The association between changes in pressure pain sensitivity and changes in cardiovascular physiological factors associated with persistent stress

Author(s):  
Søren Ballegaard ◽  
Pernille B. Petersen ◽  
Gitte S. Harboe ◽  
Benny Karpatschof ◽  
Finn Gyntelberg ◽  
...  
2017 ◽  
Vol 9 (2) ◽  
pp. 93-98 ◽  
Author(s):  
Celeste T. Tipple ◽  
Sarah Benson ◽  
Andrew Scholey

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.


2021 ◽  
pp. 1-8
Author(s):  
Daniel Viggiani ◽  
Jack P. Callaghan

Viscoelastic creep generated in the lumbar spine following sustained spine flexion may affect the relationship between tissue damage and perceived pain. Two processes supporting this altered relationship include altered neural feedback and inflammatory processes. Our purpose was to determine how low back mechanical pain sensitivity changes following seated lumbar spine flexion using pressure algometry in a repeated-measures, cross-sectional laboratory design. Thirty-eight participants underwent a 10-minute sustained seated maximal flexion exposure with a 40-minute standing recovery period. Pressure algometry assessed pressure pain thresholds and the perceived intensity and unpleasantness of fixed pressures. Accelerometers measured spine flexion angles, and electromyography measured muscular activity during flexion. The flexion exposure produced 4.4° (2.7°) of creep that persisted throughout the entire recovery period. The perception of low back stimulus unpleasantness was elevated immediately following the exposure, 20 minutes before a delayed increase in lumbar erector spinae muscle activity. Women reported the fixed pressures to be more intense than men. Sustained flexion had immediate consequences to the quality of mechanical stimulus perceived but did not alter pressure pain thresholds. Neural feedback and inflammation seemed unlikely mechanisms for this given the time and direction of pain sensitivity changes, leaving a postulated cortical influence.


2018 ◽  
Vol 47 (3) ◽  
pp. 193-200 ◽  
Author(s):  
Rami Kankaanpää ◽  
Juha Auvinen ◽  
Kari Rantavuori ◽  
Jari Jokelainen ◽  
Jaro Karppinen ◽  
...  

1989 ◽  
Vol 66 (2) ◽  
pp. 949-954 ◽  
Author(s):  
A. M. Rivera ◽  
A. E. Pels ◽  
S. P. Sady ◽  
M. A. Sady ◽  
E. M. Cullinane ◽  
...  

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.


2020 ◽  
Vol 2;23 (4;2) ◽  
pp. 219-227
Author(s):  
César Fernández-de-las-Peñas

Background: A method for assessing dynamic muscle hyperalgesia (dynamic pressure algometry) has been developed and applied in tension-type and migraine headaches. Objectives: To investigate differences in dynamic pressure pain assessment over the trigeminal area between men with cluster headache (CH) and headache-free controls, and the association between dynamic and static pressure pain sensitivity. Study Design: A case-control study. Setting: Tertiary urban hospital. Methods: Forty men with episodic CH and 40 matched controls participated. Dynamic pressure pain sensitivity was assessed with a dynamic pressure algometry set consisting of 8 rollers with different fixed levels (500, 700, 850, 1,350, 1,550, 2,200, 3,850, and 5,300 g). Each roller was moved at a speed of 0.5 cm/sec over a diagonal line covering the temporalis muscle from an anterior to posterior direction. The dynamic pressure threshold (DPT; load level of the first painful roller) and the pain intensity perceived at the DPT level (roller-evoked pain) were assessed. Static pressure pain thresholds (PPT) were also assessed with a digital pressure algometer applied statically over the mid-muscle belly of the temporalis. Patients were assessed in a remission phase, at least 3 months from the last cluster attack, and without preventive medication. Results: Side-to-side consistency between DPTs (r = 0.781, P < 0.001), roller-evoked pain on DPT (r = 0.586; P < 0.001), and PPTs (r = 0.874; P < 0.001) were found in men with CH. DPT was moderately, bilaterally, and side-to-side associated with PPTs (0.663 > r > 0.793, all P < 0.001). Men with CH had bilateral lower DPT and PPT and reported higher levels of rollerevoked pain (all P < 0.001) than headache-free controls. Limitations: Only men with episodic CH were included. Conclusions: This study supports that a dynamic pressure algometry is as valid as a static pressure algometry for assessing pressure pain sensitivity in patients with CH. Assessing both dynamic and static pain sensitivity may provide new opportunities for differentiated diagnostics. Key words: Cluster headache, dynamic pressure pain, pressure pain threshold


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