. Objectives. Because the muscle response to incremental exercise is not well documented in patients suffering from chronic fatigue syndrome (CFS), we combined electrophysiological (compound‐evoked muscle action potential, M wave), and biochemical (lactic acid production, oxidative stress) measurements to assess any muscle dysfunction in response to a routine cycling exercise. Design. This case–control study compared 15 CFS patients to a gender‐, age‐ and weight‐matched control group (n = 11) of healthy subjects. Interventions. All subjects performed an incre‐mental cycling exercise continued until exhaustion. Main outcome measures. We measured the oxygen uptake (Vo2), heart rate (HR), systemic blood pressure, percutaneous O2 saturation (SpO2), M‐wave recording from vastus lateralis, and venous blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid (LA), and three markers of the oxidative stress (thiobarbituric acid‐reactive substances, TBARS, reduced glutathione, GSH, and ascorbic acid, RAA). Results. Compared with control, in CFS patients (i) the slope of Vo2 versus work load relationship did not differ from control subjects and there was a tendency for an accentuated PvO2 fall at the same exercise intensity, indicating an increased oxygen uptake by the exercising muscles; (ii) the HR and blood pressure responses to exercise did not vary; (iii) the anaerobic pathways were not accentuated; (iv) the exercise‐induced oxidative stress was enhanced with early changes in TBARS and RAA and enhanced maximal RAA consumption; and (v) the M‐wave duration markedly increased during the recovery period. Conclusions. The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients.
Abstract. Jammes Y, Steinberg JG, Delliaux S (AixMarseille University, Marseille, France). Chronic fatigue syndrome: acute infection and history of physical activity affect resting levels and response to exercise of plasma oxidant ⁄ antioxidant status and heat shock proteins. J Intern Med 2012; 272: 74-84.Objectives. A history of high-level physical activity and ⁄ or acute infection might constitute stress factors affecting the plasma oxidant-antioxidant status and levels of heat shock proteins (HSPs) in patients with chronic fatigue syndrome (CFS).Design. This case-control study compared data from 43 CFS patients to results from a matched control group of 23 healthy sedentary subjects.Setting and subjects. Five patients had no relevant previous history (group I). Eighteen had practised high-level sport (group II), and severe acute infection had been diagnosed in nine patients (group III). A combination of sport practice and infection was noted in 11 patients (group IV).Interventions. After examination at rest, all subjects performed a maximal cycling exercise test. Plasma levels of two markers of oxidative stress [thiobarbituric acid reactive substances (TBARS) and reduced ascorbic acid (RAA)] and both HSP27 and HSP70 were measured.Results. At rest, compared with the control group, the TBARS level was higher in groups II, III and IV patients, and the RAA level was lower in groups III and IV. In addition, HSP70 levels were significantly lower in all CFS groups, compared with controls, but negative correlations were found between resting HSP27 and HSP70 levels and the history of physical activity. After exercise, the peak level of TBARS significantly increased in groups II, III and IV, and the variations in HSP27 and HSP70 were attenuated or suppressed, with the greatest effects in groups III and IV.Conclusion. The presence of stress factors in the history of CFS patients is associated with severe oxidative stress and the suppression of protective HSP27 and HSP70 responses to exercise.
Mental workload is known to alter cardiovascular function leading to increased cardiovascular risk. Nevertheless, there is no clear autonomic nervous system unbalance to be quantified during mental stress. We aimed to characterize the mental workload impact on the cardiovascular function with a focus on heart rate variability (HRV) non-linear indexes. A 1-h computerized switching task (letter recognition) was performed by 24 subjects while monitoring their performance (accuracy, response time), electrocardiogram and blood pressure waveform (finger volume clamp method). The HRV was evaluated from the beat-to-beat RR intervals (RRI) in time-, frequency-, and informational- domains, before (Control) and during the task. The task induced a significant mental workload (visual analog scale of fatigue from 27 ± 26 to 50 ± 31 mm, p < 0.001, and NASA-TLX score of 56 ± 17). The heart rate, blood pressure and baroreflex function were unchanged, whereas most of the HRV parameters markedly decreased. The maximum decrease occurred during the first 15 min of the task (P1), before starting to return to the baseline values reached at the end of the task (P4). The RRI dimension correlation (D2) decrease was the most significant (P1 vs. Control: 1.42 ± 0.85 vs. 2.21 ± 0.8, p < 0.001) and only D2 lasted until the task ended (P4 vs. Control: 1.96 ± 0.9 vs. 2.21 ± 0.9, p < 0.05). D2 was identified as the most robust cardiovascular variable impacted by the mental workload as determined by posterior predictive simulations ( p = 0.9). The Spearman correlation matrix highlighted that D2 could be a marker of the generated frustration ( R = –0.61, p < 0.01) induced by a mental task, as well as the myocardial oxygen consumption changes assessed by the double product ( R = –0.53, p < 0.05). In conclusion, we showed that mental workload sharply lowered the non-linear RRI dynamics, particularly the RRI correlation dimension.
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