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Effects of volitional wheel running on diurnal GC levels and GC responsiveness to restraint stress and ACTH challenge in male spague‐dawley rats
Author(s) -
Rakhshani Nasimeh,
Fediuc Sergiu,
Hood David Albert,
Riddell Michael Charles
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a810-b
Subject(s) - medicine , endocrinology , adrenocorticotropic hormone , glucocorticoid , circadian rhythm , stimulation , hypothalamic–pituitary–adrenal axis , turnover , stressor , psychology , hormone , clinical psychology , management , economics
Exercise is a potent activator of the hypothalamo‐pituitary adrenal (HPA) axis. In rats, the effects of voluntary training have been found to amplify the glucocorticoid (GC) response to novel stress. This suggests a possible change in adrenal sensitivity to adrenocorticotropic hormone (ACTH). We studied the effects of voluntary training on diurnal HPA‐axis rhythm, adrenal sensitivity and the response to and recovery from a novel stressor. Sprague‐Dawley rats were divided into training (T) and sedentary (S) groups (n=8/grp) for 8 weeks with T having 24h access to running wheels. A standardized restraint protocol and ACTH challenge were also done at the end of 8 week treatment. The running distance of T rose gradually from week 1 to 6 (1755±35 (X±SEM) to 9016±2068 m/day, p<0.001). Diurnal GC levels were higher for T in wk 1 (T = 229±27 vs S = 122±14 ng/ml, p<0.002) but progressively decreased to reach values similar to S by wk 6 (T = 46±11 vs S = 28±10 ng/ml, p = NS). T and S had a similar GC response during restraint. T had lower GC levels than S during the ACTH challenge (T = 132±34 vs S = 320±24 ng/ml, p<0.001; data collapsed over time). Voluntary wheel running in rats initially causes hyperactivation of the HPA axis, which normalizes by 6 weeks of training. Also, exercisers have a normal response to and recovery from a novel stressor, but a decreased adrenal sensitivity to ACTH stimulation.

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