title: Corticotropic and serotonergic responses to acute stress with/without prior exercise training in different rat strains.
abstract: The ability to cope with exercise training depends both on environmental and genetic background; however, whether the genetic status may affect (i) the hormonal status of trained subjects and, (ii) its responses to a heterotypic stressor is unknown. Herein, we have used Spontaneously Hypertensive Rats (SHR) and Lewis rats, that differ with regard to their psychoneuroendocrine profiles, to study the influences of an 8-week training programme and/or a 1-h immobilization stress on plasma adrenocorticotropin (ACTH) and corticosterone levels. In addition, brain serotonin metabolism was also measured as an index of neurochemical reactivity to stress. The amplitude of immobilization-elicited increases in ACTH levels which differed with the rat strain (Lewis > SHR), was amplified by prior training; besides, training decreased the strain difference in basal corticosterone (SHR > Lewis) and affected corticosterone response to immobilization in a strain-dependent manner. Thus, immobilization, which increased corticosterone levels in sedentary Lewis but not in SHRs, did not reveal interstrain differences in trained rats. Taken with the observation of a stimulatory effect of training on adrenal weights in SHRs, but not in Lewis, it is concluded that the effects of training on the corticotropic axis depend on the genetic profile of the individual. Lastly, training amplified the response of midbrain (but not striatum or hippocampus) serotonin metabolism to immobilization in a strain-independent manner although the levels of serotonin precursor, namely tryptophan, varied with training and immobilization in a strain-dependent manner. This study shows that some neuroendocrine and neurochemical effects of training undergo interindividual variability.
authors.affiliation: Laboratoire de Physiologie de l'Exercice Musculaire et du Sport, Université Bordeaux II, 146 rue Léo Saignat, Bordeaux Cedex, France.
authors.forename: C L
authors.initials: CL
authors.lastname: Martin
authors.forename: M
authors.initials: M
authors.lastname: Duclos
authors.forename: S
authors.initials: S
authors.lastname: Aguerre
authors.forename: P
authors.initials: P
authors.lastname: Mormede
authors.forename: G
authors.initials: G
authors.lastname: Manier
authors.forename: F
authors.initials: F
authors.lastname: Chaouloff
mesh_terms: D000311:Adrenal Glands / Q000033:anatomy & histology; D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D001835:Body Weight; D003345:Corticosterone / Q000097:blood*; D006897:Hydroxyindoleacetic Acid / Q000097:blood / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007103:Immobilization / Q000502:physiology; D008297:Male; D008636:Mesencephalon / Q000378:metabolism; D009929:Organ Size; D005082:Physical Exertion / Q000502:physiology*; D010913:Pituitary-Adrenal System / Q000502:physiology; D051381:Rats; D011917:Rats, Inbred Lew; D011918:Rats, Inbred SHR; D012701:Serotonin / Q000097:blood / Q000378:metabolism; D013045:Species Specificity; D013312:Stress, Physiological / Q000097:blood*; D014364:Tryptophan / Q000097:blood / Q000378:metabolism
chemical_list: D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D014364:Tryptophan; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone