Voluntary Exercise (voluntary + exercise)

Distribution by Scientific Domains


Selected Abstracts


Voluntary exercise induces anxiety-like behavior in adult C57BL/6J mice correlating with hippocampal neurogenesis

HIPPOCAMPUS, Issue 3 2010
Johannes Fuss
Abstract Several studies investigated the effect of physical exercise on emotional behaviors in rodents; resulting findings however remain controversial. Despite the accepted notion that voluntary exercise alters behavior in the same manners as antidepressant drugs, several studies reported opposite or no effects at all. In an attempt to evaluate the effect of physical exercise on emotional behaviors and brain plasticity, we individually housed C57BL/6J male mice in cages equipped with a running wheel. Three weeks after continuous voluntary running we assessed their anxiety- and depression-like behaviors. Tests included openfield, dark-light-box, elevated O-maze, learned helplessness, and forced swim test. We measured corticosterone metabolite levels in feces collected over a 24-h period and brain-derived neurotrophic factor (BDNF) in several brain regions. Furthermore, cell proliferation and adult hippocampal neurogenesis were assessed using Ki67 and Doublecortin. Voluntary wheel running induced increased anxiety in the openfield, elevated O-maze, and dark-light-box and higher levels of excreted corticosterone metabolites. We did not observe any antidepressant effect of running despite a significant increase of hippocampal neurogenesis and BDNF. These data are thus far the first to indicate that the effect of physical exercise in mice may be ambiguous. On one hand, the running-induced increase of neurogenesis and BDNF seems to be irrelevant in tests for depression-like behavior, at least in the present model where running activity exceeded previous reports. On the other hand, exercising mice display a more anxious phenotype and are exposed to higher levels of stress hormones such as corticosterone. Intriguingly, numbers of differentiating neurons correlate significantly with anxiety parameters in the openfield and dark-light-box. We therefore conclude that adult hippocampal neurogenesis is a crucial player in the genesis of anxiety. © 2009 Wiley-Liss, Inc. [source]


Stress differentially regulates the effects of voluntary exercise on cell proliferation in the dentate gyrus of mice

HIPPOCAMPUS, Issue 10 2009
Timal S. Kannangara
Abstract It has been well-established that cell proliferation and neurogenesis in the adult mouse dentate gyrus (DG) can be regulated by voluntary exercise. Recent evidence has suggested that the effects of voluntary exercise can in turn be influenced by environmental factors that regulate the amount of stress an animal is exposed to. In this study, we use bromodeoxyuridine and proliferating cell nuclear antigen immunohistochemistry to show that voluntary exercise produces a significant increase in cell proliferation in the adult mouse DG in both isolated and socially housed mice. This effect on proliferation translates into an increase in neurogenesis and neuronal branching of new neurons in the mice that exercised. Although social condition did not regulate proliferation in young adult mice, an effect of social housing could be observed in mice exposed to acute restraint stress. Surprisingly, only exercising mice housed in isolated conditions showed an increase in cellular proliferation following restraint stress, whereas socially housed, exercising mice, failed to show a significant increase in proliferation. These findings indicate that social housing may increase the effects of any stressful episodes on hippocampal neurogenesis in the mouse DG. © 2008 Wiley-Liss, Inc. [source]


Exercise Neuroprotection in a Rat Model of Binge Alcohol Consumption

ALCOHOLISM, Issue 3 2010
J. Leigh Leasure
Background:, Excessive alcohol intake produces structural and functional deficits in corticolimbic pathways that are thought to underlie cognitive deficits in the alcohol use disorders (AUDs). Animal models of binge alcohol administration support the direct link of high levels of alcohol consumption and neurotoxicity in the hippocampus and surrounding cortex. In contrast, voluntary wheel running enhances hippocampal neurogenesis and generally promotes the health of neurons. Methods:, We investigated whether voluntary exercise prior to binge alcohol exposure could protect against alcohol-induced cell loss. Female Long-Evans rats exercised voluntarily for 14 days before undergoing 4 days of binge alcohol consumption. Brains were harvested immediately after the last dose of alcohol and examined for various histological markers of neurodegeneration, including both cell death (FluoroJade B) and cell birth (Ki67) markers. Results:, Rats that exercised prior to binge exposure were significantly less behaviorally intoxicated, which was not a result of enhanced hepatic metabolism. Rats that exercised prior to binge alcohol consumption had reduced loss of dentate gyrus granule cells and fewer FluoroJade B positive cells in the dentate gyrus and associated entorhinal-perirhinal cortex compared to nonexercisers. However, exercise did not protect against cell death in the piriform cortex nor protect against alcohol-induced decreases in cell proliferation, evidenced by a similar alcohol-induced reduction in Ki67 labeled cells between exercise and sedentary rats. Conclusions:, We conclude that exercise can reduce behavioral sensitivity to ethanol intoxication and protect vulnerable brain areas from alcohol-induced cell death. Exercise neuroprotection of alcohol-induced brain damage has important implications in understanding the neurobiology of the AUDs as well as in developing novel treatment strategies. [source]


Functional adaptation of the femoral head to voluntary exercise

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 7 2006
Jeffrey H. Plochocki
Abstract The functional adaptation of limb joints during postnatal ontogeny is necessary to maintain proper joint function. Joint form is modified primarily through differential rates of articular cartilage proliferation across articular surfaces during endochondral growth. This process is hypothesized to be mechanically regulated by the magnitude and orientation of stresses in the articular cartilage. However, the adaptation of limb joint morphology to the mechanical environment is poorly understood. We investigate the effects of voluntary exercise on femoral head morphology in 7-week-old female mice of the inbred strain C57BL/6J. The mice were divided into a control group and a group treated with voluntary access to an activity wheel for the duration of the 4-week study. Histomorphometric comparisons of chondral and osseous joint tissue of the proximal femur were made between control and exercise treatment groups. We find that exercised mice have significantly thicker articular cartilage with greater chondral tissue area and cellularity. Exercised mice also exhibit significantly greater bone tissue area and longer and flatter subchondral surfaces. No significant difference is found in the curvature of the articular cartilage or the length of the chondral articular surface between groups. These data suggest that a complex mechanistic relationship exists between joint stress and joint form. Joint tissue response to loading is multifaceted, involving both size and shape changes. Our data support the hypothesis that joint growth is ontogenetically plastic. Mechanical loading significantly influences chondral and subchondral tissue proliferation to provide greater support against increased mechanical loading. Anat Rec Part A, 288A:776,781, 2006 © 2006 Wiley-Liss, Inc. [source]


Haemodynamic responses to exercise, ATP infusion and thigh compression in humans: insight into the role of muscle mechanisms on cardiovascular function

THE JOURNAL OF PHYSIOLOGY, Issue 9 2008
José González-Alonso
The muscle pump and muscle vasodilatory mechanims are thought to play important roles in increasing and maintaining muscle perfusion and cardiac output during exercise, but their actual contributions remain uncertain. To evaluate the role of the skeletal muscle pump and vasodilatation on cardiovascular function during exercise, we determined leg and systemic haemodynamic responses in healthy men during (1) incremental one-legged knee-extensor exercise, (2) step-wise femoral artery ATP infusion at rest, (3) passive exercise (n= 10), (4) femoral vein or artery ATP infusion (n= 6), and (5) cyclic thigh compressions at rest and during passive and voluntary exercise (n= 7). Incremental exercise resulted in progressive increases in leg blood flow (,LBF 7.4 ± 0.7 l min,1), cardiac output ( 8.7 ± 0.7 l min,1), mean arterial pressure (,MAP 51 ± 5 mmHg), and leg and systemic oxygen delivery and . Arterial ATP infusion resulted in similar increases in , LBF, and systemic and leg oxygen delivery, but central venous pressure and muscle metabolism remained unchanged and MAP was reduced. In contrast, femoral vein ATP infusion did not alter LBF, or MAP. Passive exercise also increased blood flow (,LBF 0.7 ± 0.1 l min,1), yet the increase in muscle and systemic perfusion, unrelated to elevations in aerobic metabolism, accounted only for ,5% of peak exercise hyperaemia. Likewise, thigh compressions alone or in combination with passive exercise increased blood flow (,LBF 0.5,0.7 l min,1) without altering , MAP or . These findings suggest that the skeletal muscle pump is not obligatory for sustaining venous return, central venous pressure, stroke volume and or maintaining muscle blood flow during one-legged exercise in humans. Further, its contribution to muscle and systemic peak exercise hyperaemia appears to be minimal in comparison to the effects of muscle vasodilatation. [source]