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Stressor-Induced Temporal Cortisol Deficiency as a Primary Trigger for Adaptation to Stress
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Background: Inconsistencies in measurements of cortisol response to stress have caused disagreements in the direction of the change in cortisol concentrations immediately after the onset of stress. Researchers typically observe increased cortisol levels in response to a stressor, perceiving occasional decreases as a sign of possible disorders. Reports indicate the relative ease of standardizing a physical stressor compared with a mental stressor, and cross-stressor adaptation is observable only in elite athletes. Methods: We investigated the cortisol response to top-intensity physical exertion by analyzing the course of the cortisol response, the changes in this response resulting from adaptation to intense exercise, and the possible convergence between the cortisol changes and body fat content. We examined 16 male athletes, members of the Polish National Rowing Team, competing in the World Rowing Championships, in top form, of an average training experience of seven years. The measurements were performed before and after the training camp preparatory to the Championships. We performed the measurements before and after the training camp preparatory to the Championships. Results: Before the camp, the athletes consistently reacted to the exertion test with a decrease in cortisol concentration and elevated cortisol levels after rest compared with baseline. After the camp, the post-exertion cortisol decrease as well as the post-rest cortisol elevation was much smaller and less consistent. Conclusions: The transient decrease in cortisol concentration at the onset of stress thus represents a physiological reaction, and the stress response counteracts the resulting cortisol deficiency to support cortisol availability during stress. Adaptation to stress enhanced this counteracting effect by (1) increasing the baseline cortisol concentration and (2) speeding up the response to its decline. This enhanced effect was boosted by adipose tissue.
Title: Stressor-Induced Temporal Cortisol Deficiency as a Primary Trigger for Adaptation to Stress
Description:
Background: Inconsistencies in measurements of cortisol response to stress have caused disagreements in the direction of the change in cortisol concentrations immediately after the onset of stress.
Researchers typically observe increased cortisol levels in response to a stressor, perceiving occasional decreases as a sign of possible disorders.
Reports indicate the relative ease of standardizing a physical stressor compared with a mental stressor, and cross-stressor adaptation is observable only in elite athletes.
Methods: We investigated the cortisol response to top-intensity physical exertion by analyzing the course of the cortisol response, the changes in this response resulting from adaptation to intense exercise, and the possible convergence between the cortisol changes and body fat content.
We examined 16 male athletes, members of the Polish National Rowing Team, competing in the World Rowing Championships, in top form, of an average training experience of seven years.
The measurements were performed before and after the training camp preparatory to the Championships.
We performed the measurements before and after the training camp preparatory to the Championships.
Results: Before the camp, the athletes consistently reacted to the exertion test with a decrease in cortisol concentration and elevated cortisol levels after rest compared with baseline.
After the camp, the post-exertion cortisol decrease as well as the post-rest cortisol elevation was much smaller and less consistent.
Conclusions: The transient decrease in cortisol concentration at the onset of stress thus represents a physiological reaction, and the stress response counteracts the resulting cortisol deficiency to support cortisol availability during stress.
Adaptation to stress enhanced this counteracting effect by (1) increasing the baseline cortisol concentration and (2) speeding up the response to its decline.
This enhanced effect was boosted by adipose tissue.
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