction

Chronic pain is the leading cause of disability worldwide and its prevalence continues to grow [1,2]. A potential reason is the lack of effective management for musculoskeletal conditions, leading to prolonged disability and increasing the burden related to these conditions [3].

Evidence supports the use of manual therapy, aerobic and resistance exercise to reduce pain [4–6]. Some of these interventions increase pain thresholds at remote sites of the “treated area”, suggesting they may activate endogenous pain modulation systems within the central nervous system (CNS). For example, the phenomena known as exercise-induced hypoalgesia (EIH) refer to the decrease in pain sensitivity following isometric and aerobic exercises through the activation of multiple pain modulation pathways [4–8]. Stretching is also commonly used as a part of an exercise program, as it is believed to help increase flexibility, decrease muscle tone and ultimately diminish pain [9–11]. Research in stretching has attempted to understand potential physical/biomechanical mechanisms. Some have argued that results are achieved through a change in fascial structure, hence increasing resistance to load [12]. Others have studied the biomechanical changes of muscle architecture in response to a stretch and observed a reduction in passive resistance [13]. However, few have addressed the stretching effect from a pain perspective. Emerging evidence suggests that biomechanical changes may be explained by an increase in stretch tolerance, potentially mediated by reduced pain sensitivity [14, 15]. Peripheral and central mechanisms involved in pain modulation may play an important role in increase stretch tolerance. These mechanisms could also be involved in the reduction of chronic pain following stretching program [16–19].

Few studies tested the mechanisms underlying the effect of stretching on pain. One study observed an

<footnote>*Corresponding author: Assistant Prof. Hugo Massé-Alarie, Cirris research centre, Université Laval, Quebec City, Canada; and Rehabilitation Unit, Université Laval, Centre interdisciplinaire de recherche en réadaptation et integration sociale (CIRRIS), Quebec City, Qc, Canada, E-mail: hugo.masse-alarie@fmed.ulaval.ca</footnote>

<footnote>Marie-Claude Larouche, Samuel Camiré Bernier, Rosalie Racine and Olivier Collin: McGill University, School of Occupational and Physical Therapy, Montreal, Canada</footnote>

<footnote>Mikaël Desmons and Catherine Mailloux: Cirris research centre, Université Laval, Quebec City, Canada</footnote>
immediate increase of pressure pain threshold (PPT) of the
upper trapezius and masseter muscles following a
hamstring stretch sustained for 40 s [20]. The distance
between testing and stretching sites suggests a central
component involved in this hypoalgesic response. The ef-
fect could be explained by the fact that, like aerobic or
resistance exercises, stretching can be uncomfortable and
slightly painful. A recent review [7] suggests that muscle
nociceptors may be depolarised during exercise, which
may lead to an activation of the endogenous descending
inhibitory pathways. It is possible that muscle stretching
influences pain in a similar way.

Stretching different muscle groups may have a
different impact on pain sensitivity. For example, Vaegter
et al. [21] found that a higher intensity of isometric
contraction of the *biceps brachii* muscle was necessary to
decrease temporal summation (TS) in comparison to a
*quadriceps femoris* muscle contraction. Also, studies
testing EIH following back muscle contractions reported
inconsistent hypoalegic effect [22–24] that contrasts with
the moderate-to-large effect observed after lower and up-
per limb muscle contractions [25]. This suggests that
exercising different muscle groups may produce a different
impact on pain sensitivity.

The objectives of this study are (i) to determine the
influence of stretching exercises on pain sensitivity (PPT
and TS) in healthy subjects and (ii) if response to bouts of
low back and wrist stretches differs. It was hypothesized
that forearm stretching would induce a larger hypoalgesic
effect than low back stretching.

# Methods

## Participants

Twenty-two healthy pain-free volunteers, aged between 19 and 30 years old [24.1 ± 3.1 (SD – standard deviation)], were recruited to participate in a quasi-experimental cross-sectional study with a single-group design. Recruitment was initiated through the electronic mailing list of Université Laval's community in Quebec City. Participants were excluded if they suffered from any major health condition of cardiovascular, neurological, psychological, rheumatoid or gastrointestinal origin, if they had any pain or were using pain medication (including neuroleptics, anticonvulsives, antidepressives and steroids), or if they were currently suffering from a painful musculoskeletal condition [26]. Participants aged 40 and above were excluded because older age is related to a reduction in pain modulation efficacy using conditioned pain modulation (CPM) and EIH paradigms [27, 28]. Subjects were asked to refrain from consuming tobacco or cannabis as well as partaking in physical exercise on the day of the intervention to limit any potential effect on pain sensitivity. Anthropometric data were recorded (weight, height, body mass index,

waist circumference). All participants signed informed consent before
the beginning of the procedure. The local ethics committee (CER
CIUSSS Capitale Nationale 2019-1547) provided a written ethical con-
sent to undertake the study and the study was conducted in accor-
dance with the Declaration of Helsinki.

## Experimental design

Participants attended one 2 h session at the CIRRIS research centre. Figure 1 describes the experimental design of the study. The session was divided into two components: (i) a passive stretch of the low back muscles and (ii) a passive stretch of the wrist extensor muscles. Both passive stretches were preceded and followed by three measurements of PPT (or four if large variability was present between the three measurements) and one measurement of pinprick TS at both sites. A 20 min break period was taken to prevent a possible carry-over effect [5, 29, 30].

PPT and TS were measured a total of four separate times at each
site. Once, prior to each stretching intervention and once immediately
post-intervention (Figure 1). To ensure reliability and validity of
measures, a single evaluator took every measurement during the
entire experimental process.

## Stretching conditions

Participants were instructed to maintain each stretching position for 3 min. A stretching intensity of 3/10 on the modified Borg scale (anchored as 0=no stretch and 10=extreme; 3=moderate stretching intensity) was used for both conditions. Although the modified Borg scale is usually used to rate perceived exertion, the different descriptors of fatigue may also correspond to the intensity of a stretching sensation. In pilot experiments, we noticed that low back stretch induced lower stretching intensity than wrist stretch for most individuals tested. Thus, each experiment started with the low-back stretch to be able to match the stretch intensity between conditions. If it was not possible to obtain 3/10 on the modified Borg scale, the intensity of the wrist stretch was matched to the maximum stretch sensation reached during the low back stretch. Although a stretch longer than 30 s has shown no advantage to augment muscle flexibility compared to a shorter stretch [31], our intervention focuses on central aspects of pain therefore a longer stretch time (that may induce more discomfort) was applied to maximize the possible effects on pain sensitivity. The forearm stretching intervention was applied on the left side for all participants in order to minimize the variability observed in right side PPT measures in right-hand dominant individuals [32]. Both stretches were first demonstrated to ensure comprehension and safety. Care was taken to induce a passive stretch, avoid the activation of the antagonist muscles and foster general muscle relaxation, because isometric contraction can influence pain processing [33]. During the intervention, the intensity of the stretch was assessed at the beginning of the stretch and then again at minute 1, 2 and 3 (i.e. when the stretch was completed). This procedure was done to ensure that participants maintained an approximate stretching intensity of 3/10 during the 3 min exercise.

(1) *Low-back stretch:* From a crook lying position on a plinth, participants were asked to lift their pelvis onto a foam roller placed under their sacrum (S1–S2). After bringing their knees to their chest, a traction belt was placed around their thighs and attached
<figure><img src="image_2.png" /><figcaption>**Figure 1:** Study procedure. Arrows indicate measurement of pressure pain sensitivity (PPT) and temporal summation (TS).</figcaption></figure>

under the table to maintain the stretch position and minimize muscle contraction. The position was adjusted either through external rotation of their hips and/or from increased hip flexion with the traction belt until they felt a stretch of 3/10 or the highest stretch sensation in the lumbar region (L2–L5) (Figure 2A).

(2) *Wrist stretch:* While sitting in an upright position on a chair, participants were asked to place their left arm on an adjustable table next to them (approximately 90° shoulder flexion). A foam roller was then placed adjacent to their arm in order to stabilize and maintain elbow extension. Their wrist was passively held in flexion against a cushioned ledge in front of them (Figure 2B).

After each stretching condition, participants were asked to draw the location of stretch sensation on a bodychart. Stretching locations were transposed to PowerPoint 2016 (Microsoft corp., Redmond, USA) and each bodychart was overlaid to help visualise the most common stretching locations for each stretching exercise.

## Measures/apparatus

PPT is used to quantify pressure pain sensitivity which was demonstrated to be reliable at the low back and wrist extensors muscles [34–36]. PPT was assessed using a handheld algometer (1 cm² probe-FPIX, Wagner Instruments, CT, USA). The limit of the algometer is 11.5 kg/ cm². The pressure was applied at a rate of ~0.5 kg/cm²/s. Prior to commencing the procedure, participants were familiarized with the algometer on their right thigh. The experimenter informed participants that they would feel a gradual increase in pressure and to say “stop” when the sensation first changed from pressure to pain [37]. The experimenter emphasized that pain should not be tolerated.

Two sites were tested for PPT measurements. The first site consisted of the muscle belly of the *erector spinae* 2–3 cm lateral to the L3 spinous process. The second site was 3–4 cm distal to the left lateral

epicondyle on a line from the lateral epicondyle to the styloid process of the radius, over the muscle bulk of the wrist extensors. These sites were chosen as they represent either a local or a remote effect depending on which muscles were being stretched. PPT was always measured in sets of three at each site, with 30 s intervals between each to avoid pain summation. A fourth measurement was taken if the SD was >1 kg/cm² and if one of the three measurements fell outside mean ± SD. This formula was developed to limit the impact of outlier values on the overall within-subjects average in a same series of measurements. When 4 PPT measurements were taken, the previous step was used to determine whether one of the four values was discarded or if an average of all four values would be used. A fourth PPT measurement was taken in only one participant (before and after both stretching conditions at L3).

TS was measured using a 256 mN pinprick stimulation at 1 Hz over a 1 cm² area (256 mN, MRC Systems GmbH, Germany). Participants were asked to rate their pain level using a Visual Analog Scale (VAS – anchored as 0: no pain and 10: worst imaginable pain) after the first stimulation and again after 10 repeated stimulations. A visual metronome (Visual Optical Metronome, Offenbach, Germany) was used to ensure accuracy of the stimulation frequency. Participants were familiarized with the pinprick stimulation by first testing the right hand then aminence to feel the sensation and reduce possible anxiety related to the stimulation. The two different sites were the L3 spinous process and the left lateral epicondyle. TS is considered as the difference between the maximum pain intensity felt through 10 consecutive stimulations and the pain intensity of a single stimulation. TS is a dynamic measure of pain processing, providing information about the amplification of nociceptive signals at the level of the spinal cord [38, 39].

Combining a static measure (PPT) and a dynamic measure (TS) of pain sensitivity was done to enhance the understanding of the mechanisms of stretching on pain processing.

<figure><img src="image_3.png" /></figure>

<figure><img src="image_4.png" /><figcaption>**Figure 2:** Low-back (A) and wrist (B) stretches.</figcaption></figure>
## Statistical analysis

Statistical analysis was performed using SPSS Statistics (IBM Version 23.0.0.0, SPSS inc., IL, USA). Descriptive statistics (mean and SD) of the demographic data were used to capture the characteristics of the study sample. Normality of the PPT and TS variables were assessed with the Shapiro-Wilk's test. For PPT, the data were normally distributed. For TS, the variables were not normally distributed. Due to the presence of zero in the data (i.e. pain did not increase during the repeated pinprick stimuli), a log-transformation was not possible, and the analysis was performed on the non-transformed dataset. To determine whether different types of stretches impacted pain sensitivity differently, a three-way repeated measures ANOVA was computed with factors Stretch (Back, Wrist), Site (L3, Forearm) and Time (Pre, Post) individually for PPT and TS. Pairwise comparisons with Sidak's corrections were applied to determine where differences lay. To better describe the effect of stretching on pain sensitivity, the effect size was calculated using Cohen's *d* for paired samples, the pre-post differences and 95% confidence interval (CI), and the percentage of change for each site and stretching conditions. Paired t-tests or Wilcoxon signed rank test compared the pre-Low-back stretch and the pre-Wrist stretch variables (L3 and forearm) to determine whether a carry-over effect was present. Wilcoxon's signed-rank tests were conducted to compare the average stretch intensity (measured by the modified Borg scale) between both stretches, to confirm that the stretch intensity was similar between conditions. Statistical significance was defined at an alpha level of 0.05.

## Results

### Summary of the sample

A total of 22 healthy volunteers were eligible and participated in this study. From this group, four participants were excluded due to an absence of stretch sensation during the low-back stretch. Subjects were excluded if they reported an intensity of 0/10 for more than half of the stretch duration. Also, for one participant, the PPT measured at L3 exceeded the algometer limit for the post-stretch at L3 and forearm. Since this limited the observation of hypoalgesic effect, we excluded this participant from the analysis. Baseline characteristics are summarized in Table 1.

### Stretching intensity and carry-over effect

The intensity of stretching was matched between stretches (low back: median [range]=2.5 [0.63–4.00]; wrist: 2.3 [0.50–3.50]|p=0.486) as depicted in Figure 3. This was done to minimize the influence of the intensity of stretching on results. Paired t-tests between pre-intervention confirm the absence of carry-over effects for PPT (L3: t=1.68; p=0.11|forearm: t=0.21; p=0.84) or TS (p>0.43).

For the low-back stretch, a stretching sensation was felt in the lower back area bilaterally for all participants

<table><caption>Table 1: Descriptive statistics.</caption><thead><tr><th rowspan="2">Variables</th><th>Recruited (n=22)</th><th>Analysed (n=17)</th></tr><tr><th>Mean (SD)</th><th>Mean (SD)</th></tr></thead><tbody><tr><td>Sex. n Female (n Male)</td><td>12 (10)</td><td>10 (7)</td></tr><tr><td>Age (years)</td><td>24.1 (3.1)</td><td>23.9 (3.4)</td></tr><tr><td>Height (m)</td><td>1.72 (0.08)</td><td>1.72 (0.08)</td></tr><tr><td>Weight (kg)</td><td>68.32 (11.16)</td><td>69.19 (11.86)</td></tr><tr><td>Waist circumference (cm)</td><td>78.98 (9.42)</td><td>79.41 (8.35)</td></tr><tr><td>BMI (kg/m<sup>2</sup>)</td><td>23.18 (3.37)</td><td>23.45 (3.61)</td></tr><tr><td>Hand-dominance (R(L))</td><td>20 (2)</td><td>17 (1)</td></tr></tbody></table>

SD, standard deviation; BMI, body mass index; R(L), right left.

included in the analysis, although only four reported a stretch uniquely at the lower back. Other participants reported a stretch in 2 (n=9), 3 (n=4) and 4 different regions (n=1) throughout the low-back intervention. These other regions were the groin unilaterally or bilaterally (n=9), the hip area unilaterally or bilaterally (n=8), the upper back region bilaterally (n=1), the hamstring region bilaterally (n=3), the abdominal region uni- or bi-laterally (n=2) and the buttock region (n=2). For the wrist stretch, all participants felt the stretch in the wrist extensor muscle belly region, although the stretch was isolated for only seven participants. Other participants reported a stretch in 2 (n=8) or 3 different regions (n=3) throughout the wrist extensor intervention, including distally on their forearm (n=9), at their wrist (n=9) and on the dorsum of their hand (n=2). Figure 4 depicts the areas of reported stretching sensation during both interventions.

### Comparison of stretch conditions

For PPT, repeated measures ANOVA revealed a significant interaction Stretch × Site × Time ($F_{(1,16)}$=8.73, p=0.009).

<figure><img src="image_5.png" /><figcaption>Figure 3: Stretch intensity reported every minute during low-back and wrist stretch. T0–T3: minute 0–3; Pre: before stretching started; Post: after stretching stopped.</figcaption></figure>
<figure><img src="image_6.png" /><figcaption>**Figure 4:** Visual representation of areas where stretching sensation was felt during low-back stretch (A) intervention and during wrist extensor stretch (B) intervention. Note that white represents no stretch for any participant in the group, pale grey represents one participant (n=1). The darker the visual representation, the larger numbers of participants reported stretch in one given area.</figcaption></figure>

This interaction was explained by a larger PPT after low back stretch at L3 (pre: 3.65 ± 1.42; post: 4.12 ± 1.75; % change: 13.6 ± 20.0% | p=0.002) and at forearm (pre: 1.77 ± 0.47; post: 1.99 ± 0.43; % change: 16.4 ± 19.9% |

<figure><img src="image_7.png" /><figcaption>**Figure 5:** Effect of low-back (left panel) and wrist (right panel) stretch on PPT at L3 (black bar) and forearm (white bar) sites. PPT: pressure pain threshold; \*p<0.05; \*\*p<0.01; \*\*\*p<0.001.</figcaption></figure>

p=0.007), and after wrist stretch at forearm (pre: 1.79 ± 0.46; post: 1.96 ± 0.49; % change: 10.9 ± 14.9% | p=0.009) but not at L3 (p=0.19 – Figure 5 & Table 2). Significant differences between sites were present at each timepoint and for both groups (p<0.001 for all) meaning that PPT was larger at L3 than forearm. No difference was present between stretching conditions at each timepoint for both sites (p>0.10 for all). Table 2 details the effect for each site after both stretching conditions.

The ANOVA model for TS measures (Stretch × Site × Time) revealed no significant main effect or interaction (F<1.81; p>0.20 for all). TS measures are presented in Table 3.

## Discussion

The purpose of this pilot study was to determine whether stretching influenced pain sensitivity and if stretching different muscle groups (axial vs. upper limb) would differently influence pain sensitivity. Conversely to our hypothesis, we observed that the low back stretch induced an increase in PPT at local and remote sites whereas wrist stretch only induced a PPT increase at local site. This suggests that low-back stretching produces a systemic effect whereas the wrist stretch effect was localised to the site of stretching. TS was not affected by both stretching conditions.

## Limitations

Our results need to be interpreted in light of some methodological considerations that may affect the interpretation of the results. The main limitation in this study is the non-randomized order of the stretching exercises. This was done to be able to match stretching intensity between stretching conditions but the order may have reduced the effect of wrist stretching on pain sensitivity. A parallel group study using two different groups (low back vs. wrist stretch) may help to confirm or infirm our results. The lack of a control group precludes to make strong conclusion on the presence of hypoalgesia after low back stretching that may due to the variability of PPT measures. However, a study using a test-retest within-session design suggests that the minimal detectable change (MDC) for the group for lumbar PPT is ~4% (MDC for individuals/√n) (35). This suggests that the significant change in PPT (>10.9% for L3 and forearm after low back stretch, and for forearm after wrist stretch) exceeds MDC for groups i.e. the variability of PPT measures, and probably represent true changes
<table><caption>**Table 2:** Effect of stretch on pain sensitivity measurements.</caption><thead><tr><th rowspan="2">Stretch</th><th rowspan="2"></th><th colspan="4">Low back</th><th colspan="4">Wrist</th></tr><tr><th>Δ(post-pre)</th><th>95% CI</th><th>d</th><th>%PPT</th><th>Δ(post-pre)</th><th>95% CI</th><th>d</th><th>%PPT</th></tr></thead><tbody><tr><td rowspan="2">L3</td><td>PPT (kg/cm²)</td><td>0.48</td><td>0.20-0.75</td><td>0.88</td><td>13.6 ± 20.0</td><td>-0.20</td><td>-0.36-0.08</td><td>-0.32</td><td>-4.0 ± 12.2</td></tr><tr><td>TS¹ (0/10)</td><td>0.08</td><td>-0.31-0.48</td><td>0.10</td><td></td><td>0.06</td><td>-0.35-0.46</td><td>0.07</td><td></td></tr><tr><td rowspan="2">Forearm</td><td>PPT (kg/cm²)</td><td>0.22</td><td>0.07-0.38</td><td>0.75</td><td>16.4 ± 19.9</td><td>0.16</td><td>0.03-0.24</td><td>0.72</td><td>10.9 ± 14.9</td></tr><tr><td>TS (0/10)</td><td>0.06</td><td>-0.51-0.39</td><td>-0.06</td><td></td><td>0.08</td><td>-0.52-0.35</td><td>-0.09</td><td></td></tr></tbody></table>

PPT: Pressure pain threshold; TS: temporal summation; L3: level of the spinal process of the third lumbar vertebra; Δ(post-pre): difference between pain sensitivity measured after and before stretch; CI: confidence interval; d: Cohen's d for paired sample.

<table><caption>**Table 3:** Average and standard deviation for TS.</caption><thead><tr><th rowspan="3">Stretch<br>Site<br>Time</th><th colspan="4">Low back</th><th colspan="4">Wrist</th></tr><tr><th colspan="2">L3</th><th colspan="2">Forearm</th><th colspan="2">L3</th><th colspan="2">Forearm</th></tr><tr><th>Pre</th><th>Post</th><th>Pre</th><th>Post</th><th>Pre</th><th>Post</th><th>Pre</th><th>Post</th></tr></thead><tbody><tr><td>TS<sup>a</sup> (0/10)</td><td>1.67 ± 1.18</td><td>1.75 ± 1.11</td><td>1.72 ± 1.22</td><td>1.67 ± 0.95</td><td>1.81 ± 1.27</td><td>1.86 ± 1.17</td><td>1.83 ± 1.01</td><td>1.75 ± 1.07</td></tr></tbody></table>

TS: temporal summation of pain; L3: level of the spinal process of the third lumbar vertebra.

aTS is considered as the difference between the pain produced for a single pinprick stimulus and the maximal pain felt during a series of 10 stimuli.

(hypoalgesia). The small number of participants recruited and the multiple analyses performed increased the risk of type I error. Finally, the generalization of these results is also precarious as the sample was formed of young and healthy adults from a convenience sample, which is not representative of the general population.

## Comparisons with current literature

There has been limited work investigating the immediate effect of stretching exercises on pain sensitivity. However, it is still possible to find some similarities between the results obtained in this experiment and a previous study [20] that found an increase in PPT over upper *trapezius* and masseter muscles after a unilateral hamstring stretch. These results are in agreement with our findings of the low back stretch having a hypoalgesic effect remote from the stretched site. However, this work did not measure the local effect of hamstring stretch. Another study tested the effect of a 4-week program of calf stretching on pain sensitivity measured by a computerized cuff-algometer [9], and did not report any effect. This may suggest different physiological mechanisms on pain sensitivity between bouts of stretch vs. longer-term program.

In parallel, many studies have looked at the effect of isometric exercises on PPT. While the neurophysiological

effects behind isometric and stretching exercises may differ, it can be interesting to compare their effect regarding pain sensitivity. According to a systematic review, isometric resistance exercises lead to multisegmental hypoalgesic effects in the healthy population [5]. Despite large between-study variability being present, there was a moderate-to-large effect on pain sensitivity (measured by PPT). Following isometric contraction of back and hip muscles (Biering-Sorensen exercise), Gajsar et al. [24] observed an increase in PPT post-contraction only for hamstrings but not for low back muscles. In addition, box lifting involving a strong contraction of the low back muscles did not induce hypoalgesia when performed during ~3 min [22], but did when performed during 7 min [23]. The type of isometric contraction, the duration and the muscle contracted seem to differently impact on pain sensitivity [5]. In our results, it remains unclear why the wrist and low back stretch influenced pain sensitivity differently. One possibility is that the larger effect of the low back stretch (widespread reduction in pain sensitivity) compared to the wrist stretch (local effect) was driven by a dose-response relationship [33]. During the low-back stretch, a larger total cross-sectional area of musculature was stretched in comparison to the wrist stretch, while stretching intensity and duration were kept constant. This can be further observed in Figure 4, where the low-back stretch also led to multiple other areas reported as
stretched by the participants in addition to the low back (i.e. groin, hips and hamstrings). This may be due to a lack of specificity in isolating the sensation of stretch to strictly the low back area. Therefore, the total amount of muscle fibres stretched/under tension and/or the number of joints moved may have induced a larger effect during low-back stretching perhaps triggering a systemic effect for low back stretching that was absent (only local effect) after wrist stretching. It is important to notice that some of the areas indicated as stretched by the participants cannot be physiologically stretched by the low back exercise and may rather reflect compression of these structures (e.g. anterior hip and thigh, groin).

TS was not impacted by the stretch paradigms. Conversely, Vaegter et al. [21] found that isometric arm and leg exercises induced a reduction in TS. Multiple reasons may explain this discrepancy, such as the type of exercise (isometric contraction vs. stretching), the intensity of the exercise (high vs. low) and the techniques used to measure TS (cuff algometry vs. pinprick).

## Possible mechanisms involved in stretching induced hypoalgesia

Our results suggest that stretching induced hypoalgesia. We propose that similar EIH/CPM mechanisms may be involved in this phenomenon. EIH refers to a reduction in pain sensitivity following aerobic and isometric exercises secondary to the activation of peripheral and central pain modulation mechanisms. For example, exercise leads to an increase in the circulating level of endocannabinoids and the hypoalgesia is reduced by naltrexone, an antagonist of opiate receptors [40]. A recent study also demonstrated that remote EIH may be partly induced by the circulation of analgesic agent in the blood, a potential peripheral mechanism [41]. The latter results suggest that both central and peripheral mechanisms may be involved in EIH. It has been suggested that exercise may induce hypoalgesia by “counter-irritation” mechanism i.e. by the activation of nociceptors during the isometric contraction, similar to the CPM paradigm [7]. CPM consists of the application of a noxious stimulus leading to a multisegmental decrease in pain sensitivity through serotonergic and opioidergic systems [7]. Although different, EIH and CPM paradigms reduce pain sensitivity using common pathways (e.g. opioid). We suggest that stretching may induce hypoalgesia through similar mechanisms. Given that prolonged stretching is uncomfortable, it may activate some tendon, joint, muscle and/or nerve nociceptors. For example, tendon nociceptors are preferentially depolarised by stretching [42] and may activate

the pain modulation systems. Bishop & George (2017) observed that the increase in range of motion following stretching were largely due to an increase in stretch tolerance (i.e. the ability to tolerate the discomfort) [14]. This would imply that the ability to increase range may be more related to a reduction in pain sensitivity as opposed to architectural muscle-tendon changes [15].

PPT and TS represent different characteristics of pain processing. PPT is a static measure of pain that may inform on the function of, mainly, muscle nociceptors and their central processing in pain experience. TS, on the other hand, is thought to reflect the dynamic pain processing and reflects the wind-up phenomenon (a frequency-dependent increase in neuronal excitability) that occurs in the dorsal horn neurons in response to repeated noxious stimuli [42, 43]. Our findings suggest that stretching may have an impact on PPT, but that it may not influence wind-up processing in the spinal cord.

## Clinical implications

Based on these results, stretching interventions could potentially be used to provide temporary and immediate pain relief in a clinical setting. However, it is possible than a reduction in pain sensitivity will not be associated with a reduction in clinical pain considering that pain sensitivity is different than clinical pain. For example, pain sensitivity and clinical pain are not frequently correlated and seem to be influenced by factors such as the sex [44, 45], the type of noxious stimulus, the methodology used and the definition of clinical pain (e.g. current, previous week) [46]. Further investigation must be done in individuals suffering from chronic pain to determine if they have an altered hypoalgesic response to exercise [5, 7]. Stretching exercises prescribed as a home exercise program often imply an active muscular contraction locally and/or remotely, making the completely passive intervention used in our study less suitable in a clinical setting, thus our results difficult to generalise. Future studies testing the effect of stretching on clinical pain, and on pain sensitivity in clinical population are warranted to determine the clinical value of our results.

## Conclusions

This pilot study showed that prolonged passive stretching of the low back area induced an increase in PPT at local and remote sites, whereas the wrist stretch only increased PPT locally. We suggest that this PPT increase could reflect a stretch-induced hypoalgesia, but future randomised,
controlled and parallel studies are needed to confirm our findings. Also, studies should determine if it may be secondary to an activation of peripheral and central pain modulation mechanisms, in a similar fashion as exercise induced hypoalgesia. Our results could be the premise of a larger study investigating the effects of stretching on pain sensitivity in participants with chronic pain.

**Acknowledgments:** We acknowledge the help of Jean Tittley for data collection and Richard Preuss for commenting the first version of the article.

**Research funding:** This study was funded by a collaborative grant from the Quebec Pain Research Network, Canadian Musculoskeletal Research Network and the Quebec Rehabilitation Network (REPAR). HMA is supported by a research scholar from *Fonds de recherche du Québec – Santé* (281961). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

**Author contributions:** All authors have accepted responsibility for the entire content of this manuscript and approved its submission.

**Conflict of interest:** Authors state no conflict of interest.

**Informed consent:** Informed consent has been obtained from all individuals included in this study.

**Ethical approval:** The local ethics committee (CER CIUSSS Capitale Nationale 2019-1547) provides a written ethical consent to undertake the study and the study was conducted in accordance with the Declaration of Helsinki.

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