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Pain can be defined as an unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage. Though consistent with this definition, different types of pain result in different behavioural and psychophysiological responses. For example, the transient, non‐threatening, acute muscle pain element of exercise‐induced pain (EIP) is entirely different from other pain types like delayed onset muscle soreness, muscular injury or chronic pain. However, studies often conflate the definitions or assume parity between distinct pain types. Consequently, the mechanisms through which pain might impact exercise behaviour across different pain subcategories may be incorrectly assumed, which could lead to interventions or recommendations that are inappropriate. Therefore, this review aims to distinguish EIP from other subcategories of pain according to their aetiologies and characteristics, thereby providing an updated conceptual and operational definition of EIP. Secondly, the review will discuss the experimental pain models currently used across several research domains and their relevance to EIP with a focus on the neuro‐psychophysiological mechanisms of EIP and its effect on exercise behaviour and performance. Finally, the review will examine potential interventions to cope with the impact of EIP and support wider exercise benefits. Highlights: What is the topic of this review?Considerations for future research focusing on exercise‐induced pain within endurance exercise settings.What advances does it highlight? An updated appraisal and guide of research concerning exercise‐induced pain and its impact on endurance task behaviour, particularly with reference to the aetiology, measurement, and manipulation of exercise‐induced pain. [ABSTRACT FROM AUTHOR]

Pain is a naturally occurring phenomenon that consistently inhibits exercise performance by imposing unconscious, neurophysiological alterations (e.g., corticospinal changes) as well as conscious, psychophysiological pressures (e.g., shared effort demands). Although several studies indicate that pain would elicit lower task outputs for a set intensity of perceived effort, no study has tested this. Therefore, this study investigated the impact of elevated muscle pain through a hypertonic saline injection on the power output, psychophysiological, cerebral oxygenation, and perceptual changes during fixed perceived effort exercise. Ten participants completed three visits (1 familiarization + 2 fixed perceived effort trials). Fixed perceived effort cycling corresponded to 15% above gas exchange threshold (GET) [mean rating of perceived effort (RPE) = 15 "hard"]. Before the 30-min fixed perceived effort exercise, participants received a randomized bilateral hypertonic or isotonic saline injection in the vastus lateralis. Power output, cardiorespiratory, cerebral oxygenation, and perceptual markers (e.g., affective valence) were recorded during exercise. Linear mixed-model regression assessed the condition and time effects and condition × time interactions. Significant condition effects showed that power output was significantly lower during hypertonic conditions [t107 = 208, P = 0.040, β = 4.77 W, 95% confidence interval (95% CI) [0.27 to 9.26 W]]. Meanwhile, all physiological variables (e.g., heart rate, oxygen uptake, minute ventilation) demonstrated no significant condition effects. Condition effects were observed for deoxyhemoglobin changes from baseline (t107 = −3.29, P = 0.001, β = −1.50 ΔμM, 95% CI [−2.40 to −0.61 ΔμM]) and affective valence (t127 = 6.12, P = 0.001, β = 0.93, 95% CI [0.63 to 1.23]). Results infer that pain impacts the self-regulation of fixed perceived effort exercise, as differences in power output mainly occurred when pain ratings were higher after hypertonic versus isotonic saline administration. NEW & NOTEWORTHY: This study identifies that elevated muscle pain through a hypertonic saline injection causes significantly lower power output when pain is experienced but does not seem to affect exercise behavior in a residual manner. Results provide some evidence that pain operates on a psychophysiological level to alter the self-regulation of exercise behavior due to differences between conditions in cerebral deoxyhemoglobin and other perceptual parameters. [ABSTRACT FROM AUTHOR]

This study compared the acute hypoalgesic and neurophysiological responses to low‐load resistance exercise with and without blood flow restriction (BFR), and free‐flow, high‐load exercise. Participants performed four experimental conditions where they completed baseline measures of pain pressure threshold (PPT), maximum voluntary force (MVF) with peripheral nerve stimulation to determine central and peripheral fatigue. Corticospinal excitability (CSE), corticospinal inhibition and short interval intracortical inhibition (SICI) were estimated with transcranial magnetic stimulation. Participants then performed low‐load leg press exercise at 30% of one‐repetition maximum (LL); low‐load leg press with BFR at 40% (BFR40) or 80% (BFR80) of limb occlusion pressure; or high‐load leg press of four sets of 10 repetitions at 70% one‐repetition maximum (HL). Measurements were repeated at 5, 45 min and 24 h post‐exercise. There were no differences in CSE or SICI between conditions (all P > 0.05); however, corticospinal inhibition was reduced to a greater extent (11%–14%) in all low‐load conditions compared to HL (P < 0.005). PPTs were 12%–16% greater at 5 min post‐exercise in BFR40, BFR80 and HL compared to LL (P ≤ 0.016). Neuromuscular fatigue displayed no clear difference in the magnitude or time course between conditions (all P > 0.05). In summary, low‐load BFR resistance exercise does not induce different acute neurophysiological responses to low‐load, free‐flow exercise but it does promote a greater degree of hypoalgesia and reduces corticospinal inhibition more than high‐load exercise, making it a useful rehabilitation tool. The changes in neurophysiology following exercise were not related to changes in PPT. What is the central question of this study?Does low‐load, blood flow restricted, resistance exercise promote greater hypoalgesic and neurophysiological changes in the 24 h period post‐exercise, in comparison to high‐load resistance exercise?What is the main finding and its importance?Blood flow restriction exercise augments hypoalgesia compared to free‐flow, low‐load exercise and induces similar hypoalgesia to high‐load exercise, but does not result in any different alterations to corticospinal excitability or inhibition. However, corticospinal inhibition was reduced to a greater extent with low‐load exercise, compared to high‐load exercise. Therefore, low‐load BFR resistance exercise is a suitable method for exercise rehabilitation. [ABSTRACT FROM AUTHOR]