In adolescents with anorexia nervosa, reduced maximal aerobic power appears primarily due to reduced muscle mass rather than impaired myocardial function, as stroke volume and cardiac output responses remain normal during exercise.
Preserved exercise hemodynamics in adolescent anorexia suggest intact myocardial function; hypothesis-generating for muscle mass restoration to improve aerobic capacity.
The functional and dimensional components of the oxygen transporting system was studied in 17 female and 11 male patients suffering from anorexia nervosa. Both groups were 14.9 years old, on average, and had lost about 25% of their weight. Measurements at rest included blood and heart volume, heart rate, blood pressure, oxygen uptake (VO2), RQ, blood lactate (LA) and in 6 of the patients cardiac output. During bicycle ergometry the determinations of heart rate, blood pressure, LA, VO2 and cardiac output were repeated and maximal aerobic power was determined. A low metabolic rate with bradycardia and hypotension was apparent at rest. Blood and heart volume was decreased proportionally to the weight loss. On a given work load VO2 was lowered to the same extent as the resting metabolic rate. At maximal effort VO2 was reduced out of proportion to the circulatory dimensions and maximal heart rate was low. During exercise cardiac output was normally related to VO2 and stroke volume was maintained, indicating a normokinetic circulation and an unimpaired myocardial function. The main cause of the low maximal aerobic power seems to be the reduced muscle mass.
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Fohlin et al. (1978) studied this question.
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