Treadmill exercise training augments brain norepinephrine response to familiar and novel stress.

In a test of hypothalamic-pituitary-adrenal (HPA) cortical and hypothalamic-pituitary-gonadal (HPG) interaction during familiar and novel stress, we previously reported that treadmill exercise training led to blunted plasma adrenocorticotrophin (ACTH) response to acute treadmill running but a hyper-responsiveness of ACTH after novel immobilization. In this follow-up analysis, we examined whether those results might be plausibly explained by a similar effect of treadmill exercise training on increased levels of norepinephrine (NE) in hypothalamic and limbic brain regions which synergize to modulate the release of ACTH during stress. Ovariectomized Sprague-Dawley rats that had been exercise trained by treadmill running or remained sedentary for 6 weeks received intramuscular injections of estradiol benzoate (Eb) or sesame oil on each of 3 days prior to 15 min of familiar treadmill running or novel immobilization. Treadmill exercise training, regardless of Eb treatment or type of stress, increased NE levels in the paraventricular (PVN), arcuate, medial preoptic, and ventromedial areas of the hypothalamus and protected against depletion of NE in the locus coeruleus, amygdala, and hippocampus. We conclude that treadmill exercise training has a hyperadrenergic effect in brain areas that modulate hypothalamic regulation of ACTH release during stress that is independent of HPA-HPG interaction and novelty of the stressor. To help elucidate these findings, the effects of treadmill exercise training on A1-A2 nuclei which innervate the PVN and their relationship with the limbic and hypothalamic responses we report require study.

Does acute exercise affect the susceptibility of low density lipoprotein to oxidation?

This study describes the effect of an acute exercise bout on the susceptibility of isolated low density lipoprotein (LDL) to in vitro oxidation. LDL was isolated from 23 subjects (exercisers, n = 11; sedentary, n = 12) immediately before and after a single bout of exercise (30 min of treadmill work at 55% & 70% peak oxygen consumption (VO2 peak) for exercisers and sedentary, respectively). A statistically significant decrease in lag time for LDL oxidation was observed following exercise compared to baseline (96.1+/-23.5 min vs. 92.1+/-23.3 minutes; n = 23, p < or = .03) using a 5 microM copper system. There was a statistically significant increase in plasma myeloperoxidase (MPO) levels following exercise compared to baseline values ( 1.58+/-.91 ng/dl versus 2.08+/-1.2 ng/dl; n = 12, p < or = .03). These results suggest that the 30 min exercise bout at a moderate intensity and duration was a sufficient oxidative stress to increase the susceptibility of LDL to in vitro oxidation. Additionally, the exercise bout appeared to activate neutrophils, subsequently releasing MPO protein.

Treadmill exercise training and estradiol increase plasma ACTH and prolactin after novel footshock.

We examined whether rats that were treadmill exercise trained (Tr) or chronically immobilized (CI) had similar responses by the hypothalamic-pituitary-adrenal (HPA) cortical axis to acute stress and whether the HPA responses interacted with the hypothalamic-pituitary-gonadal (HPG) axis. After 6 wk (1 h/day, 6 days/wk) of Tr or CI, plasma concentrations of adrenocorticotropic hormone ([ACTH]), [prolactin], and [corticosterone] were measured after familiar (treadmill running or immobilization) or novel (footshock) stress. Ovariectomized Sprague-Dawley females (n = 72) were implanted with capsules containing estradiol benzoate (E2) and randomly assigned in a 2-group (E2 vs. no E2) x 3 treatment (Tr vs. CI vs. sedentary) x 4 acute stressor [footshock vs. treadmill running (Run) vs. immobilization (Im) vs. no stress] x 3 recovery time (1 vs. 15 vs. 30 min) mixed-model analysis of variance. E2 capsules were removed from one-half of the animals 48 h before the first stressor session. After 10 min of acute stress, blood was drawn from a jugular catheter at 1, 15, and 30 min of recovery. [ACTH] and [prolactin] after footshock were higher in Tr rats with E2 compared with CI and sedentary rats without E2; recovery levels for sedentary animals were higher after Run compared with Im. The elevation in [corticosterone] from minute 1 to 15 of recovery was higher after the familiar Run and Im conditions. Our findings are consistent with an increased responsiveness of the HPA axis to novel footshock after treadmill exercise training that is additionally modulated by the HPG axis.

Treadmill exercise training and estradiol differentially modulate hypothalamic-pituitary-adrenal cortical responses to acute running and immobilization.

It is generally believed that physical fitness promotes health by attenuating responsiveness to other stressors. The experimental evidence for this belief is limited and does not extend to interactions between the hypothalamic-pituitary-adrenal cortical (HPA) and hypothalamic-pituitary-gonadal (HPG) axes. We tested the hypothesis that treadmill exercise training would lead to an estrogen-dependent hyporesponsiveness of the HPA axis that would generalize to immobilization stress. Ovariectomized female Sprague-Dawley rats (N = 74) that had been treadmill trained (TT) or sedentary for 6 weeks received intramuscular injections of estradiol benzoate (Eb) or sesame oil on each of 3 days prior to 15 min of acute treadmill running or immobilization. Plasma (adrenocorticotrophin) (ACTH), (corticosterone) (B) and (prolactin) (PRL) were determined from trunk blood by radioimmunoassay and compared in a 2 group (TT vs. sedentary)-by-2 treatment (Eb vs. oil)-by-2 acute stressor (running vs. immobilization) design. Home-cage (HC) animals (N = 24) provided baseline hormone levels. ACTH and B levels were elevated after stressors in animals treated with either Eb or oil compared to HC, but increases in PRL after stressors were dependent on Eb. Treadmill exercise training led to an attenuation of ACTH and prolactin to running, but the attenuation did not generalize to immobilization. In contrast, treadmill exercise training led to a hyperresponsiveness of ACTH. Treadmill training did not modulate prolactin responses to immobilization. The modulating effects of the estradiol treatment are consistent with an interaction of the HPA and HPG axes in response to stress.(ABSTRACT TRUNCATED AT 250 WORDS)