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Abstract-The potential of physical exercise to decrease body weight, alleviate depression, combat aging and enhance cognition has been well-supported by research studies. However, exercise regimens vary widely across experiments, raising the question of whether there is an optimal form, intensity and duration of exertion that would produce maximal benefits. In particular, a comparison of forced and voluntary exercise is needed, since the results of several prior studies suggest that they may differentially affect brain and behavior. In the present study, we employed a novel 8-week exercise paradigm that standardized the distance, pattern, equipment and housing condition of forced and voluntary exercisers. Exercising rats were then compared with sedentary controls on measures previously shown to be influenced by physical activity. Our results indicate that although the distance covered by both exercise groups was the same, voluntary exercisers ran at higher speed and for less total time than forced exercisers. Although evidence of the neural and behavioral benefits of exercise is accumulating, the optimal type, duration and intensity of long-term physical activity have not been established. Laboratory animal models of chronic exercise are highly variable, with many studies utilizing ad libitum access to voluntary exercise wheels, while others employ comparably short bouts of forced exercise on a treadmill. Not surprisingly, studies of the same outcome measure produce different results, depending on whether a voluntary or forced exercise paradigm is used (for a recent review of these disparities, see Ang and Gomez-Pinilla, 2007). In addition, it is becoming increasingly recognized that no single exercise paradigm is likely to fulfill all therapeutic needs (Ang and Gomez-Pinilla, 2007;Cotman et al., 2007). Thus, it is imperative to study the neural and behavioral effects of different forms of chronic exercise while holding their parameters constant.Human studies have attempted to pinpoint the optimal intensity level at which acute exercise maximally benefits cognition (Winter et al., 2007;McMorris et al., 2008, see Brisswalter et al., 2002 for a useful review), event-related brain potentials (ERP's) (Kamijo et al., 2004b(Kamijo et al., , 2007 and arousal level (Kamijo et al., 2004a). The most beneficial intensity, duration and type of long-term physical activity have not been well-studied in laboratory animals, however. The type of exercise may be particularly important, since several lines of evidence suggest that forced exercise and voluntary exercise exert different effects on the brain and behavior. For example, forced and voluntary exercise differentially affect monoamine neurotransmitters (Dishman, 1997), hippocampal parvalbumin expression (Arida et al., 2004), hippocampal brain-derived neurotrophic factor and synapsin-1 expression (Ploughman et al., 2005), longevity and body composition (Narath et al., 2001), taste aversion learning (Masaki and Nakajima, 2006) and open-field behavior (Burghardt et al., 2004...

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BackgroundLow-level developmental lead exposure is linked to cognitive and neurological disorders in children. However, the long-term effects of gestational lead exposure (GLE) have received little attention.ObjectivesOur goals were to establish a murine model of human equivalent GLE and to determine dose–response effects on body weight, motor functions, and dopamine neurochemistry in year-old offspring.MethodsWe exposed female C57BL/6 mice to water containing 0, 27 (low), 55 (moderate), or 109 ppm (high) of lead from 2 weeks prior to mating, throughout gestation, and until postnatal day 10 (PN10). Maternal and litter measures, blood lead concentrations ([BPb]), and body weights were obtained throughout the experiment. Locomotor behavior in the absence and presence of amphetamine, running wheel activity, rotarod test, and dopamine utilization were examined in year-old mice.ResultsPeak [BPb] were < 1, ≤ 10, 24–27, and 33–42 μg/dL in control, low-, moderate- and high-dose GLE groups at PN0–10, respectively. Year-old male but not female GLE mice exhibited late-onset obesity. Similarly, we observed male-specific decreased spontaneous motor activity, increased amphetamine-induced motor activity, and decreased rotarod performance in year-old GLE mice. Levels of dopamine and its major metabolite were altered in year-old male mice, although only forebrain utilization increased. GLE-induced alterations were consistently larger in low-dose GLE mice.ConclusionsOur novel results show that GLE produced permanent male-specific deficits. The nonmonotonic dose-dependent responses showed that low-level GLE produced the most adverse effects. These data reinforce the idea that lifetime measures of dose–response toxicant exposure should be a component of the neurotoxic risk assessment process.

Exercise provides a wealth of benefits to brain and body, and is regarded as a protective factor against disease. Protective factors tend to cluster together – that is, people who engage in one healthy behavior, such as exercise, also engage in other healthy behaviors, such as maintaining a nutritious diet and getting sufficient sleep. In contrast to exercise, alcohol consumption is not typically regarded as a health-promoting behavior, although moderate intake has been associated with a lower risk of cardiovascular disease. Surprisingly, several large, population-based studies have shown a positive association between physical activity and alcohol intake. The present review focuses on what is known about this relationship, including potential neural bases as well as moderating factors, and discusses important directions for further study, such as a more thorough characterization of people who both drink and exercise. We focus on ramifications for intervening with people who have alcohol use disorders, as exercise has been assessed as both a treatment and preventive measure, with mixed results. We believe that, in order for such interventions to be effective, clinical trials must distinguish treatment-seeking populations from non-treatment-seeking ones, as well as ensure that the use of exercise as a tool to decrease alcohol consumption is made explicit. We posit that a better understanding of the relationship between physical activity and alcohol intake will maximize intervention efforts by informing the design of clinical trials and research-driven prevention strategies, as well as enable individuals to make educated decisions about their health behaviors.