The Interaction Between Psychosocial Factors And Exercise-Induced Hypoalgesia in Pain-Free Nurses Part 2

Why we will be tired? How can we solve the fatigue problems?

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Regression Analysis Between Exercise-Induced Hypoalgesia and Psychosocial Factors

Multiple linear regression was carried out to investigate the relationship between all psychosocial variables and EIH at each location (Supplementary Table S3). Due to multicollinearity when MSPSS total and MSPSS subscales were included in the model, the model was refined and the MSPSS total score only was included in the primary analysis. When all psychosocial variables were included in the model, none predicted remote (F (7, 30)= 0.8771; P=0.536, adjusted R2 of −0.024), local (F (7, 30)= 0.541; P=0.797, adjusted R2 of −0.095), semi-local (F (7, 30)= 1.10; P=0.390, adjusted R2 of 0.018), or global (F (7, 30)= 0.933; P=0.496, adjusted R2 of −0.013) EIH with any certainty.

Cistanche can act as an anti-fatigue and stamina enhancer, and experimental studies have shown that the decoction of Cistanche tubulosa could effectively protect the liver hepatocytes and endothelial cells damaged in weight-bearing swimming mice, upregulate the expression of NOS3, and promote hepatic glycogen synthesis, thus exerting anti-fatigue efficacy. Phenylethanoid glycoside-rich Cistanche tubulosa extract could significantly reduce the serum creatine kinase, lactate dehydrogenase, and lactate levels, and increase the hemoglobin (HB) and glucose levels in ICR mice, and this could play an anti-fatigue role by decreasing the muscle damage and delaying the lactic acid enrichment for energy storage in mice. Compound Cistanche Tubulosa Tablets significantly prolonged the weight-bearing swimming time, increased the hepatic glycogen reserve, and decreased the serum urea level after exercise in mice, showing its anti-fatigue effect. The decoction of Cistanchis can improve endurance and accelerate the elimination of fatigue in exercising mice, and can also reduce the elevation of serum creatine kinase after load exercise and keep the ultrastructure of skeletal muscle of mice normal after exercise, which indicates that it has the effects of enhancing physical strength and anti-fatigue. Cistanchis also significantly prolonged the survival time of nitrite-poisoned mice and enhanced the tolerance against hypoxia and fatigue.

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Exploratory best subset multiple linear regression analysis was performed separately for each EIH location to determine which psychosocial variables predict EIH response. For local EIH at the calf (pooled), a two-predictor model comprising  MSPSS friends subscale and PCS total score accounted for 24% of the variance (F (2, 35) = 6.84; P=0.003, adjusted R2 of  0.24) (Table 3). Semi-local EIH response may be explained by MSPSS total, PCS total, and DASS depression; however, the model did not reach statistical significance (F (3, 34) = 2.85; P=0.052, adjusted R2 of 0.13). A similar trend was observed with the best subset model for the remote site consisting of a single variable (F (1, 36) = 4.00; P=0.053, adjusted R2 of 0.08). The best subset regression analysis to explain global EIH for all pooled sites consisted of MSPSS friends and PCS total and may explain 17% of the variance (F (2, 35) = 4.78; P=0.015, adjusted R2 of 0.17).

Discussion

This study examined the effect of cycling exercise on EIH in pain-free nurses. Pain sensitivity decreased globally and at all individual body sites following exercise, indicating EIH. Social support and pain catastrophizing presented as the most likely variables to explain up to one-quarter of the variance in EIH; however, a larger more diverse sample is required to confirm these findings.

Pain catastrophizing was found to not correlate with EIH at any site; however, some evidence for pain catastrophizing predicted EIH for the fitted model selected from the best subset regression at the local site; and a trending significant contribution for global EIH was observed. These findings may infer higher pain catastrophizing reduces endogenous pain modulation as evidenced by reduced EIH. Previous evidence showed greater levels of pain catastrophizing influenced endogenous pain modulation and increased the risk of pain onset, chronic pain development, and higher pain intensity.21 This is important because nurses have higher rates of musculoskeletal injury.27 Three previous studies reported no correlation between pain catastrophizing and EIH at the local muscle area following isometric handgrip exercise in pain-free adults.22,23,62 Our observation may partially be explained by low total pain catastrophizing scores due to the recruitment of participants without a history of musculoskeletal injury or pain. Future studies in a more representative nursing population with a broader range of pain history and pain catastrophizing are warranted.

Total MSPSS scores predicted EIH at the lumbar spine and trended toward significance at the forearm (p = 0.053), and MSPSS friends subscale predicted EIH at the lumbar spine and globally when all sites were pooled. Contrary to our expectations, the best subset linear mixed models showed that lower perceived social support predicted greater EIH following cycling. Although this is the first study to our knowledge to report the association between social support and EIH, it contrasts expectations because enhanced social support (eg, verbal support, social touch) was previously reported to reduce pain perception in pain-free and clinical pain populations.19 The effect of social support on pain sensitivity is complex, and there is evidence that, at least in the situational context, social hypoalgesia can occur (ie, exposure to social interaction with feelings of disconnectedness and general negative affect can lead to a hypoalgesic response).70 Social disconnection alone may be sufficient to evoke a stress response and therefore hypoalgesia71,72; however, we did not assess a measure of situational stress. General perceptions of stress on EIH were evaluated with the DASS stress subscale, and while there was no correlation or predictive evidence of the stress subscale on EIH, this may be due to the responses reflecting perceptions of the past week and therefore not being sensitive to situational stresses. Additionally, mental and physiological stress is associated with shift work73 and therefore may also influence the results for some participants for measures of pain processing. However, this study did not control for the influence of recent shift work on pain sensitivity measures which remains a limitation of this study. More broadly, there is evidence that social exclusion, inclusion, and social support can lead to hyperalgesia.74,75 Therefore, while we showed some evidence for lower social support to predict greater EIH in pain-free, mostly female nurses, further research on a larger scale that includes a broad range of social support is required.

Kinesiophobia was not correlated with, nor predictive of EIH at any site. These findings support previous research in pain-free adults.23,60,62 This similarity in findings could be attributed to the shared sample characteristics of low kinesiophobia scores (TSK-17 = 31 points;60 TSK-11 = 19 points;62 Fear of Pain Questionnaire-III = 77.4 points23) in previous studies. Interestingly, the change in pressure pain intensity rating assessed every 30 seconds for 2 minutes using a Forgione-Barber pressure stimulator on the forefinger but not PPT was correlated with kinesiophobia in an earlier study.23 This suggests that kinesiophobia may moderate EIH when measured as a change in pressure pain tolerance rather than a change in PPT in pain-free adults. Larger scale research is required to confirm these findings in populations where kinesiophobia has been reported to be predictive of the duration of sick leave.76

Symptoms of depression and anxiety were not found to correlate with EIH. Few studies have investigated the correlation between depressive symptoms and EIH in pain-free populations. One study23 reported total mood disturbance (Profile and Mood States questionnaire) predicted reduced EIH; however, the authors did not report depression subscales.  Further, while the aforementioned study showed a  profile of mood states was predictive of EIH, our findings are consistent with previous studies to show that anxiety does not appear to be associated with EIH.22,77,78 Our sample presented with low levels of anxiety which may partially explain the lack of prediction capability for EIH. While anxiety has been shown to moderate pain sensitivity,79 it remains unclear whether anxiety affects endogenous pain modulation.

Global work satisfaction levels in the current study had no relationship with EIH. Our study was the first to explore the relationship between work satisfaction and EIH in a pain-free population. Previous research showed that both work and family environments may lead to similar environmental stresses (eg, cohesion, control) that were predictive of pain and psychological distress.80 Brellenthin et al23 investigated the correlation between the family environment and EIH following acute isometric exercise. Negative family environment scores (Family Environment Scale Questionnaire) were predictive of EIH for PPT. This is supported by observations that negative family environments (eg, lower cohesion and marital dissatisfaction) can influence the development and maintenance of chronic pain.81,82 Although Brellenthin et al did not explicitly assess work satisfaction, social environments that lead to poorer mental health status may contribute to the dysfunction of descending pain inhibitory pathways associated with EIH.12 Therefore, future studies should further investigate the association between work satisfaction and EIH. This will be particularly important in the nursing profession where job satisfaction and staff retention are low.83

A large effect size at global and all individual local sites was observed in this study and is consistent with several previous studies examining cycling.5,36,37,61,84–91 However, our study was the first to evaluate the association between psychosocial variables in a pain-free population following an effective aerobic EIH exposure. Two previous studies in this area did not achieve EIH,60,92 but also reported that no psychosocial variables predicted EIH. Research on multi-site hypoalgesic effects of cycling is conflicting, with some studies reporting EIH at remote locations,5,61,89 while other studies have not.36,86,90,93 These studies have utilized similar exercise protocols (approximately 70–75% VO2 max; 10–30 minutes); however, in our study, participants also reached volitional fatigue. Training history related to the exercise intensity may explain some of the variability in EIH across studies more than the intensity itself. Exercise produces a physiological stress response which increases with higher exercise intensities, longer duration, and lower training history.94 Acute stress has been shown to have a hypoalgesic response via activation of opioid and endocannabinoid mechanisms,95 similar to that of EIH. The exposure to unaccustomed exercise resulting in acute situational stress may not fully explain these results because studies have shown that EIH can occur at various exercise intensities.3 Therefore, research is required to explore the effect of individual factors in addition to the absolute exercise prescription variables associated with exercise exposure on EIH.

A strength of this study is that the cycling protocol was appropriate and achieved EIH in this population. Two previous studies60,92 evaluating the effect of psychosocial factors on EIH did not achieve EIH with aerobic exercise protocols, and therefore this study is an important step towards understanding the effect of psychosocial factors on EIH in pain-free populations at high risk of musculoskeletal pain conditions. The use of valid questionnaires to measure psychosocial factors commonly associated with musculoskeletal pain conditions and the use of PPTs to measure local and remote pain sensitivity are the strengths of this study. This pilot study is limited by the cross-sectional design, and therefore threats to internal validity associated with learning, regression to the mean, contextual factors, and natural variation in response to multiple tests. The study intended to recruit adults without pain, and while this is a strength of the current study, it does preclude the application of these findings more generally. The recruitment of relatively young, pain-free participants may have also led to a lack of diversity across the psychosocial health spectrum which can influence pain-processing pathways9,16 and may have contributed to the large effect size of EIH at all body regions.1 Therefore, the findings of this research should be considered in the context of the sample studied.

Conclusion

A maximal graded exercise cycling test led to EIH at local, regional, and global body regions in pain-free, predominantly female nurses. Regression analyses between psychosocial variables and EIH show that perceived social support and pain catastrophizing are the most likely variables to explain up to one-quarter of the variance in EIH; however, these results are not conclusive due to the small sample size. Based on this pilot study, replication in a larger, more representative sample of nurses is required to confirm whether psychosocial factors moderate EIH; and further, whether these measures may be used as early predictors of lost time injury in this profession.

Acknowledgments 

The authors thank the participants for taking part in the study and their colleagues in the wider study.

Disclosure

Jessica Van Oosterwijck has a postdoctoral fellowship funded by the Research Foundation – Flanders (FWO; grant number 12L5616N). Scott Tagliaferri is supported by an Australian Government Research Training Program Scholarship.  The authors report no conflicts of interest in this work.

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