Cold-Induced Thermoregulation and Biological Aging

Abstract

Aging is associated with diminished cold-induced thermoregulation (CIT). The mechanisms accounting for this phenomenon have yet to be clearly elucidated but most likely reflect a combination of increased heat loss and decreased metabolic heat production. The inability of the aged subject to reduce heat loss during cold exposure is associated with diminished reactive tone of the cutaneous vasculature and, to a lesser degree, alterations in the insulative properties of body fat. Cold-induced metabolic heat production via skeletal muscle shivering thermogenesis and brown adipose tissue nonshivering thermogenesis appears to decline with age. Few investigations have directly linked diminished skeletal muscle shivering thermogenesis with the age-related reduction in cold-induced thermoregulatory capacity. Rather, age-related declines in skeletal muscle mass and metabolic activity are cited as evidence for decreased heat production via shivering. Reduced mass, GDP binding to brown fat mitochondria, and uncoupling protein (UCP) levels are cited as evidence for attenuated brown adipose tissue cold-induced nonshivering thermogenic capacity during aging. The age-related reduction in brown fat nonshivering thermogenic capacity most likely reflects altered cellular signal transduction rather than changes in neural and hormonal signaling. The discussion in this review focuses on how alterations in CIT during the life span may offer insight into possible mechanisms of biological aging. Although the preponderance of evidence presented here demonstrates that CIT declines with chronological time, the mechanism reflecting this attenuated function remains to be elucidated. The inability to draw definitive conclusions regarding biological aging and CIT reflects the lack of a clear definition of aging. It is unlikely that the mechanisms accounting for the decline in cold-induced thermoregulation during aging will be determined until biological aging is more precisely defined.

Cross-training in birds: cold and exercise training produce similar changes in maximal metabolic output, muscle masses and myostatin expression in house sparrows,Passer domesticus

“…However, other studies suggest that metabolic flexibility is not only due to adjustments in lean mass (e.g. muscles), but also results from alterations of the metabolic characteristics of the lean tissue (Florez-Duquet and McDonald, 1998). Further studies are needed to address the question of whether changes in cellular metabolic intensity and lipid transport capacity also contribute to cross-training effects, as they do for migratory and winter phenotypes (Guglielmo, 2010;Swanson, 2010).…”

“…In general, cold acclimation increases MMR Florez-Duquet and McDonald, 1998) and exercise training increases heat production and M sum (McDonald et al, 1988;Shechtman and Talan, 1994) in mammals. Similar experiments monitoring cross-training effects on maximal metabolic outputs for exercise and thermogenesis are less common for birds, despite the primary role of skeletal muscle in generating both M sum and MMR because of the lack of brown fat in birds (Cannon and Nedergaard, 2004;Mezentseva et al, 2008).…”

Vieillissement et rythmes biologiques chez les primates

“…En outre, les différences saisonnières dans l'expression de la torpeur diurne, normalement observées chez les animaux adultes, disparaissent chez les animaux âgés. L'affaiblissement des rythmes de température interne est à mettre en parallèle avec les déficiences observées à différents niveaux du système de thermorégulation, associant baisse de thermogenèse et augmentation des pertes énergétiques au cours du vieillissement [10,14]. Si chez les primates, les apports caloriques, la composition corporelle et les mécanismes qui les régulent évoluent avec l'âge, peu d'approches rythmiques y ont été consacrées.…”

Nitric oxide signaling regulates mitochondrial number and function

“…16 Thus, it is interesting to speculate that insulin signaling and NO-mediated mitochondrial biogenesis may regulate both body weight and lifespan. Along these lines, levels of UCP proteins and mitochrondrial density are decreased during aging, while free radicals increase (reviewed in Florez-Duquet and McDonald 20 ). Paradoxically however, insulin receptor signaling has been proposed to accelerate aging (reviewed in Guarente and Figure 1 Nitric oxide/cGMP-mediated control of mitochondrial biogenesis and energy balance.…”