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Fatigue in Persian Gulf Syndrome-Physiologic Mechanisms.
Annual rept. 15 Jun 97-14 Jun 98
TEXAS UNIV SOUTHWESTERN MEDICAL SCHOOL AT DALLAS
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We hypothesize that the common complaint of abnormal fatigue and exercise intolerance in these patients is attributable to impaired energy production via oxidative phosphorylation. Under this general hypothesis, we will address three specific questions 1 Is there an abnormality of muscle oxygen utilization or oxygen transport to muscle during exercise in affected individuals, 2 Is there exaggerated metabolic muscle fatigue in exercise consistent with impaired energy production, and 3 Is the metabolic and physiologic response to aerobic physical conditioning impaired in these patients. In order to address these questions, we will employ forearm and cycle exercise to determine maximal work and oxidative capacity and to compare fatigue and metabolic responses to similar relative workloads among patients and age and weight matched sedentary control subjects and we will compare muscle metabolic and physiologic responses to aerobic training in patients and matched control subjects. We will monitor oxidative metabolism by employing 31-phosphorus magnetic resonance spectroscopy and by utilizing near infrared spectroscopy. In a cohort of patients and control subjects we will evaluate the hypothesis that oxidative limitations detected with non-invasive testing is attributable to impaired function of the mitochondrial metabolism as assessed biochemical in biochemical muscle.
APPROVED FOR PUBLIC RELEASE