Fatigue and exercise

Myoadenylate deaminase (or AMP deaminase) deficiency is a relatively benign muscle disorder characterized by fatigue and exercise-induced muscle aches. This disorder is presumably inherited as an autosomal recessive trait. The relationship between the exercise-induced skeletal muscle dysfunction and AMP deaminase deficiency is explained by an interruption of the purine nucleotide cycle. 

Muscle fatigue during this intensity range may be due to other factors besides lack of CHO substrate. The potential mechanisms include dehydration, electrolyte imbalances, and the onset of muscle injury and soreness. As these potential fatigue factors are common to the range of intensities in this section and exercise below 60% VO2 max, they will be discussed in the following section. 

The phenomenon of muscle fatigue and pain after unaccustomed or excessive exercise is well known, and... 

In conclusion, it is apparent that the lack of definitive methods for assessment of free radicals in muscle and other tissues inhibits clear conclusions to be drawn concerning the relevance (or lack of relevance) of these substances in muscle pathology. In particular, the relevance of free radicals to the deficits in muscle function (fatigue and damage), which occur with exercise, is still unclear despite extensive study. This and other areas require much further examination. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Reduced strength and exercise capacity Defective sweating Psychological problems ° Low self-esteem ° Depression ° Fatigue/listlessness ° Sleep disturbance ° Anxiety ° Social isolation... 

Glutaric aciduria type II, which is a defect of P-oxida-tion, may affect muscle exclusively or in conjunction with other tissues. Glutaric aciduria type II, also termed multiple acyl-CoA dehydrogenase deficiency (Fig. 42-2), usually causes respiratory distress, hypoglycemia, hyperammonemia, systemic carnitine deficiency, nonketotic metabolic acidosis in the neonatal period and death within the first week. A few patients with onset in childhood or adult life showed lipid-storage myopathy, with weakness or premature fatigue [4]. Short-chain acyl-CoA deficiency (Fig. 42-2) was described in one woman with proximal limb weakness and exercise intolerance. Muscle biopsy showed marked accumulation of lipid droplets. Although... 

Left ventricular systolic dysfunction and symptoms such as dyspnea, fatigue, and reduced exercise tolerance... 

Patients experiencing a COPD exacerbation may have worsening dyspnea, increase in sputum volume, or increase in sputum purulence. Other common features of an exacerbation include chest tightness, increased need for bronchodilators, malaise, fatigue, and decreased exercise tolerance. 

Patients with sickle cell anemia suffer fatigue and pain, which is frequently localized to the extremities, upon exertion or after exercise. 

Contraindications to the use of 3 blockers are asthma and other bronchospastic conditions, severe bradycardia, atrioventricular blockade, bradycardia-tachycardia syndrome, and severe unstable left ventricular failure. Potential complications include fatigue, impaired exercise tolerance, insomnia, unpleasant dreams, worsening of claudication, and erectile dysfunction. 

Once stage C is reached, the severity of heart failure is usually described according to a scale devised by the New York Heart Association. Class I failure is associated with no limitations on ordinary activities and symptoms that occur only with greater than ordinary exercise. Class II is characterized by slight limitation of ordinary activities, which result in fatigue and palpitations with ordinary physical activity. Class III failure results in no symptoms at rest, but fatigue, shortness of breath, and tachycardia occur with less than ordinary physical activity. Class IV is associated with symptoms even when the patient is at rest. 

Her research into heart failure has given her some information about what types of variables she should collect. Patients with heart failure show symptoms of decreased exercise tolerance, shortness of breath, increased fatigue, and fluid buildup in the lungs and tissues. Patients with heart failure are also classified clinically by their level of disability so that they may be followed longitudinally and provide a reference point when compared with other patients. This classification system is the New York Heart Association (NYHA) Functional Classification system and ranges from functional class I (no limitation of physical activity) to functional class IV (unable to carry on physical activity without discomfort) (Criteria Committee, 1973). 

The ATP can then power another contraction. Eventually, the amount of ATP available approaches a level too low to be bound by myosin in the muscle, even though it is by no means exhausted. The protons (acid) from metabolism cause hemoglobin to release its oxygen more readily, promoting a switch to aerobic metabolism. Lactate and protons from glycolysis may also lead to fatigue and an inability to sustain the level of speed that was possible earlier. In most humans, this seems to occur after a run of about 400 meters, which is why running quarters is one of the most unpleasant exercises for any athlete, no matter how well conditioned. 

Clinical problems related to fatty acid metabolism. Deficiencies in carnitine lead to an inability to transport fatty acids into the mitochondria for oxidation. This can occur in newborns and particularly in pre-term infants. Treatment is by oral carnitine administration. Carnitine palmitoyltransferase I (CPT I) deficiency primarily affects the liver and leads to reduced fatty acid oxidation and ketogenesis. CPT II deficiency results in recurrent muscle pain, fatigue and myoglobinuria following strenuous exercise. 

Side effects include reduced exercise capacity, lethargy, fatigue, and impotence. Diabetics must have their insulin responses monitored regularly. 

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