Tag: exercise intolerance

Acute effect of pyridostigmine in exertional intolerance in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A randomized placebo-controlled clinical trial

Rationale: One third of patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) have evidence of small fiber neuropathy (SFN). Neurovascular dysregulation during upright exercise may be associated with impaired venoconstriction resulting in low biventricular filling pressures and impaired arteriolar constriction resulting in a mismatch between perfusion and skeletal muscle metabolism. We hypothesize that pyridostigmine, a reversible acetylcholinesterase inhibitor, may improve vascular regulation and exercise tolerance in ME/CFS by increasing sympathetic outflow.

Methods: 45 subjects (39 women, 6 men) with ME/CFS were assessed. A baseline invasive cardiopulmonary exercise test (iCPET) was performed to confirm presence of low peak exercise RAP (<6.5mmHg). Eligible subjects were blindly administered placebo (n=22) or 60mg pyridostigmine (n=23) at a 1:1 ratio. A second iCPET was performed following a 50 minute combined rest and dosing period. Serial iCPET results were compared to assess changes in oxygen uptake at peak exercise (VO2 max). Secondary outcomes included subject ventilatory efficiency (VE/VCO2), peak hemodynamic response (RAP, PCWP, SV, Qt), systemic gas exchange (Ca-vO2/Hgb), and subjective reporting of dyspnea and fatigue. Results: 39 subjects (all women) were considered in data analysis. There was a significant increase in VO2 max between iCPET 1 and iCPET 2 in the treatment group when compared with the placebo group (p = 0.043).

There was a significant decrease in the placebo group and a significant increase in the treatment group in VO2 (p = 0.008), Qt (p = 0.039), and RAP (p = 0.045) when comparing iCPET 1 peak – rest and iCPET 2 peak – rest between groups. There were no significant differences in peak arteriovenous oxygen content difference (Ca-vO2/Hgb). 38% of subjects had objective evidence of SFN with no statistically significant difference between groups.

Conclusion: Using pyridostigmine as an investigative tool, this study suggests that neurovascular dysregulation underlies acute exercise intolerance in ME/CFS. Additionally, we have new evidence that worsening vascular dysregulation results from prior exercise, which sheds insight into the post exertional malaise that is a hallmark of this syndrome.

Source: M. Stovall, P. Joseph, R. Pari, A. Warren, S. Miller, J. Squires, W. Xiao, A.B. Waxman, D.M. Systrom. Acute effect of pyridostigmine in exertional intolerance in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A randomized placebo-controlled clinical trial. American Journal of Respiratory and Clinical Care Medicine, Vol 205, p A2063, May 2022. https://www.atsjournals.org/doi/pdf/10.1164/ajrccm-conference.2022.205.1_MeetingAbstracts.A2063

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)

Lessons from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome for Long COVID: Postexertional Symptom Exacerbation is an Abnormal Response to Exercise/Activity

Prolonged symptoms after infection with the novel coronavirus 2019 (SARS-COV-2) are an emerging challenge to individual patients, society, and clinicians. In a previous post on the JOSPT Blog, we identified several lessons from research and clinical practice in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) that are important lessons for long COVID. The purpose of this post is to discuss the phenomenon of postexertional symptom exacerbation (PESE) and its clinical identification to recognize the potential onset of long COVID.

Data from a large international web-based patient survey indicate substantial symptom overlap between postacute SARS-COV-2 infection (long COVID) and ME/CFS at 6 months following the onset of first symptoms. Three quarters of respondents noted disabling fatigue and over half noted cognitive dysfunction.4 A unique finding of this survey was that 75% of respondents noted PESE, which is a worsening of symptoms after activity/exercise.4 PESE is foundational to the diagnosis of ME/CFS and it is common with long COVID.4,5 This observation suggests we can further extend lessons from ME/CFS to develop our understanding of long COVID.

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: Postexertional Symptom Exacerbation is an Abnormal Response to Exercise/Activity. Published online on February 2, 2022 https://doi.org/10.2519/jospt.blog.20220202

Persistent Exertional Intolerance After COVID-19: Insights From Invasive Cardiopulmonary Exercise Testing

Abstract:

Background: Some patients with COVID-19 who have recovered from the acute infection after experiencing only mild symptoms continue to exhibit persistent exertional limitation that often is unexplained by conventional investigative studies.

Research question: What is the pathophysiologic mechanism of exercise intolerance that underlies the post-COVID-19 long-haul syndrome in patients without cardiopulmonary disease?

Study design and methods: This study examined the systemic and pulmonary hemodynamics, ventilation, and gas exchange in 10 patients who recovered from COVID-19 and were without cardiopulmonary disease during invasive cardiopulmonary exercise testing (iCPET) and compared the results with those from 10 age- and sex-matched control participants. These data then were used to define potential reasons for exertional limitation in the cohort of patients who had recovered from COVID-19.

Results: The patients who had recovered from COVID-19 exhibited markedly reduced peak exercise aerobic capacity (oxygen consumption [VO2]) compared with control participants (70 ± 11% predicted vs 131 ± 45% predicted; P < .0001). This reduction in peak VO2 was associated with impaired systemic oxygen extraction (ie, narrow arterial-mixed venous oxygen content difference to arterial oxygen content ratio) compared with control participants (0.49 ± 0.1 vs 0.78 ± 0.1; P < .0001), despite a preserved peak cardiac index (7.8 ± 3.1 L/min vs 8.4±2.3 L/min; P > .05). Additionally, patients who had recovered from COVID-19 demonstrated greater ventilatory inefficiency (ie, abnormal ventilatory efficiency [VE/VCO2] slope: 35 ± 5 vs 27 ± 5; P = .01) compared with control participants without an increase in dead space ventilation.

Interpretation: Patients who have recovered from COVID-19 without cardiopulmonary disease demonstrate a marked reduction in peak VO2 from a peripheral rather than a central cardiac limit, along with an exaggerated hyperventilatory response during exercise.

Source: Singh I, Joseph P, Heerdt PM, Cullinan M, Lutchmansingh DD, Gulati M, Possick JD, Systrom DM, Waxman AB. Persistent Exertional Intolerance After COVID-19: Insights From Invasive Cardiopulmonary Exercise Testing. Chest. 2022 Jan;161(1):54-63. doi: 10.1016/j.chest.2021.08.010. Epub 2021 Aug 11. PMID: 34389297; PMCID: PMC8354807.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8354807/ (Full text)

Long term predictors of breathlessness, exercise intolerance, chronic fatigue and well-being in hospitalized patients with COVID-19: A cohort study with 4 months median follow-up

Abstract:

Background: Post-acute COVID-19 syndrome (PACS) is an emerging healthcare burden. We therefore aimed to determine predictors of different functional outcomes after hospital discharge in patients with COVID-19.

Methods: An ambidirectional cohort study was conducted between May and July 2020, in which PCR-confirmed COVID-19 patients underwent a standardized telephone assessment between 6 weeks and 6 months post discharge. We excluded patients who died, had a mental illness or failed to respond to two follow-up phone calls. The medical research council (MRC) dyspnea scale, metabolic equivalent of task (MET) score for exercise tolerance, chronic fatigability syndrome (CFS) scale and World Health Organization-five well-being index (WHO-5) for mental health were used to evaluate symptoms at follow-up.

Results: 375 patients were contacted and 153 failed to respond. The median timing for the follow-up assessment was 122 days (IQR, 109-158). On multivariate analyses, female gender, pre-existing lung disease, headache at presentation, intensive care unit (ICU) admission, critical COVID-19 and post-discharge ER visit were predictors of higher MRC scores at follow-up. Female gender, older age >67 years, arterial hypertension and emergency room (ER) visit were associated with lower MET exercise tolerance scores. Female gender, pre-existing lung disease, and ER visit were associated with higher risk of CFS. Age, dyslipidemia, hypertension, pre-existing lung disease and duration of symptoms were negatively associated with WHO-5 score.

Conclusions: Several risk factors were associated with an increased risk of PACS. Hospitalized patients with COVID-19 who are at risk for PACS may benefit from a targeted pre-emptive follow-up and rehabilitation programs.

Source: Tleyjeh IM, Saddik B, Ramakrishnan RK, AlSwaidan N, AlAnazi A, Alhazmi D, Aloufi A, AlSumait F, Berbari EF, Halwani R. Long term predictors of breathlessness, exercise intolerance, chronic fatigue and well-being in hospitalized patients with COVID-19: A cohort study with 4 months median follow-up. J Infect Public Health. 2021 Nov 18;15(1):21-28. doi: 10.1016/j.jiph.2021.11.016. Epub ahead of print. PMID: 34861604; PMCID: PMC8600938. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8600938/ (Full text)

Investigating Fatigue and Exercise Intolerance in a University Immunology Clinic

Abstract:

Purpose: This manuscript reviews the experience of a University Immunology clinic with the evaluation of patients with idiopathic fatigue and exercise intolerance for the presence of metabolic disorders. Laboratory, biochemical and genetic studies were utilized in the evaluation.

Recent Findings: Of the 372 patients evaluated, 95% were found to have a treatable metabolic disorder. A defect in the glycogen storage pathway was found in 78 patients. Mitochondrial disorders were found in 258 patients. Myoadenylate deaminase deficiency was found in 7 patients. Various congenital myopathies were identified in 11 patients. Inflammatory myopathies were identified in 25 patients, 6 of whom had normal muscle enzymes on the initial evaluation.

Summary: The majority of patients (95%) referred with idiopathic fatigue and exercise intolerance after extensive evaluations were found to have underlying metabolic dysfunction. Frequently associated problems included gastrointestinal dysmotility disorders, recurrent infections, Raynaud’s, migraine headaches and various autoimmune diseases. Most patients showed symptomatic improvement with treatment of their metabolic dysfunction.

Source: Julian L A, Paul I, Molly M, John B, Lucia B. Investigating Fatigue and Exercise Intolerance in a University Immunology Clinic. Arch Rheum & Arthritis Res. 1(1): 2020. ARAR.MS.ID.000505. https://irispublishers.com/arar/fulltext/Investigating-Fatigue-and-Exercise-Intolerance-in-a-University.ID.000505.php (Full study)

Persistent Exertional Intolerance After COVID-19

Abstract:

Background: Some patients with COVID-19 who have recovered from the acute infection after experiencing only mild symptoms continue to exhibit persistent exertional limitation that often is unexplained by conventional investigative studies.

Research question: What is the pathophysiologic mechanism of exercise intolerance that underlies the post-COVID-19 long-haul syndrome after COVID-19 in patients without cardiopulmonary disease?

Study design and methods: This study examined the systemic and pulmonary hemodynamics, ventilation, and gas exchange in 10 patients who recovered from COVID-19 and were without cardiopulmonary disease during invasive cardiopulmonary exercise testing (iCPET) and compared the results with those from 10 age- and sex-matched control participants. These data then were used to define potential reasons for exertional limitation in the cohort of patients who had recovered from COVID-19.

Results: The patients who had recovered from COVID-19 exhibited markedly reduced peak exercise aerobic capacity (oxygen consumption [VO2]) compared with control participants (70 ± 11% predicted vs 131 ± 45% predicted; P < .0001). This reduction in peak VO2 was associated with impaired systemic oxygen extraction (ie, narrow arterial-mixed venous oxygen content difference to arterial oxygen content ratio) compared with control participants (0.49 ± 0.1 vs 0.78 ± 0.1; P < .0001), despite a preserved peak cardiac index (7.8 ± 3.1 L/min vs 8.4±2.3 L/min; P > .05). Additionally, patients who had recovered from COVID-19 demonstrated greater ventilatory inefficiency (ie, abnormal ventilatory efficiency [VE/VCO2] slope: 35 ± 5 vs 27 ± 5; P = .01) compared with control participants without an increase in dead space ventilation.

Interpretation: Patients who have recovered from COVID-19 without cardiopulmonary disease demonstrate a marked reduction in peak VO2 from a peripheral rather than a central cardiac limit, along with an exaggerated hyperventilatory response during exercise.

Source: Singh I, Joseph P, Heerdt PM, Cullinan M, Lutchmansingh DD, Gulati M, Possick JD, Systrom DM, Waxman AB. Persistent Exertional Intolerance After COVID-19: Insights From Invasive Cardiopulmonary Exercise Testing. Chest. 2021 Aug 11:S0012-3692(21)03635-7. doi: 10.1016/j.chest.2021.08.010. Epub ahead of print. PMID: 34389297; PMCID: PMC8354807. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8354807/  (Full text)

Skeletal muscle alterations in patients with acute Covid-19 and post-acute sequelae of Covid-19

Abstract:

Background and methods: Skeletal muscle-related symptoms are common in both acute Covid-19 and Post-Acute Sequelae of Covid-19 (PASC). In this narrative review, we discuss cellular and molecular pathways that are affected, and consider these in regard to skeletal muscle involvement in other conditions, such as acute respiratory distress syndrome, critical illness myopathy and post-viral fatigue syndrome.
Results: Patients with severe Covid-19 and PASC suffer from skeletal muscle weakness and exercise intolerance. Histological sections present muscle fiber atrophy, metabolic alterations, and immune cell infiltration. Contributing factors to weakness and fatigue in patients with severe Covid-19 include systemic inflammation, disuse, hypoxemia, and malnutrition. These factors also contribute to post-ICU syndrome and ICU-acquired weakness, and likely explain a substantial part of Covid-19-acquired weakness. The skeletal muscle weakness and exercise intolerance associated with PASC are more obscure and different factors likely contribute. Direct SARS-CoV-2 viral infiltration into skeletal muscle or an aberrant immune system likely contribute. Similarities between skeletal muscle alterations in PASC and chronic fatigue syndrome deserve further study.
Conclusion: Both SARS-CoV-2 specific factors and generic consequences of acute disease likely underlie the observed skeletal muscle alterations in both acute Covid 19 and PASC.
Source: Soares, M., Eggelbusch, M., Naddaf, E., Gerrits, K., van der Schaaf, M., van den Borst, B., Wiersinga, W. J., et al. Skeletal muscle alterations in patients with acute Covid-19 and post-acute sequelae of Covid-19. Journal of Cachexia, Sarcopenia and Muscle. https://doi.org/10.17863/CAM.78509 https://www.repository.cam.ac.uk/handle/1810/331064

Investigating Fatigue and Exercise Intolerance in a University Immunology Clinic

Abstract:

Purpose: This manuscript reviews the experience of a University Immunology clinic with the evaluation of patients with idiopathic fatigue and exercise intolerance for the presence of metabolic disorders. Laboratory, biochemical and genetic studies were utilized in the evaluation.

Recent Findings: Of the 372 patients evaluated, 95% were found to have a treatable metabolic disorder. A defect in the glycogen storage pathway was found in 78 patients. Mitochondrial disorders were found in 258 patients. Myoadenylate deaminase deficiency was found in 7 patients. Various congenital myopathies were identified in 11 patients. Inflammatory myopathies were identified in 25 patients, 6 of whom had normal muscle enzymes on the initial evaluation.

Summary: The majority of patients (95%) referred with idiopathic fatigue and exercise intolerance after extensive evaluations were found to have underlying metabolic dysfunction. Frequently associated problems included gastrointestinal dysmotility disorders, recurrent infections, Raynaud’s, migraine headaches and various autoimmune diseases. Most patients showed symptomatic improvement with treatment of their metabolic dysfunction.

Source: Julian L A, Paul I, Molly M, John B, Lucia B. Investigating Fatigue and Exercise Intolerance in a University Immunology Clinic. Arch Rheum & Arthritis Res. 1(1): 2020. ARAR.MS.ID.000505. https://irispublishers.com/arar/fulltext/Investigating-Fatigue-and-Exercise-Intolerance-in-a-University.ID.000505.php (Full text)

Comparing Idiopathic Chronic Fatigue and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) in Males: Response to Two-Day Cardiopulmonary Exercise Testing Protocol

Abstract:

(1) Introduction: Multiple studies have shown that peak oxygen consumption is reduced in the majority of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS )patients, using the gold standard for measuring exercise intolerance: cardiopulmonary exercise testing (CPET). A 2-day CPET protocol has shown different results on day 2 in ME/CFS patients compared to sedentary controls. No comparison is known between ME/CFS and idiopathic chronic fatigue (ICF) for 2-day CPET protocols. We compared ME/CFS patients with patients with chronic fatigue who did not fulfill the ME/CFS criteria in a male population and hypothesized a different pattern of response would be present during the 2nd day CPET.

(2) Methods: We compared 25 male patients with ICF who had completed a 2-day CPET protocol to an age-/gender-matched group of 26 male ME/CFS patients. Measures of oxygen consumption (VO2), heart rate (HR), systolic and diastolic blood pressure, workload (Work), and respiratory exchange ratio (RER) were collected at maximal (peak) and ventilatory threshold (VT) intensities.

(3) Results: Baseline characteristics for both groups were similar for age, body mass index (BMI), body surface area, (BSA), and disease duration. A significant difference was present in the number of patients with fibromyalgia (seven ME/CFS patients vs. zero ICF patients). Heart rate at rest and the RER did not differ significantly between CPET 1 and CPET 2. All other CPET parameters at the ventilatory threshold and maximum exercise differed significantly (p-value between 0.002 and <0.0001). ME/CFS patients showed a deterioration of performance on CPET2 as reflected by VO2 and workload at peak exercise and ventilatory threshold, whereas ICF patients showed improved performance on CPET2 with no significant change in peak workload.

(4) Conclusion: This study confirms that male ME/CFS patients have a reduction in exercise capacity in response to a second-day CPET. These results are similar to published results in male ME/CFS populations. Patients diagnosed with ICF show a different response on day 2, more similar to sedentary and healthy controls.

Source: van Campen CLMC, Visser FC. Comparing Idiopathic Chronic Fatigue and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) in Males: Response to Two-Day Cardiopulmonary Exercise Testing Protocol. Healthcare (Basel). 2021 Jun 5;9(6):683. doi: 10.3390/healthcare9060683. PMID: 34198946. https://pubmed.ncbi.nlm.nih.gov/34198946/