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. 2024 Oct 26;29(3):e4750. doi: 10.1002/ejp.4750

The effect of stretching intensity on pain sensitivity: A randomized crossover study on healthy adults

Morten Pallisgaard Støve 1,2,✉, Line Ørum Hansen 1, Kristian Kloppenborg Elmbæk 1, Stig Peter Magnusson 3,4, Janus Laust Thomsen 2, Allan Riis 1,2
PMCID: PMC11755707  PMID: 39460597

Abstract

Background

Stretching exercises have effects on local and widespread pain sensitivity. A dose–response relationship may exist between the analgesic effect and the intensity of stretching, such that a higher intensity of stretching may generate a larger reduction in analgesic response, but this remains to be studied. This study aimed to examine the dose–response relationship between stretching intensity and the analgesic effect.

Methods

A randomized, repeated‐measures crossover study was performed to examine the effect of stretching to the first point of pain onset and stretching to the point of a sensation of stretching (discomfort). The primary outcome was regional and distant pressure pain thresholds.

Results

Thirty‐one participants (n = 24 female) were available for analysis. We observed a 22.2% increase in regional pressure pain thresholds (93.2 kPa, p = 0.001) and a 15.0% increase in distant pressure pain thresholds (50.9 kPa, p = 0.012) following stretching to the point of stretch. We observed a 20.0% increase in regional pressure pain thresholds (90.3 kPa, p = 0.001) and a 15.1% increase in distant pressure pain thresholds (52.1 kPa, p = 0.004) following stretching to the point of pain.

Conclusions

The results showed that local and widespread pain sensitivity decreased following acute stretching, regardless of stretching intensity. No differences in pain sensitivity were found between stretching to the point of stretch or stretching to the first onset of pain. Thus, the results showed no evidence of a dose–response relationship between stretching intensity and the analgesic effect.

Significance

The study showed a significant acute hypoalgesic effect of stretching exercises regardless of stretching intensity. This may have appropriate clinical implications for patients with musculoskeletal and nociplastic pain.

1. INTRODUCTION

Stretching exercises are a well‐known intervention to maintain or improve joint range of motion (Behm et al., 2016; Konrad et al., 2023). In addition, stretching exercises may positively affect musculoskeletal pain (Behm et al., 2021) and nociplastic pain (Ferro Moura Franco et al., 2020). Stretching exercises have positive acute and long‐term effects on regional (i.e. local) and widespread (i.e. a remote site of the body) pain sensitivity [5–8], resulting in stretch‐induced hypoalgesia (SIH) (Larouche et al., 2020; Støve et al., 2021). So far, different pain modulation mechanisms have been suggested to explain the impact of stretching on overall pain sensitivity (Behm et al., 2021). Recent evidence suggests that the analgesic effect of stretching exercises is generated by endogenous modulation of somatosensory input (Støve, Hirata, & Palsson, 2024; Støve, Thomsen, et al., 2024), resulting in modulation of the perceived magnitude of afferent stimuli similar to that of exercise‐induced hypoalgesia (EIH) or conditioned pain modulation (CPM) (Larouche et al., 2020; Støve, Hirata, & Palsson, 2024). Due to their analgesic effect, stretching exercises may be implemented in the treatment of individuals suffering from acute or chronic pain as long as the stretching exercises do not contribute to the pathology underlying the pain (Behm et al., 2021).

Endogenous modulation of somatosensory input is likely a saturable phenomenon, which suggests that the inhibitory range may reach a ceiling effect (Granot et al., 2008). Also, current evidence indicates that intensity (e.g. exercise and conditioning stimulus) is a key factor in determining the EIH (Vaegter & Jones, 2020) and CPM response (Coulombe‐Lévêque et al., 2021). Therefore, it is plausible that such an association also exists for SIH. Current evidence suggests a dose–response relationship between the intensity of stretching exercises and acute changes in flexibility (Thomas et al., 2018). What is less clear is the effect over time (Bryant et al., 2023). Little is known about SIH's temporal properties (i.e. duration and magnitude). Still, the intensity of stretching may influence the effectiveness of SIH, inviting the hypothesis that a higher intensity of stretching may generate a larger analgesic response than lower intensity stretching.

This study examined the dose–response relationship between stretching intensity and the analgesic effect. We hypothesized the existence of a dose–response relationship between local and widespread pain sensitivity and stretching intensity.

2. METHODS

This is a randomized, repeated‐measures crossover study. The study is reported according to the Consolidated Standards of Reporting Trials (CONSORT) extension to randomized crossover trials (Dwan et al., 2019). The trial was approved by the North Denmark Region Committee on Health Research Ethics (N‐20210044), reported to the Danish Data Protection Agency and registered at ClinicalTrials.gov (09.08.2023) (Trial registration number NCT05989490). Participants provided written informed consent before participation. Enrolment began on 13 September 2023 and ended on 30 November 2023.

2.1. Participants

Participants were recruited through social media and advertisements at local universities. Healthy subjects between 18 and 55 years old with no previous participation in experimental pain studies were eligible for inclusion. Exclusion criteria were as follows. (1) All participants had to be pain‐free (including delayed onset of muscle soreness, DOMS) and have no current medical conditions such as cognitive impairments, neurological, orthopaedic or neuromuscular problems that impede stretching exercises or range of motion testing at the knee. (2) Regular use (i.e. during the week before participation) of prescription medicines or over‐the‐counter medications that affect the somatosensory systems, such as psychotropic medicines, analgesics or anti‐inflammatory drugs.

Participants were asked to refrain from physical exercise on the days with experimental sessions. The participants were familiarized with the testing procedures before the start of the experimental sessions.

2.2. Intervention

The participants were assigned to two sessions (i.e. stretching to the point of stretch (discomfort) and stretching to the first onset of pain). Both sessions consisted of four bouts of 30‐s unilateral static stretching of the right knee flexors with a 30‐s rest period between bouts in line with a previous study (Støve, Hirata, & Palsson, 2024). Stretches were performed with the participants seated in the Biodex System 4 Pro isokinetic dynamometer (Biodex Medical Systems, Shirley, New York, USA). The participants were instructed to relax the limb as the lower leg was passively moved towards extension (Figure 1). The movements were stopped when the participants felt that the stretching sensation reached the point of stretch/discomfort (stretch to the point of a stretching sensation) or the point of pain (stretch to the first onset of pain). This position was maintained for 30 s. Possible carryover effects were negated by using a washout period of at least 24 h between sessions.

FIGURE 1.

FIGURE 1

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An illustration of the experimental set‐up using the Biodex system 4 pro.

2.3. Outcomes

The primary outcome measure was pain sensitivity expressed as regional (local) and distant (widespread) pressure pain thresholds. Assessments were performed before and within 2 min after the stretching exercises. Pressure pain thresholds were assessed using a handheld digital pressure algometer (Algometer Type 2, SBMEDIC, Hörby, Sweden) with a probe size of 1 cm2. The rate of pressure increase was applied perpendicular to the tissue and retained at 30 kPa/s. The first time the sensation of pressure was perceived as pain, the participant pressed a stop button, thereby stopping the stimulation. At that time, the pressure value was defined as the pressure pain threshold. Pressure pain thresholds were assessed at two sites. The right tibialis anterior site (regional site) was located at 1/3 on the line connecting the fibula's tip and the medial malleolus's tip. The left deltoid site (distant site) was located in the middle of the most prominent muscle bulge on the line connecting the acromion and the lateral epicondyle of the elbow in accordance with previous procedures (Støve, Thomsen, et al., 2024). Pressure pain thresholds were assessed in an alternating fashion three times at each site. Twenty‐second intervals between assessments were kept to avoid pain summation. Mean values were used for the analysis. Before the assessments started, the participant was familiarized with the pressure algometer through assessments of pressure pain thresholds at a site not included for outcome measuring (i.e. the left m. rectus femoris).

Passive knee extension range of motion and passive resistive torque were assessed before and immediately after the stretching exercises using the Biodex. Participants were seated fixed to the chair (a hip flexion angle of 100° and a knee extension angle of 90°) (Figure 1). Posterior pelvic tilt was averted by placing a firm wedge (22.5*6*5 cm) at the low back (the level of L5). The seated position ensured that tension was placed primarily on the muscle‐tendon unit of the knee flexors to prevent hyperextension of the knee during testing (Magnusson et al., 1996). The dynamometer lever arm passively extended the knee at an angular velocity of 5°/s (Støve et al., 2021). Participants were instructed to stop the movement by pressing a stop button when the sensation changed from stretch to the first onset of pain. All testing was completed at the musculoskeletal laboratory at the University College of Northern Denmark.

2.4. Sample size

A between‐group difference in pressure pain thresholds of 15% was used as the minimal detectable difference (Nascimento et al., 2020; Walton et al., 2011). A two‐tailed power analysis was performed using a two‐way repeated‐measures analysis of variance (ANOVA). G*Power V.3.1.9.4 (Heinrich‐Heine‐Universität Düsseldorf, Düsseldorf, Germany) was used for calculation. According to the analysis, a sample size of 31 participants would be sufficient to detect a 15% difference in PPT, assuming a between‐groups correlation of 0.9 (Black et al., 2017; Nascimento et al., 2020), β = 0.1 (90% power), an α‐level of 0.05 and a 20% loss to follow‐up.

2.5. Randomisation

The order of sessions (pain first or stretch first) was randomized a priori to ensure that order effects did not systematically bias the results. Counterbalanced block randomisation on a 1:1 ratio in blocks of four was performed a priori by the investigator (MPS). The allocation was distributed and stored in sealed opaque envelopes handled only by the two experimenters (LØH and KKE), who assigned participants to the intervention. Experimenters 1 and 2 enrolled participants. All outcome measurements (pain sensitivity, range of motion and passive resistive torque measures) were performed by Experimenters 1 and 2. The participants and Experimenters 1 and 2 were blind to the range of motion and passive resistive torque measurements. Participants were blind to the results of the pressure pain threshold measurements. The investigator (MPS), blinded to the assessments and group allocations, performed the statistical analyses and interpretation of the results.

2.6. Statistical analysis

The data were analysed with descriptive and inferential statistics using SPSS 29 (SPSS Inc., Chicago, IL, USA). Continuous variables are presented with mean ± SD and 95% CIs. Variables were tested for normality using a visual inspection of histograms and Q‐Q plots and a test of deviation from normality (Shapiro–Wilk test). The homogeneity‐of‐variance assumption was assessed by testing for sphericity. Parameters that did not meet the assumption of sphericity were corrected using the Greenhouse–Geisser adjustment. Two‐way repeated measures analysis of variance were used to examine the absolute effect of time (two levels: pre‐stretch and post‐stretch) × intensity (two levels: point of stretch and first onset of pain), with session order as group factor, on the primary outcome measures regional and distant pressure pain thresholds and secondary outcome measures range of motion and passive resistive torque. In case of significant factors or interactions in the RM‐ANOVAs, Bonferroni corrected post hoc paired comparisons of pairs of each independent factor were performed. Effect size estimates were calculated using partial eta square (ηp2) for ANOVA and were interpreted as small (ES 0.01), moderate (ES 0.06) and large (ES 0.14) (Cohen, 1973). The percentage of change between measurements was calculated to depict the effect of stretching on pain sensitivity. Wilcoxon signed rank sum tests were used to compare the relative (percentage) change in pressure pain thresholds from baseline to post‐stretch at the regional and distant sites between stretching to the point of stretch and stretching to the first onset of pain. Spearman's rank correlations were calculated to describe the association between pressure pain thresholds following stretching at different intensities (i.e. stretching to the point of stretch and stretching to the first onset of pain). An alpha level of 0.05 was defined for the statistical significance of all tests.

3. RESULTS

Thirty‐one participants (n = 24 female) were available for analysis. The participants had a mean ± standard deviation (range) age of 29.7 ± 10 (20–54) years, height of 1.72 ± 0.07 (1.55–1.85) m, weight of 69.3 ± 9.6 (55–90) kg and BMI of 23.4 ± 2.3 (18–28.4) kg/m2. The average number of days between sessions was 4 ± 3 days.

Mean values for range of motion are presented in Table 1.

TABLE 1.

Absolute values (means (SD) and 95% CI) for range of motion.

Point of stretch First onset of pain
Pres‐stretch Post‐stretch Pre‐stretch Post‐stretch
Range of motion (deg.) 182.5 ± 17.0 deg. 183.6 ± 18.8 deg. 179.6 ± 19.6 deg. 189.9 ± 17.3 deg.*
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Note: Knee extension range of motion measured before (pre‐stretch) and after stretching (post‐stretch) to the first sensation of stretch and the first onset of pain. Data are reported as absolute (mean ± SD). Significantly different compared with pre‐stretch (*) (p < 0.05).

No significant interactions were found for pressure pain thresholds at the regional site (F[1,30] = 0.026, p > 0.874, ηp2 = 0.001). There was a main effect of time on pressure pain thresholds at the regional site (F[1,317] = 36.526, p = 0.001, ηp2 = 0.549). Post hoc tests demonstrated a 22% increase in pressure pain thresholds from baseline to post‐stretch following stretching to the point of stretch (93.2 kPa, 95% CI: 41.9–144.5, p = 0.001) and a 20% increase in pressure pain thresholds from baseline to post‐stretch following stretching to the first onset of pain (90.3 kPa, 95% CI: 41.8–138.8, p = 0.001) (Figure 2).

FIGURE 2.

FIGURE 2

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Pressure pain thresholds at the tibialis anterior site (regional site) measured before (pre‐stretch) and after stretching (post‐stretch) to the first sensation of stretch and the first onset of pain. Data are reported as absolute mean ± SD. Significantly different compared with pre‐stretch (*) (p < 0.05).

No significant interactions were found for pressure pain thresholds at the distant site (F[1,30] = 0.005, p > 0.945, ηp2 = 0.001). A main effect of time was found with a significant difference in pressure pain thresholds at the distant site (F[1,590] = 18,406, p = 0.001, ηp2 = 0.380). Post hoc tests demonstrated a 15% increase in pressure pain thresholds from baseline to post‐stretch following stretching to the point of stretch (50.9 kPa, 95% CI: 8.4–93.4, p = 0.012) and a 15% increase in pressure pain thresholds from baseline to post‐stretch following stretching to the first onset of pain (52.1 kPa, 95 %CI: 12.9–91.2, p = 0.004) (Figure 3).

FIGURE 3.

FIGURE 3

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Pressure pain thresholds at the deltoid site (widespread site) measured before (pre‐stretch) and after stretching (post‐stretch) to the first sensation of stretch and the first onset of pain. Data are reported as absolute mean ± SD. Significantly different compared with pre‐stretch (*) (p < 0.05).

Significant interactions for range of motion were found between intensity and time (F[1,30] = 22.247, p < 0.001 ηp2 = 0.431) and intensity and session order (F[1,29] = 9.961, p = 0.013 ηp2 = 0.194). Therefore, analyses of simple main effects were run. Post hoc tests demonstrated a 5.4% increase in range of motion from baseline to post‐stretch following stretching to the first onset of pain (10.3°, 95%CI: 2.3–10.5, p = 0.001). Post hoc tests demonstrated no significant increase in passive knee extension range of motion from baseline to post‐stretch following stretching to the point of stretch (1.1°, 95% CI: −2.4–4.5, p = 1.00).

Post hoc tests showed no evidence of between‐group order effects p = 0.169 .

No significant interactions were found for passive resistive torque (F[1, 3] = 1.554, p = 0.206, ηp2 = 0.051). No significant main effect of time was found for passive resistive torque (F[1,3] = 1.048, p = 0.376, ηp2 = 0.035).

There were no significant differences in the relative (percentage) change in pressure pain thresholds from baseline to post‐stretch at the regional or distant sites between stretching to the point of stretch and stretching to the point of pain (p > 0.991).

Significant correlations for post‐stretch pressure pain thresholds between the regional and distant sites were found following stretching to the point of stretch (Rho = 0.898, p = 0.001) and stretching to the point of pain (Rho = 0.836, p = 0.001).

No harm or adverse events were reported .

4. DISCUSSION

The present study investigated the effect of two different stretching intensities on the primary outcome of regional and distant pain sensitivity and secondary outcomes, range of motion and passive resistive torque. The main findings demonstrated that regional and distant pain sensitivity decreased following stretching. However, in contrast to our expectations, stretching intensity did not affect the hypoalgesic effect of stretching in a dose–response relationship.

The present results showed a significant widespread analgesic effect following acute bouts of stretching. These results add to the growing body of research suggesting the existence of a systemic response to stretching exercises that produce SIH (Larouche et al., 2020; Støve, Hirata, & Palsson, 2024; Støve, Thomsen, et al., 2024). The present findings may have important clinical implications and may translate to rehabilitation efforts in patients with chronic pain. However, applying stretching exercises for pain management requires understanding the intensity thresholds necessary to elicit a clinically significant analgesic effect. The present results show that a higher intensity of acute stretching did not generate a larger analgesic response than lower intensity stretching. The present findings, therefore, do not support a dose–response relationship between local and distant pain sensitivity and stretching intensity following acute bouts of stretching.

Current evidence suggests that the analgesic effect of stretching exercises is generated by endogenous modulation of somatosensory input [6, 7], indicating that SIH and EIH could be mediated through common mechanisms. Although the underlying mechanisms behind EIH are insufficiently understood, they are likely multifaceted (Song et al., 2022; Tomschi et al., 2022). It has been suggested that EIH occurs partially due to the activation of descending inhibitory pathways (Rice et al., 2019). However, evidence also shows spatial and temporal differences between EIH and CPM, suggesting that local and segmental mechanisms may play an essential role in EIH (Kosek & Lundberg, 2003; Vaegter et al., 2013). Consistent with previous findings (Larouche et al., 2020; Støve, Hirata, & Palsson, 2024; Støve, Thomsen, et al., 2024), the present study showed that the hypoalgesic effect of stretching exercises occurred with multisegmental manifestations. The present results thus further support the presumption that stretching exercises activate central inhibitory mechanisms (Larouche et al., 2020; Støve, Hirata, & Palsson, 2024; Støve, Thomsen, et al., 2024). However, when interpreting the point estimates, the present results suggest that the SIH response at the regional site was more pronounced than at the distant site. This is in agreement with previous findings (Støve, Thomsen, et al., 2024) and may also suggest the involvement of both central and local/segmental pain mechanisms in SIH. These results support the hypothesis that SIH and EIH could be mediated through common mechanisms.

Endogenous modulation of somatosensory input is likely a saturable phenomenon. Therefore, the inhibitory range of central pain modulation may reach a ceiling effect (Granot et al., 2008). Evidence suggests that the efficacy of EIH may be intensity‐dependent and high‐intensity exercise generally produces more significant EIH effects than moderate to low‐intensity exercises (Naugle et al., 2014; Rice et al., 2019; Wu et al., 2022). Surprisingly, the present results showed no intensity dependency of SIH. This may indicate that the intensity threshold required to elicit SIH is lower than that of EIH. The present results indicate that low‐intensity stretching may significantly modulate pain and that increased intensity may not yield a greater inhibitory response.

Previous research has found that an acute bout of stretching will most often increase ROM regardless of stretching intensity (Behm et al., 2023). However, no statistically significant differences in ROM were found following stretching to the point of stretch in the present study. Although this finding was unexpected, the present results reflect previous observations suggesting that higher intensity acute static stretching results in significantly greater acute increases in ROM (Bryant et al., 2023; Fukaya et al., 2020, 2022; Takeuchi et al., 2021). Taken together, the present results seem consistent with previous research, which suggests that the changes in the range of motion following acute bouts of stretching are associated with but not linearly dependent on the extent of the analgesic effect (Støve et al., 2021).

Although extensive research has shown positive effects of acute and regular stretching on musculoskeletal and nociplastic pain, there is little evidence to support applicable protocol prescriptions for pain reduction (Behm et al., 2021). The present findings showed a significant acute hypoalgesic effect of stretching exercises regardless of stretching intensity. This invites the hypothesis that for pain relief, stretching at a lesser intensity (i.e. the sensation of stretch) may be preferable to higher intensities (i.e. the first onset of pain).

5. LIMITATIONS

This study only assessed the acute effect of stretching intensity on regional and distant pain sensitivity. Therefore, it is not possible to reject the potential existence of a dose–response relationship between stretching intensity and the analgesic effect following regular stretching.

Determining the causal effect of acute bouts of static stretches and pain reduction would require a comparative study design. Current recommendations for the development and reporting of control interventions in mechanistic trials recommend designing control interventions that are as similar as possible to the tested intervention, apart from the components examined by the study (i.e. placebo/sham interventions) (Hohenschurz‐Schmidt et al., 2023). However, as most people have prior experience with stretching exercises, designing a true placebo/sham stretching intervention may be challenging. Accordingly, further research is warranted to assess how statistic stretching compares with a no‐treatment/control group. It is imperative, however, that future comparative trials use large(r) sample sizes, given that small studies are inherently biased to find larger effects (Dechartres et al., 2013).

The study population consisted of healthy participants. Considering that the efficiency of endogenous pain inhibitory mechanisms is reduced in patients suffering from chronic pain, it is unclear whether patients with pain would experience similar acute analgesic effects of muscle stretching as demonstrated in the present study.

6. CONCLUSION

The results showed that local and widespread pain sensitivity decreased following acute stretching, regardless of stretching intensity. No differences in pain sensitivity were found between stretching to the point of stretch (discomfort) or stretching to the first onset of pain. Thus, the results showed no evidence of a dose–response relationship between stretching intensity and the analgesic effect. However, further research is needed to investigate the hypoalgesic effects of stretching exercises in clinical populations.

AUTHOR CONTRIBUTIONS

I have added a paragraph at the end of my manuscript (between the Discussion and the References). MPS conceived the study. MPS, AR, JLT and SPM were involved in planning the study. LØH and KKE performed the data collection. MPS conducted the analyses and interpretation, wrote the paper's first draft and prepared Figures 1, 2, 3, which AR, LØH, KKE, JLT and SPM critically revised in multiple rounds. All authors contributed to the interpretation of the findings. All authors have read and approved the final manuscript.

FUNDING INFORMATION

This project was funded by the Frimodt‐Heinecke Foundation. The funding body had no role in the design, collection, analysis, interpretation of data or in writing the manuscript.

CONFLICT OF INTEREST STATEMENT

The authors declare that they have no competing interests.

CONSENT TO PARTICIPATE

Participants provided written informed consent to participate in the study. The trial was reported to the Danish Data Protection Agency (Project ID 24000509), registered at ClinicalTrials.gov (Trial registration number NCT05989490) and approved by the North Denmark Region Committee on Health Research Ethics (N‐20210044).

CONSENT FOR PUBLICATION

Not applicable.

USE OF ARTIFICIAL INTELLIGENCE

Artificial Intelligence Generated Content (AIGC) tools—such as ChatGPT and others based on large language models (LLMs) were not used in any part of the preparation of this manuscript.

ACKNOWLEDGEMENTS

Not applicable.

Støve, M. P. , Hansen, L. Ø. , Elmbæk, K. K. , Magnusson, S. P. , Thomsen, J. L. , & Riis, A. (2025). The effect of stretching intensity on pain sensitivity: A randomized crossover study on healthy adults. European Journal of Pain, 29, e4750. 10.1002/ejp.4750

DATA AVAILABILITY STATEMENT

The datasets used and analysed during the current study are available from the corresponding author upon reasonable request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The datasets used and analysed during the current study are available from the corresponding author upon reasonable request.

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