Tag: exercise

The Qigong of Prolong Life With Nine Turn Method Relieve Fatigue, Sleep, Anxiety and Depression in Patients With Chronic Fatigue Syndrome: A Randomized Controlled Clinical Study

Abstract

Background: Chronic fatigue syndrome (CFS) is a complex disease of unknown etiology and mechanism. The purpose of this study was to investigate the effect of Prolong Life with Nine Turn Method (PLWNT) Qigong exercise on CFS focusing on fatigue, sleep quality, depression, and anxiety.

Methods: A total of 90 participants diagnosed with CFS were randomly assigned into two parallel groups: PLWNT and cognitive behavioral therapy (CBT). The participants in the PLWNT or CBT group participated in qigong exercise or cognitive behavior education program, respectively, once a week in-person and were supervised online during the remaining 6 days at home, over 12 consecutive weeks. The primary outcome was fatigue (Multi-dimensional Fatigue Inventory 20 [MFI-20]), and secondary outcomes were sleep quality (Pittsburgh Sleep Quality Index [PSQI]), anxiety, depression (Hospital Anxiety and Depression Scale [HADS]), and changes in the Neuropeptide Y (NPY) of peripheral blood.

Results: The within-group comparisons of the PLWNT and CBT groups revealed significant improvement in both groups in MFI-20, PSQI, and HADS scores (P < 0.05). No significant difference were found between the PLWNT and CBT groups, even though the effective rate of the PLWNT group was 62.22%, which is slightly than 50.00% of the CBT group. The fatigue scores in the PLWNT group were positively correlated with sleep degree (r = 0.315) and anxiety degree (r = 0.333), only anxiety degree (r = 0.332) was found to be positively correlated with fatigue in the CBT group. The analysis of peripheral blood showed that NPY decreased after PLWNT intervention but increased significantly in the CBT.

Conclusion: The PLWNT qigong exercise has potential to be an effective rehabilitation method for CFS symptoms including fatigue, sleep disturbance, anxiety, and depression. Future studies should expand study sample size for in-depth investigation to determine the optimal frequency and intensity of PLWNT qigong intervention in CFS patients. The study was registered in the ClinicalTrials.gov database on April 12, 2018, with registration number NCT03496961.

Source: Xie F, You Y, Guan C, Xu J, Yao F. The Qigong of Prolong Life With Nine Turn Method Relieve Fatigue, Sleep, Anxiety and Depression in Patients With Chronic Fatigue Syndrome: A Randomized Controlled Clinical Study. Front Med (Lausanne). 2022 Jun 30;9:828414. doi: 10.3389/fmed.2022.828414. PMID: 35847786; PMCID: PMC9280429. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9280429/ (Full text)

Impaired Cardiac Autonomic Control in Women With Fibromyalgia Is Independent of Their Physical Fitness

Abstract:

Background/objective: Evidence has suggested abnormal cardiac autonomic responses to exercise in patients with fibromyalgia (FM). However, it is not clear whether the dysautonomia represents a reduced physical fitness rather directly related to FM pathogenesis. Thus, we aimed to verify the cardiac autonomic responses before, during, and after a maximal incremental exercise in women with FM and whether these hypothesized alterations would be dependent with their physical fitness.

Methods: This is a cross-sectional study with 23 FM women and 17 healthy women. The participants performed a maximal incremental cycling test to determine their maximal workload (Wmax) and were further matched by their Wmax (14 FM patients, Wmax: 128.6 ± 16.2 W; and 14 healthy women, Wmax: 131.9 ± 15.9 W). Beat-to-beat heart rate (HR) was continuously monitored to calculate HR variability indexes at rest, chronotropic reserve during exercise, and HR recovery.

Results: Heart rate variability indexes related to vagal modulation were significantly lower in FM patients than in healthy women (p < 0.05). The chronotropic reserve and the HR recovery at 30, 120, 180, 300, and 600 seconds after exercise were all lower in FM patients compared with those of healthy women (p < 0.05). Similar findings were found when analysis was performed using the matched physical fitness subgroup.

Conclusions: The documented cardiac autonomic abnormalities at rest, during, and after exercise in FM patients persist even when physical fitness status is taken in account. Thus, strategies to attenuate the dysautonomia in FM patients must be considered.

Source: Schamne JC, Ressetti JC, Lima-Silva AE, Okuno NM. Impaired Cardiac Autonomic Control in Women With Fibromyalgia Is Independent of Their Physical Fitness. J Clin Rheumatol. 2021 Sep 1;27(6S):S278-S283. doi: 10.1097/RHU.0000000000001518. PMID: 32826659. https://pubmed.ncbi.nlm.nih.gov/32826659/

Neurovascular Dysregulation and Acute Exercise Intolerance in ME/CFS: A Randomized, Placebo-Controlled Trial of Pyridostigmine

Abstract:

Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by intractable fatigue, post-exertional malaise, and orthostatic intolerance, but its pathophysiology is poorly understood. Pharmacologic cholinergic stimulation was used to test the hypothesis that neurovascular dysregulation underlies exercise intolerance in ME/CFS.

Research Question: Does neurovascular dysregulation contribute to exercise intolerance in ME/CFS and can its treatment improve exercise capacity?

Methods: Forty-five subjects with ME/CFS were enrolled in a single-center, randomized, double-blind, placebo-controlled trial. Subjects were assigned in a 1:1 ratio to receive a 60 mg dose of oral pyridostigmine or placebo after an invasive cardiopulmonary exercise test (iCPET). A second iCPET was performed 50 minutes later. The primary end point was the difference in peak exercise oxygen uptake (VO2). Secondary end points included exercise pulmonary and systemic hemodynamics and gas exchange.

Results: Twenty-three subjects were assigned to pyridostigmine and 22 to placebo. The peak VO2 increased after pyridostigmine but decreased after placebo (13.3 ± 13.4 mL/min vs. -40.2 ± 21.3 mL/min, P<0.05). The treatment effect of pyridostigmine was 53.6 mL/min (95% CI, -105.2 to -2.0). Peak versus rest VO2 (25.9 ± 15.3 mL/min vs. -60.8 ± 25.6 mL/min, P<0.01), cardiac output (-0.2 ± 0.6 L/min vs. -1.9 ± 0.6 L/min, P<0.05), and RAP (1.0 ± 0.5 mm Hg vs. -0.6 ± 0.5 mm Hg, P<0.05) were greater in the pyridostigmine group compared to placebo.

Interpretation: Pyridostigmine improves peak VO2 in ME/CFS by increasing cardiac output and right ventricular filling pressures. Worsening peak exercise VO2, Qc, and RAP after placebo may signal the onset of post-exertional malaise. We suggest treatable neurovascular dysregulation underlies acute exercise intolerance in ME/CFS.

Abbreviations List: Ca-vO2 (arterial-venous oxygen content difference), iCPET (Invasive cardiopulmonary exercise test), MAP (Mean arterial pressure), mPAP (Mean pulmonary artery pressure), ME/CFS (Myalgic encephalomyelitis/chronic fatigue syndrome), PASC (Post-acute sequelae of SARS-CoV-2 infection), PAWP (Pulmonary arterial wedge pressure), POTS (Postural orthostatic tachycardia syndrome), Qc (Cardiac output), RAP (Right atrial pressure), SE (Standard error), SFN (Small fiber neuropathy), VE/VCO2 (Ventilatory efficiency), VO2 (Oxygen uptake)

Source: Phillip Joseph, MD, Rosa Pari, MD, Sarah Miller, BS, Arabella Warren, BS, Mary Catherine Stovall, BS, Johanna Squires, MSc, Chia-Jung Chang, PhD, Wenzhong Xiao, PhD, Aaron B. Waxman, MD, PhD, David M. Systrom, MD. Neurovascular Dysregulation and Acute Exercise Intolerance in ME/CFS: A Randomized, Placebo-Controlled Trial of Pyridostigmine. Chest, Published: May 05, 2022. DOI: https://doi.org/10.1016/j.chest.2022.04.146

The Relationship between Physical Activity and Long COVID: A Cross-Sectional Study

Abstract:

The relationship between Long Covid (LC) symptoms and physical activity (PA) levels are unclear. In this cross-sectional study, we examined this association, and the advice that individuals with LC received on PA. Adults with LC were recruited via social media. The New Zealand physical activity questionnaire short form (NZPAQ-SF) was adapted to capture current and pre-COVID-19 PA levels and activities of daily living (ADLs).
Participants reported how PA affected their symptoms, and what PA recommendations they had received from healthcare professionals and other resources; 477 participants completed the survey. Mean age (SD) was 45.69 (10.02) years, 89.1% female, 92.7% white, and median LC duration was 383.5 days (IQR: 168.25,427). Participants were less active than pre-COVID-19 (26.88 ± 74.85 vs. 361.68 ± 396.29 min per week, p < 0.001) and required more assistance with ADLs in a 7-day period compared to pre-COVID-19 (2.23 ± 2.83 vs. 0.11 ± 0.74 days requiring assistance, p < 0.001). No differences were found between the number of days of assistance required with ADLs, or the amount of PA, and the different durations of LC illness (p > 0.05).
Participants reported the effect of PA on LC symptoms as: worsened (74.84%), improved (0.84%), mixed effect (20.96%), or no effect (28.72%). Participants received contradictory advice on whether to be physically active in LC. LC is associated with a reduction in PA and a loss of independence, with most participants reporting PA worsened LC symptoms. PA level reduction is independent of duration of LC. Research is needed to understand how to safely return to PA without worsening LC symptoms.
Source: Wright J, Astill SL, Sivan M. The Relationship between Physical Activity and Long COVID: A Cross-Sectional Study. International Journal of Environmental Research and Public Health. 2022; 19(9):5093. https://doi.org/10.3390/ijerph19095093  https://www.mdpi.com/1660-4601/19/9/5093/htm (Full text)

Risk factors and multidimensional assessment of long COVID fatigue: a nested case-control study

Abstract:

Background: Fatigue is the most prevalent and debilitating long COVID symptom, however risk factors and pathophysiology of this condition remain unknown. We assessed risk factors for long COVID fatigue and explored its possible pathophysiology.

Methods: Nested case-control study in a COVID recovery clinic. Individuals with (cases) and without (controls) significant fatigue were included. We performed a multidimensional assessment evaluating various parameters, including pulmonary function tests and cardiopulmonary exercise testing, and implemented multivariable logistic regression to assess risk factors for significant long COVID fatigue.

Results: Total of 141 individuals were included. Mean age was 47 (SD 13) years; 115 (82%) were recovering from mild COVID-19. Mean time for evaluation was 8 months following COVID-19. Sixty-six (47%) individuals were classified with significant long COVID fatigue. They had significantly higher number of children, lower proportion of hypothyroidism, higher proportion of sore throat during acute illness and long COVID symptoms, and of physical limitation in daily activities. Individuals with fatigue had poorer sleep quality and higher degree of depression. They had significantly lower heart rate [153.52 (22.64) vs 163.52 (18.53), p=0.038] and oxygen consumption per Kg [27.69 (7.52) vs 30.71 (7.52), p=0.036] at peak exercise. The two independent risk factors for fatigue identified in multivariable analysis were peak exercise heart rate (odds ratio [OR] 0.79 per 10 beats/minute, 95% confidence interval [CI] 0.65-0.96, p=0.019); and long COVID memory impairment (OR 3.76, 95% CI 1.57-9.01, p=0.003).

Conclusions: Long COVID fatigue may be related to autonomic dysfunction, impaired cognition and decreased mood. This may suggest a limbic-vagal pathophysiology. Clinical Trial registration: NCT04851561.

Source: Margalit I, Yelin D, Sagi M, Rahat MM, Sheena L, Mizrahi N, Gordin Y, Agmon H, Epstein NK, Atamna A, Tishler O, Daitch V, Babich T, Abecasis D, Yarom Y, Kazum S, Shitenberg D, Baltaxe E, Elkana O, Shapira-Lichter I, Leibovici L, Yahav D. Risk factors and multidimensional assessment of long COVID fatigue: a nested case-control study. Clin Infect Dis. 2022 Apr 11:ciac283. doi: 10.1093/cid/ciac283. Epub ahead of print. PMID: 35403679.  https://pubmed.ncbi.nlm.nih.gov/35403679/

Autonomic dysfunction and post-COVID-19 syndrome: A still elusive link

Editorial:

Infection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the long-lasting pandemic coronavirus disease 2019 (COVID-19), with dramatic clinical, social, and economic implications. Importantly, evolving experience consistently shows that, in addition to issues related to the acute phase, patients who recover from COVID-19 may present a wide variety of bothersome symptoms, which may be debilitating and significantly impair their quality of life. This condition, when it persists beyond 12 weeks after recovery, is defined as “post–COVID-19” or “long COVID-19” syndrome.

Some of the symptoms, including tachycardia/palpitations, chest pain, fatigue, and dyspnea with reduced effort tolerance, suggest a possible cardiovascular cause, whereas others (eg, muscle and/or joint pain, headache, memory loss, nausea, mood disturbances) suggest involvement of other systems. Symptoms may occur independently of the severity of COVID-19, although patients with more severe symptoms in the acute phase experience a higher rate of symptom persistence during follow-up. , 

Importantly, careful diagnostic assessment usually fails to identify specific causes of post–COVID-19 syndrome. However, it has been suggested that at least some post–COVID-19 symptoms, including those of potential cardiovascular origin, might be related to abnormalities of the autonomic nervous system (ANS). The pathophysiological mechanisms responsible for ANS impairment remain speculative and might include direct damage of the ANS (ganglia and/or nerve terminations) by the virus, a toxic effect of inflammatory cytokines released during the acute infection, and an immune-mediated response triggered by some viral component(s). ,  Independent of the mechanism, the possibility of ANS involvement in SARS-CoV-2 infection is supported by the frequent occurrence of neurologic symptoms (eg, anosmia, dysgeusia) as well as the sporadic occurrence of clinical conditions typically related to ANS dysfunction (eg, orthostatic hypotension, orthostatic tachycardia) in post–COVID-19 syndrome. Furthermore, patients with COVID-19, compared to healthy subjects, have been found to show reduced heart rate variability (HRV) parameters 20 weeks after recovery from the illness. However, a pathogenetic relationship between dysautonomia and post–COVID-19 syndrome remains to be demonstrated. Establishing such a relationship would be of importance because it might help guide the management of this clinical condition.

The study by Ladlow et al in this issue of Heart Rhythm Journal is welcome because it attempts to clarify whether any association exists between dysautonomia and symptoms, as well as objective evidence of exercise intolerance, in patients with post–COVID-19 syndrome. In their study, Ladlow et al enrolled 205 patients referred to a post–COVID-19 clinic who fulfilled specific eligibility criteria (hospitalization and desaturation ≤95% on a Harvard step test or chest pain with electrocardiographic [ECG] changes during acute illness and life-limiting symptoms persisting for >12 weeks). All patients underwent bicycle cardiopulmonary exercise testing (CPET) and were divided into 1 of 2 groups according to evidence or no evidence of dysautonomia.

Dysautonomia was diagnosed based on 3 heart rate (HR) parameters that Jouven et al found to be associated with total mortality and sudden death in a population of asymptomatic subjects: (1) resting HR >75 bpm; (2) increase in HR during exercise <89 bpm; and (3) HR reduction <25 bpm during the first minute of recovery from peak exercise. HRV was also assessed by calculating the root mean square of the squared differences of adjacent RR intervals (RMSSD) on a 1-minute 12-lead ECG at rest and on 30-second ECGs during the first 3 minutes of recovery after peak exercise.

Patients were studied 183 ± 77 days (∼6 months) from COVID-19 disease, and dysautonomia was found in 51 patients (25%). Per definition, these patients had higher HR at rest (95 ± 12 bpm vs 81 ± 12 bpm; P <.001) and lower HR increase during CPET (75 ± 12 bpm vs 96 ± 13 bpm; P <.001) and HR recovery after peak exercise (17 ± 4 bpm vs 31 ± 17 bpm; P <.001) compared to those without dysautonomia.

Patients with dysautonomia were older, had a higher body mass index (BMI) (P = .013) and waist circumference (WC) (P = .003), and had a lower basal RMSSD (P <.001). Furthermore, at rest, dysautonomic patients showed a higher breathing rate (P = .006) and lower forced vital capacity (P = .031), forced expiratory volume in 1 second (P = .036), and ventilatory efficiency (Ve/Vco 2) (P = .036).

When assessing symptoms that showed prevalence >25%, a significant association with dysautonomia was found for low mood (P = .007), headache (P = .026), and poor attention (P = .047). However, other symptoms, including some of potential cardiovascular origin (eg, shortness of breath, fatigue), showed no significant association with dysautonomia.

Patients with dysautonomia, however, showed a lower performance on CPET. In particular, HR at peak exercise (170 ± 13 bpm vs 177 ± 15 bpm; P = .003), maximal work rate (219 ± 37 W vs 253 ± 52 W; P <.001), and maximal oxygen consumption (V⋅O2) (30.6 ± 5.5 mL/kg/min vs 35.8 ± 7.6 mL/kg/min; P <.001) all were significantly lower in patients with dysautonomia than in those without dysautonomia, suggesting a role of ANS dysfunction in their physical limitation.

Ladlow et al should be congratulated for performing this large study on post–COVID-19 syndrome. However, possible alternative interpretations of the data suggest caution in deriving definitive conclusions from their results.

Although the study shows the lack of significant relationship between dysautonomia and most post–COVID-19 symptoms, including, in particular, some symptoms of possible cardiovascular origin, the method applied to identify patients with an impairment of ANS function presents some limitations. Both higher HR at rest and lower HR recovery after exercise suggest an imbalance of sympathovagal tone toward adrenergic predominance in their patients with dysautonomia. However, rather than reflecting a primary impairment of the ANS, these findings simply might have been related to differences between the 2 groups with regard to some basal clinical characteristics, including higher BMI/WC, lower efficiency in respiratory function, and lower mood in dysautonomic patients. In addition, the lower increase in HR during maximal exercise in patients with dysautonomia might have been a mere consequence of their having a higher HR at rest and, given their older age, a lower maximal theoretical HR for age. The percent of predicted maximal HR for age achieved during CPET, in fact, did not differ between the 2 groups. The possibility that the differences in HR behavior might have not been related to a primary abnormality of the ANS is also suggested by the fact that, despite the basal difference, RMSSD values were similar during exercise recovery in the 2 groups of patients, suggesting a similar ANS response to exercise interruption in the 2 groups.

Future studies should clarify whether different results regarding the relationship between ANS dysfunction and post–COVID-19 symptoms might be obtained using more comprehensive and better validated methods for the diagnosis of ANS dysfunction, such as standard tests of autonomic function and HRV assessed from its multiple (short-term and long-term) components.

Of note, although the results of CPET in the study by Ladlow et al suggest lower performance by patients classified with dysautonomia, exercise tolerance was largely normal in these subjects, who achieved >100% of the predicted maximal oxygen consumption and an average maximal work rate of 219 W, with only small differences compared to patients without dysautonomia, possibly explained, again, and at least in part, by some demographic (age) and clinical (BMI, respiratory function) differences.

In conclusion, the study by Ladlow et al provides interesting data on the clinical characteristics and objective physical performance of patients with post–COVID-19 syndrome. However, the role of ANS in determining symptoms (particularly those of potential cardiovascular origin) and physical limitation in these patients still has not been fully elucidated by their data, making necessary further studies applying more comprehensive and valuable methods for the assessment of ANS function.

Source: Lanza GA. Autonomic dysfunction and post-COVID-19 syndrome: A still elusive link. Heart Rhythm. 2022 Apr;19(4):621-622. doi: 10.1016/j.hrthm.2021.12.027. Epub 2021 Dec 28. PMID: 34968741; PMCID: PMC8712711. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8712711/ (Full study)

Plasma metabolomics reveals disrupted response and recovery following maximal exercise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Abstract:

Post-exertional malaise (PEM) is a hallmark symptom of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). We monitored the evolution of 1,157 plasma metabolites in 60 ME/CFS cases (45 females, 15 males) and in 45 matched healthy control subjects (30 females, 15 males) before and after two maximal Cardiopulmonary Exercise Test (CPET) challenges separated by 24 hours, with the intent of provoking PEM in patients. Four timepoints allowed exploration of the metabolic response to maximal energy-producing capacity and the recovery pattern of ME/CFS cases compared to the healthy control group.

Baseline comparison identified several significantly different metabolites, along with an enriched percentage of yet-to-be identified compounds. Additionally, temporal measures demonstrated an increased metabolic disparity between cohorts, including unknown metabolites. The effects of exertion in the ME/CFS cohort predominantly highlighted lipid- as well as energy-related pathways and chemical structure clusters, which were disparately affected by the first and second exercise sessions.

The 24-hour recovery period was distinct in the ME/CFS cohort, with over a quarter of the identified pathways statistically different. The pathways that are uniquely different 24 hours after an exercise challenge provide clues to metabolic disruptions that lead to PEM. Numerous altered pathways were observed to depend on glutamate metabolism, a crucial component to the homeostasis of many organs in the body, including the brain.

Source: Germain A, Giloteaux L, Moore GE, Levine SM, Chia JK, Keller BA, Stevens J, Franconi CJ, Mao X, Shungu DC, Grimson A, Hanson MR. Plasma metabolomics reveals disrupted response and recovery following maximal exercise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. JCI Insight. 2022 Mar 31:e157621. doi: 10.1172/jci.insight.157621. Epub ahead of print. PMID: 35358096. https://pubmed.ncbi.nlm.nih.gov/35358096/

Lessons from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome for Long COVID Part 4: Heart Rate Monitoring to Manage Postexertional Symptom Exacerbation

The physiology underlying postexertional symptom exacerbation (PESE) is abnormal in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and likely long COVID. Activity pacing approaches appear warranted to accommodate the unusual physiological deficits of PESE.

The Rationale for Heart Rate Monitoring

Similar to people living with ME/CFS,7 people living with long COVID have reported finding activity pacing to be helpful. This idea is reflected in current safe rehabilitation guidelines for this condition.8 PESE is challenging to self-manage because of the variability in onset, duration, and nature from person to person.2,6 Social stigma associated with PESE may lead people to overexert to meet the demands of their daily tasks. This stigma may be exacerbated by people telling patients that “it’s all in their head” or they “just need to exercise.” Variability and stigma, in turn, make it difficult to identify important activity triggers in the early stages of learning to manage PESE.

PESE is characterized by aerobic system dysfunction. Pacing based on heart rate can help the patient avoid the dysfunctional aerobic system by keeping their activity intensity at a level anaerobic metabolism will dominate. Heart rate monitoring (HRM) provides an element of predictive potential for the patient to understand when their activities exceed physiological limits and eventually may result in PESE. In this post, we will discuss activity pacing to manage PESE that is based on HRM.

Source: Todd E. Davenport, Staci R. Stevens, Jared Stevens, Christopher R. Snell, J. Mark Van Ness. Lessons from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome for Long COVID Part 4: Heart Rate Monitoring to Manage Postexertional Symptom Exacerbation. Published online on February 23, 2022. https://doi.org/10.2519/jospt.blog.20220223 (Full text)

Lessons from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome for Long COVID Part 2: Physiological Characteristics During Acute Exercise Are Abnormal in People With Postexertional Symptom Exacerbation

In a previous post on the JOSPT Blog, we outlined the connection between postacute sequalae to novel coronavirus (long COVID) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) through their common clinical presentation: postexertional symptom exacerbation (PESE). PESE suggests the presence of abnormal physiological responses to exercise/activity. These physiological responses may be measured using cardiopulmonary exercise testing (CPET), which allows for careful characterization of cardiac, pulmonary, and metabolic functioning during exercise. We will review the characteristic findings on CPET in people with PESE.

The Physiology of PESE

One well-established protocol involves consecutive-day CPETs.8 In deconditioned people and people with a whole host of health conditions, CPET measurements demonstrate low error variance. Yet, CPET measurements are known to vary between tests in people with PESE.2 The observed variation in people with PESE reflects the biological variance associated with PESE.2 Clues about biological variance can provide important information about the underlying pathoetiology, severity, and functional limitations present.2,8 CPET data from peak exertion and ventilatory anaerobic threshold (VAT) provide important snapshots of physiological functioning. Data from peak exertion tells us about the physiology of a person’s “top-end” performance, and data from VAT elucidates the physiology of more “everyday” levels of exertion.

Read the rest of this article HERE.

Source: Todd E. Davenport, Staci R. Stevens, Jared Stevens, Christopher R. Snell, J. Mark Van Ness. Lessons from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome for Long COVID Part 2: Physiological Characteristics During Acute Exercise Are Abnormal in People With Postexertional Symptom Exacerbation. JOSPT blog, Published online on February 9, 2022. https://doi.org/10.2519/jospt.blog.20220209 (Full text)

Differential Effects of Exercise on fMRI of the Midbrain Ascending Arousal Network Nuclei in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) in a Model of Postexertional Malaise (PEM)

Abstract:

Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), Gulf War Illness (GWI) and control subjects underwent fMRI during difficult cognitive tests performed before and after submaximal exercise provocation (Washington 2020). Exercise caused increased activation in ME/CFS but decreased activation for GWI in the dorsal midbrain, left Rolandic operculum and right middle insula. Midbrain and isthmus nuclei participate in threat assessment, attention, cognition, mood, pain, sleep, and autonomic dysfunction.

Methods: Activated midbrain nuclei were inferred by a re-analysis of data from 31 control, 36 ME/CFS and 78 GWI subjects using a seed region approach and the Harvard Ascending Arousal Network.

Results: Before exercise, control and GWI subjects showed greater activation during cognition than ME/CFS in the left pedunculotegmental nucleus. Post exercise, ME/CFS subjects showed greater activation than GWI ones for midline periaqueductal gray, dorsal and median raphe, and right midbrain reticular formation, parabrachial complex and locus coeruleus. The change between days (delta) was positive for ME/CFS but negative for GWI, indicating reciprocal patterns of activation. The controls had no changes.

Conclusions: Exercise caused the opposite effects with increased activation in ME/CFS but decreased activation in GWI, indicating different pathophysiological responses to exertion and mechanisms of disease. Midbrain and isthmus nuclei contribute to postexertional malaise in ME/CFS and GWI.

Source: Baraniuk JN, Amar A, Pepermitwala H, Washington SD. Differential Effects of Exercise on fMRI of the Midbrain Ascending Arousal Network Nuclei in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) in a Model of Postexertional Malaise (PEM). Brain Sci. 2022 Jan 5;12(1):78. doi: 10.3390/brainsci12010078. PMID: 35053821. https://pubmed.ncbi.nlm.nih.gov/35053821/