Differences in metabolite-detecting, adrenergic, and immune gene expression after moderate exercise in patients with chronic fatigue syndrome, patients with multiple sclerosis, and healthy controls

Psychosom Med. 2012 Jan;74(1):46-54. doi: 10.1097/PSY.0b013e31824152ed. Epub 2011 Dec 30.

Abstract

Objective: Chronic fatigue syndrome (CFS) and multiple sclerosis (MS) are characterized by debilitating fatigue, yet evaluation of this symptom is subjective. We examined metabolite-detecting, adrenergic, and immune gene expression (messenger ribonucleic acid [mRNA]) in patients with CFS (n = 22) versus patients with MS (n = 20) versus healthy controls (n = 23) and determined their relationship to fatigue and pain before and after exercise.

Methods: Blood samples and fatigue and pain ratings were obtained at baseline and 0.5, 8, 24, and 48 hours after sustained moderate exercise. Leukocyte mRNA of four metabolite-detecting receptors (acid-sensing ion channel 3, purinergic type 2X4 and 2X5 receptors, and transient receptor potential vanilloid type 1) and four adrenergic (α-2a, β-1, and β-2 receptors and catechol-O-methyltransferase) and five immune markers (CD14, toll-like receptor 4 [TLR4], interleukin [IL] 6, IL-10, and lymphotoxin α) was examined using quantitative polymerase chain reaction.

Results: Patients with CFS had greater postexercise increases in fatigue and pain (10-29 points above baseline, p < .001) and greater mRNA increases in purinergic type 2X4 receptor, transient receptor potential vanilloid type 1, CD14, and all adrenergic receptors than controls (mean ± standard error = 1.3 ± 0.14- to 3.4 ± 0.90-fold increase above baseline, p = .04-.005). Patients with CFS with comorbid fibromyalgia (n = 18) also showed greater increases in acid-sensing ion channel 3 and purinergic type 2X5 receptors (p < .05). Patients with MS had greater postexercise increases than controls in β-1 and β-2 adrenergic receptor expressions (1.4 ± 0.27- and 1.3 ± 0.06-fold increases, respectively, p = .02 and p < .001) and greater decreases in TLR4 (p = .02). In MS, IL-10 and TLR4 decreases correlated with higher fatigue scores.

Conclusions: Postexercise mRNA increases in metabolite-detecting receptors were unique to patients with CFS, whereas both patients with MS and patients with CFS showed abnormal increases in adrenergic receptors. Among patients with MS, greater fatigue was correlated with blunted immune marker expression.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic Agents / metabolism
  • Adult
  • Analysis of Variance
  • Biomarkers / metabolism
  • Case-Control Studies
  • Disease Susceptibility
  • Exercise Test
  • Exercise Tolerance / physiology
  • Fatigue / genetics
  • Fatigue / physiopathology
  • Fatigue Syndrome, Chronic / genetics
  • Fatigue Syndrome, Chronic / immunology
  • Fatigue Syndrome, Chronic / metabolism
  • Fatigue Syndrome, Chronic / physiopathology*
  • Female
  • Fibromyalgia / genetics
  • Fibromyalgia / immunology
  • Fibromyalgia / physiopathology
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Gene-Environment Interaction
  • Humans
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Ion Channels / genetics
  • Ion Channels / metabolism
  • Leukocytes / metabolism*
  • Male
  • Multiple Sclerosis / genetics
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis / metabolism
  • Multiple Sclerosis / physiopathology*
  • Pain / genetics
  • Pain / physiopathology
  • Polymerase Chain Reaction
  • RNA, Messenger / metabolism
  • Receptors, Adrenergic / genetics
  • Receptors, Adrenergic / metabolism
  • Receptors, Purinergic / genetics
  • Receptors, Purinergic / metabolism
  • Severity of Illness Index
  • TRPV Cation Channels
  • Time Factors
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism

Substances

  • Adrenergic Agents
  • Biomarkers
  • Ion Channels
  • RNA, Messenger
  • Receptors, Adrenergic
  • Receptors, Purinergic
  • TRPV Cation Channels
  • Toll-Like Receptor 4
  • Interleukin-10