1. The diencephalon of the unanaesthetized macaque monkey was radio-labelled with calcium by a microinjection of 6-8 muC (45)Ca(2+) into the third cerebral ventricle through a permanently implanted cannula. Successive 5 min push-pull perfusions of the mid-line hypothalamic region with an artificial C.S.F. were carried out at a rate of 28 mul./min every 20 min. A washout curve of declining (45)Ca(2+) radioactivity was thus generated.2. When the monkey exercised strenuously on a special ;rowing machine' to obtain highly palatable banana pellets, its body temperature rose sharply. As the monkey exercised, during a sequence of push-pull perfusions, the concurrent efflux of (45)Ca(2+) ions increased markedly in the corresponding samples of diencephalic perfusate. This enhanced activity of calcium ions continued throughout a 30 min work period and persisted as long as the monkey's temperature was elevated in the interval immediately following exercise.3. Exposure of the monkey's trunk, between neck and thigh to cold air of 5 degrees C likewise augmented the amount of (45)Ca(2+) ions in the diencephalic push-pull perfusates; however, a similar exposure to air warmed to 35 degrees C failed to alter the pattern of (45)Ca(2+) efflux from the animal's diencephalon. If a fasted monkey consumed only the banana pellets but was not exercised, the level of (45)Ca(2+) in the perfusate also increased transiently, just at the onset of feeding.4. We conclude that a local change in calcium transport, binding or other cellular activity of the cation within the diencephalon could play an important role in the central mechanism underlying the set-point rise in a primate's temperature which accompanies vigorous exercise. Further, the results support the idea that this cation functions in the diencephalic control of metabolic heat production as well as in the overall processes of energy metabolism, particularly in relation to feeding.