CFS/ME and Exercise
Exercise Bad for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis?
Dec 22, 2008
CFS/ME, Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, is an inflammatory disease, but unlike many other inflammatory diseases that display high levels of inflammatory cytokines, this disease shows elevated levels of the receptors for the inflammatory cytokines. Enhanced receptors may explain the enhanced sensitivity of people with CFS/ME to the exercise-induced inflammatory cytokine, IL-6.
Inflammation Means Cytokines and Prostaglanoids
Inflammation is usually associated with infected splinters embedded in a finger with reddening, swelling, heating and pain. The symptoms of a localized infection result from a dilation of the affected capillaries. The capillary surface also changes, because of new proteins that are exposed to the blood, and snags passing white blood cells. The white blood cells of the immune system can accumulate to form pus and also migrate toward the source of the infection along a gradient of signaling molecules, cytokines, released by leukocytes already in contact with bacteria or foreign materials. The inflammatory cytokines are also responsible for changes in the capillaries.
Inflammatory Cytokines are IL-1, IL-6 and TNF
Many cells of the immune system, as well as cells related to the endothelial cells that line internal surfaces of blood vessels, respond to bacterial cell wall components by triggering an inflammatory response. The inflammatory response involves the expression of dozens of genes that code for cytokines and enzymes that signal other neighboring cells to participate in defense of the tissue. Typical inflammatory cytokines are IL-1 (interleukin-1), IL-6 and TNF. The inflammatory enzymes, e.g. COX-2 and iNOS, are involved in the synthesis of small, readily-diffusible signals, such as prostaglandins and nitric oxide (NO). COX-2 is the target of anti-inflammatory aspirin, and converts the omega-6 arachidonic acid into inflammatory prostaglandins/leukotriene. Omega-3 fatty acids, e.g. EPA and DHA, block this process and/or yield anti-inflammatory prostaglandins.
Exercise Produces Fatigue and More Muscle via IL-6
CFS/ME is a chronic inflammatory disease with expected elevated inflammatory cytokines. The exception is IL-6. IL-6 is associated with inflammation, but like C-reactive protein, it may be a signal that helps the body adapt to inflammation. Intense exercise results in IL-6 production and exercise fatigue symptoms can be duplicated experimentally by muscle injections of IL-6. IL-6 production following intense exercise results in muscle enhancement, as a result of IL-6-stimulated myoblast cell division. Inflammatory IL-6 is needed for muscle development. In the absence of exercise, IL-6 results in muscle atrophy. Thus, exercise can protect muscle from continuous IL-6 application or chronic inflammation. These results are consistent with the positive effects of exercise therapy for many inflammatory diseases. Unfortunately, CFS/ME is not like most inflammatory diseases.
Response to Cytokines Requires Corresponding Receptors
A recent study of the expression pattern of genes in CFS/ME obtained some interesting results on inflammation in this disease. CFS/ME results in increased levels of the receptors for IL-6 and TNF, but not for the corresponding cytokines, IL-6 and TNF, which trigger fatigue and wasting associated with chronic inflammatory diseases. These findings suggest that people with CFS/ME should be very sensitive to activities or conditions that produce inflammatory cytokines
Exercise Produces Fatigue in CFS/ME
People with CFS/ME do not seem to benefit from exercise, but rather the combination of exercise-induced IL-6, together with enhanced preexisting IL-6 receptors, produces extreme fatigue. Many doctors discourage CFS/ME sufferers from exercising, because the exercise-based IL-6 never reaches therapeutic levels required for muscle enhancement. These recent studies explain what people with CFS/ME have experienced -- exercise is bad for CFS/ME. Hopefully, therapy will follow the new insights.
references:
Kerr JR, Petty R, Burke B, Gough J, Fear D, Sinclair LI, Mattey DL, Richards SC, Montgomery J, Baldwin DA, Kellam P, Harrison TJ, Griffin GE, Main J, Enlander D, Nutt DJ, Holgate ST. 2008. Gene expression subtypes in patients with chronic fatigue syndrome/myalgic encephalomyelitis. J Infect Dis. 197(8):1171-84.
Bodell PW, Kodesh E, Haddad F, Zaldivar FP, Cooper DM, Adams GR. 2008. Skeletal muscle growth in young rats is inhibited by chronic exposure to IL-6, but preserved by concurrent voluntary endurance exercise. J Appl Physiol. Dec 4. [Epub ahead of print]
 |
