scholarly journals Occlusion of blood flow attenuates exercise-induced hypoalgesia in the occluded limb of healthy adults

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.

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.


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.


2019 ◽  
Vol 30 (2) ◽  
pp. 525-533 ◽  
Author(s):  
J J Steventon ◽  
C Foster ◽  
H Furby ◽  
D Helme ◽  
R G Wise ◽  
...  

Abstract Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels’ ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10–12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.


2006 ◽  
Vol 101 (1) ◽  
pp. 289-297 ◽  
Author(s):  
D. Merrill Dane ◽  
Connie C. W. Hsia ◽  
Eugene Y. Wu ◽  
Richard T. Hogg ◽  
Deborah C. Hogg ◽  
...  

The spleen acts as an erythrocyte reservoir in highly aerobic species such as the dog and horse. Sympathetic-mediated splenic contraction during exercise reversibly enhances convective O2 transport by increasing hematocrit, blood volume, and O2-carrying capacity. Based on theoretical interactions between erythrocytes and capillary membrane (Hsia CCW, Johnson RL Jr, and Shah D. J Appl Physiol 86: 1460–1467, 1999) and experimental findings in horses of a postsplenectomy reduction in peripheral O2-diffusing capacity (Wagner PD, Erickson BK, Kubo K, Hiraga A, Kai M, Yamaya Y, Richardson R, and Seaman J. Equine Vet J 18, Suppl: 82–89, 1995), we hypothesized that splenic contraction also augments diffusive O2 transport in the lung. Therefore, we have measured lung diffusing capacity (DlCO) and its components during exercise by a rebreathing technique in six adult foxhounds before and after splenectomy. Splenectomy eliminated exercise-induced polycythemia, associated with a 30% reduction in maximal O2 uptake. At any given pulmonary blood flow, DlCO was significantly lower after splenectomy owing to a lower membrane diffusing capacity, whereas pulmonary capillary blood volume changed variably; microvascular recruitment, indicated by the slope of the increase in DlCO with respect to pulmonary blood flow, was also reduced. We conclude that splenic contraction enhances both convective and diffusive O2 transport and provides another compensatory mechanism for maintaining alveolar O2 transport in the presence of restrictive lung disease or ambient hypoxia.


2014 ◽  
Vol 5 (4) ◽  
pp. 258-267 ◽  
Author(s):  
Silvia Lo Vecchio ◽  
Lars J. Petersen ◽  
Sara Finocchietti ◽  
Parisa Gazerani ◽  
Lars Arendt-Nielsen ◽  
...  

AbstractBackground and aimsThe ultraviolet-B (UVB) inflammatory model is a well-established model of inflammatory pain. This study investigated whether UVB-induced cutaneous inflammation would enhance pain responses from the underlying deep somatic areas.MethodsSkin inflammation was induced, in 24 healthy volunteers, by UVB irradiation (three times of the individual minimal erythema UVB dose) in square-shaped areas on the forearm and lower back. Assessments of cutaneous blood flow, pin-prick thresholds, pressure pain thresholds and tolerance, stimulus–response functions relating graded pressure stimulations and pain intensity (visual analogue scale, VAS) were performed within and outside the irradiated area.ResultsTwenty-four hours after UVB irradiation, a significant increase in superficial blood flow in the irradiated skin area was demonstrated compared with baseline (P < 0.01) indicating that inflammation was induced. Compared with baseline, UVB irradiation significantly reduced the pin-prick thresholds, pressure pain thresholds and tolerance within and outside of the irradiated area (P < 0.05). The stimulus–response function was left-shifted compared with baseline both within and outside the irradiated area (P < 0.05) with a more pronounced left-shift within the irradiated area (P < 0.01). Application of topical anaesthesia 24h after irradiation in 5 subjects, both within and outside the irradiated area, could only increase the pin-prick thresholds outside the irradiated area.ConclusionThe UVB irradiation of the skin not only provokes cutaneous primary and secondary hyper-algesia but also causes hyperalgesia to blunt pressure stimulations 24h after the UVB exposure.ImplicationsThe presented UVB model can be used as a translational model from animals into healthy subjects. This model can potentially be used to screen drug candidates with anti-inflammatory properties in early stages of drug development.


2011 ◽  
Vol 27 (6) ◽  
pp. 495-501 ◽  
Author(s):  
Steven J. Kamper ◽  
Christopher G. Maher ◽  
Julia M. Hush ◽  
Ashley Pedler ◽  
Michele Sterling

1999 ◽  
Vol 276 (2) ◽  
pp. H663-H670 ◽  
Author(s):  
Stephen J. Duffy ◽  
Gishel New ◽  
Binh T. Tran ◽  
Richard W. Harper ◽  
Ian T. Meredith

Although many factors are thought to contribute to the regulation of metabolic vasodilation in skeletal muscle vasculature, recent interest has focused on the role of the endothelium. We examined the relative roles of nitric oxide (NO) and of vasodilator prostanoids in the control of metabolically induced functional hyperemia in the forearm of humans. In 43 healthy volunteers [24 ± 5 (SD) yr] we assessed resting and functional hyperemic blood flow (FHBF) in response to 2 min of isotonic forearm exercise before and after inhibition of NO and/or vasodilator prostanoid production with intra-arterial N G-monomethyl-l-arginine (l-NMMA, 2 mg/min) and aspirin (ASA, 3 mg/min), respectively. Blood flow was measured using venous occlusion plethysmography.l-NMMA and ASA decreased resting forearm blood flow by 42% ( P < 0.0001) and 23% ( P < 0.0001), respectively, whereas infusion of ASA followed byl-NMMA reduced flow by a further 24% ( P < 0.05).l-NMMA reduced peak FHBF by 18% [from 13.9 ± 1.0 to 11.4 ± 1.1 (SE) ml ⋅ 100 ml forearm−1 ⋅ min−1, P = 0.003] and the volume “repaid” after 1 and 5 min by 25% (8.9 ± 0.7 vs. 6.7 ± 0.7 ml/100 ml, P < 0.0001) and 37% (26.6 ± 1.8 vs. 16.8 ± 1.6 ml/100 ml, P < 0.0001). ASA similarly reduced peak FHBF by 19% (from 14.5 ± 1.1 to 11.8 ± 0.9 ⋅ 100 ml forearm−1 ⋅ min−1, P < 0.001) and the volume repaid after 1 and 5 min by 14% (7.5 ± 0.6 vs. 6.4 ± 0.6 ml/100 ml, P = 0.0001) and 20% (21.2 ± 1.5 vs. 16.9 ± 1.5 ml/100 ml, P < 0.0001), respectively. The coinfusion of ASA andl-NMMA did not decrease FHBF to a greater extent than either agent alone. These data suggest that endothelium-derived NO and vasodilator prostanoids contribute to resting blood flow and metabolic vasodilation in skeletal muscle vasculature in healthy humans. Although these vasodilator mechanisms operate in parallel in exercise-induced hyperemia, they appear not to be additive. Other mechanisms must also be operative in metabolic vasodilation.


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 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.


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