scholarly journals The Role of Autonomic Function in Exerciseinduced Endogenous Analgesia: A Case-control Study in Myalgic Encephalomyelitis⁄Chronic Fatigue Syndrome and Healthy People

2017 ◽  
Vol 3 (20;3) ◽  
pp. E389-E399 ◽  
Author(s):  
Jo Nijs

Background: Patients with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) are unable to activate brain-orchestrated endogenous analgesia (or descending inhibition) in response to exercise. This physiological impairment is currently regarded as one factor explaining postexertional malaise in these patients. Autonomic dysfunction is also a feature of ME/CFS. Objectives: This study aims to examine the role of the autonomic nervous system in exerciseinduced analgesia in healthy people and those with ME/CFS, by studying the recovery of autonomic parameters following aerobic exercise and the relation to changes in self-reported pain intensity. Study Design: A controlled experimental study. Setting: The study was conducted at the Human Physiology lab of the Vrije Universiteit Brussel. Methods: Twenty women with ME/CFS- and 20 healthy, sedentary controls performed a submaximal bicycle exercise test known as the Aerobic Power Index with continuous cardiorespiratory monitoring. Before and after the exercise, measures of autonomic function (i.e., heart rate variability, blood pressure, and respiration rate) were performed continuously for 10 minutes and self-reported pain levels were registered. The relation between autonomous parameters and self-reported pain parameters was examined using correlation analysis. Results: Some relationships of moderate strength between autonomic and pain measures were found. The change (post-exercise minus pre-exercise score) in pain severity was correlated (r = .580, P = .007) with the change in diastolic blood pressure in the healthy group. In the ME/CFS group, positive correlations between the changes in pain severity and low frequency (r = .552, P = .014), and between the changes in bodily pain and diastolic blood pressure (r = .472, P = .036), were seen. In addition, in ME/CHFS the change in headache severity was inversely correlated (r = -.480, P = .038) with the change in high frequency heart rate variability. Limitations: Based on the cross-sectional design of the study, no firm conclusions can be drawn on the causality of the relations. Conclusions: Reduced parasympathetic reactivation during recovery from exercise is associated with the dysfunctional exercise-induced analgesia in ME/CFS. Poor recovery of diastolic blood pressure in response to exercise, with blood pressure remaining elevated, is associated with reductions of pain following exercise in ME/CFS, suggesting a role for the arterial baroreceptors in explaining dysfunctional exercise-induced analgesia in ME/CFS patients. Key words: Aerobic exercise, aerobic power index, autonomic nervous system, exercise-induced analgesia, exercise-induced hypoalgesia, fibromyalgia, heart rate variability, stress-induced analgesia, pain Pain

2022 ◽  
Vol 28 (1) ◽  
Author(s):  
Linda P. Bolin ◽  
Amelia D. Saul ◽  
Lauren L. Bethune Scroggs ◽  
Carolyn Horne

Abstract Background Cardiovascular disease is one of the leading causes of death globally with hypertension being a primary cause of premature death from this disease process. Individuals with a family history of cardiovascular disease and hypertension are at a greater risk for developing the same sequela. Autonomic cardiac control is important in the level of cardiac function. One intervention that is effective in improving cardiovascular function is heart rate variability biofeedback training. The purpose of our study was to determine the effectiveness of heart rate biofeedback training on HRV and blood pressure in individuals with a family history of cardiovascular disease. Methods Thirty-four participants (76.5% female, 22.7 ± 4.3 years) completed a baseline assessment and training using an established short-term HRV protocol followed by two weeks of at-home paced breathing employing a smartphone application. The participants were then reassessed in a biofeedback clinic. Results The participants physiological measures showed a significant increase in means between pre and post intervention of SDNN (t (32) = 2.177, p =.037) and TP, (t (32) = 2.327 p = .026). Correlation noted a medium effect on diastolic blood pressure and high frequency heart rate variability, F, r = .41, n =33, p < .05. A multiple regression with all predictor variables in the model found no significance with diastolic and systolic blood pressure. Conclusions The findings from this pilot study demonstrated that a two-week paced breathing intervention may assist in reducing heart rate and diastolic blood pressure while improving heart rate variability.


2021 ◽  
Author(s):  
Rada R Veeneman ◽  
Jentien M Vermeulen ◽  
Abdel Abdellaoui ◽  
Eleanor Sanderson ◽  
Robyn E Wootton ◽  
...  

Importance: Individuals with schizophrenia have a reduced life-expectancy compared to the general population, largely due to an increased risk of cardiovascular disease (CVD). Clinical and epidemiological studies have been unable to fully unravel the nature of this relationship. Objective: Investigate genetic correlations and potential bi-directional effects between liability to schizophrenia and CVD. Design, setting, and participants: We obtained summary-data of genome-wide-association studies of schizophrenia (N=130,644), heart failure (N=977,323), coronary artery disease (N=332,477), systolic and diastolic blood pressure (N=757,601), heart rate variability (N=46,952), QT interval (N=103,331), early repolarization and dilated cardiomyopathy ECG patterns (N=63,700). We computed genetic correlations with linkage disequilibrium score regression and conducted bi-directional Mendelian randomization (MR). With multivariable MR, we investigated whether associations were mediated by smoking, body mass index, physical activity, lipid levels, or type 2 diabetes. To ensure robustness, we applied a range of sensitivity methods. Main outcomes and measures: Schizophrenia, heart failure, coronary artery disease, systolic blood pressure, diastolic blood pressure, heart rate variability, QT interval, early repolarization, dilated cardiomyopathy. Results: Genetic correlations between liability to schizophrenia and CVD were close to zero (-0.02 to 0.04). With MR, we found robust evidence that liability to schizophrenia increases heart failure risk. This effect remained consistent with multivariable MR. There was also evidence that liability to schizophrenia increases early repolarization risk, largely mediated by BMI and lipid levels. Finally, there was evidence that liability to schizophrenia increases heart rate variability, a direction of effect contrasting previous studies. In the other direction, there was weak evidence that higher systolic, but not diastolic, blood pressure increases schizophrenia risk. Conclusions and relevance: Our findings indicate that liability to schizophrenia increases the risk of heart failure, and that this is not mediated by key health behaviours. This is consistent with the notion that schizophrenia is characterised by a systemic dysregulation of the body (including inflammation and oxidative stress) with detrimental effects on the heart. To decrease cardiovascular mortality among schizophrenia patients, priority should lie with optimal treatment and interventions in early stages of psychoses. We also identified early repolarization, currently understudied, as a potential CVD marker among patients with schizophrenia.


2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Rosa María Escorihuela ◽  
Lluís Capdevila ◽  
Juan Ramos Castro ◽  
María Cleofé Zaragozà ◽  
Sara Maurel ◽  
...  

Abstract Background Heart rate variability (HRV) is an objective, non-invasive tool to assessing autonomic dysfunction in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). People with CFS/ME tend to have lower HRV; however, in the literature there are only a few previous studies (most of them inconclusive) on their association with illness-related complaints. To address this issue, we assessed the value of different diurnal HRV parameters as potential biomarker in CFS/ME and also investigated the relationship between these HRV indices and self-reported symptoms in individuals with CFS/ME. Methods In this case–control study, 45 female patients who met the 1994 CDC/Fukuda definition for CFS/ME and 25 age- and gender-matched healthy controls underwent HRV recording-resting state tests. The intervals between consecutive heartbeats (RR) were continuously recorded over three 5-min periods. Time- and frequency-domain analyses were applied to estimate HRV variables. Demographic and clinical features, and self-reported symptom measures were also recorded. Results CFS/ME patients showed significantly higher scores in all symptom questionnaires (p < 0.001), decreased RR intervals (p < 0.01), and decreased HRV time- and frequency-domain parameters (p < 0.005), except for the LF/HF ratio than in the healthy controls. Overall, the correlation analysis reached significant associations between the questionnaires scores and HRV time- and frequency-domain measurements (p < 0.05). Furthermore, separate linear regression analyses showed significant relationships between self-reported fatigue symptoms and mean RR (p = 0.005), RMSSD (p = 0.0268) and HFnu indices (p = 0.0067) in CFS/ME patients, but not in healthy controls. Conclusions Our findings suggest that ANS dysfunction presenting as increased sympathetic hyperactivity may contribute to fatigue severity in individuals with ME/CFS. Further studies comparing short- and long-term HRV recording and self-reported outcome measures with previous studies in larger CFS/ME cohorts are urgently warranted.


1991 ◽  
Vol 9 (6) ◽  
pp. S429
Author(s):  
C. Cerutti ◽  
M. Lo ◽  
Claude Julien ◽  
Madelaine Vincent ◽  
C. Paultre ◽  
...  

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