Circadian rhythms and patterns of running-wheel activity, feeding and drinking behaviors of old male rats

Peng, Michael Yao‐Ping; Kang, Ming-Yuan

doi:10.1016/0031-9384(84)90380-9

Cited by 56 publications

(17 citation statements)

References 21 publications

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“…Although chronobiological theory appears to contribute little to understanding the amount of running, the observed patterns of daily running in our study are consistent with a chronobiological model of running becoming entrained to both light/dark cycles and periodic feeding (1,2,12,18,19). We observed a substantial increase in running 2 h prior to feeding/ animal care in deprived rats and a smaller increase in raks with unlimited access to food.…”

Section: Discussionsupporting

confidence: 79%

An analysis of excessive running in the development of activity anorexia

Beneke

Schulte

Tuig

1995

Physiology & Behavior

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analysis of excessive running in the development of activity anorexia. PHYSIOL BEHAV 58(3) 451-457, 1995.--Food restriction combined with activity wheel access produces activity anorexia: a combination of excessive running, reduced food intake and rapid weight loss. Temporal distributions of running in activity anorexia were examined in a reversal design with one of 2 × 2 × 2 factorial combinations (pelleted-vs-powdered food × deprivation × wheel access) as the treatment condition. Wheel revolutions were recorded in 30 min intervals; body weights, food and water intakes were measured daily. Only wheel access combined with food deprivation reliably produced activity anorexia. Excessive running occurred in the absence of schedule-induced polydipsia, was unaffected by food form, and showed distributional characteristics of facultative behavior. These results are inconsistent with schedule-induced behavior explanations. Running distributions appeared consistent with chronobiological models with light/dark onset and feeding serving as zeitgebers. Activity anorexia Activity Temporal running distribution Food deprivationSchedule-induced behavior Rats RATS (8,13,20,21), mice (8), and golden hamsters (4,5) allowed access to running wheels combined with food deprivation schedules (60-90 min daily food access), ran excessively, ate little and eventually starved. The phenomenon, labelled activity anorexia (7), is characterized by dramatic increases in activity paradoxically associated with decreased food consumption, and has also been observed in some humans diagnosed with anorexia nervosa (10,15,27) as well as some athletes (14,23,26,28). These observations have led researchers (7,9) to suggest that activity anorexia, induced experimentally in rodents, might serve as a useful model for the understanding of anorexia nervosa and its treatment in humans. Consistent with this notion, Epling and Pierce (7) also observed dramatic increases in running immediately before and after scheduled feeding. They suggested that the running might be a schedule-induced behavior. If water is continuously available during a variable interval schedule of food reinforcement, rats become polydipsic, drinking several times their normal daily water intake (11). The behavior typically manifests itself as an interim schedule-induced behavior, as described by Staddon (24), and has also been obtained with fixed time schedules of reinforcement [e.g., (25)]. If one were to postulate water availability as somewhat analogous to availability of a running wheel, then one could also postulate the excessive wheel running as scheduleinduced under the same conditions that produce schedule-induced polydipsia (17,25). Although studies of schedule-induced behavior have utilized small food portions as reinforcers and brief (commonly 1 min) periodic schedules, at least by analogy, activity anorexia might be a special case of schedule-induced behavior, or the behaviors might share common underlying mechanisms. If true, variables influencing schedule-induced behavior...

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Section: Discussionsupporting

confidence: 79%

An analysis of excessive running in the development of activity anorexia

Beneke

Schulte

Tuig

1995

Physiology & Behavior

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“…Differential responsivity to the SPA- and NEAT-promoting effects of orexin-A between OP and OR rats suggests that sensitivity to orexin-A SPA promotion is an inherent trait that may be critically important to body weight regulation. The idea that orexin neurons are important for mediating energy balance is supported by studies in aged animals showing age-related declines in both SPA [260] and hypothalamic orexin receptor mRNA [261]. Although not demonstrated by these studies, a decline in orexin neuronal activity [262], receptor mRNA [261] and receptor signaling during aging may explain the reduction in SPA [260] and increased propensity for obesity observed during aging.…”

Section: Role Of Neat In Obesity Resistancementioning

confidence: 62%

Neuropeptidergic Mediators of Spontaneous Physical Activity and Non-Exercise Activity Thermogenesis

Teske¹,

Billington

Kotz³

2007

Neuroendocrinology

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Lean individuals have high levels of spontaneous physical activity (SPA) and the energy expenditure derived from that activity, termed non-exercise activity thermogenesis or NEAT, appears to protect them from obesity. Conversely, obesity in different human populations is characterized by low levels of SPA and NEAT. Like in humans, elevated SPA in rats appears to protect against obesity: obesity-resistant rats have significantly greater SPA and NEAT than obesity-prone rats. We review the literature on brain mechanisms important in mediating SPA and NEAT. The focus is on neuropeptides, including cholecystokinin, corticotropin-releasing hormone (also known as corticotropin-releasing factor), neuromedin U, neuropeptide Y, leptin, agouti-related protein, orexin-A (also known as hypocretin-1), and ghrelin. We also review information regarding interactions between these neuropeptides and dopamine, a neurotransmitter important in mediating motor function. Finally, we present evidence that elevated signaling of pathways mediating SPA and NEAT may protect against weight gain and obesity.

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“…Because orexin A can pass the blood-brain barrier (26), peripheral orexin A levels might reflect its CNS levels. In the mouse hypothalamus, age-related decline in OX 2 R messenger RNA levels has been shown (59), and it is known that old rats have decreased activity (43). The decline in orexin with obesity and aging may support the hypothesis that orexin A in the PVN is a mediator of NEAT.…”

Section: Discussionmentioning

confidence: 85%

Orexin A (hypocretin 1) injected into hypothalamic paraventricular nucleus and spontaneous physical activity in rats

Kiwaki¹,

Kotz²,

Wang³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

135

134

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The mediator of the interaction between positive energy balance and physical activity is unknown. In this study, we address the hypothesis that orexin A acts in the hypothalamic paraventricular nucleus (PVN) to increase nonfeeding-associated physical activity. PVN-cannulated rats were injected with either orexin A or vehicle during the light and dark cycle. Spontaneous physical activity (SPA) was measured using arrays of infrared activity sensors and night vision videotaped recording (VTR). O2 consumption and CO2 production were measured by indirect calorimetry. Feeding behavior was assessed by VTR. Regardless of the time point of injection, orexin A (1 nmol) was associated with dramatic increases in SPA for 2 h after injection (orexin A: 6.27 Ϯ 1.95 ϫ 10 3 beam break count, n ϭ 24; vehicle: 1.85 Ϯ 1.13 ϫ 10 3 , n ϭ 38). This increase in SPA was accompanied by compatible increase in O2 consumption. Duration of feeding was increased only when orexin A was injected in the early light phase and accounted for only 3.5 Ϯ 2.5% of the increased physical activity. In a dose-response experiment, increases in SPA were correlated with dose of orexin A linearly up to 2 nmol. PVN injections of orexin receptor antagonist SB-334867 were associated with decreases in SPA and attenuated the effects of PVN-injected orexin A. Thus orexin A can act in PVN to increase nonfeeding-associated physical activity, suggesting that this neuropeptide might be a mediator of NEAT. energy expenditure; hypothalamus; obesity; nonexercise activity thermogenesis OBESITY AFFECTS ONE-THIRD of the American population and is the second leading cause of death in the United States after smoking (1). Treatment of obesity has proven difficult, and this intractability may be due to the fact that energy balance is regulated through multiple and complex mechanisms that are not fully understood (4). Maintenance of body weight is achieved by an intricate balance between energy intake and expenditure. We found that changes in nonexercise activity thermogenesis (NEAT) mediate resistance to weight gain with overfeeding in sedentary adults (32). There is evidence that "spontaneous" physical activity (SPA) is familial (63) and shows marked interindividual differences in its contribution to daily energy expenditure (49); however, the mediator of the interaction between overfeeding and physical activity is unknown.Orexins (A and B, also known as hypocretin 1 and 2) are recently identified neuropeptides synthesized exclusively in the lateral hypothalamus, an area classically believed to be a crucial "feeding" center (25). Initial interest in these neuropeptides concentrated on their orexigenic actions, since central injection of orexins increased food intake, and prepro-orexin mRNA was shown to be upregulated with fasting (50). Apart from appetite regulation, orexins have been implicated in the central nervous system (CNS) regulation of arousal and sleep, cardiovascular function, temperature, metabolic rate, locomotor activity, pituitary secretion, glucose homeostasis, ...

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Circadian rhythms and patterns of running-wheel activity, feeding and drinking behaviors of old male rats

Cited by 56 publications

References 21 publications

An analysis of excessive running in the development of activity anorexia

An analysis of excessive running in the development of activity anorexia

Neuropeptidergic Mediators of Spontaneous Physical Activity and Non-Exercise Activity Thermogenesis

Orexin A (hypocretin 1) injected into hypothalamic paraventricular nucleus and spontaneous physical activity in rats

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