Abnormalities in pH handling by peripheral muscle and potential regulation by the autonomic nervous system in chronic fatigue syndrome
Article first published online: 20 AUG 2009
© 2010 Blackwell Publishing Ltd
Journal of Internal Medicine
Volume 267, Issue 4, pages 394–401, April 2010
How to Cite
Jones, D. E. J., Hollingsworth, K. G., Taylor, R., Blamire, A. M. and Newton, J. L. (2010), Abnormalities in pH handling by peripheral muscle and potential regulation by the autonomic nervous system in chronic fatigue syndrome. Journal of Internal Medicine, 267: 394–401. doi: 10.1111/j.1365-2796.2009.02160.x
- Issue published online: 11 MAR 2010
- Article first published online: 20 AUG 2009
- autonomic dysfunction;
- chronic fatigue syndrome;
- magnetic resonance spectroscopy;
- muscle bioenergetics
Abstract. Jones DEJ, Hollingsworth KG, Taylor R, Blamire AM, Newton JL (From the Institute of Cellular Medicine, Newcastle Magnetic Resonance Centre, and Institute for Ageing and Health, Newcastle University, UK). Abnormalities in pH handling by peripheral muscle and potential regulation by the autonomic nervous system in chronic fatigue syndrome. J Intern Med 2010; 267: 394–401.
Objectives. To examine muscle acid handling following exercise in chronic fatigue syndrome (CFS/ME) and the relationship with autonomic dysfunction.
Design. Observational study.
Setting. Regional fatigue service.
Subjects & interventions. Chronic fatigue syndrome (n = 16) and age and sex matched normal controls (n = 8) underwent phosphorus magnetic resonance spectroscopy (MRS) to evaluate pH handling during exercise. Subjects performed plantar flexion at fixed 35% load maximum voluntary contraction. Heart rate variability was performed during 10 min supine rest using digital photophlethysmography as a measure of autonomic function.
Results. Compared to normal controls, the CFS/ME group had significant suppression of proton efflux both immediately postexercise (CFS: 1.1 ± 0.5 mmol L−1 min−1 vs. normal: 3.6 ± 1.5 mmol L−1 min−1, P < 0.001) and maximally (CFS: 2.7 ± 3.4 mmol L−1 min−1 vs. control: 3.8 ± 1.6 mmol L−1 min−1, P < 0.05). Furthermore, the time taken to reach maximum proton efflux was significantly prolonged in patients (CFS: 25.6 ± 36.1 s vs. normal: 3.8 ± 5.2 s, P < 0.05). In controls the rate of maximum proton efflux showed a strong inverse correlation with nadir muscle pH following exercise (r2 = 0.6; P < 0.01). In CFS patients, in contrast, this significant normal relationship was lost (r2 = 0.003; P = ns). In normal individuals, the maximum proton efflux following exercise were closely correlated with total heart rate variability (r2 = 0.7; P = 0.007) this relationship was lost in CFS/ME patients (r2 < 0.001; P = ns).
Conclusion. Patients with CFS/ME have abnormalities in recovery of intramuscular pH following standardised exercise degree of which is related to autonomic dysfunction. This study identifies a novel biological abnormality in patients with CFS/ME which is potentially open to modification.