Exercise promotes positive impression formation towards both men and women.

Exercise is endorsed for its physiological and psychological benefits, and has been proposed to have positive effects on impression formation. To test this proposal, 62 female and 44 male college students read one of three brief descriptions of either a fictitious male or female "target" student. The descriptions varied only in exercise level: no exercise; moderate exercise and intensive exercise. Participants then rated the fictitious student on 38 personality traits. Ratings of characteristics that are associated with exercise (e.g. athletic; energetic) increased, while ratings associated with the lack of exercise (e.g. lazy; weak) decreased as a function of the reported level of exercise. Exercise level also positively influenced ratings of characteristics not related to exercise. These data show that even minimal information about exercise is an important component of first impressions in both men and women.

Architecture of energy balance traits in emerging lines of the Collaborative Cross.

The potential utility of the Collaborative Cross (CC) mouse resource was evaluated to better understand complex traits related to energy balance. A primary focus was to examine if genetic diversity in emerging CC lines (pre-CC) would translate into equivalent phenotypic diversity. Second, we mapped quantitative trait loci (QTL) for 15 metabolism- and exercise-related phenotypes in this population. We evaluated metabolic and voluntary exercise traits in 176 pre-CC lines, revealing phenotypic variation often exceeding that seen across the eight founder strains from which the pre-CC was derived. Many phenotypic correlations existing within the founder strains were no longer significant in the pre-CC population, potentially representing reduced linkage disequilibrium (LD) of regions harboring multiple genes with effects on energy balance or disruption of genetic structure of extant inbred strains with substantial shared ancestry. QTL mapping revealed five significant and eight suggestive QTL for body weight (Chr 4, 7.54 Mb; CI 3.32-10.34 Mb; Bwq14), body composition, wheel running (Chr 16, 33.2 Mb; CI 32.5-38.3 Mb), body weight change in response to exercise (1: Chr 6, 77.7Mb; CI 72.2-83.4 Mb and 2: Chr 6, 42.8 Mb; CI 39.4-48.1 Mb), and food intake during exercise (Chr 12, 85.1 Mb; CI 82.9-89.0 Mb). Some QTL overlapped with previously mapped QTL for similar traits, whereas other QTL appear to represent novel loci. These results suggest that the CC will be a powerful, high-precision tool for examining the genetic architecture of complex traits such as those involved in regulation of energy balance.

Advances in comparative genetics: influence of genetics on obesity.

Obesity has reached epidemic proportions and is recognised as a significant global health problem. Increased food intake and decreased physical activity are traditionally to blame for the development of obesity; however, many variables such as behaviour, diet, environment, social structures and genetics also contribute to this multifactorial disease. Complex interactions among these variables (for example, gene-environment, gene-diet and gene-gene) contribute not only to individual differences in the development of obesity, but also in treatment response. Mouse models have historically played valuable roles in understanding the genetics of traits related to energy balance and obesity. In the present review, we survey past use and examine new advances in mouse models designed to uncover the genetic architecture of obesity and its component traits. We discuss traditional models such as inbred strains and selectively bred lines and their contributions and shortcomings. We consider the evolution of mouse models into more informative resources such as outbred crosses and the Hybrid Mouse Diversity Panel, as well as novel next-generation approaches such as the Collaborative Cross. Moreover, the genetic architecture of voluntary exercise and the interactive relationship between host genetics and the gut microbiome are presented as novel phenotypes that augment studies using body weight and body fat percentage as endpoints. Understanding the intricate network of phenotypic, genotypic and environmental variables that predispose individuals to obesity will elucidate biological networks involved in the development of obesity. Knowledge obtained from advances in mouse models will inform human health and provide insight into inter-individual variability in the aetiology of obesity-related diseases.

The biology of binge eating.

OBJECTIVE: To examine the literature on binge eating to gain a better understanding of its biological foundations and their role in eating disorders. METHOD: Literature review and synthesis. RESULTS: Research using animal models has revealed several factors that contribute to the development and maintenance of binge eating. These factors, including stress, food restriction, the presence of palatable foods, and environmental conditioning, parallel many of the precursory circumstances leading to binge eating in individuals with bulimia nervosa and binge eating disorder. DISCUSSION: The animal literature has opened a new avenue to aid in the understanding of the neurobiological basis of binge eating. Future endeavors examining the genetic and environmental correlates of binge eating behavior will further contribute to the understanding of the biological foundations of binge eating and assist with establishing diagnostic criteria and the development of novel treatments for eating disorders marked by binge eating.

Persistent exercise attenuates nicotine- but not clonidine-induced antinociception in female rats.

Exercise decreases the antinociceptive effects of opiate drugs. It has been hypothesized that the exercise-induced attenuation of opiate drug action is the result of the development of cross-tolerance between endogenous opioids released during exercise and exogenous opiates. The present study was designed to evaluate the role of exercise on non-opiate antinociception. Female Long-Evans rats were allowed ad lib access to running wheels. After 3 weeks, antinociceptive responses of animals were measured using the tail flick test following the administration of clonidine or nicotine. Nicotine and clonidine both produced dose-dependent increases in antinociceptive responses. Active animals were significantly less sensitive to nicotine-induced antinociception than inactive animals. There was no difference between the two groups in clonidine-induced antinociception. The results of these experiments suggest that exercise does not attenuate non-opioid, clonidine-induced antinociception. However, exercise does attenuate nicotine-induced antinociception. Therefore, the effect of persistent exercise on analgesic drugs is not specific to opiates.

Chronic running wheel activity attenuates the antinociceptive actions of morphine and morphine-6-glucouronide administration into the periaqueductal gray in rats.

Chronic exercise in a running wheel increases baseline pain sensitivity while attenuating the antinociceptive effects of peripherally administered opiate agonists in laboratory rodents. To determine if these effects are due to exercise-induced changes in the central nervous system (CNS) or an artifact of exercise-induced alterations in peripheral physiology, the present study evaluated the antinociceptive actions of centrally administered opiate agonists in active and inactive female rats. Rats were implanted with cannula into the right periaqueductal gray (PAG) area of the midbrain. After the completion of the surgery, the animals were allowed ad libitum access to running wheels or housed in standard cages for three weeks. Pain sensitivity was measured on the tail flick test before and immediately following microinjections of either morphine (0, 2.5, 5.0, 10.0, 20.0 microg/rat) or the more potent morphine metabolite, morphine-6-glucuronide (M6G) (0, 0.03, 0.1, 0.3, 1.0 microg/rat). Baseline tail flick latencies were significantly shorter in active than in inactive rats. Additionally, active animals were less sensitive to the antinociceptive effects of morphine and M6G than inactive rats. These findings provide evidence for the involvement of the CNS in exercise-mediated alterations in pain sensitivity and opiate drug actions.

Dopaminergic dysregulation in mice selectively bred for excessive exercise or obesity.

Dysregulation of the dopamine system is linked to various aberrant behaviors, including addiction, compulsive exercise, and hyperphagia leading to obesity. The goal of the present experiments was to determine how dopamine contributes to the expression of opposing phenotypes, excessive exercise and obesity. We hypothesized that similar alterations in dopamine and dopamine-related gene expression may underly obesity and excessive exercise, as competing traits for central reward pathways. Moreover, we hypothesized that selective breeding for high levels of exercise or obesity may have influenced genetic variation controlling these pathways, manifesting as opposing complex traits. Dopamine, dopamine-related peptide concentrations, and gene expression were evaluated in dorsal striatum (DS) and nucleus accumbens (NA) of mice from lines selectively bred for high rates of wheel running (HR) or obesity (M16), and the non-selected ICR strain from which these lines were derived. HPLC analysis showed significantly greater neurotransmitter concentrations in DS and NA of HR mice compared to M16 and ICR. Microarray analysis showed significant gene expression differences between HR and M16 compared to ICR in both brain areas, with changes revealed throughout the dopamine pathway including D1 and D2 receptors, associated G-proteins (e.g., Golf), and adenylate cyclase (e.g., Adcy5). The results suggest that similar modifications within the dopamine system may contribute to the expression of opposite phenotypes in mice, demonstrating that alterations within central reward pathways can contribute to both obesity and excessive exercise.

Running and addiction: precipitated withdrawal in a rat model of activity-based anorexia.

Exercise improves cardiovascular health, strengthens muscles and bones, stimulates neuroplasticity, and promotes feelings of well-being. However, when taken to extremes, exercise can develop into an addictive-like behavior. To assess the addictive potential of exercise, withdrawal symptoms following injections of 1.0 mg/kg naloxone were compared in active and inactive male and female rats. Active and inactive rats were given food for 1 hr or 24 hr/day. Additionally, a group of inactive rats was pair-fed the amount of food consumed on the previous day by food-restricted active rats. Rats fed for 1 hr/day decreased food intake and lost weight. Additionally, food-restricted active rats increased wheel running. There was a direct relationship between the intensity of running and the severity of withdrawal symptoms. Active food-restricted rats displayed the most withdrawal symptoms, followed by active rats given 24-hr access to food. Only minimal withdrawal symptoms were observed in inactive rats. These findings support the hypothesis that exercise-induced increases in endogenous opioid peptides act in a manner similar to chronic administration of opiate drugs.