Journal of IiME Volume 2 Issue 2 www.investinme.org The Physiology of Exercise Intolerance in Patients with Myalgic Eencephalomyelitis (ME) and the Utility of Graded Exercise Therapy concentrations to the point where viral RNA is no longer prevented from replicating, aiding either an initial infection or the renewed replication of previously blocked viral RNA present in muscle tissue and blood27, 29. Thus glutathione depletion is a strong candidate for ‘the trigger for reactivation of endogenous latent viruses’ in ME30. A small number of studies demonstrate that foods rich in glutathione or direct glutathione injection help to relieve fatigue in ME patients, and may clear active viral infections31, 32. Although the above studies have concentrated on skeletal muscle, the heart (and the postural leg muscle involved in pumping blood back to the heart) is not exempt from glutathione depletion. Thus the above mechanism can also account for the range of cardiovascular problems associated with ME, including orthostatic (standing) intolerance (reviewed by Spence and Stewart33). Patients with orthostatic intolerance ‘have continuous disability and commonly have exercise intolerance’33. Together, this evidence suggests that chronic fatigue in ME is symptomatic of the following sequence of events: a period of infection or strenuous physical or mental activity results in glutathione depletion; this renders the immune system relatively ineffective, particularly against enterovirus infection; the immune system becomes constantly activated (and inefficiently governed) because it has insufficient resources (glutathione) to completely rid the body of viral particles; the constantly elevated energy demand of the immune system detracts from other metabolic functions (particularly energy-demanding systems such as skeletal muscles and the cardiovascular system); limitation of respiratory and cardiovascular systems further locks the patient into a vicious cycle of inefficient energy production and use; increased reliance on anaerobic metabolism leads to lactic acid production and associated muscle pain. Invest in ME (Charity Nr. 1114035) Clearly, the performance of energydemanding activities such as exercise can only aggravate this situation. Indeed, 82 % of ME patients in a recent study stated that graded exercise therapy worsened their condition, and only 5 % found it useful (compared to 70 – 75 % of patients who found either pain management or ‘pacing’ of daily activities useful)34. Furthermore, the Canadian Clinical Treatment Protocol warns that “externally paced ‘Graded Exercise Programs’ or programs based on the premise that patients are misperceiving their activity limits or illness must be avoided”35. If exercise is so detrimental, why is graded exercise therapy often recommended as a treatment for ME? Firstly, many of the studies cited here are recent, and the information and implications have perhaps not yet filtered up to policy makers. Secondly, the reclassification of ME as an ambiguous ‘chronic fatigue syndrome’ (CFS) by members of the psychiatric profession assumes that the symptoms have no physiological basis and are best treated with the traditional psychiatric method of facing and overcoming a problem, rather than direct removal of the problem at source. However, this approach jumps from hypothesis to treatment without investigating the mechanisms involved, perhaps explaining why “no psychiatrist has ever cured an ME patient using psychiatric treatments”19. Psychiatry, by definition, should not have authority over the treatment of physiological disorders, particularly those that occur chiefly in muscle tissues. Graded exercise therapy is founded on, and perpetuates, the myth that ME patients are simply malingering, while most are frustrated by their incapacity to satisfactorily conduct critical aspects of daily life34. ME is a heterogeneous disorder that affects different patients to varying degrees and with (continued on page 58) Page 57/74

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