Recent published work showed post-exercise (PostEx) esophageal temperature (Tes) recovered rapidly to a persistent plateau that was significantly elevated (0.5$\sp\circ$C or more) above pre-exercise (PreEx) values. Non-acral skin temperatures, except over exercised muscle, returned rapidly to PreEx levels. Rectal temperatures (Tre) fell gradually during recovery reaching a plateau late in recovery (45 min) equal in magnitude of difference from Tes to PreEx values. Surface temperatures over the quadriceps remained high, indicating that heat was trapped in muscle. A similarity between the exercise Tes at which skin surface dilation occurred (Tdil) and the PostEx Tes was identified. These observations contradict the widely accepted "load-error" prinicple of thermoregulation which predicts that displacement of core temperature (Tco) from a hypothalamic set point (SPhy) will induce defense reflexes until the displacement is reversed. These data lead to the hypothesis that there was some residual influence related to exercise that retained the modulation of thermal reflex thresholds during recovery. Testing of the hypothesis was conducted with experiments to establish if: (1) the PostEx Tes was related to PreEx temperature; (2) exogenous thermal loading would produce the same post treatment elevation; (3) PostEx Tes elevation followed by exogenous thermal loading would result in an increase in the Tes elevation and (4) a 5 min exercise generating Tes below Tdil would result in a PostEx elevation of Tes. It was demonstrated that repeated running-recovery cycles produced patterns of rise and then fall of Tes to an elevated PostEx plateau that was equal to Tdil. This was similar to previous results except that the second exercise was begun at an elevated Tes and produced further elevation of Tdil with a comparable effect on PostEx Tes. Similarly, the third exercise further increased Tes following which it recovered to an even higher plateau equal in magnitude to Tdil. We observed that exogenous heat loading, by immersion of subjects in a bath of water at 44$\sp\circ$C to produce a rate of increase and peak elevation of Tes equal to exercise, did not result in a post-treatment elevation in Tes. Similarly, the PostEx Tes elevated plateau, equal to Tdil, remained unchanged following water immersion at 44$\sp\circ$C despite a larger total heat gain during the immersion. These observations eliminate whole body heat content changes as the primary cause of the Tes elevation and support the hypothesis that the homeothermic defense mechanisms become inoperative during recovery at a temperature above resting values as defined by Tdil. The physiological importance of Tdil in defining upper limits of resting temperature cannot be determined at this point. However, the physiological relationship of Tdil with PostEx Tes suggests that neuro-muscular activity significantly influences thermolytic controls which persist in recovery. That Tdil may represent the upper limit of a range of "normal temperatures" is supported by data from a 5 min exercise performed to a Tes elevation below Tdil. Within minutes of exercise termination Tes achieved a stable elevated PostEx Tes (0.3$\sp\circ$C or greater) which was maintained with no change over 65 min of recovery. The data suggest the possibility of: (1) a metabolically induced change in SPhy thermosensitivity, (2) a decreased sensitivity to an increase LE, or (3) a range of temperature regulation defined by an upper threshold control for thermolytic temperature defense reflexes.
| Identifer | oai:union.ndltd.org:uottawa.ca/oai:ruor.uottawa.ca:10393/6486 |
| Date | January 1994 |
| Creators | Kenny, Glen |
| Contributors | Thoden, James |
| Publisher | University of Ottawa (Canada) |
| Source Sets | Université d’Ottawa |
| Detected Language | English |
| Type | Thesis |
| Format | 201 p., application/pdf |
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