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Metabolic Heat Production (metabolic + heat_production)

Distribution by Scientific Domains

Life Sciences	80%

Selected Abstracts

Metabolic Heat Production, Heat Loss and the Circadian Rhythm of Body Temperature in the Rat

EXPERIMENTAL PHYSIOLOGY, Issue 3 2003
Roberto Refinetti
Metabolic heat production (calculated from oxygen consumption), dry heat loss (measured in a calorimeter) and body temperature (measured by telemetry) were recorded simultaneously at 6 min intervals over five consecutive days in rats maintained in constant darkness. Robust circadian rhythmicity (confirmed by chi square periodogram analysis) was observed in all three variables. The rhythm of heat production was phase-advanced by about half an hour in relation to the body temperature rhythm, whereas the rhythm of heat loss was phase-delayed by about half an hour. The balance of heat production and heat loss exhibited a daily oscillation 180 deg out of phase with the oscillation in body temperature. Computations indicated that the amount of heat associated with the generation of the body temperature rhythm (1.6 kJ) corresponds to less than 1% of the total daily energy budget (172 kJ) in this species. Because of the small magnitude of the fraction of heat balance associated with the body temperature rhythm, it is likely that the daily oscillation in heat balance has a very slow effect on body temperature, thus accounting for the 180 deg phase difference between the rhythms of heat balance and body temperature. [source]

Central control of thermogenesis in mammals

EXPERIMENTAL PHYSIOLOGY, Issue 7 2008
Shaun F. Morrison
Thermogenesis, the production of heat energy, is an essential component of the homeostatic repertoire to maintain body temperature in mammals and birds during the challenge of low environmental temperature and plays a key role in elevating body temperature during the febrile response to infection. The primary sources of neurally regulated metabolic heat production are mitochondrial oxidation in brown adipose tissue, increases in heart rate and shivering in skeletal muscle. Thermogenesis is regulated in each of these tissues by parallel networks in the central nervous system, which respond to feedforward afferent signals from cutaneous and core body thermoreceptors and to feedback signals from brain thermosensitive neurons to activate the appropriate sympathetic and somatic efferents. This review summarizes the research leading to a model of the feedforward reflex pathway through which environmental cold stimulates thermogenesis and discusses the influence on this thermoregulatory network of the pyrogenic mediator, prostaglandin E2, to increase body temperature. The cold thermal afferent circuit from cutaneous thermal receptors ascends via second-order thermosensory neurons in the dorsal horn of the spinal cord to activate neurons in the lateral parabrachial nucleus, which drive GABAergic interneurons in the preoptic area to inhibit warm-sensitive, inhibitory output neurons of the preoptic area. The resulting disinhibition of thermogenesis-promoting neurons in the dorsomedial hypothalamus and possibly of sympathetic and somatic premotor neurons in the rostral ventromedial medulla, including the raphe pallidus, activates excitatory inputs to spinal sympathetic and somatic motor circuits to drive thermogenesis. [source]

Partial-body exposure of human volunteers to 2450,MHz pulsed or CW fields provokes similar thermoregulatory responses,

BIOELECTROMAGNETICS, Issue 4 2001
Eleanor R. Adair
Abstract Many reports describe data showing that continuous wave (CW) and pulsed (PW) radiofrequency (RF) fields, at the same frequency and average power density (PD), yield similar response changes in the exposed organism. During whole-body exposure of squirrel monkeys at 2450 MHz CW and PW fields, heat production and heat loss responses were nearly identical. To explore this question in humans, we exposed two different groups of volunteers to 2450,MHz CW (two females, five males) and PW (65,,s pulse width, 104,pps; three females, three males) RF fields. We measured thermophysiological responses of heat production and heat loss (esophageal and six skin temperatures, metabolic heat production, local skin blood flow, and local sweat rate) under a standardized protocol (30,min baseline, 45,min RF or sham exposure, 10,min baseline), conducted in three ambient temperatures (Ta,=,24, 28, and 31°C). At each Ta, average PDs studied were 0, 27, and 35,mW/cm2 (Specific absorption rate (SAR),=,0, 5.94, and 7.7,W/kg). Mean data for each group showed minimal changes in core temperature and metabolic heat production for all test conditions and no reliable differences between CW and PW exposure. Local skin temperatures showed similar trends for CW and PW exposure that were PD-dependent; only the skin temperature of the upper back (facing the antenna) showed a reliably greater increase (P,=,.005) during PW exposure than during CW exposure. Local sweat rate and skin blood flow were both Ta - and PD-dependent and showed greater variability than other measures between CW and PW exposures; this variability was attributable primarily to the characteristics of the two subject groups. With one noted exception, no clear evidence for a differential response to CW and PW fields was found. Bioelectromagnetics 22:246,259, 2001. © 2001 Wiley-Liss, Inc. [source]

Kinetics of the Action of Na2SeO3 on Bacillus subtilis Growth as Studied by Microcalorimetry

CHINESE JOURNAL OF CHEMISTRY, Issue 2 2002
Yi Liu
Abstract Microcalorimetric bioassay for acute cellular toxicity is based on metabolic heat production from cultured cells. The biological response to toxicants is the inhibition of the heat production rate in cells, and toxicity is expressed as the concentration of toxicant that is 50% effective in this inhibition (IC50). In mis paper, the effect of Na2SeO3 on Bacillus subtilis growth was investigated at 37 °C by microcalorimetry. The relationship between growth rate constants (k) and concentration of Na2SeO3 (c) shows a logarithmic normal distribution, and lC50 is 20.3 ,g/mL. All these thermokinetic information is readily obtained by an LKB 2277,204 heat conduction microcalorimeter. Microcalorimetry is a quantitative, inexpensive, and versatile method for toxicology research. [source]