Skip to main content
NCBI home page
Wiley Open Access Collection logoLink to Wiley Open Access Collection
. 2026 Apr 10;63(7):e70475. doi: 10.1111/ejn.70475

Neural and Mechanical Adaptations During Static Stretching With Different Amplitudes

Denis César Leite Vieira 1,2,✉, Martim Bottaro 2, Marion Hitier 1, João Luiz Quaglioti Durigan 3, Nicolas Babault 1
PMCID: PMC13066921  PMID: 41958299

ABSTRACT

This study examined neural and mechanical responses at the onset of prolonged static stretching performed at different amplitudes, their progression during the stretching period, and alterations immediately after its completion. Thirteen healthy adults completed three randomized sessions: control (15‐min rest in neutral ankle angle), 15 min of submaximal stretching (ROMmax − 5°), and 15 min of supramaximal stretching (ROMmax + 5°). Spinal excitability (H max/M max), evoked contractile properties (PTT), voluntary strength (MVC), passive torque, and maximal range of motion (ROMmax) were assessed at baseline (PRE), during stretching (T00, T05, T10, and T15), and immediately after stretching (POST). Spinal excitability decreased at stretch onset but progressively increased during stretching (T00–T15, p < 0.05), with greater facilitation in supramaximal (soleus and gastrocnemius, p < 0.001) than submaximal conditions (soleus only, p < 0.001). These changes were transient, returning to baseline at POST (p < 0.001). Passive torque increased during both stretching (p < 0.05); however, in supramaximal, it declined after 5 min and stabilized until 15 min (p = 0.001), while in submaximal, it declined only at 15 min (p = 0.043). Both conditions reduced PTT (p < 0.05), with slightly greater decreases in the supramaximal condition. MVC decreased similarly after both protocols (p < 0.05). ROMmax improved in both (p < 0.05), with slightly greater gains in the supramaximal condition. Static stretching amplitude modulates neuromechanical adaptations. Both supramaximal and submaximal protocols reduced voluntary strength but improved flexibility, with greater spinal excitability after the initial decrease and slightly larger ROMmax gains at supramaximal amplitude.

Keywords: muscle performance, neural adaptations, peripheral adaptations, stretch, warm‐up

Prolonged static stretching elicits biphasic modulation of spinal excitability characterized by initial suppression followed by progressive facilitation that is amplitude‐dependent, with supramaximal stretching producing greater neural adaptations in both soleus and gastrocnemius muscles. In contrast, submaximal stretching only affects the soleus. Concurrently, passive torque initially increased during stretch application but subsequently declined more rapidly under supramaximal conditions (5 min) compared to submaximal conditions (15 min), indicating differential viscoelastic adaptations within the muscle‐tendon unit.

graphic file with name EJN-63-0-g006.jpg

Abbreviations

CON

control condition

EMG

electromyography

E reflex/M max

exteroceptive reflex normalized by maximal M wave

ES

effect size

GM

gastrocnemius medial

H max/M max

maximal Hoffman reflex normalized by maximal M wave

H reflex

Hoffman reflex

MEP/M max

motor evoked potential normalized by maximal M wave

M max

maximal M wave

MVC

maximal voluntary contraction

PIC

persistant inward current

POST

post moment measures

PRE

PRE moment measures

PT

passive torque

PTT

peak twitch torque

ROMmax

maximal range of motion

Submaximal

submaximal static stretching condition

Supramaximal

supramaximal static stretching condition

T00

measures at the beginning of static stretching

T05

measures 5 min after the beginning of stretching

T10

measures 10 min after the beginning of stretching

T15

measures 15 min after the beginning of stretching

T reflex

tendon reflex

T reflex/M max

tendon reflex normalized by maximal M wave

1. Introduction

Static stretching has been consistently reported to impair muscle strength and power acutely (Behm and Chaouachi 2011; Behm et al. 2016; Warneke et al. 2025). Despite this evidence, it remains widely employed by physically active individuals, primarily due to its effectiveness in enhancing joint range of motion (ROM) (Babault et al. 2021). Indeed, evidence from the literature consistently demonstrates that static stretching elicits acute increases in joint ROM and flexibility (Behm and Chaouachi 2011; Behm et al. 2016; Warneke et al. 2025). Moreover, these effects appear to be duration‐dependent, with longer stretching protocols producing greater improvements compared to shorter ones (Matsuo et al. 2013). Consequently, prolonged static stretching with varying amplitudes has been widely implemented in clinical practice to improve joint flexibility (Behm et al. 2001; Warneke et al. 2025). However, the influence of stretching amplitude on acute flexibility adaptations following long‐lasting static stretching (i.e., > 5 min) remains uncertain. This uncertainty largely arises because most previous studies have investigated different amplitudes only within shorter protocols (i.e., 20 s to ~3 min), and their results have been inconsistent (Kataura et al. 2017; Santos et al. 2020; Takeuchi, Sato, Kiyono, et al. 2021; Marchetti et al. 2022).

It has been proposed that neural mechanisms, particularly spinal excitability, play a key role in determining muscle flexibility and may thus contribute to adaptations in joint ROM (Guissard et al. 2001). For instance, spinal excitability mediated by afferent pathways conveys input from muscle spindles, that is, proprioceptive receptors arranged in parallel with muscle fibers and innervated by group Ia and II afferent fibers, to spinal motor neurons (Matthews 1931; Trajano and Blazevich 2021). These receptors can mediate stretch reflexes during stretching maneuvers, theoretically increasing motor neuron excitability and muscle activation, thereby influencing ROM assessments (Gollhofer and Rapp 1993; Blazevich et al. 2014; Mizuno 2017). Consequently, most assessments of passive maximal ROM and muscle–tendon stiffness are performed at low angular velocities to minimize stretch reflex activation from muscle spindle afferents, which could otherwise elevate spinal excitability and, consequently, passive tension during muscle lengthening (Blazevich et al. 2014; Bouvier et al. 2017; Mizuno 2017; Vieira et al. 2021, 2025).

However, evidence regarding the effects of static stretching on spinal excitability remains inconsistent (Budini et al. 2019; Pulverenti et al. 2020). For example, studies using the Hoffman reflex normalized to the maximal M wave (H max/M max) to control for changes in efferent muscle fiber excitability and/or the tendon reflex (T reflex) have reported that static stretching can acutely modulate spinal excitability (Budini et al. 2017, 2019). These effects, however, appear to be transient, returning to baseline within minutes after stretching cessation (Budini et al. 2019). Conversely, other investigations assessing the tendon reflex normalized by the maximal M wave (T reflex/M max) have found no significant changes in spinal excitability following static stretching (Pulverenti et al. 2021), and protocols involving five 60‐s bouts of static stretching have similarly shown no effect on H max/M max (Pulverenti et al. 2020). These inconsistencies may be partly attributable to methodological differences, including variations in normalization procedures (e.g., normalization to M max), heterogeneity in stimulation protocols used to assess H max/M max, T reflex, and T reflex/M max, as well as differences in stretching volume across the studies (Budini et al. 2017, 2019; Pulverenti et al. 2020, 2021). Beyond these inconsistencies, the acute effects of long‐lasting static stretching performed at amplitudes above or below the maximal point of discomfort, an approach widely implemented in clinical practice to improve joint flexibility, remain unclear (Behm et al. 2001; Warneke et al. 2025).

In addition to neural mechanisms, peripheral adaptations within the muscle–tendon unit are thought to contribute to acute increases in joint ROM (Matsuo et al. 2013; Hirata et al. 2017). The acute mechanical responses of the muscle–tendon unit to prolonged static stretching are relatively well established (Matsuo et al. 2013; Hirata et al. 2016). For instance, reductions in evoked contractile responses have been observed following 20 min of static stretching (Behm et al. 2001), which may reflect alterations in cross‐bridge function and muscle–tendon stiffness (Ryan et al. 2011). Supporting this, both shear‐wave elastography and torque–angle analyses consistently demonstrate that 5 min of stretching performed at maximal tolerable discomfort decreases muscle–tendon stiffness (Matsuo et al. 2013; Hirata et al. 2017). These findings suggest that static stretching can reduce the viscoelastic properties of the muscle–tendon unit, thereby lowering passive tension during muscle lengthening and contributing to improvements in joint ROM. However, as with neural mechanisms, the available evidence is limited to stretching protocols performed up to the maximal point of discomfort (Matsuo et al. 2013; Hirata et al. 2016, 2017); therefore, the influence of different static stretching amplitudes on muscle–tendon stiffness responses remains insufficiently understood.

While most investigations have focused on the acute outcomes observed following static stretching (Hirata et al. 2017; Budini et al. 2019; Pulverenti et al. 2021), the neurophysiological and mechanical adaptations that occur during the stretching maneuver itself remain less well characterized (Guissard et al. 2001; Opplert and Babault 2018). Current evidence suggests that spinal excitability decreases during muscle lengthening (Guissard et al. 2001) and passive static stretching (Budini et al. 2018), with the magnitude of inhibition being proportional to the extent of muscle lengthening throughout the stretching maneuver (Guissard et al. 2001; Guissard and Duchateau 2006). Additionally, muscle–tendon stiffness may transiently increase with muscle lengthening (Mizuno and Umemura 2016; Mizuno 2017). However, these findings are primarily derived from protocols involving short‐duration static stretches and/or single muscle‐lengthening movements (Guissard et al. 2001; Mizuno and Umemura 2016; Mizuno 2017; Budini et al. 2018), which in turn may not represent the most effective stretching protocols to be applied in sports and rehabilitation settings to acutely enhance the ROM (Babault et al. 2021; Warneke et al. 2025). Indeed, as previously reported, despite inconsistent findings concerning stretching amplitude (Kataura et al. 2017; Santos et al. 2020; Takeuchi, Sato, Kiyono, et al. 2021; Marchetti et al. 2022), greater improvements in flexibility have been observed with longer‐duration static stretching protocols (Matsuo et al. 2013).

Therefore, the neurophysiological and mechanical responses elicited by the most adequate protocols for acute ROM improvements, particularly prolonged static stretching performed at varying amplitudes, remain poorly understood. Thus, given the importance of characterizing these responses to optimize the safety and effectiveness of stretching prescriptions (Guissard et al. 2001; Vianna et al. 2009), and considering that the acute effects of long‐lasting static stretching performed at amplitudes above or below the maximal point of discomfort remain unclear. This study was designed to examine neural and mechanical responses at the onset, during, and immediately after prolonged static stretching performed at different amplitudes. We hypothesized that static stretching would transiently reduce spinal excitability, particularly at higher amplitudes, but would progressively increase throughout the stretching period with larger enhancements at higher amplitudes. Conversely, muscle‐tendon stiffness was hypothesized to decrease during stretching, with greater reductions at larger amplitudes.

2. Methods

2.1. Ethical Approval

The study received approval from the Ethics Committee for Research in STAPS (CERSTAPS IRB00012476‐2023‐17‐02‐229). All individuals were fully informed about the experimental procedure and purpose of the study, and they read and signed an informed consent form. The study followed the standards set out by the Declaration of Helsinki.

2.2. Participants

Thirteen volunteers (7 women and 6 men) participated in this study. The mean age ± standard deviation (SD), height, body mass, and physical activity per week were 27.2 ± 6.8 years, 170.7 ± 9.7 cm, 69.9 ± 16.9 kg and 5.6 ± 2.8 h. None of the participants reported any lower limb injuries or back pain in the last 3 months, nor any specific hamstrings or triceps surae injuries in the previous 2 years. During the present experiment, participants were asked to maintain their regular physical activities and dietary intake. They were also advised to refrain from intensive activity for at least 2 days before an experimental session.

2.3. Experimental Procedures

A randomized, controlled, and crossover design was used to explore acute neuromechanical adaptations during and immediately after 15 min of static stretching performed at different amplitudes. Participants visited our lab on four occasions separated by 72 h. The first visit was used to familiarize volunteers with all test procedures and static stretching protocols. The following three other experimental sessions (randomly presented) were: (1) control session (control); (2) 15 min of static stretching performed at supramaximal amplitudes (supramaximal); and (3) 15 min of static stretching performed at submaximal amplitudes (submaximal).

During all experimental sessions, no warm‐up was performed to avoid any influence on pretests and to verify the effect of static stretching as an isolated warm‐up component. Initially, the recruitment curves from tibial nerve electrical stimulation were performed to identify the intensities relative to H max and M max. Subsequently, participants remained at rest for 10 min. After this rest period, the pre‐tests (PRE) were conducted, with the ankle at neutral position (i.e., 0°), to determine spinal excitability (H max/M max), muscle performance (maximal isometric voluntary contraction [MVC] and maximal range of motion [ROMmax]), and muscle‐tendon stiffness (passive torque [PT] and peak twitch torque). These test procedures were repeated immediately after (POST) each experimental condition (Figure 1).

FIGURE 1.

FIGURE 1

Open in a new tab

Experimental design. Control = experimental protocol with ankle positioned at neutral, that is, no stretching, H max = maximal Hoffman reflex, M max = maximal M wave, MVC = maximal voluntary contraction, POST = measurements immediately after experimental protocol, PRE: measurements before the experimental protocol, ROMmax = maximal range of motion, Submaximal = experimental protocol with ankle position during the stretching at ROMmax − 5°, Supramaximal = experimental protocol with ankle position during the stretching at ROMmax + 5°, T00 = measurement at the onset of experimental protocol, T05 = measurement 5 min after the onset of experimental protocol, T10 = measurement 10 min after the onset of experimental protocol, T15 = measurement 15 min after the onset of experimental protocol.

Additionally, during the experimental protocols, at each 5 min from the begin of the protocol (T00, T05, T10, and T15), six tibial nerve electrical stimulation were done at intensities relative to H max and M max (three electrical stimulation at each intensity), and PT were register to measure the dynamics of changes in spinal excitability, muscle‐evoked contractile properties, and muscle‐tendon stiffness during prolonged static stretching performed at different amplitudes and control conditions. The PRE and POST measures were done with ankle at neutral position, that is, 0° of plantarflexion/dorsiflexion in all experimental conditions, and T00, T05, T10, and T15 measures were done with the ankle positioned according to the daily experimental protocol, that is, supramaximal (ROMmax + 5°), submaximal (ROMmax − 5°), or control (neutral position). Therefore, the experimental protocol was not interrupted to perform the assessment.

All experimental procedures were completed on the right plantar flexor muscles using an isokinetic dynamometer (Biodex System 4, BIODEX Corporation, Shirley, NY, USA). The participants were positioned in the supine position, with the hip in a neutral position (0° flexion/extension), the right knee fully extended, and the left knee flexed at 90° in all experimental sessions. To minimize heel displacements, the foot was positioned and fastened inside a shoe and firmly attached to the footplate of the dynamometer with straps. The lateral malleolus was aligned to the center of rotation of the dynamometer. Volunteers' positioning was carefully registered and reproduced to permit consistent measurements during the different experimental sessions.

2.4. Electromyography

Surface electromyography (EMG) activity was recorded from the soleus (SOL) and gastrocnemius medialis (GM) muscles of the right leg. The skin was shaved and cleaned with alcohol to minimize impedance. Bipolar silver–chloride electrodes (10‐mm diameter, 2‐cm interelectrode distance) were used. For SOL, electrodes were placed 2 cm distal to the Achilles tendon intersection, while for GM, they were positioned over the muscle belly. The reference electrode was placed over the contralateral patella (Pulverenti et al. 2020). The EMG signal was amplified with a bandwidth frequency range from 10 Hz to 5 kHz (gain = 500). EMG traces were recorded using a Biopac MP 200 system (Biopac System, Santa Barbara, CA, USA) at a sampling rate of 10 kHz and stored for analysis with the AcqKnowledge software (Ver. 6.0, Biopac System, Santa Barbara, CA, USA).

2.5. H‐Reflex, M‐Wave, Peak Twitch Torque, and PT Assessments

Transcutaneous electrical nerve stimulation was used to assess the H‐reflex, M‐wave, and Peak Twitch Torque (Opplert and Babault 2019; Vieira et al. 2021, 2025). Additionally, PT assessment was performed immediately prior to the transcutaneous electrical nerve stimulation (Vieira et al. 2025). The posterior tibial nerve was stimulated with rectangular pulses (1 ms) using a Digitimer stimulator (DS7R, Hertfordshire, UK). The cathode electrode (10 mm in diameter) was placed in the popliteal fossa, and the anode electrode (5 × 10 cm) was placed over the patella on the anterior surface of the knee. The optimal stimulation site was determined by eliciting the largest M‐wave at a given intensity using a handheld stimulation probe. Then, the stimulation electrode was pasted to the site (Vieira et al. 2025).

The recruitment curve was obtained by increasing stimulation intensity in 2‐mA increments from 0 mA to the SOL maximal peak‐to‐peak H‐reflex amplitude (H max). After reaching H max, 5‐mA increments were used until the SOL maximal peak‐to‐peak M‐wave amplitude (M max). For PRE and POST measures, as well as for measures during experimental protocols (T00, T05, T10, and T15), three electrical stimuli were delivered at an intensity relative to the SOL H max, and three electrical stimuli at 120% of the SOL M max were delivered, with a 10‐s rest interval (Figure 2). The intensities were the same for PRE, T00, T05, T10, T15, and POST moments of each experimental session. The use of a constant current intensity throughout an experimental session is common in the literature (Opplert et al. 2020; Vieira et al. 2025). The order of stimuli (i.e., H max or M max) was randomized for each participant. The mean H‐reflex and M‐wave amplitudes of the SOL and GM, obtained from the three stimuli at each intensity relative to the SOL H max and SOL M max, were considered the H max and M max of each muscle. H max was then normalized by M max (H max/M max) to minimize the influence of peripheral changes. Additionally, the torque was recorded for the three electrical stimuli delivered at 120% of M max, and the mean peak torque induced by plantar flexion across the three attempts was used for PTT analysis (Opplert and Babault 2019; Vieira et al. 2021, 2025).

FIGURE 2.

FIGURE 2

Open in a new tab

Representative waveforms from raw data of one participant (i.e., same individual in all time points of all experimental conditions). Control = experimental protocol with ankle positioned at neutral, that is, no stretching, H max = maximal Hoffman reflex, M max = maximal M wave, mV = millivolts, N*m = Newton/m, POST = measurements immediately after experimental protocol, PRE: measurements before the experimental protocol, Submaximal = experimental protocol with ankle position during the stretching at ROMmax − 5°, Supramaximal = experimental protocol with ankle position during the stretching at ROMmax + 5°, T00 = measurement at the onset of experimental protocol, T05 = measurement 5 min after the onset of experimental protocol, T10 = measurement 10 min after the onset of experimental protocol, T15 = measurement 15min after the onset of experimental protocol.

Moreover, for PT analysis, ankle torque was recorded from a 10‐millisecond window immediately preceding the first electrical stimulation at each time point (i.e., PRE, T00, T05, T10, T15, and POST) in each experimental condition (Vieira et al. 2025). PT is often considered a marker of muscle–tendon stiffness, and evoked contractile properties (i.e., peak twitch torque), although primarily reflecting contractile capacity, may also indicate changes in muscle and tendon stiffness. Therefore, both PT and peak twitch torque were considered as surrogate markers of muscle‐tendon stiffness for our purpose (Ryan et al. 2011; Vieira et al. 2021).

2.6. Maximal Voluntary Contraction

Two isometric plantar flexor Maximal voluntary contractions (MVCs) with the ankle at a neutral position were performed, respecting a rest interval of 1 min to determine the maximal voluntary peak torque. The individuals were verbally encouraged to produce maximal force during MVCs; the peak torque for each MVC was recorded, and the highest value was used for analysis.

2.7. Range of Motion

ROMmax was assessed using an isokinetic dynamometer (Biodex System 4, BIODEX Corporation, Shirley, NY, USA). Participants were positioned supine, with the hip in neutral (0° flexion/extension), the right knee fully extended, and the left knee flexed to 90°. During the ROMmax assessment, the ankle was passively dorsiflexed by the dynamometer at a constant angular velocity of 5°·s−1, starting from the neutral ankle position (0° plantarflexion/dorsiflexion). Participants were instructed to press a handheld button to voluntarily terminate the movement at the point of maximal stretch discomfort. ROMmax was defined as the ankle dorsiflexion angle at which the participant pressed the button to stop the movement (Vieira et al. 2025).

2.8. Experimental Protocols

During static stretching, participants lay supine with the hip in a neutral position (0° flexion/extension), the left knee flexed at 90°, the right knee fully extended, and the right foot secured to the isokinetic dynamometer. In both stretching conditions, the ankle was passively rotated at a slow velocity (5°·s−1) from the neutral position to either 5° beyond (supramaximal) or 5° short of (submaximal) the previously determined maximal passive dorsiflexion at the beginning of each experimental session. Participants then remained in the stretched position for 15 min. During the control session (CON), participants rested in the supine position for 15 min with the ankle secured to the dynamometer in the neutral position.

2.9. Statistical Analysis

The data were reported as mean ± standard deviation (SD). Data reliability was assessed using the intraclass correlation coefficient (ICC3,3), with ICC scores < 0.5 considered poor, 0.5–0.74 moderate, 0.75–0.9 good, and > 0.9 excellent (Atkinson and Nevill 1998; Koo and Li 2016). Moreover, a generalized mixed model with preintervention measurements for each condition (supramaximal, submaximal, and control) as fixed factors, and participants as a random intercept to account for interindividual variability, was also used to assess systematic error (Atkinson and Nevill 1998). The main aim of the study was assessed using the generalized mixed model analysis with condition (supramaximal, submaximal, and control), and time (PRE, T00, T05, T10, T15, and POST for SOL and GM H max/M max, PTT and PT; and PRE, and POST for MVC and ROMmax) as fixed factors, and participants as random intercept to account for interindividual variability. In addition, for SOL and GM H max/M max, PTT, and PT, the T00 values were included as covariates. Additionally, only for PTT, the PT of all moments (i.e., PRE, T00, T05, T10, T15, and POST) were also included as covariates, since all experimental protocols were performed with the ankle in different positions, which could affect both H max/M max, PTT, and PT measures (Guissard et al. 2001). When a significant main effect or interaction was detected, a Tukey post hoc test was conducted. The significance level for all comparisons was set at p < 0.05. The effect size between PRE and POST, and between T00 and T15 measures were calculated from the following formulas: POST mean − PRE mean/PRE SD, T15 mean − T00 mean/T00 SD, respectively, and classified as trivial (< 0.35), small (0.35–0.80), moderate (0.80–1.50), and large (> 1.5) effect size (Rhea 2004). All statistical procedures were performed using Jamovi Software (Version 2.6.44, The Jamovi Project, Sydney, Australia, available free at http://jamovi.org). Additionally, sample size power was determined a posteriori using RStudio (Ver 2023.03.1, Posit Software, PBC, Boston, MA, USA), following the recommendations of Kumle et al. (2021) for power analyses with the available data as the starting point. We defined the SOL H max/M max as the primary dependent variable. Our sample of 13 subjects was used as a random intercept. The subjects were assessed at 6 time points (PRE, T00, T05, T10, T15, and POST) across three conditions (control, submaximal, and supramaximal), with time and condition treated as fixed factors of the generalized mixed model. Therefore, we had 234 measures for the primary variable. Thus, considering the procedures of Kumle et al. (2021) for power analyses with the available data as the starting point, the power was 0.89 and 0.94 for 12 and 13 subjects, respectively. Given that a power > 0.80 is considered good to excellent (Kumle et al. 2021), we deemed that the sample size of 12–13 subjects was sufficient. The dataset, custom RStudio code for power analyses, and figures showing individual data points are available at https://github.com/denisclvieira/STRETCHAMPLITUDE.git.

3. Results

There were no significant differences between the pre‐intervention conditions for SOL H max/M max (p = 0.362), GM H max/M max (p = 0.409), PTT (p = 0.196), PT (p = 0.072), MVC (p = 0.349), and ROMmax (p = 0.125), reporting no systematic error between the measures. Additionally, data reliability was good to excellent, as ICC3,3 values were 0.848 (good), 0.780 (good), 0.847 (good), 0.941 (excellent), 0.980 (excellent), and 0.973 (excellent) for SOL H max/M max, GM H max/M max, PTT, PT, MVC, and ROMmax, respectively.

For SOL H max/M max, there was no significant effect of condition (χ2 = 1.14, p = 0.565). However, there was a significant main effect of time (χ2 = 60.40, p = 0.001) and a significant time × condition interaction (χ2 = 91.03, p = 0.001). SOL H max/M max at T15 was greater than T00 and T05 in the supramaximal condition (p < 0.05), and T00 in the submaximal condition (p = 0.013). Additionally, SOL H max/M max at T10 was greater than T00 in the submaximal condition (p = 0.004). SOL H max/M max at T00, T05, T10, and T15 were significantly lower than at PRE and POST in both supramaximal (p < 0.01) and submaximal (p = 0.01) conditions. Conversely, there were no significant differences between PRE and POST SOL H max/M max in any experimental condition (p > 0.05), nor between T00, T05, T10, and T15, in the control condition (p > 0.05, Figure 3, Table 1). SOL H max/M max effect sizes between PRE and POST were 0.05 (trivial), 0.24 (trivial), and 0.26 (trivial) for control, submaximal, and supramaximal conditions, respectively. Additionally, SOL H max/M max effect sizes between T00 and T15 were −0.02 (trivial), 0.26 (trivial), and 0.42 (small) for control, submaximal, and supramaximal conditions, respectively.

FIGURE 3.

FIGURE 3

Open in a new tab

Neural adaptations (n = 13 participants). Control = control session, ES PREvs.POST = effect size between PRE and POST moments, ES T00vs.T15 = effect size between T00 and T15 moments, GM H max/M max = gastrocnemius medial maximal H reflex normalized by maximal M wave, POST = posttest, PRE = pretest, SOL H max/M max = soleus maximal H reflex normalized by maximal M wave, Submaximal = static stretching submaximal, Supramaximal = static stretching supramaximal, T00 = measure immediately at the begin of the experimental condition, T05 = measure 5 min after the begin of the experimental condition, T10 = measure 10 min after the begin of the experimental condition, T15 = measure 15 min after the begin of the experimental condition. #Significant differences with the T00 (p < 0.05). $Significant differences with T00, T05, T10, and T15 (p < 0.01).

TABLE 1.

Summary of statistical effects (time, condition, and interaction).

Comparisons/variables SOL H max/M max GM H max/M max PTT Passive torque MVC ROMmax
TIME MAIN EFFECT
PRE vs. POST ↔ ↔ ↓ ↔ ↑ ↓
T00 vs. PRE ↓ ↓ ↑ ↑ — —
T00 vs. T05 ↔ ↔ ↔ ↑ — —
T10 vs. T00 ↔ ↔ ↓ ↓ — —
T15 vs. T00 ↑ ↑ ↓ ↓ — —
POST vs. T15 ↑ ↑ ↓ ↓ — —
CONDITION MAIN EFFECT
Control vs. submaximal ↔ ↔ ↔ ↓ ↓ ↓
Control vs. supramaximal ↔ ↔ ↔ ↓ ↓ ↔
Submaximal vs. supramaximal ↔ ↔ ↔ ↓ ↔ ↔
INTERRATION TIME × CONDITION
Control PRE vs. POST ↔ ↔ ↔ ↔ — ↔
T00 vs. PRE ↔ ↔ ↔ ↔ — —
T00 vs. T05 ↔ ↔ ↔ ↔ — —
T10 vs. T00 ↔ ↔ ↔ ↔ — —
T15 vs. T00 ↔ ↔ ↔ ↔ — —
POST vs. T15 ↔ ↔ ↔ ↔ — —
Submaximal PRE vs. POST ↔ ↔ ↓ ↔ — ↓
T00 vs. PRE ↓ ↓ ↑ ↑ — —
T00 vs. T05 ↔ ↔ ↔ ↔ — —
T10 vs. T00 ↑ ↔ ↔ ↔ — —
T15 vs. T00 ↑ ↔ ↔ ↓ — —
POST vs. T15 ↑ ↑ ↓ ↓ — —
Supramaximal PRE vs. POST ↔ ↔ ↓ ↔ — ↓
T00 vs. PRE ↓ ↓ ↑ ↑ — —
T00 vs. T05 ↔ ↔ ↔ ↑ — —
T10 vs. T00 ↔ ↔ ↔ ↓ — —
T15 vs. T00 ↑ ↑ ↔ ↓ — —
POST vs. T15 ↑ ↑ ↓ ↓ — —
Open in a new tab

Abbreviations: − = no comparison performed in the statistical model or no significant main effect or interaction (p > 0.05), ↑ = Post hoc reported that first condition of the comparison were greater than second reported condition of the comparison (p < 0.05), ↓ = post hoc reported that first condition of the comparison were lesser than second reported condition of the comparison (p < 0.05), ↔ = post hoc reported that both conditions of the comparison were similar (p > 0.05), CON = control session, GM H max/M max = gastrocnemius medial maximal H reflex normalized by maximal M wave, MVC = maximal voluntary contraction, POST = posttest, PRE = pretest, PT = passive torque, PTT = peak twitch torque, ROMmax = maximal range of motion, SOL H max/M max = soleus maximal H reflex normalized by maximal M wave, Submaximal = static stretching submaximal, Supramaximal = static stretching supramaximal, T00 = measure immediately at the begin of the experimental condition, T05 = measure 5 min after the begin of the experimental condition, T10 = measure 10 min after the begin of the experimental condition, T15 = measure 15 min after the begin of the experimental condition.

For GM H max/M max, there was no significant effect of condition (χ2 = 5.59, p = 0.061). However, there was a significant main effect of time (χ2 = 93.94, p = 0.001) and a significant time × condition interaction (χ2 = 57.86, p = 0.001). GM H max/M max at T15 was greater than at T00 only in the supramaximal condition (p = 0.008). Additionally, GM H max/M max at T00, T05, T10, and T15 were significantly lower than at PRE and POST in both supramaximal (p < 0.01) and submaximal (p = 0.01) conditions. Conversely, no significant differences were found in GM H max/M max between T05, T10, and T15 (p > 0.05), nor between PRE and POST in any experimental condition (p > 0.05). GM H max/M max effect sizes between PRE and POST were 0.10 (trivial), 0.01 (trivial), and 0.12 (trivial) for control, submaximal, and supramaximal conditions, respectively. Additionally, GM H max/M max effect sizes between T00 and T15 were −0.04 (trivial), 0.50 (small), and 1.06 (moderate) for control, submaximal, and supramaximal conditions, respectively.

For PTT, there was no significant effect of condition (χ2 = 4.77, p = 0.092). However, there were significant main effects of time (χ2 = 284.08, p = 0.001) and a significant time × condition interaction (χ2 = 194.39, p = 0.001). PTT at PRE was greater than POST in both supramaximal (p = 0.001) and submaximal (p = 0.006) conditions. Additionally, PTT at T00, T05, T10, and T15 was greater than PRE and POST in both supramaximal (p = 0.001) and submaximal (p = 0.001) conditions (Figure 4). Conversely, there were no significant differences for PTT at T00, T05, T10, and T15 in all experimental conditions (p > 0.05), nor between PRE and POST at the control condition (p = 0.054). PTT effect size between PRE and POST moments was −0.61 (small), −0.71 (small), and −1.19 (moderate) for control, submaximal, and supramaximal conditions, respectively. Additionally, PTT effect size between T00 and T15 moments was −0.67 (small), −0.35 (trivial), and −0.19 (trivial) for control, submaximal, and supramaximal conditions, respectively.

FIGURE 4.

FIGURE 4

Open in a new tab

Mechanical adaptations (n = 12 participants). Control = control condition, ES PREvs.POST = effect size between PRE and POST moments, ES T00vs.T15 = effect size between T00 and T15 moments, POST = posttest, PRE = pretest, PT = passive torque, PTT = peak twitch torque, Submaximal = static stretching submaximal condition, Supramaximal = static stretching supramaximal condition, T00 = measure immediately at the begin of the experimental condition, T05 = measure 5 min after the begin of the experimental condition, T10 = measure 10 min after the begin of the experimental condition, T15 = measure 15 min after the begin of the experimental condition. *Significant differences from PRE moment (p < 0.05). #Lesser than T00 moment (p < 0.05). $Greater than both PRE and POST moments (p < 0.01).

For PT, there were significant main effects of condition (χ2 = 1140.89, p = 0.001) and time (χ2 = 942.96, p = 0.001), as well as a significant time × condition interaction (χ2 = 537.49, p < 0.001). In the supramaximal condition, PT at T00 was lower than at T05, T10, and T15 (p < 0.001). Nonetheless, for the submaximal condition, PT at T00 was lower than only at T15 (p = 0.043). Additionally, T00, T05, T10, and T15 were significantly greater than PRE and POST in both supramaximal (p < 0.01) and submaximal (p = 0.01) conditions. Conversely, no significant differences were found in PT between T05, T10, and T15 (p > 0.05), nor between PRE and POST in any experimental condition (p > 0.05). PT effect sizes between PRE and POST were −0.30 (trivial), −0.10 (trivial), and −0.49 (small) for control, submaximal, and supramaximal conditions, respectively. Additionally, PT effect sizes between T00 and T15 were 0.15 (trivial), −0.55 (small), and −0.68 (small) for control, submaximal, and supramaximal conditions, respectively.

For MVC, there was no significant time × condition interaction (χ2 = 2.36, p = 0.307, Figure 5). However, there were significant main effects of time (χ2 = 12.61, p = 0.001) and condition (χ2 = 9.20, p = 0.010). MVC at POST was lower than PRE (p = 0.001). The MVC decrease was greater in both supramaximal (p = 0.016) and submaximal (p = 0.035) conditions when compared to the control condition. No differences were found between supramaximal and submaximal conditions (p = 0.959). MVC effect sizes between PRE and POST were −0.20 (trivial), −0.28 (trivial), and −0.37 (small) for control, submaximal, and supramaximal conditions, respectively.

FIGURE 5.

FIGURE 5

Open in a new tab

Muscle strength and flexibility adaptations (n = 13 participants). Control = control condition, MVC = maximal voluntary contraction, PRE = pretest, POST = posttest; Submaximal = submaximal static stretching condition, Supramaximal = supramaximal static stretching condition. *Significant differences from PRE moment (p < 0.05). &Main effect for condition with significant differences from control.

For ROMmax, there were significant main effects of time (χ2 = 27.18, p = 0.001), condition (χ2 = 8.69, p = 0.013), and time × condition interaction (χ2 = 15.89, p = 0.001). ROMmax at POST was greater than at PRE in both supramaximal (p = 0.001) and submaximal (p = 0.001) conditions. Conversely, there were no significant differences between PRE and POST ROMmax in the control condition (p = 1.000). ROMmax effect sizes between PRE and POST were 0.02 (trivial), −0.36 (small), and −0.50 (small) for control, submaximal, and supramaximal conditions, respectively.

4. Discussion

This study demonstrates that prolonged static stretching elicits biphasic modulation of spinal excitability, characterized by initial suppression followed by progressive facilitation that is amplitude‐dependent; supramaximal stretching elicits greater neural adaptations in both the SOL and gastrocnemius muscles. In contrast, submaximal stretching only affects the SOL. Concurrently, PT initially increased during stretch application but subsequently declined more rapidly under supramaximal conditions (5 min) compared to submaximal conditions (15 min), indicating differential viscoelastic adaptations within the muscle‐tendon unit. Despite these neural and mechanical differences, both stretching amplitudes similarly reduced voluntary muscle strength while improving joint ROM, and slightly greater flexibility gains are observed under supramaximal conditions.

The initial decrease in spinal excitability during static stretching aligns with previous findings reporting reduced H max or H max/M max during passive stretching maneuvers (Guissard et al. 2001; Budini et al. 2018). Since the reduction in reflex responses may contribute to greater muscle flexibility (Guissard and Duchateau 2006), it supports the notion that stretching may induce changes in both neural and peripheral inputs to the motoneuron pool, thereby facilitating muscle lengthening (Guissard et al. 2001; Guissard and Duchateau 2006). The amplitude H max/M max is modulated by excitatory and inhibitory mechanisms in the α‐motor neurons (Clark et al. 2014; Stevanovic et al. 2019). For instance, a previous study measured SOL H max every 3 s during a 30‐s static stretch of the calf muscles and reported a decrease at the onset of stretching. However, because of the recovery characteristics of H max measurements, the responses showed an enhancement from 21 s onward compared with the first stimulus at 3 s. The authors attributed this early reduction in H max to decreased neurotransmitter release, suggesting homosynaptic depression (Budini et al. 2018). Nevertheless, postactivation depression of the Hoffman reflex is typically observed when stimuli are delivered at short intervals because recovery of H‐reflex responses generally requires 8 s (Vitry et al. 2021). Therefore, in the absence of a control condition in the previous study (Budini et al. 2018), the observed depression may have resulted from the stimulation protocol itself rather than from the stretching intervention (Budini et al. 2018; Vitry et al. 2021). Thus, although evidence suggested that homosynaptic depression may play an important role in the modulation of spinal excitability during stretching (Budini et al. 2018; Datoussaid et al. 2021), the reduction in the H max/M max at the onset of stretching observed in the present study cannot be unequivocally attributed to this mechanism, as it remains uncertain whether homosynaptic depression was specifically induced by the stretching exercise or by the stimulation protocol itself (Budini et al. 2018; Vitry et al. 2021). Accordingly, other neurophysiological mechanisms likely contributed to the attenuation of the reflex response.

Consistent with this interpretation, a previous study reported reductions in both the exteroceptive reflex (E reflex/M max) and the motor evoked potential (MEP/M max) in the calf muscles during ankle dorsiflexion at 20° compared to the neutral position (Guissard et al. 2001). Because spinal motor neurons integrate afferent inputs originating from both cortical and peripheral sources (Aagaard et al. 2002; Heckman et al. 2005), and E reflex/M max and MEP/M max are considered to reflect, respectively, afferent input from nociceptive nerve endings and corticospinal drive to the spinal motoneuron pool (Guissard et al. 2001; Pulverenti et al. 2020; Vieira et al. 2025), the initial decrease in spinal excitability during static stretching could result from concurrent reductions in both peripheral afferent feedback from nociceptive nerve endings and cortical excitatory input (Guissard et al. 2001; Guissard and Duchateau 2006). However, reductions in H max amplitude during stretching induced by tendon pressure have been observed even after local anesthesia of the skin (Robinson et al. 1982), suggesting that nociceptive nerve endings' activity may not play a predominant role in spinal excitability modulation during muscle lengthening (Robinson et al. 1982; Masugi et al. 2017). Conversely, Ia afferent transmission from muscle spindles during muscle lengthening is suppressed by presynaptic inhibition (Guissard and Duchateau 2006), providing an additional inhibitory contribution to spinal motoneuron excitability. Collectively, these mechanisms suggest that static stretching transiently engages multiple inhibitory pathways to reduce motoneuron output (Guissard et al. 2001; Guissard and Duchateau 2006), and thereby, it could help explain the decline in H max/M max observed at the onset of stretching in our study.

Despite an initial decline in spinal excitability at the onset of stretching, H max/M max progressively increased throughout the static stretching period, independent of stretching magnitude. Notably, this facilitation was observed in both the SOL and medial gastrocnemius under supramaximal conditions, and it was limited to the SOL under submaximal conditions. A plausible explanation is that adaptations within the muscle–tendon unit contributed to the observed increase in spinal excitability. Consistent with this, our study reported that PT decreased across all stretching conditions, with a greater reduction during supramaximal stretching (effect size = 0.68; ~30% decrease from T00 to T15) compared with submaximal stretching (effect size = 0.55; ~22% decrease from T00 to T15). Previous studies have shown that static stretching promotes elongation at the myotendinous junction (Mizuno et al. 2012; Maeda et al. 2017). Importantly, such extensibility appears to originate primarily from adaptations in the muscle fibers rather than the tendon itself, as elongation of the calf muscles can occur without measurable displacement of the Achilles tendon following static stretching (Morse et al. 2008). Therefore, muscle elongation required to maintain the ankle joint at the target stretching angle may enhance muscle spindle activity, potentially increase afferent feedback, and contribute to the elevations in H max/M max observed throughout the stretching (Blum et al. 2017; Kröger and Watkins 2021). In line with this interpretation, Datoussaid et al. (2021) reported that changes in the H max/M max ratio during the loading and unloading phases of stretching were inversely related to PT, suggesting a mechanistic link between stretch‐induced reductions in muscle stiffness and modulation of spinal excitability.

However, the elevations in H max/M max observed during stretching appear to be transient (Guissard et al. 2001; Budini et al. 2018, 2019). For example, previous studies have reported that a pronounced decrease in H max/M max during passive stretching rapidly returned to baseline values once stretching ceased (Guissard et al. 2001; Budini et al. 2018). Likewise, other investigations demonstrated that although H max/M max responses increased immediately after one or 5 min of static stretching, they reverted to baseline within 2 min (Budini et al. 2017, 2019). Despite the longer duration applied in our protocol (i.e., 15 min), our results were consistent with these previous findings across different stretching volumes (Budini et al. 2017, 2019). Taken together, this evidence suggests that the adaptations in H max/M max responses observed during or immediately after static stretching are short‐lived and return to baseline within minutes following the cessation of stretching (Guissard et al. 2001; Budini et al. 2018).

In contrast to the H max/M max responses, PT increased immediately at the onset of stretching, with a greater increase observed during the supramaximal compared with the submaximal stretching condition. These findings are consistent with previous studies reporting higher PT at greater ankle dorsiflexion ranges of motion during muscle lengthening (Mizuno and Umemura 2016; Mizuno 2017). Despite the initial increase in PT at the onset of stretching, PT progressively decreased throughout the stretching period, with slightly greater reductions in the supramaximal than in the submaximal condition (effect sizes of −0.68 vs. −0.55 for supramaximal and submaximal stretching conditions, respectively). Previous evidence suggested that decreases in PT may result from a reduction in afferent input from nociceptive nerve endings and mechanoreceptors (Guissard et al. 2001; Guissard and Duchateau 2006; Lévenéz et al. 2023). As the activity of both nociceptive afferents and mechanoreceptors decreases during muscle lengthening, particularly at higher ankle dorsiflexion ranges of motion, such changes could, in principle, reduce spinal excitability and decrease PT (Guissard et al. 2001). However, in the present study, spinal excitability increased throughout the stretching protocol, as evidenced by a higher H max/M max ratio at the end compared to the onset of stretching. This dissociation suggests that the observed changes in PT were unlikely to be mediated by alterations in spinal excitability associated with nociceptive or mechanoreceptive afferent input. Accordingly, the reduction in PT observed during stretching is more likely attributable to changes in the stiffness of the muscle and surrounding connective tissues within the muscle–tendon unit (Opplert et al. 2016; Opplert and Babault 2019; Vieira et al. 2021; Lévenéz et al. 2023). In this context, greater static stretching amplitudes are known to induce larger reductions in muscle–tendon stiffness (Takeuchi and Nakamura 2020; Takeuchi, Akizuki, and Nakamura 2021), and therefore, it could help to explain the slightly greater decrease in PT throughout the stretching period, observed under the supramaximal compared with the submaximal stretching condition.

Similarly, both protocols increased joint ROM, with slightly greater improvements following supramaximal compared with submaximal stretching (effect sizes of 0.50 vs. 0.35, respectively), which is consistent with previous studies reporting flexibility gains after stretching performed at high or moderate amplitudes (Takeuchi, Akizuki, and Nakamura 2021; Marchetti et al. 2022). Enhancements in ROM are commonly attributed to reductions in muscle–tendon viscoelasticity (Bouvier et al. 2017). Elastography studies have shown decreases in shear‐wave velocity following static stretching (Morrin and Redding 2013; Reiner et al. 2022), and other investigations using stiffness indices have also reported reductions in muscle–tendon stiffness (Nojiri et al. 2019; Palmer et al. 2022). Our study observed reductions in PT under both conditions, with slightly greater decreases after supramaximal than submaximal stretching (effect sizes of 0.68 and 0.55, respectively, between the T00 and T15 measures). Moreover, although evoked contractile properties (i.e., peak twitch torque) increased during the stretching protocol, possibly due to the length–tension relationship (Maffiuletti and Lepers 2003), greater impairments in evoked contractile properties were observed after supramaximal compared with submaximal stretching (effect size of −1.19 and −0,71, respectively). PT is often considered a surrogate marker of muscle–tendon stiffness, and evoked contractile properties, though primarily reflecting contractile capacity, may also indicate changes in muscle and tendon stiffness (Ryan et al. 2011; Vieira et al. 2021). Therefore, the combined reductions in PT and peak twitch torque suggest that stretching decreased muscle–tendon stiffness, particularly when performed at greater amplitudes. Consequently, given the established relationship between muscle–tendon stiffness and ROM (Bouvier et al. 2017), the greater reductions in these stiffness‐related markers following stretching observed in our study, especially after the greater stretching amplitudes, may help explain the slightly greater improvements in ROM observed in this condition compared with the submaximal condition.

In addition, our results demonstrated a similar reduction in voluntary muscle strength following both supramaximal and submaximal static stretching compared with the control condition. Previous systematic review indicates that greater impairments in strength may occur after short‐duration static stretching (e.g., 2 × 30 s) when performed at maximal rather than submaximal amplitudes. However, when stretching volume is higher, different amplitudes may induce similar deficits (Bryant et al. 2023). The physiological mechanisms underlying these impairments remain incompletely understood, but intrinsic motoneuron properties, particularly persistent inward currents (PICs), are thought to play a key role. PICs amplify synaptic input and enhance the input–output relationship of motoneurons, thereby supporting sustained force production during voluntary contractions, such as those assessed in our study (Heckman et al. 2005). Prolonged static stretching has been shown to reduce PIC activity (Trajano and Blazevich 2021), which provides a plausible explanation for the attenuation of voluntary strength observed in the present findings. Although we observed slightly greater impairments in evoked contractile properties following supramaximal compared with submaximal stretching, possibly reflecting disturbances in cross‐bridge function, prior evidence suggests that static stretching–induced reductions in muscle strength are primarily of neural rather than peripheral origin (Trajano et al. 2013). This may explain the absence of significant voluntary strength differences between conditions despite divergent evoked contractile responses.

Our study has some limitations that should be acknowledged. The H max/M max, PTT, and PT measures during the experimental protocols (T00 to T15) were obtained with the ankle positioned differently across conditions (i.e., ROMmax + 5°, ROMmax − 5°, or neutral), which could have an impact on the results (Guissard et al. 2001; Vieira et al. 2025). In addition, during the stretching sessions, PRE and POST measures were assessed in the neutral position, whereas measures obtained during stretching were performed at ROMmax + 5° or ROMmax − 5°. Although these methodological discrepancies may introduce variability, the generalized mixed model provides a robust statistical framework accounting for interindividual variability (Cnaan et al. 1997), and covariate inclusion was intended to minimize type I error and enhance analytical conservatism (Hernández et al. 2006). Moreover, the H max and M max intensities were determined from the recruitment curve at the beginning of each experimental session. Therefore, intensities were the same for PRE, T00, T05, T10, T15, and POST moments. Additionally, performing a recruitment curve at each time point to measure H max and M max would be time‐consuming and therefore mask potential immediate and transient stretch effects (Budini et al. 2017; Opplert et al. 2020; Vieira et al. 2025). Indeed, the use of a constant intensity throughout an experimental session is usually conducted in the literature on the acute effect of stretching on the H max/M max ratio (Opplert et al. 2020; Vieira et al. 2025).

5. Conclusion

Static stretching amplitude plays a key role in modulating neuromechanical adaptations. Both supramaximal and submaximal stretching improved joint flexibility, likely through reductions in muscle–tendon stiffness, with slightly greater ROM gains observed under supramaximal conditions. Spinal excitability initially decreased but subsequently increased to a greater extent during supramaximal stretching compared with submaximal protocols. Nevertheless, both conditions elicited similar decreases in voluntary muscle strength. These findings highlight the importance of considering stretching amplitude when designing flexibility or rehabilitation programs. By demonstrating that higher amplitudes can acutely enhance flexibility without inducing additional strength impairments, this study provides novel insights into the neural and mechanical mechanisms underlying static stretching. Additionally, it informs safer and more effective stretching programs to be applied in sports and clinical contexts.

Author Contributions

Conception and design of the work: D.C.L.V. and N.B. Acquisition, analysis, or interpretation of the data for the work: D.C.L.V., M.H., J.L.Q.D., N.B., and M.B. Drafting the work or revising it critically for important intellectual content: all authors. All authors have read and approved the final version of this manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed.

Funding

The study was supported by the Centre d'Expertise de la Performance from the Université́ of Bourgogne, by the Region Bourgogne Franche‐Comté (2020Y‐22065 and 2022Y‐13186), by the National Council for Scientific and Technological Development–CNPq (304136/2020‐4, 200391/2022‐4, and 446576/2024‐7), Coordination for the Improvement of High Education Personnel (88887.188974/2025‐00), and by the Foundation for Support of Research in the Federal District‐FAP/DF (00193‐00001261/2021‐23, 00193‐00001661/2024‐81, and 00193‐00001372/2024‐82).

Ethics Statement

The study received approval from the Ethics Committee for Research in STAPS (CERSTAPS IRB00012476‐2023‐17‐02‐229).

Consent

All individuals were fully informed about the experimental procedure and purpose of the study, and they read and signed an informed consent form. The study followed the standards set out by the Declaration of Helsinki.

Conflicts of Interest

The authors declare no conflicts of interest.

Acknowledgements

The authors thank all individuals who participated in this study. Additionally, we are grateful to Camila Tomaz Pereira for their assistance during data acquisition, and Centre d'Expertise de la Performance from the Université́ of Bourgogne, by the Region Bourgogne Franche‐ Comté (2020Y‐22065 and 2022Y‐13186), by the National Council for Scientific and Technological Development–CNPq (304136/2020‐4, 200391/2022‐4, and 446576/2024‐7), Coordination for the Improvement of High Education Personnel (88887.188974/2025‐00) and by Foundation for Support of Research in the Federal District‐FAP/DF (00193‐00001261/2021‐23, 00193‐00001661/2024‐81, and 00193‐00001372/2024‐82). Open access publication funding provided by COUPERIN CY26.

Vieira, D. C. L. , Bottaro M., Hitier M., Durigan J. L. Q., and Babault N.. 2026. “Neural and Mechanical Adaptations During Static Stretching With Different Amplitudes.” European Journal of Neuroscience 63, no. 7: e70475. 10.1111/ejn.70475.

Associate Editor: Yoland Smith

Data Availability Statement

Source data for this study are openly available at: https://github.com/denisclvieira/STRETCHAMPLITUDE.git.

References

  1. Aagaard, P. , Simonsen E. B., Andersen J. L., Magnusson P., and Dyhre‐Poulsen P.. 2002. “Neural Adaptation to Resistance Training: Changes in Evoked V‐Wave and H‐Reflex Responses.” Journal of Applied Physiology 92: 2309–2318. [DOI] [PubMed] [Google Scholar]
  2. Atkinson, G. , and Nevill A. M.. 1998. “Statistical Methods for Assessing Measurement Error (Reliability) in Variables Relevant to Sports Medicine.” Sports Medicine 26: 217–238. [DOI] [PubMed] [Google Scholar]
  3. Babault, N. , Rodot G., Champelovier M., and Cometti C.. 2021. “A Survey on Stretching Practices in Women and Men From Various Sports or Physical Activity Programs.” International Journal of Environmental Research and Public Health 18: 3928. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Behm, D. G. , Blazevich A. J., Kay A. D., and McHugh M.. 2016. “Acute Effects of Muscle Stretching on Physical Performance, Range of Motion, and Injury Incidence in Healthy Active Individuals: A Systematic Review.” Applied Physiology, Nutrition, and Metabolism 41: 1–11. [DOI] [PubMed] [Google Scholar]
  5. Behm, D. G. , Button D. C., and Butt J. C.. 2001. “Factors Affecting Force Loss With Prolonged Stretching.” Canadian Journal of Applied Physiology 26: 261–272. [PubMed] [Google Scholar]
  6. Behm, D. G. , and Chaouachi A.. 2011. “A Review of the Acute Effects of Static and Dynamic Stretching on Performance.” European Journal of Applied Physiology 111: 2633–2651. [DOI] [PubMed] [Google Scholar]
  7. Blazevich, A. J. , Cannavan D., Waugh C. M., et al. 2014. “Range of Motion, Neuromechanical, and Architectural Adaptations to Plantar Flexor Stretch Training in Humans.” Journal of Applied Physiology 117: 452–462. [DOI] [PubMed] [Google Scholar]
  8. Blum, K. P. , Lamotte D'Incamps B., Zytnicki D., and Ting L. H.. 2017. “Force Encoding in Muscle Spindles During Stretch of Passive Muscle.” PLoS Computational Biology 13: e1005767. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Bouvier, T. , Opplert J., Cometti C., and Babault N.. 2017. “Acute Effects of Static Stretching on Muscle–Tendon Mechanics of Quadriceps and Plantar Flexor Muscles.” European Journal of Applied Physiology 117: 1309–1315. [DOI] [PubMed] [Google Scholar]
  10. Bryant, J. , Cooper D. J., Peters D. M., and Cook M. D.. 2023. “The Effects of Static Stretching Intensity on Range of Motion and Strength: A Systematic Review.” Journal of Functional Morphology and Kinesiology 8: 37. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Budini, F. , Christova M., Gallasch E., Rafolt D., and Tilp M.. 2018. “Soleus H‐Reflex Inhibition Decreases During 30 s Static Stretching of Plantar Flexors, Showing Two Recovery Steps.” Frontiers in Physiology 9: 935. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Budini, F. , Gallasch E., Christova M., Rafolt D., Rauscher A. B., and Tilp M.. 2017. “One Minute Static Stretch of Plantar Flexors Transiently Increases H Reflex Excitability and Exerts No Effect on Corticospinal Pathways.” Experimental Physiology 102: 901–910. [DOI] [PubMed] [Google Scholar]
  13. Budini, F. , Kemper D., Christova M., Gallasch E., Rafolt D., and Tilp M.. 2019. “Five Minutes Static Stretching Influences Neural Responses at Spinal Level in the Background of Unchanged Corticospinal Excitability.” Journal of Musculoskeletal & Neuronal Interactions 19: 30–37. [PMC free article] [PubMed] [Google Scholar]
  14. Clark, L. , O'Leary B C., Hong J., and Lockard M.. 2014. “The Acute Effects of Tretching on Presynaptic Inhibition and Peak Power.” Journal of Sports Medicine and Physical Fitness 54: 605–610. [PubMed] [Google Scholar]
  15. Cnaan, A. , Laird N. M., and Slasor P.. 1997. “Using the General Linear Mixed Model to Analyse Unbalanced Repeated Measures and Longitudinal Data.” Statistics in Medicine 16: 2349–2380. [DOI] [PubMed] [Google Scholar]
  16. Datoussaid, M. , El Khalouqi H., Dahm C., Guissard N., and Baudry S.. 2021. “Passive Torque Influences the Hoffmann Reflex Pathway During the Loading and Unloading Phases of Plantar Flexor Muscles Stretching.” Physiological Reports 9: e14834. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Gollhofer, A. , and Rapp W.. 1993. “Recovery of Stretch Reflex Responses Following Mechanical Stimulation.” European Journal of Applied Physiology 66: 415–420. [DOI] [PubMed] [Google Scholar]
  18. Guissard, N. , and Duchateau J.. 2006. “Neural Aspects of Muscle Stretching.” Exercise and Sport Sciences Reviews 34: 154–158. [DOI] [PubMed] [Google Scholar]
  19. Guissard, N. , Duchateau J., and Hainaut K.. 2001. “Mechanisms of Decreased Motoneurone Excitation During Passive Muscle Stretching.” Experimental Brain Research 137: 163–169. [DOI] [PubMed] [Google Scholar]
  20. Heckman, C. J. , Gorassini M. A., and Bennett D. J.. 2005. “Persistent Inward Currents in Motoneuron Dendrites: Implications for Motor Output.” Muscle & Nerve 31: 135–156. [DOI] [PubMed] [Google Scholar]
  21. Hernández, A. V. , Eijkemans M. J. C., and Steyerberg E. W.. 2006. “Randomized Controlled Trials With Time‐to‐Event Outcomes: How Much Does Prespecified Covariate Adjustment Increase Power?” Annals of Epidemiology 16: 41–48. [DOI] [PubMed] [Google Scholar]
  22. Hirata, K. , Kanehisa H., and Miyamoto N.. 2017. “Acute Effect of Static Stretching on Passive Stiffness of the Human Gastrocnemius Fascicle Measured by Ultrasound Shear Wave Elastography.” European Journal of Applied Physiology 117: 493–499. [DOI] [PubMed] [Google Scholar]
  23. Hirata, K. , Miyamoto‐Mikami E., Kanehisa H., and Miyamoto N.. 2016. “Muscle‐Specific Acute Changes in Passive Stiffness of Human Triceps Surae After Stretching.” European Journal of Applied Physiology 116: 911–918. [DOI] [PubMed] [Google Scholar]
  24. Kataura, S. , Suzuki S., Matsuo S., et al. 2017. “Acute Effects of the Different Intensity of Static Stretching on Flexibility and Isometric Muscle Force.” Journal of Strength and Conditioning Research 31: 3403–3410. [DOI] [PubMed] [Google Scholar]
  25. Koo, T. K. , and Li M. Y.. 2016. “A Guideline of Selecting and Reporting Intraclass Correlation Coefficients for Reliability Research.” Journal of Chiropractic Medicine 15: 155–163. [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Kröger, S. , and Watkins B.. 2021. “Muscle Spindle Function in Healthy and Diseased Muscle.” Skeletal Muscle 11: 3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  27. Kumle, L. , Võ M. L.‐H., and Draschkow D.. 2021. “Estimating Power in (Generalized) Linear Mixed Models: An Open Introduction and Tutorial in R.” Behavior Research Methods 53: 2528–2543. [DOI] [PMC free article] [PubMed] [Google Scholar]
  28. Lévenéz, M. , Moeremans M., Booghs C., et al. 2023. “Architectural and Mechanical Changes After Five Weeks of Intermittent Static Stretch Training on the Medial Gastrocnemius Muscle of Active Adults.” Sports 11: 73. [DOI] [PMC free article] [PubMed] [Google Scholar]
  29. Maeda, N. , Urabe Y., Tsutsumi S., et al. 2017. “The Acute Effects of Static and Cyclic Stretching on Muscle Stiffness and Hardness of Medial Gastrocnemius Muscle.” Journal of Sports Science and Medicine 16: 514–520. [PMC free article] [PubMed] [Google Scholar]
  30. Maffiuletti, N. A. , and Lepers R.. 2003. “Quadriceps Femoris Torque and EMG Activity in Seated Versus Supine Position.” Medicine and Science in Sports and Exercise 35: 1511–1516. [DOI] [PubMed] [Google Scholar]
  31. Marchetti, P. H. , Miyatake M. M. S., Magalhaes R. A., et al. 2022. “Different Volumes and Intensities of Static Stretching Affect the Range of Motion and Muscle Force Output in Well‐Trained Subjects.” Sports Biomechanics 21: 155–164. [DOI] [PubMed] [Google Scholar]
  32. Masugi, Y. , Obata H., Inoue D., Kawashima N., and Nakazawa K.. 2017. “Neural Effects of Muscle Stretching on the Spinal Reflexes in Multiple Lower‐Limb Muscles.” PLoS ONE 12: e0180275. [DOI] [PMC free article] [PubMed] [Google Scholar]
  33. Matsuo, S. , Suzuki S., Iwata M., et al. 2013. “Acute Effects of Different Stretching Durations on Passive Torque, Mobility, and Isometric Muscle Force.” Journal of Strength and Conditioning Research 27: 3367–3376. [DOI] [PubMed] [Google Scholar]
  34. Matthews, B. H. C. 1931. “The Response of a Muscle Spindle During Active Contraction of a Muscle.” Journal of Physiology 72: 153–174. [DOI] [PMC free article] [PubMed] [Google Scholar]
  35. Mizuno, T. 2017. “Changes in Joint Range of Motion and Muscle–Tendon Unit Stiffness After Varying Amounts of Dynamic Stretching.” Journal of Sports Sciences 35: 2157–2163. [DOI] [PubMed] [Google Scholar]
  36. Mizuno, T. , Matsumoto M., and Umemura Y.. 2012. “Decrements in Stiffness Are Restored Within 10 Min.” International Journal of Sports Medicine 34: 484–490. [DOI] [PubMed] [Google Scholar]
  37. Mizuno, T. , and Umemura Y.. 2016. “Dynamic Stretching Does Not Change the Stiffness of the Muscle‐Tendon Unit.” International Journal of Sports Medicine 37: 1044–1050. [DOI] [PubMed] [Google Scholar]
  38. Morrin, N. , and Redding E.. 2013. “Acute Effects of Warm‐Up Stretch Protocols on Balance, Vertical Jump Height, and Range of Motion in Dancers.” Journal of Dance Medicine & Science 17: 34–40. [DOI] [PubMed] [Google Scholar]
  39. Morse, C. I. , Degens H., Seynnes O. R., Maganaris C. N., and Jones D. A.. 2008. “The Acute Effect of Stretching on the Passive Stiffness of the Human Gastrocnemius Muscle Tendon Unit.” Journal of Physiology 586: 97–106. [DOI] [PMC free article] [PubMed] [Google Scholar]
  40. Nojiri, S. , Ikezoe T., Nakao S., et al. 2019. “Effect of Static Stretching With Different Rest Intervals on Muscle Stiffness.” Journal of Biomechanics 90: 128–132. [DOI] [PubMed] [Google Scholar]
  41. Opplert, J. , and Babault N.. 2018. “Acute Effects of Dynamic Stretching on Muscle Flexibility and Performance: An Analysis of the Current Literature.” Sports Medicine 48: 299–325. [DOI] [PubMed] [Google Scholar]
  42. Opplert, J. , and Babault N.. 2019. “Acute Effects of Dynamic Stretching on Mechanical Properties Result From Both Muscle‐Tendon Stretching and Muscle Warm‐Up.” Journal of Sports Science and Medicine 18: 351–358. [PMC free article] [PubMed] [Google Scholar]
  43. Opplert, J. , Genty J. B., and Babault N.. 2016. “Do Stretch Durations Affect Muscle Mechanical and Neurophysiological Properties?” International Journal of Sports Medicine 37: 673–679. [DOI] [PubMed] [Google Scholar]
  44. Opplert, J. , Paizis C., Papitsa A., Blazevich A. J., Cometti C., and Babault N.. 2020. “Static Stretch and Dynamic Muscle Activity Induce Acute Similar Increase in Corticospinal Excitability.” PLoS ONE 15: e0230388. [DOI] [PMC free article] [PubMed] [Google Scholar]
  45. Palmer, T. B. , Farrow A. C., Agu‐Udemba C. C., and Mitchell E. A.. 2022. “The Time Course of Passive Stiffness Responses Following an Acute Bout of Static Stretching in Healthy, Elderly Men.” Physiotherapy Theory and Practice 38: 695–703. [DOI] [PubMed] [Google Scholar]
  46. Pulverenti, T. S. , Trajano G. S., Kirk B. J. C., Bochkezanian V., and Blazevich A. J.. 2021. “Plantar Flexor Muscle Stretching Depresses the Soleus Late Response but Not Tendon Tap Reflexes.” European Journal of Neuroscience 53: 3185–3198. [DOI] [PubMed] [Google Scholar]
  47. Pulverenti, T. S. , Trajano G. S., Walsh A., Kirk B. J. C., and Blazevich A. J.. 2020. “Lack of Cortical or Ia‐Afferent Spinal Pathway Involvement in Muscle Force Loss After Passive Static Stretching.” Journal of Neurophysiology 123: 1896–1906. [DOI] [PubMed] [Google Scholar]
  48. Reiner, M. M. , Tilp M., Guilhem G., Morales‐Artacho A., and Konrad A.. 2022. “Comparison of A Single Vibration Foam Rolling and Static Stretching Exercise on the Muscle Function and Mechanical Properties of the Hamstring Muscles.” Journal of Sports Science and Medicine 21: 287–297. [DOI] [PMC free article] [PubMed] [Google Scholar]
  49. Rhea, M. R. 2004. “Determining the Magnitude of Treatment Effects in Strength Training Research Through the Use of the Effect Size.” Journal of Strength and Conditioning Research 18: 918–920. [DOI] [PubMed] [Google Scholar]
  50. Robinson, K. L. , McComas A. J., and Belanger A. Y.. 1982. “Control of Soleus Motoneuron Excitability During Muscle Stretch in Man.” Journal of Neurology, Neurosurgery, and Psychiatry 45: 699–704. [DOI] [PMC free article] [PubMed] [Google Scholar]
  51. Ryan, E. D. , Thompson B. J., Herda T. J., et al. 2011. “The Relationship Between Passive Stiffness and Evoked Twitch Properties: The Influence of Muscle CSA Normalization.” Physiological Measurement 32: 677–686. [DOI] [PubMed] [Google Scholar]
  52. Santos, C. X. , Beltrão N. B., Pirauá A. L. T., Durigan J. L. Q., Behm D., and de Araújo R. C.. 2020. “Static Stretching Intensity Does Not Influence Acute Range of Motion, Passive Torque, and Muscle Architecture.” Journal of Sport Rehabilitation 29: 1–6. [DOI] [PubMed] [Google Scholar]
  53. Stevanovic, V. B. , Jelic M. B., Milanovic S. D., Filipovic S. R., Mikic M. J., and Stojanovic M. D. M.. 2019. “Sport‐Specific Warm‐Up Attenuates Static Stretching‐Induced Negative Effects.Pdf.” Journal of Sports Science and Medicine 18: 282–289. [PMC free article] [PubMed] [Google Scholar]
  54. Takeuchi, K. , Akizuki K., and Nakamura M.. 2021. “Time Course of Changes in the Range of Motion and Muscle‐Tendon Unit Stiffness of the Hamstrings After Two Different Intensities of Static Stretching.” PLoS ONE 16: e0257367. [DOI] [PMC free article] [PubMed] [Google Scholar]
  55. Takeuchi, K. , and Nakamura M.. 2020. “Influence of High Intensity 20‐Second Static Stretching on the Flexibility and Strength of Hamstrings.” Journal of Sports Science and Medicine 19: 429–435. [PMC free article] [PubMed] [Google Scholar]
  56. Takeuchi, K. , Sato S., Kiyono R., et al. 2021. “High‐Intensity Static Stretching in Quadriceps Is Affected More by Its Intensity Than Its Duration.” Frontiers in Physiology 12: 709655. [DOI] [PMC free article] [PubMed] [Google Scholar]
  57. Trajano, G. S. , and Blazevich A. J.. 2021. “Static Stretching Reduces Motoneuron Excitability: The Potential Role of Neuromodulation.” Exercise and Sport Sciences Reviews 49: 126–132. [DOI] [PubMed] [Google Scholar]
  58. Trajano, G. S. , Seitz L., Nosaka K., and Blazevich A. J.. 2013. “Contribution of Central vs. Peripheral Factors to the Force Loss Induced by Passive Stretch of the Human Plantar Flexors.” Journal of Applied Physiology 115: 212–218. [DOI] [PubMed] [Google Scholar]
  59. Vianna, L. C. , Araújo C. G. S., and Fisher J. P.. 2009. “Influence of Central Command and Muscle Afferent Activation on Anterior Cerebral Artery Blood Velocity Responses to Calf Exercise in Humans.” Journal of Applied Physiology 107: 1113–1120. [DOI] [PubMed] [Google Scholar]
  60. Vieira, D. C. L. , Babault N., Hitier M., Durigan J. L. Q., and Bottaro M.. 2025. “The Acute Effects of Dynamic Stretching on the Neuromuscular System Are Independent of the Velocity.” Experimental Physiology 110: 494–505. [DOI] [PMC free article] [PubMed] [Google Scholar]
  61. Vieira, D. C. L. , Opplert J., and Babault N.. 2021. “Acute Effects of Dynamic Stretching on Neuromechanical Properties: An Interaction Between Stretching, Contraction, and Movement.” European Journal of Applied Physiology 121: 957–967. [DOI] [PubMed] [Google Scholar]
  62. Vitry, F. , Papaiordanidou M., and Martin A.. 2021. “Mechanisms Modulating Spinal Excitability After Nerve Stimulation Inducing Extra Torque.” Journal of Applied Physiology 131: 1162–1175. [DOI] [PubMed] [Google Scholar]
  63. Warneke, K. , Thomas E., Blazevich A. J., et al. 2025. “Practical Recommendations on Stretching Exercise: A Delphi Consensus Statement of International Research Experts.” Journal of Sport and Health Science 14: 101067. [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

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

Data Availability Statement

Source data for this study are openly available at: https://github.com/denisclvieira/STRETCHAMPLITUDE.git.

Articles from The European Journal of Neuroscience are provided here courtesy of Wiley

RESOURCES