Exploring the Mechanisms of Exercise-Induced Hypoalgesia Using Somatosensory and Laser Evoked Potentials

Abstract

Exercise-induced hypoalgesia is well described, but the underlying mechanisms are unclear. The aim of this study was to examine the effect of exercise on somatosensory evoked potentials, laser evoked potentials, pressure pain thresholds and heat pain thresholds. These were recorded before and after 3-min of isometric elbow flexion exercise at 40% of the participant's maximal voluntary force, or an equivalent period of rest. Exercise-induced hypoalgesia was confirmed in two experiments (Experiment 1–SEPs; Experiment 2–LEPs) by increased pressure pain thresholds at biceps brachii (24.3 and 20.6% increase in Experiment 1 and 2, respectively; both d > 0.84 and p < 0.001) and first dorsal interosseous (18.8 and 21.5% increase in Experiment 1 and 2, respectively; both d > 0.57 and p < 0.001). In contrast, heat pain thresholds were not significantly different after exercise (forearm: 10.8% increase, d = 0.35, p = 0.10; hand: 3.6% increase, d = 0.06, p = 0.74). Contrasting effects of exercise on the amplitude of laser evoked potentials (14.6% decrease, d = −0.42, p = 0.004) and somatosensory evoked potentials (10.9% increase, d = −0.02, p = 1) were also observed, while an equivalent period of rest showed similar habituation (laser evoked potential: 7.3% decrease, d = −0.25, p = 0.14; somatosensory evoked potential: 20.7% decrease, d = −0.32, p = 0.006). The differential response of pressure pain thresholds and heat pain thresholds to exercise is consistent with relative insensitivity of thermal nociception to the acute hypoalgesic effects of exercise. Conflicting effects of exercise on somatosensory evoked potentials and laser evoked potentials were observed. This may reflect non-nociceptive contributions to the somatosensory evoked potential, but could also indicate that peripheral nociceptors contribute to exercise-induced hypoalgesia.

Exercise-induced hypoalgesia after acute and regular exercise: experimental and clinical manifestations and possible mechanisms in individuals with and without pain

“…The perceived pain intensity of a suprathreshold stimulus is consistently reduced by aerobic, isometric, and dynamic resistance exercises, 42 , 64 , 98 and acute exercise can reduce ratings of pain unpleasantness even in the absence of a change in pain intensity. 80 In addition, low-intensity nonpainful aerobic and isometric exercises also increase the tolerance to a painful stimulus. A 20% increase in pain tolerance was observed by Vaegter et al 199 after a 3-minute submaximal isometric knee extension exercise, and after a 6-minute walking exercise 73 compared with rest in 35 pain-free individuals.…”

“… 130 Controlled studies using similar methodology but different designs (eg, crossover trials and parallel trials) have also been conducted. 80 , 162 , 195 , 204 The results of these studies, especially those where participants were randomized to exercise or control, or where the order of exercise and control were randomized and counterbalanced for crossover trials, give a less biased estimate of the effect of a single bout of exercise on pain.…”

“…Although not an assessment of pain per se, techniques that assess the function of the nociceptive pathways have sometimes been used to investigate EIH. 38 , 80 These more complex methods, which include evoked potentials and neuroimaging, may provide greater insight into the mechanisms of EIH compared to more commonly used quantitative sensory tests. Evoked potentials are cortical responses recorded at the scalp using electroencephalography in response to brief and intense stimuli.…”

Exercise does not produce hypoalgesia when performed immediately after a painful stimulus

“…In pain-free individuals, acute exercise can transiently reduce pain sensitivity, known as exerciseinduced hypoalgesia (EIH) [2]. EIH is often reported when assessed at non-exercising muscles, but greater increases in pressure pain thresholds (PPTs) are seen at the exercising muscles [3][4][5][6][7]. This suggests that EIH involves -in addition to peripheral or segmental pain modulatory processes -a systemic component of central descending inhibition, which is reflected in EIH effects at non-exercising muscles.…”

Exercise-induced pain threshold modulation in healthy subjects: a systematic review and meta-analysis.

“…Studies have suggested that exercise can induce hypoalgesia by peripherally modulating the transduction, transmission, and processing of noxious stimuli (Jones, Taylor, Booth, & Barry, 2016). Some other hypotheses include the systemic activation of the endogenous opioid, serotoninergic and immune system, and the central activation of the corticothalamic descending inhibitory pathways (K. F. Koltyn, 2000), assuming that these physiological mechanisms could be assessed by quantitative sensory testing, such as paint threshold (PT).…”