Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy

Baschetti, Riccardo

doi:10.1111/j.1365-2796.2005.01526.x

Cited by 4 publications

(3 citation statements)

References 18 publications

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“…Lastly, the potential mechanisms responsible for the reported adrenal insufficiency remained unclear. Two possible underlying mechanisms could be at play: 1) an Addison-type syndrome, in which the adrenal glands are no longer able to synthesize cortisol and epinephrine despite normal stimulation by the adrenocorticotropic hormone (ACTH) (3,4,17); or 2) reduced adrenal responsiveness to ACTH stimulation (11,22). As we did not measure ACTH or serum cortisol concentrations in the present study, we did not have the possibility to test these hypotheses.…”

Section: Discussionmentioning

confidence: 88%

Maximal exercise limitation in functionally overreached triathletes: role of cardiac adrenergic stimulation

Meur

Louis

Aubry

et al. 2014

Journal of Applied Physiology

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Functional overreaching (F-OR) induced by heavy load endurance training programs has been associated with reduced heart rate values both at rest and during exercise. Because this phenomenon may reflect an impairment of cardiac response, this research was conducted to test this hypothesis. Thirty-five experienced male triathletes were tested (11 control and 24 overload subjects) before overloading (Pre), immediately after overloading (Mid), and after a 2-wk taper period (Post). Physiological responses were assessed during an incremental cycling protocol to volitional exhaustion, including catecholamines release, oxygen uptake (V̇o2), arteriovenous O2 difference, cardiac output (Q̇), and systolic (SBP) and diastolic blood pressure (DBP). Twelve subjects of the overload group developed signs of F-OR at Mid (decreased performance with concomitant high perceived fatigue), while 12 others did not [acute fatigue group (AF)]. V̇o2max was reduced only in F-OR subjects at Mid. Lower Q̇ and SBP values with greater arteriovenous O2 difference were reported in F-OR subjects at all exercising intensities, while no significant change was observed in the control and AF groups. A concomitant decrease in epinephrine excretion was reported only in the F-OR group. All values returned to baseline at Post. Following an overload endurance training program leading to F-OR, the cardiac response to exhaustive exercise is transiently impaired, possibly due to reduced epinephrine excretion. This finding is likely to explain the complex process of underperformance syndrome experienced by F-OR endurance athletes during heavy load programs.

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Section: Discussionmentioning

confidence: 88%

Maximal exercise limitation in functionally overreached triathletes: role of cardiac adrenergic stimulation

Meur

Louis

Aubry

et al. 2014

Journal of Applied Physiology

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“…176 Some authors have even asserted that exerciseparticularly at high initial intensity -might be harmful in CFS, by precipitating abnormal immune activation and lowering pain threshold. 34,177,178 However, negative effects of graded exercise therapy have never been empirically demonstrated. 55,170 Yet, in clinical practice this therapy often forms an essential part of a multidisciplinary treatment package, under the supervision of a rehabilitation clinician.…”

Section: For a Critical Review)mentioning

confidence: 99%

“…107,155,164,165 As stated above, this may promote a pathological sickness response, prolonged recovery and pain threshold lowering through immune-related sensitization mechanisms, leading to generalized hyperalgesia, musculoskeletal pain and tenderness. 34,177,178,195 Influencing psychosocial variables Several studies have found that graded exercise therapy not only improved the physical condition of CFS patients, but also had a positive influence on psychological variables such as self-esteem, mood, perceived control over symptoms, cognitive functioning and symptom-focusing. [166][167][168][169][170][171][172] Our own multidisciplinary treatment study in CFS has shown that unfit patients (who also had the most severe psychosocial disturbances) derived most benefit from graded exercise therapy -physically as well as psychosocially.…”

Section: Restoring Stress System Functionmentioning

confidence: 99%

Rehabilitation of decreased motor performance in patients with chronic fatigue syndrome: should we treat low effort capacity or reduced effort tolerance?

Houdenhove

Verheyen²,

Pardaens³

et al. 2007

Clin Rehabil

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Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

Sorensen

Jones

Vernon

et al. 2009

Mol Med

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Complement activation resulting in significant increases of C4a split product may be a marker of postexertional malaise in individuals with chronic fatigue syndrome (CFS). This study focused on identification of the transcriptional control that may contribute to the increased C4a in CFS subjects after exercise. We used quantitative reverse-transcription polymerase chain reaction to evaluate differential expression of genes in the classical and lectin pathways in peripheral blood mononuclear cells (PBMCs). Calibrated expression values were normalized to the internal reference gene peptidylpropyl isomerase B (PPIB), the external reference gene ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit (rbcL), or the geometric mean (GM) of the genes ribosomal protein, large, P0 (RPLP0) and phosphoglycerate kinase 1 (PGK1). All nine genes tested, except mannose-binding lectin 2 (MBL2), were expressed in PBMCs. At 1 hour postexercise, C4, mannan-binding lectin serine protease 2 (MASP2) and ficolin 1 (FCN1) transcripts were detected at higher levels (≥2-fold) in at least 50% (4 of 8) of CFS subjects and were detected in 88% (7 of 8) CFS subjects when subjects with overexpression of either C4 or MASP2 were combined. Only an increase in the MASP2 transcript was statistically significant (PPIB, P = 0.001; GM, P = 0.047; rbcL, P = 0.045). This result may be due to the significant but transient downregulation of MASP2 in control subjects (PPIB, P = 0.023; rbcL, P = 0.027). By 6 hours postexercise, MASP2 expression was similar in both groups. In conclusion, lectin pathway responded to exercise differentially in CFS than in control subjects. MASP2 downregulation may act as an antiinflammatory acute-phase response in healthy subjects, whereas its elevated level may account for increased C4a and inflammation-mediated postexertional malaise in CFS subjects.

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Chronic fatigue syndrome, exercise, cortisol and lymphadenopathy

Cited by 4 publications

References 18 publications

Maximal exercise limitation in functionally overreached triathletes: role of cardiac adrenergic stimulation

Maximal exercise limitation in functionally overreached triathletes: role of cardiac adrenergic stimulation

Rehabilitation of decreased motor performance in patients with chronic fatigue syndrome: should we treat low effort capacity or reduced effort tolerance?

Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome

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