Vitamin E differentially affects short term exercise induced changes in oxidative stress, lipids, and inflammatory markers.

BACKGROUND AND AIM: Physical activity or exercise is a proven deterrent of cardiovascular diseases. The purpose of this study was to examine whether vitamin E supplementation interfere with the potential benefits of exercise. METHODS AND RESULTS: A total of 455 apparently healthy men and women were recruited, for a 2-month aerobic/cardiovascular exercise program. Subjects were randomly assigned for soft gel vitamin E or placebo (800 IU), and required to give blood at 0, 2, 4 and 8 weeks of exercise. Levels of lipid and markers of oxidative stress and inflammation were measured along with the VO2 and duration time spent on treadmill. Statistical analysis did not show significant changes in the levels of lipids and markers of oxidative stress and inflammation. Favorable trends among both of the randomization groups were observed in lipids, and some of the oxidative stress and inflammatory markers. This study also established several interesting correlations between VO2, and lipids on one hand and markers of oxidation and inflammation on the other hand. Reduction in LDL levels positively associated with increased levels of MCP-1 (P < 0.008) among placebo group, and also decreased hCRP levels strongly correlated with the increases in VO2 (P < 0.0004) among the placebo, and vitamin E subjects (P < 0.01). CONCLUSIONS: Exercise training induces oxidative stress might be instrumental in favorable lipid reduction and markers of oxidative stress and inflammation. However interestingly, vitamin E didn't demonstrate favorable effects on the level of oxidative stress and inflammation associated with exercise.

Perceived exertion during incremental cycling is not influenced by the Type A behavior pattern.

Recent publications have perpetuated a concern that the Type A Behavior Pattern (TABP) influences ratings of perceived exertion (RPE) during exercise testing. Previous studies of this topic used the Jenkins Activity Survey (JAS) which lacks validity for predicting the criterion Structured Interview (SI) for TABP and used exercise protocols that were unstandardized or yielded results that were uninterpretable for clinical exercise prescription. We used the SI to classify 44 normotensive men (18-35 y) according to TABP and compared their RPE during an incremental cycling test to peak oxygen uptake (VO2peak). Groups did not differ on maximal test performance or RPE at any stage of the test, even after adjusting RPE for small group variations in % VO2peak and ventilatory equivalent for oxygen, which are strong correlates of RPE during incremental exercise. The findings agree with our prior report [14] that no relationship existed between RPE and several self-report measures of TABP. We conclude that there is no empirical basis for the view that the Type A Behavior Pattern affects cycling performance or ratings of perceived exertion during standard exercise testing in young white men.

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.

Exercise and cardiovascular disease: a new perspective.

The oxidation of low density lipoprotein (LDL) has been suggested as a key event in atherogenesis. Paradoxically, exercise, which imposes an oxidative stress, is an important deterrent of cardiovascular disease. In study 1 the oxidizability of LDL was enhanced in exercisers compared with sedentary controls. The lag time of isolated LDL subjected to copper-induced in vitro oxidation was significantly shortened in the exercisers compared with sedentary subjects. This increased sensitivity was not due to a decreased presence of vitamin E. Instead, these findings suggested that the LDL of exercisers may contain increased amounts of preformed lipid peroxides, which account for the increased oxidizability. In study 2, a group x sex ANOVA revealed that male exercisers had a significantly longer mean lag time than male sedentary subjects and that females had similar mean lag times regardless of exercise group. This remained the case when statistical adjustment was made for age, body mass index, blood lipid levels, LDL, and plasma alpha-tocopherol levels. Study 1 exercisers had been in training for a shorter time (< 1 year) than study 2 exercisers (> 2 years). These findings suggest that truly "chronic" exercise (aerobic intensity over several months) decreases the susceptibility of a male exerciser's LDL to undergo oxidation. Conversely, regular aerobic stress during an overall shorter time span creates a more oxidative environment in the body, thus increasing the susceptibility of LDL to undergo oxidation. The oxidative stress of aerobic exercise does not appear to adversely affect the oxidizability of LDL in women.

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)