Aerobic Exercise Reduces Pressure More Than Heat Pain Sensitivity in Healthy Adults

Pain Medicine ◽  
2019 ◽  
Vol 20 (8) ◽  
pp. 1534-1546 ◽  
Author(s):  
Matthew D Jones ◽  
James L Nuzzo ◽  
Janet L Taylor ◽  
Benjamin K Barry

Abstract Objectives The hypoalgesic effects of exercise are well described, but there are conflicting findings for different modalities of pain; in particular for mechanical vs thermal noxious stimuli, which are the most commonly used in studies of exercise-induced hypoalgesia. The aims of this study were 1) to investigate the effect of aerobic exercise on pressure and heat pain thresholds that were well equated with regard to their temporal and spatial profile and 2) to identify whether changes in the excitability of nociceptive pathways—measured using laser-evoked potentials—accompany exercise-induced hypoalgesia. Subjects Sixteen healthy adults recruited from the University of New South Wales. Methods Pressure and heat pain thresholds and pain ratings to laser stimulation and laser-evoked potentials were measured before and after aerobic cycling exercise and an equivalent period of light activity. Results Pressure pain thresholds increased substantially after exercise (rectus femoris: 29.6%, d = 0.82, P < 0.001; tibialis anterior: 26.9%, d = 0.61, P < 0.001), whereas heat pain thresholds did not (tibialis anterior: 4.2%, d = 0.30, P = 0.27; foot: 0.44%, d = 0.02, P = 1). Laser-evoked potentials and laser heat pain ratings also changed minimally after exercise (d = −0.59 to 0.3, P > 0.06). Conclusions This is the first investigation to compare the effects of exercise on pressure and heat pain using the same stimulation site and pattern. The results show that aerobic exercise reduces mechanical pain sensitivity more than thermal pain sensitivity.

2017 ◽  
Vol 122 (5) ◽  
pp. 1284-1291 ◽  
Author(s):  
Matthew D. Jones ◽  
Janet L. Taylor ◽  
Benjamin K. Barry

Animal studies have demonstrated an important role of peripheral mechanisms as contributors to exercise-induced hypoalgesia (EIH). Whether these same mechanisms contribute to EIH in humans is not known. In the current study, pain thresholds were assessed in healthy volunteers ( n = 36) before and after 5 min of high-intensity leg cycling exercise and an equivalent period of quiet rest. Pressure pain thresholds (PPTs) were assessed over the rectus femoris muscle of one leg and first dorsal interosseous muscles (FDIs) of both arms. Blood flow to one arm was occluded by a cuff throughout the 5-min period of exercise (or rest) and postexercise (or rest) assessments. Ratings of pain intensity and pain unpleasantness during occlusion were also measured. Pain ratings during occlusion increased over time (range, 1.5 to 3.5/10, all d > 0.63, P < 0.001) similarly in the rest and exercise conditions ( d < 0.35, P > 0.4). PPTs at all sites were unchanged following rest (range, −1.3% to +0.9%, all d < 0.05, P > 0.51). Consistent with EIH, exercise significantly increased PPT at the leg (+29%, d = 0.69, P < 0.001) and the nonoccluded (+23%, d = 0.56, P < 0.001) and occluded (+8%, d = 0.19, P = 0.003) unexercised arms. However, the increase in the occluded arm was significantly smaller ( d = −1.03, P < 0.001). These findings show that blocking blood flow to a limb during exercise attenuates EIH, suggesting that peripheral factors contribute to EIH in healthy adults. NEW & NOTEWORTHY This is the first demonstration in humans that a factor carried by the circulation and acting at the periphery is important for exercise-induced hypoalgesia. Further understanding of this mechanism may provide new insight to pain relief with exercise as well as potential interactions between analgesic medications and exercise.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Morten Pallisgaard Støve ◽  
Rogerio Pessoto Hirata ◽  
Thorvaldur Skuli Palsson

Abstract Objectives The effect of stretching on joint range of motion is well documented, and although sensory perception has significance for changes in the tolerance to stretch following stretching the underlining mechanisms responsible for these changes is insufficiently understood. The aim of this study was to examine the influence of endogenous pain inhibitory mechanisms on stretch tolerance and to investigate the relationship between range of motion and changes in pain sensitivity. Methods Nineteen healthy males participated in this randomized, repeated-measures crossover study, conducted on 2 separate days. Knee extension range of motion, passive resistive torque, and pressure pain thresholds were recorded before, after, and 10 min after each of four experimental conditions; (i) Exercise-induced hypoalgesia, (ii) two bouts of static stretching, (iii) resting, and (iv) a remote, painful stimulus induced by the cold pressor test. Results Exercise-induced hypoalgesia and cold pressor test caused an increase in range of motion (p<0.034) and pressure pain thresholds (p<0.027). Moderate correlations in pressure pain thresholds were found between exercise-induced hypoalgesia and static stretch (Rho>0.507, p=0.01) and exercise-induced hypoalgesia and the cold pressor test (Rho=0.562, p=0.01). A weak correlation in pressure pain thresholds and changes in range of motion were found following the cold pressor test (Rho=0.460, p=0.047). However, a potential carryover hypoalgesic effect may have affected the results of the static stretch. Conclusions These results suggest that stretch tolerance may be linked with endogenous modulation of pain. Present results suggest, that stretch tolerance may merely be a marker for pain sensitivity which may have clinical significance given that stretching is often prescribed in the rehabilitation of different musculoskeletal pain conditions where reduced endogenous pain inhibition is frequently seen.


Pain ◽  
1996 ◽  
Vol 65 (2) ◽  
pp. 189-196 ◽  
Author(s):  
A. Beydoun ◽  
D. B.S. Dyke ◽  
T. J. Morrow ◽  
K. L. Casey

2017 ◽  
Author(s):  
EJ. Hird ◽  
D. Talmi ◽  
AKP. Jones ◽  
W. El-Deredy

AbstractBackgroundPain is modulated by expectation. Event-related potential (ERP) studies of the influence of expectation on pain typically utilise laser heat stimulation to provide a controllable nociceptive-specific stimulus. Short painful electric stimulation has a number of practical advantages, but is less nociceptive-specific. We compared the modulation of electric versus laser-evoked pain by expectation, and their corresponding pain-evoked and anticipatory ERPs.New MethodWe developed understanding of recognised methods of laser and electric stimulation. We tested whether pain perception and neural activity induced by electric stimulation was modulated by expectation, whether this expectation elicited anticipatory neural correlates, and how these measures compared to those associated with laser stimulation. We elicited cue-evoked expectations of high and low pain and compared subjective ratings and corresponding ERPs in response to the delivery of laser and electric stimulation in a within-participant design.ResultsDespite sensory and affective differences between laser and electric pain, intensity ratings and pain-evoked potentials were modulated equivalently by expectation, though ERPs only correlated with pain ratings in the laser pain condition. Anticipatory correlates significantly differentiated pain intensity expectation to laser but not electric pain.Comparison with Existing MethodPrevious studies have consistently shown that laser-evoked potentials are modulated by expectation. We extend this by showing electric pain-evoked potentials are equally modulated by expectation, within the same participants. We also show a difference between the pain types in anticipation.ConclusionsThough laser-evoked potentials express a stronger relationship with pain perception, both laser and electric stimulation may be used to study the modulation of pain-evoked potentials by expectation. Anticipatory-evoked potentials are elicited by both pain types, but they may reflect different processes and did not correlate with pain perception.


Cephalalgia ◽  
2021 ◽  
pp. 033310242110565
Author(s):  
Jan Petter Neverdahl ◽  
Martin Uglem ◽  
Dagfinn Matre ◽  
Johannes Orvin Hansen ◽  
Morten Engstrøm ◽  
...  

Objective There is an unexplained association between disturbed sleep and migraine. In this blinded crossover study, we investigate if experimental sleep restriction has a different effect on pain thresholds and suprathreshold pain in interictal migraineurs and controls. Methods Forearm heat pain thresholds and tolerance thresholds, and trapezius pressure pain thresholds and suprathreshold pain were measured in 39 interictal migraineurs and 31 healthy controls after two consecutive nights of partial sleep restriction and after habitual sleep. Results The effect of sleep restriction was not significantly different between interictal migraineurs and controls in the primary analyses. Pressure pain thresholds tended to be lower (i.e., increased pain sensitivity) after sleep restriction in interictal migraineurs compared to controls with a 48-hour preictal-interictal cut-off (p = 0.061). We found decreased pain thresholds after sleep restriction in two of seven migraine subgroup comparisons: heat pain thresholds decreased in migraineurs with lower pain intensity during attacks (p = 0.005) and pressure pain thresholds decreased in migraineurs with higher severity of photophobia during attacks (p = 0.031). Heat pain thresholds tended to decrease after sleep restriction in sleep-related migraine (p = 0.060). Sleep restriction did not affect suprathreshold pain measurements in either group. Conclusion This study could not provide strong evidence for an increased effect of sleep restriction on pain sensitivity in migraineurs compared to healthy controls. There might be a slightly increased effect of sleep restriction in migraineurs, detectable using large samples or more pronounced in certain migraine subgroups.


2018 ◽  
Vol 18 (3) ◽  
pp. 513-523 ◽  
Author(s):  
Samuel Harris ◽  
Michele Sterling ◽  
Scott F. Farrell ◽  
Ashley Pedler ◽  
Ashley D. Smith

Abstract Background and aims Impairment of endogenous analgesia has been associated with the development, maintenance and persistence of pain. Endogenous analgesia can be evaluated using exercise-induced hypoalgesia (EIH) and offset analgesia (OffA) paradigms, which measure temporal filtering of sensory information. It is not clear if these paradigms are underpinned by common mechanisms, as EIH and OffA have not previously been directly compared. A further understanding of the processes responsible for these clinically relevant phenomena may have future diagnostic and therapeutic utility in management of individuals with persistent pain conditions. The primary aim of this study was to investigate if there is a correlation between the magnitudes of EIH and OffA. The secondary aim of the study was to examine whether exercise influences OffA. Methods Thirty-six healthy, pain-free participants were recruited. EIH was evaluated using pressure pain thresholds (PPT) and pain ratings to suprathreshold pressure stimuli over tibialis anterior and the cervical spine. OffA evaluation utilised a three-step protocol, whereby individualised heat pain thermal stimuli [Numerical Rating Scale (NRS)=50/100] were applied (T1), before increasing 1 °C (T2), followed by 1 °C reduction (T3). The magnitude of OffA was calculated as the percentage reduction in the NRS from T2 to T3. PPT/suprathreshold pain ratings and OffA measures were recorded, before and after 5 min of isometric quadriceps exercise performed at 20–25% maximum voluntary contraction (MVC); and following a 15 min rest period. Data were analysed using repeated measures (RM) ANCOVA and correlational analyses. Results There was no correlation between EIH measures (PPTs or pain ratings to suprathreshold pressure stimuli over tibialis anterior or the cervical spine) and OffA (p>0.11 for all). OffA was induced and not modulated by exercise (p=0.28). Conclusions Five minutes of 20–25% MVC lower limb isometric exercise provided non-pharmacological pain modulation in young, active adults. Magnitude of EIH was not correlated with that of OffA, and exercise did not influence magnitude of OffA. Implications These results suggest that in young, pain-free individuals, separate testing of these two paradigms is required to comprehensively evaluate efficacy of endogenous analgesia. If these results are replicated in patient populations, alternative or complementary methods to exercise interventions may be required to modulate impaired OffA.


2021 ◽  
Vol 2 ◽  
Author(s):  
Jessica F. McDougall ◽  
Nicole G. N. Bailey ◽  
Rohan Banga ◽  
Lukas D. Linde ◽  
John L. K. Kramer

Background: The influence of examiner gender on pain reporting has been previously explored in both research and clinical settings. However, previous investigations have been limited, with the majority of studies employing single, static assessments of pain (e.g., cold pressor test, verbal pain ratings). The impact of examiner gender on both static and dynamic heat-based pain assessments is currently unknown.Methods: Thirty eight participants (20 females aged 24.1 ± 4.44, and 18 males, aged 24.8 ± 4.54) completed two identical testing sessions, randomized to a male and female examiner in a cross-over design. Pain sensitivity was examined using heat pain thresholds, verbal pain ratings to tonic heat, computerized visual analog scale (CoVAS) rating to tonic heat, and participant-controlled temperature (PCT) heat pain assessments.Results: Female participants reported higher verbal pain to tonic heat with a female examiner compared to male participants, with similar trends for CoVAS responses to tonic heat. Conversely heat pain thresholds and PCT were not significantly influenced by experimenter gender.Conclusions: Overall, verbal ratings were the most impacted by examiner gender, with temperature-based methods such as PCT and pain thresholds showing little to no examiner gender effects. While the gender of the examiner may be an important consideration in the measurement of sex and gender differences in pain research, the choice of pain assessment method may be of similar consequence.


2021 ◽  
pp. 1-6
Author(s):  
Chang-Chia Liu ◽  
Shayan Moosa ◽  
Mark Quigg ◽  
W. Jeffrey Elias

OBJECTIVE Chronic pain results in an enormous societal and financial burden. Opioids are the mainstay of treatment, but opioid abuse has led to an epidemic in the United States. Nonpharmacological treatment strategies like deep brain stimulation could be applied to refractory chronic pain if safe and effective brain targets are identified. The anterior insula is a putative mediator of pain-related affective-motivational and cognitive-evaluative cerebral processing. However, the effect of anterior insula stimulation on pain perception is still unknown. Here, the authors provide behavioral and neurophysiological evidence for stimulating the anterior insula as a means of potential therapeutic intervention for patients with chronic pain. METHODS Six patients with epilepsy in whom intracerebral electrodes had been implanted for seizure localization were recruited to the study. The direct anterior insula stimulations were performed in the inpatient epilepsy monitoring unit while subjects were fully awake, comfortable, and without sedating medications. The effects of anterior insula stimulation were assessed with quantitative sensory testing for heat pain threshold, nociceptive-specific cutaneous laser-evoked potentials, and intracranial electroencephalogram (EEG) recordings. Control stimulation of noninsular brain regions was performed to test stimulation specificity. Sham stimulations, in which no current was delivered, were also performed to control for potential placebo effects. The safety of these stimulations was evaluated by bedside physicians, real-time intracranial EEG monitoring, and electrocardiogram recordings. RESULTS Following anterior insula stimulations, the heat pain threshold of each patient significantly increased from baseline (p < 0.001) and correlated with stimulation intensity (regression analysis: β = 0.5712, standard error 0.070, p < 0.001). Significant changes in ongoing intracranial EEG frequency band powers (p < 0.001), reduction in laser pain intensity, and attenuated laser-evoked potentials were also observed following stimulations. Furthermore, the observed behavioral and neurophysiological effects persisted beyond the stimulations. Subjects were not aware of the stimulations, and there were no cardiovascular or untoward effects. CONCLUSIONS Additional, nonpharmacological therapies are imperative for the future management of chronic pain conditions and to mitigate the ongoing opioid crisis. This study suggests that direct stimulation of the anterior insula can safely alter cerebral pain processing in humans. Further investigation of the anterior insula as a potential target for therapeutic neuromodulation is underway.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Hannah Gajsar ◽  
Marcel Meyer ◽  
Monika I. Hasenbring ◽  
Henrik B. Vaegter

Abstract Objectives Cognitive inhibition, which denotes the ability to suppress predominant or automatic responses, has been associated with lower pain sensitivity and larger conditioned pain modulation in humans. Studies exploring the association between cognitive inhibition and other pain inhibitory phenomena, like exercise-induced hypoalgesia (EIH), are scarce. The primary aim was to explore the association between cognitive inhibition and EIH at exercising (local) and non-exercising (remote) muscles after isometric exercise. The secondary aim was to explore the association between cognitive inhibition and pressure pain sensitivity. Methods Sixty-six pain-free participants (28.3 ± 8.9 years old, 34 women) completed two cognitive inhibition tasks (stop-signal task and Stroop Colour-Word task), a 3-min isometric wall squat exercise, and a quiet rest control condition with pre- and post-assessments of manual pressure pain thresholds at a local (thigh) and a remote site (shoulder). In addition, cuff pressure pain thresholds, pain tolerance and temporal summation of pain were assessed at baseline. Results No association was found between remote EIH and cognitive inhibition (Stroop interference score: r=0.12, [−0.15; 0.37], p=0.405, BF01=6.70; stop-signal reaction time: r=−0.08, [−0.32; 0.17], p=0.524, BF01=8.32). Unexpectedly, individuals with worse performance on the Stroop task, as indicated by a higher Stroop interference score, showed higher local EIH (r=0.33; [0.10; 0.53], p=0.007, BF01=0.29). No associations were observed between pain sensitivity and any of the cognitive inhibition performance parameters. Conclusions The present findings do not support previous evidence on positive associations between exercise-induced hypoalgesia and cognitive inhibition, as well as baseline pain sensitivity and cognitive inhibition.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Maxime Billot ◽  
Cécilia Neige ◽  
Martin Gagné ◽  
Catherine Mercier ◽  
Laurent J. Bouyer

Previous studies have shown that pain can interfere with motor control. The neural mechanisms underlying these effects remain largely unknown. At the upper limb, mounting evidence suggests that pain-induced reduction in corticospinal excitability is involved. No equivalent data is currently available at the lower limb. The present study therefore examined the effect of thermal pain on the corticospinal drive to tibialis anterior (TA) at rest and during an isometric submaximal dorsiflexion. Transcranial magnetic stimulation was used to induce motor-evoked potentials (MEPs) in the TA at rest and during contraction in the presence or absence of cutaneous heat pain induced by a thermode positioned above the TA (51°C during 1 s). With similar pain ratings between conditions (3.9/10 at rest and 3.6/10 during contraction), results indicate significant decreases in MEP amplitude during both rest (−9%) and active conditions (−13%) (main effect of pain, p=0.02). These results therefore suggest that cutaneous heat pain can reduce corticospinal excitability in the TA muscle and that such reduction in corticospinal excitability could contribute to the interference of pain on motor control/motor learning.


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