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Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
So how do we maintain our core body temperature? Several processes either increase or decrease our body temperature. Body temperature is increased mainly by two processes (Figure 11.5 (36)): Non-shivering thermogenesis: While most of our adipose tissue is white adipose tissue, we have two types that can generate heat via the “short cut” protein UCP1. These are brown (37) and so-called beige (or brite) adipose tissue (38). Hormones such as catecholamines, secretin (39) as well as metabolites, myokines and miRNAs regulate the expression of the UCP1 gene or the activity of the heat-generating UCP1 protein which generates heat, raises energy expenditure and has beneficial metabolic effects (39, 40).Muscle contraction in the form of exercise or shivering: Skeletal muscle is an organ that converts the chemical energy of nutrients into work (i.e. muscle contraction and exercise) and heat. For example, during cycling only approximately 20% of the chemical energy is converted into work, whereas 80% of it is typically converted into heat. This is why we become warm when we exercise. Moreover, involuntary muscle contractions during shivering also generate heat via the same mechanism.
Fuel Metabolism in the Fetus
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
Since the fetus is maintained at a controlled temperature, the newborn has to respond to an abrupt decrease in environmental temperature. Thermogenesis is then necessary to maintain body temperature. The anatomical site of this thermogenesis, so-called “nonshivering thermogenesis”, has been recognized as Brown Adipose Tissue.22
Temperature Regulation
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Non-shivering thermogenesis (Figure 68.3) increases metabolic heat production without mechanical work. Heat production is activated by β3-sympathetic activity, which uncouples oxidative phosphorylation in brown fat and skeletal muscle. In adults, lipolysis of adipose tissue releases glycerol and free fatty acids, and the free fatty acids are energy sources for skeletal muscle and myocardium. In the newborn, brown fat is found in interscapular areas, perinephric fat and around intra-abdominal vessels. Brown fat is highly vascular with abundant mitochondria and is richly innervated by adrenergic fibres. In the neonate, non-shivering thermogenesis involving brown fat can increase the metabolic rate twofold above the resting value. In the newborn, triglycerides are hydrolysed to glycerol and free fatty acids, the latter then being re-esterified with the formation of fatty acid acyl CoA. The CoA moiety is replaced by glycerol derived from glucose, whereas the acyl CoA is broken down with the liberation of heat. As each molecule of fatty acid recycles, one ATP is converted to heat. Thus, a small fraction of fatty acid is oxidized rather than re-esterified, and this is reflected by the raised oxygen consumption.
CORM-401, an orally active carbon monoxide-releasing molecule, increases body temperature by activating non-shivering thermogenesis in rats
Published in Temperature, 2022
Mateus R. Amorim, Roberta Foresti, Djamal Eddine Benrahla, Roberto Motterlini, Luiz G. S. Branco
In this study, we have shown that oral administration of CORM-401 to rats leads to an increase in Tb caused by augmented non-shivering thermogenesis without affecting neither the amount of heat loss through the tail skin nor blood pressure. Thus, the present data are consistent with the notion that delivery of controlled amounts of CO to the body causes an increase in Tb associated with an elevated heat production, indicating that this thermoeffector is specifically activated after systemic CO liberation. Moreover, these thermoregulatory responses were not associated with any significant changes in arterial blood pressure. Non-shivering thermogenesis is defined as an increased metabolic heat production (above the basal metabolism) that is not associated with muscle activity but rather resulting mainly from the increased metabolism of brown fat [25].
Human cold habituation: Physiology, timeline, and modifiers
Published in Temperature, 2022
Beau R. Yurkevicius, Billie K. Alba, Afton D. Seeley, John W. Castellani
Human beings, when exposed to cold environments, exhibit a range of adaptations that are dependent on the number, duration, and severity of cold exposures. The primary adaptations that have been documented include a) hypermetabolic, b) insulative, and c) habituated responses [1,2]. A hypermetabolic adaptation has traditionally been defined as an enhancement in metabolic heat production, often through increased shivering thermogenesis, though the data supporting this type of response are sparse [3]. Recent data suggest that non-shivering thermogenesis may be a part of this increased heat production. An insulative adaptation is characterized by a greater degree of cutaneous vasoconstriction, resulting in lower skin temperatures and a reduction in peripheral heat loss. Insulative and hypermetabolic adaptations to the cold are not frequently observed in modern society as humans today typically engage in behavioral thermoregulation aided by the development of modern clothing, heated buildings, and vehicles that allow for the maintenance of thermoneutral microenvironments and comfort in the winter months. Interested readers are referred to excellent reviews for additional information on hypermetabolic and insulative adaptations to chronic cold stress [1,2,4,5].
Skeletal muscle plasticity and thermogenesis: Insights from sea otters
Published in Temperature, 2022
Traver Wright, Melinda Sheffield-Moore
Although the metabolic rate in resting skeletal muscle is low, it can rapidly increase to support metabolic demand. In skeletal muscle, this increased demand often powers muscle contractions for movement during physical activity, but can also increase for thermogenesis. Increased metabolic heat production can result from shivering (thermogenic muscle contractions that do not support functional movement), or nonshivering thermogenesis. Nonshivering thermogenesis has the advantage of not requiring muscle contraction to increase cellular energy expenditure. Instead, the sequestration of ions in membrane-bound intracellular chambers is made less efficient by “leaky” membranes. This leak requires additional energy expenditure to maintain trans-membrane concentration gradients, and includes proton leak across the inner mitochondrial membrane (where the proton gradient is used to generate ATP) as well as sarcolipin-mediated leak of sequestered calcium from the sarcoplasmic reticulum [4]. Through these mechanisms, skeletal muscle tissue contributes significantly to thermogenesis. Skeletal muscle metabolic capacity must be maintained at a level adequate to support not only thermogenesis, but also peak simultaneous demands for sustained physical activity and cellular maintenance. While increased demand for physical activity (e.g. endurance exercise training) is recognized as the primary work-producing stimulus to upregulate skeletal muscle aerobic capacity, the role of cold exposure is often underappreciated for its ability to stimulate an upregulation of metabolic capacity and thermogenic leak.