To determine whether aging results in reduced accumulation of the 70-kDa heat shock protein (HSP70) in response to a thermal challenge, experiments were conducted in conscious and freely moving mature (12-mo-old) and senescent (24-mo-old) male Fischer 344 rats. Rats were assigned to a euthermic control group or a nonexertionally heated group that was exposed to an ambient temperature of 42 degrees C until colonic temperature reached 41 degrees C. Samples were subsequently obtained from the liver and myocardium, and absolute levels of both the constitutive and inducible forms of HSP70 were quantitated. Heat-stressed rats had significantly elevated HSP70 levels in the liver compared with the euthermic groups. Post hoc comparisons revealed that heat stress elicited marked elevations in liver HSP70 in mature rats compared with age-matched control animals. In contrast, HSP70 values were unchanged in the senescent heated group vs. the control group. In the myocardium, heat stress produced marked increases in HSP70 levels in both the mature and senescent groups compared with age-matched control animals, with accumulation significantly blunted in the senescent vs. mature rats. Thus the increases in liver and myocardial HSP70 accumulation in response to nonexertional heat stress are attenuated with senescence. Because these proteins are postulated to protect cells from injury and enhance cellular recovery from heat stress, the data suggest that an aging organism has a reduced ability to properly maintain cellular function and integrity after a thermal challenge.