Both hypo- and hyperthyroidism are characterised by exercise intoleran
ce. In hypothyroidism, inadequate cardiovascular support appears to be
the principal factor involved. Insufficient skeletal muscle blood flo
w compromises exercise capacity via reduced oxygen delivery, and endur
ance through decreased delivery of blood-borne substrates. The latter
effect results in increased dependence on intramuscular glycogen. Addi
tionally, decreased mobilisation of free fatty acids from adipose tiss
ue and, consequently, lower plasma free fatty acid levels compound the
problem of reduced lipid delivery to active skeletal muscle in the hy
pothyroid state. In contrast, cardiovascular support is enhanced in hy
perthyroidism, implicating other factors in exercise intolerance. Grea
ter reliance on muscle glycogen appears to be the primary reason for d
ecreased endurance. Biochemical changes with hyperthyroidism that woul
d favour enhanced flux through glycolysis may account for this depende
nce on glycogen. Deviations from normal thyroid function, and the ensu
ing exercise intolerance, require appropriate medical therapy to attai
n euthyroid status.