Re: Why should ME/CFS-patients be cautious with physical exercise?

[Guest guest]

Absolutely fascinating explanation of what happens when you exercise. I tried to get into better shape before Christmas by using the exercise bike for only ten minutes a day, and not too strong a tension. Just got the heart rate up to about 130. I was doing this for about three weeks when, one morning, my knee suddenly seized up and I could barely straighten it or bend it. Extremely painful to walk on. This lasted a full 5 days. Now I'm afraid to exercise.I'm going to try some yoga. Maybe the slower pace will be beneficial. Helen Shari Ferbert <shari23@...> wrote: Source: Co-Cure Why should ME/CFS-patients be cautious with physical exercise?*Why should ME/CFS-patients be cautious with physical exercise?Who risks decline after a forced reconditioning program?__________________________________________________________*Most ME/CFS-patients have chronically activated immune systems, as is thecase in Rheumatoid Arthritis patients. This problem is not detected inroutine laboratory tests because these are mainly indicators forinflammation and do not reveal an altered 'innate immunity'.Nevertheless, there are laboratory

tests available which indicate thepresence of these maladjustments and which worsen under the influence ofphysical exertion. The parameters are: hCRP (high sensitivity CRP), elastase(index of immune activity), NO (nitric oxide) and presence in the serum ofDNA, RNA, LPS (lipopolysaccharides), and/or antibodies for bowel bacteria inthe blood.If ME/CFS-patients are systematically examined for these markers, one findsthat the majority of them have one or more abnormal values, and it istherefore probable that they will have a slow recovery after physicalexercise. Furthermore, patients will sometimes feel worse after exertionbecause the underlying anomalies continue to become worse as a consequenceof the physical exertion.The case of nitric oxide (NO) is interesting. As a result of disruption innormal bowel flora in these patients, there is sometimes an increasedNO-production by these bacteria. Also, due to an

activated nonspecificimmune system, the enzyme iNOS is responsible for higher NO-values in theserum. This, among other things, is responsible for a lowered blood pressurebecause it expands the larger blood vessels. As a result, the peripheralblood vessels must contract, which causes a maladapted circulation indifferent parts of the body.Nitric monoxide, or simply NO, plays an important role in physical exertion.An acceleration of the heartbeat causes the blood flow to increase. As aresponse to this, endothelial cells trigger a number of processes to raisethe production of NO. This leads to several processes which raiseNO-production and activity and keep it going: the eNOS (endothelial enzymethat stimulates NO-production) becomes more active and there is a drop inthe inactivation of NO caused by a decrease in production of free oxygenradicals and by activation of the anti-oxidizing ESA. NO is toxic fornatural

killer cells and T-cells because they lose their ability to functionif there is too much NO circulating. This is one of the reasons whyME/CFS-patients easily become ill after they have engaged in physicalactivity.Sports is beneficial to healthy individuals because NO has a protectiveimpact against arteriosclerosis and bacterial infections. However, an excessof NO is detrimental and patients should be advised that physical exertionhas been shown to lead to a build up of NO in people suffering from ME/CFS.Furthermore, these patients show exercise intolerance because the bloodsupply cannot adapt to the increased exercise-induced demand for oxygen inthe tissues .The case of NO is just one of the many imbalanced systems which createexercise intolerance and/or delayed recovery. Typically, an ME/CFS-patientof the Rheumatoid Arthritis type will have a much lower exercise capacity 24hours after undergoing an exercise

test till exhaustion. Also, a lot ofpatients do not reach their target heart rate when they are pushed toperform an exercise test, due to muscle weakness or pain in the lowerextremities. This muscle weakness is a result of the binding of NO to theryanodine receptors in the muscles. The pain is a result of maladapted bloodflow in the muscles of the same extremities, which results in a prematureaccumulation of lactic acid. A portion of the NO will oxidize: NO + O2 ->ONOO - (peroxynitrate). This is a very strong free radical which damagescell membranes.*What can we learn from this ?*ME/CFS-patients must *never *be forced to do compulsory exercise; they mustlisten to their bodies and not to other people who think they know betterbut are not familiar with the biology of these disorders. Physical exercisemust be adapted to the individual, based on the severity and consequences ofthe illness.

Therefore, the individual patient evaluation should beextensive, specific and adapted to the disorder.Leo Trower*References:***. Ito et al. Cell.Immunol. 1996 : 174 ; 13. Englebienne & De Meirleir 2002 - book (291 pages) - CRC press. Mihylova et al. Neuro.Endocrinol.Letters 2007 : 11 ; 28. Connolly et al. J.Appl.Physiol. 2004 : 97 ; 1461. Sobko et al. Free Radical Biology & Medicine 2006 : 41 ; 985. VanNess et al. J. Chronic Fatigue Syndrome 2007 : 14(2) ; 77

[Guest guest]

This is a great article. I've added it to the files for future reference. I wonder how many pwc may also have the same genetic clotting disorder that I have which predisposes one to Nitric Oxide buildup in the first place? (No wonder I've always crashed so badly after a couple days of activity.) My guess is quite a few of us may have it since hypercoagulation seems to be an issue for so many with this disease. penny Hope 4all <hope.4.you.and.me@...> wrote: Why should ME/CFS-patients be cautious with physical exercise? Who risks decline after a forced reconditioning program? __________________________________________________________ Most ME/CFS-patients have chronically activated immune systems, as is the case in Rheumatoid Arthritis patients. This problem is not detected in routine laboratory tests because these are mainly indicators for inflammation and do not reveal an altered 'innate immunity'. Nevertheless, there are laboratory tests available which indicate the presence of these maladjustments and which worsen under the influence of physical exertion. The parameters are: hCRP (high sensitivity CRP), elastase (index of immune

activity), NO (nitric oxide) and presence in the serum of DNA, RNA, LPS (lipopolysaccharides), and/or antibodies for bowel bacteria in the blood. If ME/CFS-patients are systematically examined for these markers, one finds that the majority of them have one or more abnormal values, and it is therefore probable that they will have a slow recovery after physical exercise. Furthermore, patients will sometimes feel worse after exertion because the underlying anomalies continue to become worse as a consequence of the physical exertion. The case of nitric oxide (NO) is interesting. As a result of disruption in normal bowel flora in these patients, there is sometimes an increased NO-production by these bacteria. Also, due to an activated nonspecific immune system, the enzyme iNOS is responsible for higher NO-values in the serum. This, among other things, is responsible for a lowered blood pressure because it expands the

larger blood vessels. As a result, the peripheral blood vessels must contract, which causes a maladapted circulation in different parts of the body. Nitric monoxide, or simply NO, plays an important role in physical exertion. An acceleration of the heartbeat causes the blood flow to increase. As a response to this, endothelial cells trigger a number of processes to raise the production of NO. This leads to several processes which raise NO-production and activity and keep it going: the eNOS (endothelial enzyme that stimulates NO-production) becomes more active and there is a drop in the inactivation of NO caused by a decrease in production of free oxygen radicals and by activation of the anti-oxidizing ESA. NO is toxic for natural killer cells and T-cells because they lose their ability to function if there is too much NO circulating. This is one of the reasons why ME/CFS-patients easily become ill after they have engaged in physical activity.

Sports is beneficial to healthy individuals because NO has a protective impact against arteriosclerosis and bacterial infections. However, an excess of NO is detrimental and patients should be advised that physical exertion has been shown to lead to a build up of NO in people suffering from ME/CFS. Furthermore, these patients show exercise intolerance because the blood supply cannot adapt to the increased exercise-induced demand for oxygen in the tissues . The case of NO is just one of the many imbalanced systems which create exercise intolerance and/or delayed recovery. Typically, an ME/CFS-patient of the Rheumatoid Arthritis type will have a much lower exercise capacity 24 hours after undergoing an exercise test till exhaustion. Also, a lot of patients do not reach their target heart rate when they are pushed to perform an exercise test, due to muscle weakness or pain in the lower extremities. This muscle weakness is

a result of the binding of NO to the ryanodine receptors in the muscles. The pain is a result of maladapted blood flow in the muscles of the same extremities, which results in a premature accumulation of lactic acid. A portion of the NO will oxidize: NO + O2 -> ONOO - (peroxynitrate). This is a very strong free radical which damages cell membranes. What can we learn from this ? ME/CFS-patients must never be forced to do compulsory exercise; they must listen to their bodies and not to other people who think they know better but are not familiar with the biology of these disorders. Physical exercise must be adapted to the individual, based on the severity and consequences of the illness. Therefore, the individual patient evaluation should be extensive, specific and adapted to the disorder. Leo Trower References: . Ito et al. Cell.Immunol. 1996 : 174 ; 13 . Englebienne & De Meirleir 2002 - book (291 pages) - CRC press . Mihylova et al. Neuro.Endocrinol.Letters 2007 : 11 ; 28 . Connolly et al. J.Appl.Physiol. 2004 : 97 ; 1461 . Sobko et al. Free Radical Biology & Medicine 2006 : 41 ; 985 . VanNess et al. J. Chronic Fatigue Syndrome 2007 : 14(2) ; 77