Abstract
There is a rising medical need for novel therapeutic targets of physical activity. Physical activity spans from spontaneous, low intensity movements to voluntary, high-intensity exercise. Regulation of spontaneous and voluntary movement is distributed over many brain areas and neural substrates, but the specific cellular and molecular mechanisms responsible for mediating overall activity levels are not well understood. The hypothalamus plays a central role in the control of physical activity, which is executed through coordination of multiple signaling systems, including the orexin neuropeptides. Orexin producing neurons integrate physiological and metabolic information to coordinate multiple behavioral states and modulate physical activity in response to the environment. This review is organized around three questions: (1) How do orexin peptides modulate physical activity? (2) What are the effects of aging and lifestyle choices on physical activity? (3) What are the effects of aging on hypothalamic function and the orexin peptides? Discussion of these questions will provide a summary of the current state of knowledge regarding hypothalamic orexin regulation of physical activity during aging and provide a platform on which to develop improved clinical outcomes in age-associated obesity and metabolic syndromes.
Highlights
PHYSICAL ACTIVITY AND THE OREXIN NEUROPEPTIDE SYSTEM Physical activity can improve overall health
This review describes recent advances in our understanding of neuronal processes that regulate spontaneous physical activity (SPA), with a specific focus on changes that occur in the orexin neuropeptide system during normal and pathological aging
Our work suggests that orexin A in the rostral lateral hypothalamus (LH) has the greatest effect on SPA
Summary
PHYSICAL ACTIVITY AND THE OREXIN NEUROPEPTIDE SYSTEM Physical activity can improve overall health. In turn, regulate physiological and behavioral processes that have major impacts on energy balance and metabolic state, physical activity, blood glucose levels, and food intake (Sakurai et al, 1998; Akiyama et al, 2004; Alam et al, 2005; Kotz et al, 2006; Inutsuka et al, 2014).
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