Effects Of Voluntary Exercise Research Articles

Exercise and time-dependent benefits to learning and memory

While it is well established that exercise can improve cognitive performance, it is unclear how long these benefits endure after exercise has ended. Accordingly, the effects of voluntary exercise on cognitive function and brain-derived neurotrophic factor (BDNF) protein levels, a major player in the mechanisms governing the dynamics of memory formation and storage, were assessed immediately after a 3-week running period, or after a 1-week or 2-week delay following the exercise period. All exercised mice showed improved performance on the radial arm water maze relative to sedentary animals. Unexpectedly, fastest acquisition (fewest errors and shortest latency) occurred in animals trained following a 1-week delay, while best memory performance in the probe trial was observed in those trained immediately after the exercise period. Assessment of the time course of hippocampal BDNF availability following exercise revealed significant elevations of BDNF immediately after the exercise period (186% of sedentary levels) and at 1 and 2 weeks after exercise ended, with levels returning to baseline by 3–4 weeks. BDNF protein levels showed a positive correlation with cognitive improvement in radial water maze training and with memory performance on day 4, supporting the idea that BDNF availability contributes to the time-dependent cognitive benefits of exercise revealed in this study. Overall, this novel approach assessing the temporal endurance of cognitive and biochemical effects of exercise unveils new concepts in the exercise-learning field, and reveals that beneficial effects of exercise on brain plasticity continue to evolve even after exercise has ended.

P5.2 The effect of voluntary exercise and high fat diet on tyrosine hydroxylase phosphorylation in male Sprague–Dawley rats exposed to early life stress

P5.2 The effect of voluntary exercise and high fat diet on tyrosine hydroxylase phosphorylation in male Sprague–Dawley rats exposed to early life stress

P3.16 Effects of voluntary exercise on cardiac responses to stress and on cardiac contractility and excitability in rats

P3.16 Effects of voluntary exercise on cardiac responses to stress and on cardiac contractility and excitability in rats

118. Effects of voluntary exercise on acute stress responses in white adipose tissue

118. Effects of voluntary exercise on acute stress responses in white adipose tissue

The Effect Of Voluntary Exercise On Cardiac Remodeling In Apc Min/+ Mice

ApcMin/+ mice experience intestinal adenomas and chronic inflammation that lead to cachexia and cardiac enlargement. Physical activity can maintain overall physical function, lower chronic inflammation and attenuate cardiac enlargement. PURPOSE: To determine whether lifetime voluntary exercise attenuates cardiac enlargement and related changes in gene expression in ApcMin/+ mice. METHODS: C57BL/6 (wt) and ApcMin/+ mice given access to running wheels or served as cage controls beginning at 4 wks of age and mice were sacrificed at 26 wks of age. Body weights, heart, gastrocnemius, mammary fat pads, and spleens wts were determined and hearts were frozen. Collagen 1a, TGFb, myosin heavy chain (MHC)a, and MHCb were determined by RT-PCR. STAT3 activation was determined by western blot analysis. RESULTS: Body wts were 10% lower in ApcMin/+ than wt mice (21.5±.5 vs 24.2±.7 g) (P≤0.05) and were not altered by exercise. Gastrocnemius muscle wts were 37% lower in ApcMin/+ than wt mice (68±5 vs 108±4 mg) (P≤0.05) but were not altered by exercise. Mammary fat pad wts were lower in ApcMin/+ than wt mice (28±11 vs 262±49 mg) (P≤0.05), and were not altered by exercise. Heart wts were 25% heavier in ApcMin/+ than wt mice (9.0±.3 vs 7.6±.3 mg/mm) (P≤0.05) but were not altered by exercise. Procollagen 1a gene expression was 300% greater in ApcMin/+ than wt mice (3.6±.9 vs 1±.1) (P≤0.05), but exercise attenuated this expression by 48% in ApcMin/+ mice (1.9±.2) (P≤0.05). MHCa gene expression was not different between ApcMin/+ and wt mice, nor was it altered by exercise. However, MHCb gene expression was attenuated by exercise in both ApcMin/+ and wt mice (0.5±.1 vs 1±.1) (P≤0.05) but was not different between ApcMin/+ and wt mice. CONCLUSIONS: These results demonstrate that increased exercise altered cardiac extracellular matrix and myocyte gene expression. The exercise-induced changes altered the physiological function of the heart during cancer-cachexia that were independent of heart and body weight in ApcMin/+ mice.

Effects of voluntary physical exercise on learning and memory: an U-inverted relationship?

Event Abstract Back to Event Effects of voluntary physical exercise on learning and memory: an U-inverted relationship? Sílvia Garcia-Capdevila1, Isabel Portell-Cortes1, Margalida Coll-Andreu1, Meritxell Torras-Garcia1 and David Costa-Miserachs1* 1 Universitat Autònoma de Barcelona, Department of Psicobiologia i Metodologia , Spain Previous work from our laboratory suggested that voluntary exercise affected memory for a recognition object task in a U-inverted manner. To further explore this possibility rats were maintained in an standard home cage (SED) or in a home cage with an attached running wheel for 40 days. From day 1 to 11 running wheel was permanently unblocked, but from day 12 to 40, exercised animals had either the wheel unblocked only during the first 6 nightly hours (6hr) or for 18 hours (18hr) (12 nightly hours plus six daily hours). After these 40 days, a subset of animals were tested in an object recognition task with a 24 hours (RT1) and a 72 hours (RT2) retention sessions, and a different subset were sacrificed to analyse BDNF in hippocampus and perirhinal cortex. Within each condition of restricted running behaviour, we divided the animals into low- and high-runners according to the median of daily running from day 18 to 40. The final groups were 6hr-low (214 m/day), 18hr-low (472 m/day), 6hr-high (546 m/day), 18hr-high (945 m/day) and an additional group 6hr-out (4794 m/day) that includes 7 animals of the 6-hr conditions that showed a very high (outliers) running behaviour during the restriction period. 18hr-high (p=0.015) and 6hr-out (p=0.008) showed less exploration than SED in the neophobia test previous to the recognition object task. There were no differences between groups in exploration time during sample session. On RT1 none of the groups showed significant recall. On RT2 only 18hr-high group showed significant recall of the sample (p=0.009). Moreover, when considering only non-outlier subjects there was a linear relationship (p=0.039) between the amount of exercise and the object recognition memory on RT2, but when including the outlier subjects the relationship was U-inverted (p=0.038). Regarding BDNF, levels of the protein were nearly undetectable in the perirhinal cortex of most of the animals. BDNF levels in the hippocampus showed no differences between groups. Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009. Presentation Type: Poster Presentation Topic: Poster presentations Citation: Garcia-Capdevila S, Portell-Cortes I, Coll-Andreu M, Torras-Garcia M and Costa-Miserachs D (2009). Effects of voluntary physical exercise on learning and memory: an U-inverted relationship?. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.08.2009.09.154 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 09 Jun 2009; Published Online: 09 Jun 2009. * Correspondence: David Costa-Miserachs, Universitat Autònoma de Barcelona, Department of Psicobiologia i Metodologia, Barcelona, Spain, david.costa@uab.cat Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Sílvia Garcia-Capdevila Isabel Portell-Cortes Margalida Coll-Andreu Meritxell Torras-Garcia David Costa-Miserachs Google Sílvia Garcia-Capdevila Isabel Portell-Cortes Margalida Coll-Andreu Meritxell Torras-Garcia David Costa-Miserachs Google Scholar Sílvia Garcia-Capdevila Isabel Portell-Cortes Margalida Coll-Andreu Meritxell Torras-Garcia David Costa-Miserachs PubMed Sílvia Garcia-Capdevila Isabel Portell-Cortes Margalida Coll-Andreu Meritxell Torras-Garcia David Costa-Miserachs Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Voluntary physical exercise alters attentional orienting and social behavior in a rat model of attention-deficit/hyperactivity disorder.

The effects of voluntary physical exercise on attentional function and social behavior were examined in male and female spontaneously hypertensive rats (SHR), a commonly used animal model of attention-deficit/hyperactivity disorder (ADHD). Rats in the exercise groups had free access to a running wheel for 2 weeks and then all rats received nonreinforced presentations of a visual stimulus (light) during the 1st training session, followed by daily sessions in which the light was paired with food. Nonexercising male and female SHR rats exhibited more unconditioned orienting behavior than Wistar-Kyoto rats. SHRs also exhibited impaired conditioning when the light was paired with food. Exercise reduced orienting in female SHRs but not in male SHRs. In the social interaction task, nonexercising male and female SHRs interacted more with an unfamiliar rat than Wistar-Kyoto rats. Exercise reduced the number of social interactions in female SHRs but not male SHRs. There were no differences in general locomotor activity observed between the nonexercising and exercising SHRs. These data indicate that exercise may preferentially benefit female SHRs, and has implications for using exercise as an intervention for ADHD and for understanding sex differences in the effects of exercise on behavior.

Effect of voluntary exercise on number and volume of cardiomyocytes and their mitochondria in the mouse left ventricle

Voluntary exercise (VE) has a beneficial influence on the heart and mean lifespan. The present study evaluates structural adaptations of cardiomyocytes and their mitochondria due to VE by new, unbiased stereological methods. Female, 7-9-week-old mice were randomly assigned to a control (CG, n = 7) or VE group (EG, n = 7). EG animals were housed in cages with free access to a running wheel and had a mean running distance of 6.7 (1.8) km per day. After 4 weeks, the hearts of all mice were processed for light and electron microscopy. We estimated the number and volume of cardiomyocytes by the disector method and the number and volume of mitochondria by estimation of the Euler number. In comparison to CG, VE did not have an effect on the myocardial volume of the left ventricle (CG: 93 (10), EG: 103 (17) (mm(3))), the number of cardiomyocytes (CG: 2.81 (0.27), EG: 2.82 (0.43) (x10(6))) and their number-weighted mean volume. However, the composition of the cardiomyocytes changed due to VE. The total volume of mitochondria (CG: 21.8 (4.9), EG: 32.2 (4.3) (mm(3)), P < 0.01) and the total number (CG: 3.76 (0.44), EG: 7.02 (1.13) (x10(10)), P < 0.001) were significantly higher in EG than in CG. The mean number-weighted mitochondrial volume was smaller in EG than in CG (P < 0.05). In summary, VE does not alter ventricular volume nor cardiomyocyte volume or number but the oxidative capacity of cardiomyocytes by an increased mitochondrial number and total volume in the left ventricle. These structural changes may participate in the beneficial effects of VE.

Effects of voluntary exercise on heart function in streptozotocin (STZ) – induced diabetic rat

Exercise training improves cardiac performance and has been utilized as an effective adjunct to pharmacotherapy in themanagement of diabetes mellitus. The aims of this study were to characterize voluntary exercise habits in streptozotocin(STZ)-induced diabetic rats and investigate whether attained levels of voluntary exercise induce effects on diabetic heartfunction. Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg). Animals were divided into 4 groups:Control Sedentary (CS), Diabetic Sedentary (DS), Control Running (CR) and Diabetic Running (DR). DR and CR rats wereprovided with running wheels. Body weight and blood glucose were measured in running rats at the start and end of the 60-day exercise period. Ventricular action potentials were measured in spontaneously beating heart. Shortening and intracellularCa2+ were measured in electrically stimulated ventricular myocytes. DR rats exercised less than CR rats. At 60 days the meandistance covered by DR rats was 1027 ± 289 m compared to 5975 ± 1117 m in CR rats. CR gained whilst DR rats lost weightat the end of the exercise period. Mean blood glucose in CR and DR rats at the start of the exercise period was 71 ± 4 and 426± 21 mg/dl, respectively. Glucose levels were not altered in CR rats but were reduced in DR rats at the end of the exerciseperiod. The time to peak shortening and peak Ca2+ transient and time to half relaxation of the Ca2+ transient were prolongedin myocytes from DS compared to CS rats and were not additionally altered by voluntary exercise. In conclusion, diabeticrats were less inclined to partake in voluntary exercise compared to controls and the levels and duration of exercise wereinsufficient to significantly alter cardiac performance in either control or diabetic rats. (Int J Diabetes Metab 15: 32-37,2007)

Differential effects of voluntary physical exercise on behavioral and brain-derived neurotrophic factor expression deficits in huntington’s disease transgenic mice

Huntington’s disease is a fatal neurodegenerative disorder caused by a mutation of the huntingtin gene and involves progressive motor abnormalities (including chorea), cognitive deficits (dementia) as well as psychiatric symptoms. We have previously demonstrated that environmental enrichment slows the onset and progression of Huntington’s disease in transgenic mice. Here, we investigated the effects of enhanced physical exercise on disease progression and brain-derived neurotrophic factor expression. Standard-housed Huntington’s disease mice developed phenotypic rear-paw clasping by 16 weeks of age, displayed abnormal rearing behavior, deficits in motor co-ordination and of spatial working memory. Huntington’s disease mice with access to running wheels exhibited delayed onset of rear-paw clasping, normalized levels of rearing behavior and amelioration of the cognitive deficits. However, in contrast to our previous environmental enrichment studies, there was no rescue of motor coordination deficits in wheel-running Huntington’s disease mice. An abnormal accumulation of brain-derived neurotrophic factor protein in the frontal cortex of Huntington’s disease mice was unaffected by running. Striatal and hippocampal brain-derived neurotrophic factor protein levels were unchanged. Brain-derived neurotrophic factor mRNA levels were reduced in the anterior cortex, striatum and hippocampus of Huntington’s disease mice, and only striatal deficits were ameliorated by running. Overall, we show that voluntary physical exercise delays the onset of Huntington’s disease and the decline in cognitive ability. In addition, our results reveal that some aspects of hippocampal dependent memory are not entirely reliant on sustained hippocampal brain-derived neurotrophic factor expression.

Effect of voluntary exercise on peripheral tissue glucocorticoid receptor content and the expression and activity of 11β-HSD1 in the Syrian hamster

Recent findings indicate that elevated levels of glucocorticoids (GC), governed by the expression of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) and GC receptors (GR), in visceral adipose tissue and skeletal muscle lead to increased insulin resistance and the metabolic syndrome. Paradoxically, evidence indicates that aerobic exercise attenuates the development of the metabolic syndrome even though it stimulates acute increases in circulating GC levels. To investigate the hypothesis that training alters peripheral GC action to maintain insulin sensitivity, young male hamsters were randomly divided into sedentary (S) and trained (T) groups (n = 8 in each). The T group had 24-h access to running wheels over 4 wk of study. In muscle, T hamsters had lower 11beta-HSD1 protein expression (19.2 +/- 1.40 vs. 22.2 +/- 0.96 optical density, P < 0.05), similar 11beta-HSD1 enzyme activity (0.9 +/- 0.27% vs. 1.1 +/- 0.26), and lower GR protein expression (9.7 +/- 1.86 vs. 15.1 +/- 1.78 optical density, P < 0.01) than S hamsters. In liver, 11beta-HSD1 protein expression tended to be lower in T compared with S (19.2 +/- 0.56 vs. 21.4 +/- 1.05, P = 0.07), whereas both enzyme activity and GR protein expression were similar. In contrast, visceral adipose tissue contained approximately 2.7-fold higher 11beta-HSD1 enzyme activity in T compared with S (12.9 +/- 3.3 vs. 4.8 +/- 1.5% conversion, P < 0.05) but was considerably smaller in mass (0.24 +/- 0.02 vs. 0.71 +/- 0.06 g). Thus the intracellular adaptation of GC regulators to exercise is tissue specific, resulting in decreases in GC action in skeletal muscle and increases in GC action in visceral fat. These adaptations may have important implications in explaining the protective effects of aerobic exercise on insulin resistance and other symptoms of the metabolic syndrome.

EFFECTS OF VOLUNTARY EXERCISE ON CEREBRAL THROMBOSIS and ENDOTHELIAL FUNCTION IN SPONTANEOUSLY HYPERTENSIVE RATS (SHRSP/IZM)

1. Effects of voluntary exercise on blood pressures, oxidative stress, urinary nitric oxide (NO) level and expression of endothelial NO synthase (eNOS) mRNA were studied in stroke-prone spontaneously hypertensive rats (SHRSP/Izm). 2. SHRSP at the age of 6 weeks were divided into four groups: (i) the control group, sedentary group; (ii) the L-NAME group, which was the sedentary control group given L-NAME (5 mg/kg per day) in drinking water; (iii) the exercise group, which was allowed to run voluntarily on running wheel attached to the metal cages; and (iv) the exercise plus L-NAME group which was loaded exercise and given L-NAME solution for 3 weeks. 3. The bodyweight and systolic pressure of rats were increased with age and the bodyweight of the rats in an exercise plus L-NAME group was less than control but systolic pressure in the exercise group were significantly lower than control. 4. Thrombotic tendency assessed by He-Ne laser method in an exercise group was significantly decreased compared with the rest of the groups. 5. Urinary nitrite/nitrate level was significantly increased in the exercise group compared with before (6 weeks) and after exercise (9 weeks), but there were no significant differences in the rest of groups. 6. eNOS mRNA expression of aorta in the exercise group measured after exercise was significantly higher than the other groups. 7. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) level after exercise was significantly decreased in the exercise group compared with before exercise. 8. These results suggested that voluntary exercise decreased thrombotic tendency by increasing NO level through enhanced expression of eNOS mRNA and antioxidative effects.

Voluntary physical exercise-induced vascular effects in spontaneously hypertensive rats

Forced training has been shown to have beneficial vascular effects in various animal exercise models. In the present study, we explored possible physiological and molecular effects of voluntary physical exercise on various vascular beds. SHR (spontaneously hypertensive rats) performed voluntary exercise for 5 weeks in a computerized wheel cage facility. Ex vivo myograph studies revealed an increased sensitivity of the ACh (acetylcholine)-mediated vasodilation in resistance arteries of the exercised animals (ED50=15.0+/-3.5 nmol/l) compared with the controls (ED50=37.0+/-8.8 nmol/l; P=0.05). The exercise/control difference was abolished after scavenging reactive oxygen radicals. In conduit arteries, ACh induced a similar vasodilatory response in both groups. The in vivo aortic wall stiffness, assessed by means of Doppler tissue echography, was significantly lower in the exercising animals than in controls. This was demonstrated by significantly increased peak systolic aortic wall velocity (P=0.03) and the velocity time integral (P=0.01) in exercising animals compared with controls. The relative gene expression of eNOS (endothelial nitric oxide synthase) was similar in both groups of animals, whereas Cu/ZnSOD (copper/zinc superoxide dismutase) gene expression was significantly increased (+111%; P=0.0007) in the exercising animal compared with controls. In conclusion, voluntary physical exercise differentially improves vascular function in various vascular beds. Increased vascular compliance and antioxidative capacity may contribute to the atheroprotective effects associated with physical exercise in conduit vessels.

Changes in lipids and glucose concentration after voluntary wheel-exercise, high magnesium diet and magnesium fortification in rats

In this study, the effects of voluntary exercise and magnesium fortification on lipid and glucose concentrations in growing rats were examined. Thirty-six 5-week old male wistar rats were divided into 4 groups; CR, SR, EG and ESG (N=9) respectively. 500ppm of elemental magnesium as MgCl2 was provided in the drinking water of Mg- fortified groups. After one week of acclimatization and four weeks of Mg-fortification and/or exercise, the animals were fasted and sacrificed. Total magnesium concentration was similar in EG, ESG, and CR rats, but were all-lower than the concentration in SR rats (p The combination of exercise and magnesium fortification resulted in significant reduction in the concentrations of glucose, triglyceride and total cholesterol. This could prove to be a more effective way of control of metabolic indexes. Key Word: Voluntary exercise-Magnesium fortification-Lipids-Glucose metabolism. Journal of Biomedical Investigation Vol.1 2003: 40-47

Effect of voluntary exercise on the expression of IGF-I and androgen receptor in three rat skeletal muscles and on serum IGF-I and testosterone levels.

The effects of anabolic agents and training on skeletal muscle are believed to be mediated by a variety of growth and transcription factors. Among these regulatory proteins, insulin-like growth factor-I (IGF-I) and androgen receptor (AR) play a crucial role. The purpose of this study was to investigate the effects of wheel running on IGF-I and AR mRNA expression in three distinct rat skeletal muscles (i.e., gastrocnemius, vastus lateralis, and soleus), as well as on the serum levels of IGF-I and testosterone. Twenty male Wistar rats were housed in cages with free access to running wheels for 12 weeks, while nine rats served as controls. Analysis of the mRNA expression of IGF-I and AR using real time RT-PCR revealed no significant differences between the trained and untrained rats in any of the muscles studied. Enzyme immunoassay showed significantly lower serum levels of IGF-I and testosterone in the trained compared to the untrained animals. These results suggest that chronic exercise in wheels does not affect IGF-I and AR mRNA levels in rat skeletal muscle, while decreasing the circulating levels of two anabolic factors, i.e., IGF-I and testosterone. It is concluded that IGF-I, AR and testosterone seem to play a marginal role during the adaptation process of rat skeletal muscle to long-term wheel running.

Effects of voluntary exercise on synaptic plasticity and gene expression in the dentate gyrus of adult male sprague–dawley rats in vivo

We have previously shown that voluntary exercise produces enhanced neurogenesis and long-term potentiation (LTP) in the dentate gyrus (DG) of mice in vitro. In the present experiments we show that rats given access to a running wheel (Runners) exhibit significantly more short-term potentiation and LTP with θ-patterned conditioning stimulation in vivo than do age-matched litter mates (Controls). This increase in LTP appears to reflect an alteration in the induction threshold for synaptic plasticity that accompanies voluntary exercise. Weak θ-patterned stimulation, which did not produce LTP in control subjects, produced a robust and long-lasting LTP in Runners. LTP induction in both groups was dependent upon the activation of N -methyl- d-aspartate (NMDA) receptors, and could be blocked by the competitive antagonist [±]-3-[2-carboxypiperazin-4-yl] propanephosphonic acid. Consistent with these findings, we found that mRNA levels for NR2B subtype of NMDA receptor were increased specifically in the DG of Runners. In addition to changes in NR2B mRNA levels, quantitative polymerase chain reaction analysis revealed that brain-derived neurotrophic factor (BDNF) and glutamate receptor 5 mRNA levels were also significantly elevated in the DG of Runners, but not in other areas of the hippocampus. Thus, alterations in the expression of BDNF, and specific glutamate receptor subtypes, may underlie the ability of exercise to enhance neurogenesis and reduce the threshold for LTP in the DG.

Effects of voluntary exercise and genetic selection for high activity levels on HSP72 expression in house mice.

We studied expression of heat shock protein 72 (HSP72) in female mice from four replicate lines that had been selectively bred for high voluntary wheel running (S) and from four random-bred control lines (C). Mice from generation 23 were sampled after 6 days of wheel access, and those from generation 14 were sampled after 8 wk of access to wheels either free to rotate or locked. Mice from S lines ran approximately 2.6 times as many revolutions per day as did those from C lines. Western blotting of tissues from generation 23 mice indicated that S mice had elevated HSP72 expression in triceps surae muscle, but levels in spleen, kidney, heart, and lung were similar in S and C mice. HSP72 expression in triceps surae from generation 14 mice was measured by ELISA and analyzed with a two-way analysis of covariance. The interaction between wheel type and line type (S vs. C) was statistically significant, and subsequent analyses indicated that S mice had significantly elevated HSP72 expression only when housed with free wheels. Mice with the previously described mini-muscle phenotype (Houle-Leroy P, Guderley H, Swallow JG, and Garland T Jr. Am J Physiol Regul Integr Comp Physiol 284: R433-R443, 2003) occurred in both generations and had elevated HSP72 expression in triceps surae. For the generation 23 sample, wheel running as a covariate had a significant negative association with HSP72 expression, and the effect of line type was still statistically significant. Therefore, the increased HSP72 expression of S mice is not a simple proximate effect of their increased wheel running.

Effect of voluntary exercise on H2O2 release by subsarcolemmal and intermyofibrillar mitochondria.

Previous data have demonstrated that, to handle the oxidative stress encountered with training at high intensity, skeletal muscle relies on an increase in mitochondrial biogenesis, a reduced H(2)O(2) production, and an enhancement of antioxidant enzymes. In the present study, we evaluated the influence of voluntary running on mitochondrial O(2) consumption and H(2)O(2) production by intermyofibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM) isolated from oxidative muscles in conjunction with the determination of antioxidant capacities. When mitochondria are incubated with succinate as substrate, both maximal (state 3) and resting (state 4) O(2) consumption were significantly lower in SSM than in IFM populations. Mitochondrial H(2)O(2) release per unit of O(2) consumed was 2-fold higher in SSM than in IFM. Inhibition of H(2)O(2) formation by rotenone suggests that complex I of the electron transport chain is likely the major physiological H(2)O(2)-generating system. In Lou/C rats (an inbred strain of rats of Wistar origin), neither O(2) consumption nor H(2)O(2) release by IFM and SSM were affected by long-term, voluntary wheel training. In contrast, glutathione peroxidase and catalase activity were significantly increased despite no change in oxidative capacities with long-term, voluntary exercise. Furthermore, chronic exercise enhanced heat shock protein 72 accumulation within skeletal muscle. It is concluded that the antioxidant status of muscle can be significantly improved by prolonged wheel exercise without necessitating an increase in mitochondrial oxidative capacities.

Long-Term Voluntary Access to Running Wheels Decreases Kappa-Opioid Antinociception

D'ANCI, K. E., GERSTEIN, A. V. AND KANAREK, R. B. Long-term voluntary access to running wheels decreases kappa-opioid antinociception. PHARMACOL BIOCHEM BEHAV 66(2) 343–346, 2000.—Previous research has demonstrated that voluntary exercise is associated with a reduction in mu-opioid-induced antinociception. To determine if the effects of voluntary exercise on opioid-induced antinociception were limited to drugs that affect the mu opioid receptor or were more general, the analgesic effects of the kappa opioid agonist U50,488H were compared in active and sedentary rats. Eight adult male Long-Evans rats were housed in standard hanging cages and eight in cages with attached running wheels for 20 days prior to antinociceptive testing. Pain thresholds were determined using a tail-flick procedure, and antinociception was expressed as percent maximal possible effect (%MPE). In the first study, U50,488H was administered in a cumulative dosing procedure (5.0, 10.0, 20.0 mg/kg). Tail-flick latencies were measured immediately prior to and 30 min following each injection. In the second study, the time course of U50,488H effects was examined in animals from the first experiment. Tail-flick latencies were measured immediately prior to and 30, 60, and 90 min following 10.0 mg/kg U50,488H. In the first study, U50,488H produced significant antinociception in both groups of rats. However, antinociceptive responses were significantly reduced for rats given access to running wheels relative to inactive rats. In the second study, antinociceptive responses to U50,488H continued for 90 min. Again, antinociceptive responses were lower for rats given access to running wheels relative to inactive rats. These results indicate that long-term voluntary exercise decreases the antinociceptive properties of the kappa agonist U50,488H, as well as the mu agonist morphine.

The Effects of Voluntary Exercise and Immobilization on Humoral Immunity and Endocrine Responses in Rats

Baldwin, D. R., Z. C. Wilcox and G. Zheng. The effects of voluntary exercise and immobilization on humoral immunity and endocrine responses in rats. Physiol Behav 61(3) 447–453, 1997.—This research examined the effect of type of stressor (physical vs. psychological) on humoral immunity and neuroendocrine responses in male and female rats. Eighty adult Sprague–Dawley rats were assigned to one of the four stress conditions ( n = 20 animals/group): 1. Voluntary running (high physical/low psychological stress); 2. immobilization (low physical/high psychological stress); 3. mixed stress (running and immobilization); and 4. cage control group. The experimental manipulations were conducted over a 6-week period for 4 h/day. Five weeks after the start of the study, all animals were immunized with 1 ml of a 10% suspension of sheep red blood cells (SRBC) in saline and sacrificed 1 week later. Data analyses revealed no main effect of stress on any of the immune or endocrine parameters. However, strong gender differences emerged within the stress conditions on these physiological parameters. The stressed female rats displayed an enhanced antibody response to SRBC and a higher percentage of peripheral blood lymphocytes than their male counterparts. However, there were no significant differences between the male and female control animals with respect to these variables. Female rats consistently displayed elevated levels of plasma corticosterone and adrenal norepinephrine across all conditions. In addition, female rats displayed heavier relative organ weights (adrenal and spleen). Taken together, the notion of differential immunity with respect to physical or psychological stress is not supported by the present study.