Purpose It has been well established in mammals that circadian behavior as well as the molecular clockwork can be synchronized to the light-dark (LD) cycle via the suprachiasmatic nucleus of the hypothalamus (SCN). In addition to light, it has been demonstrated that non-photic time cues, such as restricting the time of food availability, can alter circadian behavior and clock gene expression in selected peripheral tissues such as liver. Studies have also suggested that scheduled physical activity (exercise) can alter circadian rhythms in behavior and clock gene expression, however currently the effects of exercise alone are largely unknown and have not been explored in skeletal muscle. Methods Period2∷Luciferase (Per2∷Luc) mice were maintained under 12 hours of light followed by 12 hours of darkness (12L:12D) then exposed to 2 hours of voluntary or involuntary exercise during the light phase for 4 weeks. Control mice were left in home cages or moved to the exercise environment (sham). A second group of mice had restricted access to food (4 hours per day for 2 weeks) in order to compare the effects of two non-photic cues on PER2∷LUC bioluminescence. Skeletal muscles, lung and SCN tissue explants were cultured for 5-6 days to study molecular rhythms. Results In the exercised mice, the phase of peak PER2∷LUC bioluminescence was shifted in the skeletal muscle and lung explants but not the SCN suggesting a specific synchronizing effect of exercise on the molecular clockwork in peripheral tissues. Conclusions These data provide evidence that the molecular circadian clock in peripheral tissues can respond to the time of exercise suggesting that physical activity contributes important timing information for synchronization of circadian clocks throughout the body.

Emerging research has shown that subtle factors during pregnancy and gestation can influence long-term health in offspring. In an attempt to be proactive, we set out to explore whether a nonpharmacological intervention, perinatal exercise, might improve offspring health. Female mice were separated into sedentary or exercise cohorts, with the exercise cohort having voluntary access to a running wheel prior to mating and during pregnancy and nursing. Offspring were weaned, and analyses were performed on the mature offspring that did not have access to running wheels during any portion of their lives. Perinatal exercise caused improved glucose disposal following an oral glucose challenge in both female and male adult offspring (P Ͻ 0.05 for both). Blood glucose concentrations were reduced to lower values in response to an intraperitoneal insulin tolerance test for both female and male adult offspring of parents with access to running wheels (P Ͻ 0.05 and P Ͻ 0.01, respectively). Male offspring from exercised dams showed increased percent lean mass and decreased fat mass percent compared with male offspring from sedentary dams (P Ͻ 0.01 for both), but these parameters were unchanged in female offspring. These data suggest that short-term maternal voluntary exercise prior to and during healthy pregnancy and nursing can enhance long-term glucose homeostasis in offspring.running; pregnancy; programming; mice IN 2007, 23.5 MILLION PEOPLE in the US were estimated to have diabetes, and this number is increasing (4). Interestingly, and what is often underappreciated, is that the metabolic status of an individual is decided not only by their inherited genes, nutritional intake, and physical exercise but also by maternal nutrition and obesity during pregnancy. In 1992, Hales and Barker (18) put forth the thrifty phenotype hypothesis that suggested that malnourished pregnant mothers produce smaller offspring that have a higher incidence of obesity, diabetes, and heart disease in adulthood. This hypothesis has since been modified to the developmental origins of health and disease (DOHaD) (15,17,18).The DOHaD suggests that the maternal environment and fetal programming lead to a higher incidence of several diseases later in life (14, 16). A growing number of studies have been designed to provide evidence for the negative impact of DOHaD, using mice, rats, and sheep as animal models (11,12,31,38). Many of these studies are directed at malnutrition through protein restriction or physical stressors that produce similar effects (8,11,34,44,45), but more recent studies are elucidating the metabolic effects of high-fat diet consumption during pregnancy on offspring (22,38,44,48).It has been known since Hippocrates and Galen that physical activity is an important component of a healthy lifestyle (33). However, knowledge about the contributions of maternal exercise during pregnancy and the long-term consequences on offspring is minimal. In both rats and mice, maternal exercise during pregnancy can improve brain physiology and cognition...

No abstract