Resting Heat Production Research Articles

A mathematical model to quantify RYR Ca2+ leak and associated heat production in resting human skeletal muscle fibers.

Cycling of Ca2+ between the sarcoplasmic reticulum (SR) and myoplasm is an important component of skeletal muscle resting metabolism. As part of this cycle, Ca2+ leaks from the SR into the myoplasm and is pumped back into the SR using ATP, which leads to the consumption of O2 and generation of heat. Ca2+ may leak through release channels or ryanodine receptors (RYRs). RYR Ca2+ leak can be monitored in a skinned fiber preparation in which leaked Ca2+ is pumped into the t-system and measured with a fluorescent dye. However, accurate quantification faces a number of hurdles. To overcome them, we developed a mathematical model of Ca2+ movement in these preparations. The model incorporated Ca2+ pumps that move Ca2+ from the myoplasm to the SR and from the junctional space (JS) to the t-system, Ca2+ buffering by EGTA in the JS and myoplasm and by buffers in the SR, and Ca2+ leaks from the SR into the JS and myoplasm and from the t-system into the myoplasm. The model accurately simulated Ca2+ uptake into the t-system, the relationship between myoplasmic [Ca2+] and steady-state t-system [Ca2+], and the effect of blocking RYR Ca2+ leak on t-system Ca2+ uptake. The magnitude of the leak through the RYRs would contribute ∼5% of the resting heat production of human muscle. In normal resting fibers, RYR Ca2+ leak makes a small contribution to resting metabolism. RYR-focused pathologies have the potential to increase RYR Ca2+ leak and the RYR leak component of resting metabolism.

Compensating for changes in heart muscle resting heat production in a microcalorimeter.

The heat production of cardiac muscle, determined by calorimetry, can be used as a measure of cardiac metabolism. However, heat produced while a muscle is actively-shortening, thereby performing force-length work, comprises both active and basal metabolic processes. In this paper, we present a method for post-experimental processing of calorimetric measurements of muscle heat production, that uncovers and compensates for the measured basal heat rate during work. In this method, the relationships between muscle length, velocity of length change and muscle heat output are coupled with a simulation of the measurement instrument, providing a model-based estimate of change of measured basal heat while the muscle is performing work. We demonstrate the use of this technique in an experiment conducted on a working cardiac muscle sample. The ability to identify the various components of heat release in these muscles provides useful insight into their mechanical and energetic capabilities.

Great Hornbill Casque Functions as a Thermoregulatory Radiator

Hornbills (Bucerotidae) are defined by their casques, structures that are extensions of the beak. The purpose of these structures, which take diverse forms, has been subject to speculation. In this study, it is asserted that a primary function of the casque is thermoregulation, its large vascularised surface area functioning as a structure to facilitate heat exchange. Infrared thermography on a Great Hornbill (Buceros bicornis) revealed that the bird’s casque exhibited significant percentage of heat loss in relation to the body's resting heat production along a temperature gradient of 19.2 to 34.2°C. The results indicate that the casque is capable of dissipating a disproportionate amount of heat in relation to the rest of its body and even comparable to major thermal windows in other animals.

Human energy expenditure: advances in organ‐tissue prediction models

Humans expend energy at rest (REE), and this major energy exchange component is now usually estimated using statistical equations that include weight and other predictor variables. While these formulas are useful in evaluating an individual's or group's REE, an important gap remains: available statistical models are inadequate for explaining underlying organ-specific and tissue-specific mechanisms accounting for resting heat production. The lack of such systems level REE prediction models leaves many research questions unanswered. A potential approach that can fill this gap began with investigators who first showed in animals and later in humans that REE reflects the summated heat production rates of individual organs and tissues. Today, using advanced imaging technologies, REE can be accurately estimated from the measured in vivo mass of 10 organ-tissue mass components combined with their respective mass-specific metabolic rates. This review examines the next frontier of energy expenditure models and discusses how organ-tissue models have the potential not only to better predict REE but also to provide insights into how perturbations in organ mass lead to structure-function changes across other interacting organ systems. The introductory ideas advanced in this review provide a framework for future human energy expenditure modelling research.

Body size and human energy requirements: reduced mass-specific resting energy expenditure in tall adults

Two observations favor the presence of a lower mass-specific resting energy expenditure (REE/weight) in taller adult humans: an earlier report of height (H)-related differences in relative body composition; and a combined model based on Quetelet and Kleiber's classic equations suggesting that REE/weight proportional, variantH(-0.5). This study tested the hypothesis stating that mass-specific REE scales negatively to height with a secondary aim exploration of related associations between height, weight (W), surface area (SA), and REE. Two independent data sets (n = 344 and 884) were evaluated, both with REE measured by indirect calorimetry and the smaller of the two including fat estimates by dual-energy X-ray absorptiometry. Results support Quetelet's equation (W proportional, variantH(2)), but Kleiber's equation approached the interspecific mammal form (REE proportional, variantW(0.75)) only after adding adiposity measures to weight and age as REE predictors. REE/weight scaled as H( approximately (-0.5)) in support of the hypothesis with P values ranging from 0.17 to <0.001. REE and SA both scaled as H( approximately 1.5), and REE/SA was nonsignificantly correlated with height in all groups. These observations suggest that adiposity needs to be considered when evaluating the intraspecific scaling of REE to weight; that relative to their weight, taller subjects require a lower energy intake for replacing resting heat losses than shorter subjects; that fasting endurance, approximated as fat mass/REE, increases as H(0.5); and that thermal balance is maintained independent of stature by evident stable associations between resting heat production and capacity of external heat release. These observations have implications for the modeling of adult human energy requirements and associate with anthropological concepts founded on body size.

Metabolism after injury. 2. Effect of a dryish and warm environment on skin temperatures and electrolyte responses.

Abstract Patients with moderate to severe fractures of the major long bones of the lower limb had generally warmer extremities if nursed in cubicles with a dryish (35–45 per cent relative humidity) and warm (29–30° C.) environment than if maintained at a normal temperature of 20–24° C. The additional heat was applied soon after the period of shock was over and was then provided for a further 10–12 days thereafter. The effect of a higher temperature in reducing the protein catabolic response to injury–which seems mainly to involve an increase in the catabolism of some muscle proteins accompanied by increased urinary excretions of potassium, creatine, and zinc–has already been described (Cuthbertson, Fell, Smith, and Tilstone, 1972). The effects of a warmer atmosphere on oral and skin temperatures over various surfaces are described in the present paper and these effects are compared with those found when extra bed coverings are applied under normal ward environmental conditions (20–22° C.). By the application of such heat the skin temperature of the extremities can be raised several degrees; that of the large toes by as much as 12° C. By the use of extra bed coverings conductive losses can undoubtedly be diminished, particularly at normal temperatures. Oral, axillary, and frontal and mastoid process temperatures are not apparently influenced by a higher environmental temperature but appear to be mainly related to the degree of traumatic fever. The advantage of the higher environmental temperature over extra bed coverings is presumed to be mainly in reducing total resting heat production from resting to basal values by providing thermoneutral conditions. Apart from a significant reduction in the rise in serum potassium around the fifth day after injury and a reduction in the normal increased urinary excretion of potassium previously noted, there were no significant changes in the concentration of other serum electrolytes as a result of the higher environmental temperature, nor were the other characteristic electrolyte patterns of urinary excretion altered by the change in the ambient temperature. There were also no distinctive differences in the pattern of urinary amino-acids at the two temperatures.

Effect of once daily 5-h or 10-h cold-exposures on body temperature and resting heat production of beef cattle

Twelve yearling crossbred beef heifers weighing 454 ± 31 kg were randomly assigned to either 0 h (control), 5 h (5CE; 0800 to 1300) or 10 h (10CE; 0800 to 1800) of cold exposure (-20°C) daily to determine the effect of daily cold exposures of different durations on body core temperature and resting heat production of beef cattle. Treatments were imposed for a 21-d period (seven intervals of 3 d duration) using two replications with two heifers per treatment × replication combination. Heifers were group housed outdoors in a pen with overhead shade at one end and were moved daily at 0800 to a group pen in either a control room or an environmental chamber set at -20°C. After the 21-d period was completed, resting heat production was measured in a thermal neutral environment for 5 h. Vaginal temperature (Tvag) was continuously monitored using radiotransmitters. Treatment did not affect daily maximum, mean or minimum Tvag, the amount of time spent at Tvag exceeding daily mean Tvag, or the variability of Tvag (P ≥ 0.29). However, when examined within specific phases of the day, treatment effects on Tvag were found. Tvag was elevated 0.24°C (5CE) and 0.35°C (10CE) during the daily first 5 h of cold-exposure (10CE = 5CE &gt; control; P = 0.02) throughout the entire 21-d trial. During other times of the day there was no effect of treatment on Tvag but treatment × interval was significant (P ≤ 0.02) during the 6–10 h from initiation of cold-exposure when the 10CE group remained in the cold but the 5CE group had been returned to the outdoor pen. The Tvag of the 10CE and 5CE heifers was elevated at this time of day compared to control heifers, but only during the first 4 to 6 d (5CE) or 7 to 9 d (10CE) of the trial. These results indicate that thermoregulatory mechanisms that control core body temperature undergo habituation and the timecourse of habituation depends on the duration of daily cold- exposure. Resting heat production was unaffected by the two durations of cold-exposure examined (P = 0.55), suggesting that metabolic acclimation does not occur in response to intermittent cold-exposure of beef cattle. Key words: Beef heifers, vaginal temperature, resting heat production, environment, cold duration

Metabolic rate is not reduced by dietary-restriction or by lowered insulin/IGF-1 signalling and is not correlated with individual lifespan in Drosophila melanogaster

The link between resting metabolic rate and aging, measured as adult lifespan, was investigated in Drosophila melanogaster by (i) comparing lifespan and metabolic rate of individual flies, (ii) examining the effect of dietary-restriction on the metabolic rate of adult flies, and (iii) comparing the metabolic rate of wild-type and insulin/IGF-1 signalling mutant chico 1 flies. The resting oxygen consumption of 65 individually housed and fully fed Drosophila was measured weekly throughout their lifetime. There was no significant difference in the mass-specific rate of oxygen consumption between cohorts that differed in lifespan. Nor was there any statistical correlation between mass-specific oxygen consumption and lifespan of individual Drosophila. The average mass-specific rate of oxygen consumption at 25 °C was 3.52±0.07 μl O 2 mg −1 h −1. Variation in mass-specific metabolic rate explained only 4% of variation in individual life span in these flies. Contrary to predictions from the ‘rate of living’ theory of aging lifetime oxygen consumption was not constant and the lifespan of individual flies accounted for 91% of their lifetime oxygen consumption. An average Drosophila consumes about 3 ml O 2 during its adult life. Dietary-restriction had no effect on mass-specific resting metabolic rate both when measured as oxygen consumption by respirometry and when measured as heat production by microcalorimetry. The mass-specific resting heat production of fully fed adult flies at 25 °C averaged 17.3±0.3 μW mg −1. Similarly there was no difference in mass-specific metabolic rate of wild-type flies and longliving chico 1 insulin/IGF-1 signalling mutant flies, either when measured as oxygen consumption or heat production. Thus, individual variation in lifespan in wild-type flies, and life extension by dietary-restriction and reduced insulin/IGF-1 signalling is not attributable to differences in metabolic rate.

Rhoads Lecture. Heat and life: the ongoing scientific odyssey.

The source of body heat has fascinated philosophers and scientists for millennia. Resting heat production is a major component of human energy requirements in health and disease. This review traces through mankind's attempts to understand the nature of resting heat production in humans and animals and its relationships to body mass and composition. Far from being fully understood, the study of heat production is an area of intense research interest bridging the gap between modern biology and physics.

Ontogeny of thermoregulatory mechanisms in king penguin chicks ( Aptenodytes patagonicus)

The rapid maturation of thermoregulatory mechanisms may be of critical importance for optimising chick growth and survival and parental energy investment under harsh climatic conditions. The ontogeny of thermoregulatory mechanisms was studied in growing king penguin chicks from hatching to the full emancipation observed at 1 month of age in the sub-Antarctic area (Crozet Archipelago). Newly hatched chicks showed small, but significant regulatory thermogenesis (21% rise in heat production assessed by indirect calorimetry), but rapidly became hypothermic. Within a few days, both resting (+32%) and peak (+52%) metabolic rates increased. The first week of life was characterised by a two-fold rise in thermogenic capacity in the cold, while thermal insulation was not improved. During the second and third weeks of age, thermal insulation markedly rose (two-fold drop in thermal conductance) in relation to down growth, while resting heat production was slightly reduced (−13%). Shivering (assessed by electromyography) was visible right after hatching, although its efficiency was limited. Thermogenic efficiency of shivering increased five-fold with age during the first weeks of life, but there was no sign of non-shivering thermogenesis. We conclude that thermal emancipation of king penguin chicks may be primarily determined by improvement of thermal insulation after thermogenic processes have become sufficiently matured. Both insulative and metabolic adaptations are required for the rapid ontogeny of thermoregulation and thermal emancipation in growing king penguin chicks.

Effects of intermittent cold exposure varying in intensity on core body temperature and resting heat production of beef cattle

Crossbred beef heifers (n = 18) fed at 1.3× maintenance were exposed to summer daytime temperatures (20 ± 0.2°C) for 8 h (08:00 until 16:00) and to control (22°C), moderate (–6°C) or cold (–15°C) environments for 16 h daily (16:00 until 08:00) for a minimum 21-d adaptation period to investigate the effects of in tensity of intermittent cold exposure on vaginal temperature and resting heat production. Resting heat production was measured at the end of the adaptation period. Vaginal temperature was continuously monitored throughout the experiment using radiotelemetry. Vaginal temperature increased immediately after the onset of cold exposure in both moderate and cold treatments, peaked after 3 h, and returned to pre-exposure levels by the time the 16-h treatment ended. In contrast, vaginal temperatures of control heifers peaked only after feeding at 08:30. Treatment did not affect daily maximum (P= 0.60), mean (P = 0.72) or minimum (P = 0.34) vaginal temperatures, but heifers in both cold-exposed treatments spent more time (P = 0.03) with vaginal temperatures exceeding the daily mean vaginal temperature than control heifers. Compared to control heifers, the variability of vaginal temperature increased 1.8- and 2.2-fold in the moderate and cold treatments, respectively (P = 0.04), and did not change with time (P = 0.98 ). Resting heat production did not increase following 21 d of exposure to moderate and cold conditions. Results of this study indicate that intermittent cold exposure influenced circadian body temperature rhythms without increasing resting heat production. Key words: Beef cattle, thermoregulation, vaginal temperature, heat production.

A comparison of no-flow and low-flow ischemia in the rat heart: an energetic study

Heat production under no-flow ischemia (ISCH) and under hypoperfusion (HYP) conditions was measured in single isovolumetric contractions of perfused rat ventricles at 25°C. Resting heat production (Hr) and resting pressure decreased when the perfusion rate was reduced from 6 to 1.5 mL·min-1 or lower flows (HYP) and by ISCH. Maximal developed pressure (P) decreased to 29% and 20% of control by HYP at 0.8 mL·min–1 and ISCH, respectively. The tension-independent heat (TIH) fraction attributed to Ca2+-binding, measured during single contractions, decreased under HYP with an increase in the ratio between the maximum relaxation rate and P (–P/P ratio). The TIH fractions (attributed to Ca2+ binding and Ca2+ removal processes) decreased under ISCH. The long duration TIH fraction associated with Ca2+-dependent mitochondrial activity disappeared at flow rates of 1.5 mL·min–1 or lower. The ratio between the tension-dependent energy release and P was decreased by ISCH but not by HYP, indicating that under ISCH there was an improvement in contractile economy, but this was not modified by HYP. Overall, the results indicate that no-flow and low-flow ischemias are energetically different models. While the contractile failure under HYP seems to be related to a decrease in myofilament Ca2+ sensitivity, under ISCH it appears to be related to decreased cytosolic Ca2+ availability combined with a more noticeable effect on a fraction of energy that has been attributed to mitochondrial activity. Furthermore, mechanical and energetic responses of both models (i.e., ISCH and HYP) found in the present work were not the same as those previously observed in severe hypoxia so that all these models should not be used indistinctly.Key words: calorimetry, hypoperfusion, ischemia, muscle economy, tension-dependent heat, tension-independent heat.

A comparison of no-flow and low-flow ischemia in the rat heart: an energetic study

Heat production under no-flow ischemia (ISCH) and under hypoperfusion (HYP) conditions was measured in single isovolumetric contractions of perfused rat ventricles at 25 degrees C. Resting heat production (Hr) and resting pressure decreased when the perfusion rate was reduced from 6 to 1.5 mL min(-1) or lower flows (HYP) and by ISCH. Maximal developed pressure (P) decreased to 29% and 20% of control by HYP at 0.8 mL min(-1) and ISCH, respectively. The tension-independent heat (TIH) fraction attributed to Ca2+-binding, measured during single contractions, decreased under HYP with an increase in the ratio between the maximum relaxation rate and P (-P/P ratio). The TIH fractions (attributed to Ca2+ binding and Ca2+ removal processes) decreased under ISCH. The long duration TIH fraction associated with Ca2+-dependent mitochondrial activity disappeared at flow rates of 1.5 mL min(-1) or lower. The ratio between the tension-dependent energy release and P was decreased by ISCH but not by HYP, indicating that under ISCH there was an improvement in contractile economy, but this was not modified by HYP. Overall, the results indicate that no-flow and low-flow ischemias are energetically different models. While the contractile failure under HYP seems to be related to a decrease in myofilament Ca2+ sensitivity, under ISCH it appears to be related to decreased cytosolic Ca2+ availability combined with a more noticeable effect on a fraction of energy that has been attributed to mitochondrial activity. Furthermore, mechanical and energetic responses of both models (i.e., ISCH and HYP) found in the present work were not the same as those previously observed in severe hypoxia so that all these models should not be used indistinctly.

Increased myocardial oxygen consumption and resting heat production, as measured by microcalorimetry, after propranolol and carvedilol treatment: Is there a partial agonistic effect in the rat?

This study investigated the influence of β-blockade on the resting heat production of myocardial tissue by microcalorimetry. During one week, propranolol (β1β2-adrenoceptor antagonist) was orally given to 14 rats − 5 mg kg−1 once daily, and carvedilol (β1β2- and α1-antagonist) to eight rats − 3 mg kg−1 once daily; 36 rats were controls. Thin slices of cardiac tissue, ≈10 mg, were removed from the apex. Carbogen-saturated Krebs-Ringer bicarbonate buffer with glucose as substrate was pumped through the microcalorimetric ampoule during the measurement at 37°C. Unexpectedly, the mean resting heat production was higher after both propranolol, 1.25 mW g−1 wet tissue (p < 0.01, ANOVA) and carvedilol, 1.19 mW g−1 (p < 0.05) treatments, than in the control group, 1.01 mW g−1. The same applied to oxygen consumption. The calculated anaerobic fractions were 16, 8 and 24% in the respective groups, but differences were not significant. Also, when added in vitro, propranolol caused an enhanced myocardial resting heat production by an average of 23%. As resting myocardial metabolism contributes to the overall cardiac energetics to a relatively minor extent, the net result of treatment will probably be of only marginal physiological importance. The experimental outcome is indicative of a stimulation of resting myocardial metabolic activity after propranolol and carvedilol, rather than a predicted decrease. We hypothesize that the absence of anything to depress in the non-beating heart tissue, reveals a small degree of partial β-agonist activity, possibly via the newly discovered β3-adrenoceptor.

The energetics of the quiescent heart muscle: high potassium cardioplegic solution and the influence of calcium and hypoxia on the rat heart

Heart basal metabolism has been classically studied as the energy expenditure of those processes unrelated to mechanical activity and often measured by rendering the heart inactive using cardioplegic solutions (usually by increasing extracellular K concentration ([Kle]). In arterially perfused rat heart (at 25 degrees C), raising [K]e from 7 to 25 mM at a constant extracellular Ca concentration ([Ca]e) (0.5 mM), induced an increase in resting heat production (Hr) from 4.1 +/- 0.3 to 5.1 +/- 0.3 mol. wt g-1. Under 25 mM K additional increase in [Ca]e further increased Hr to 6.0 +/- 0.4, 7.0 +/- 0.4 and 8.3 +/- 0.9 mol. wt g-1 for 1, 2 and 4 mM Ca, respectively. While under 7 mM K perfusion Hr was not affected by 4 microM verapamil, under 25 mM K and 2 mM Ca 0.4 microM verapamil induced a decrease in Hr (-1.6 +/- 0.2 mol. wt g-1, n = 5, P < 0.001). Caffeine increased Hr under 0.5 mM Ca and 7 mM K perfusion (+0.32 +/- 0.06 and +1.19 +/- 0.25 mol. wt g-1 for 1 and 5 mM caffeine respectively), but under 25 mM K conditions Hr was not affected by caffeine 2 mM. Severe hypoxia decreased Hr under both 7 and 25 mM K (3.7 +/- 0.5 to 2.7 +/- 0.4 mol. wt g-1 and 7.0 +/- 0.4 to 2.2 +/- 0.5 mol. wt g-1, respectively) suggesting that the increased Hr associated with the verapamil sensitive fraction of heat released is associated to a mitochondrial mechanism. Therefore, the use of high [K]e overestimates basal values by increasing a verapamil sensitive fraction of the energy released. In addition, high [K]e modifies a caffeine sensitive energy component probably due to a depletion of caffeine-dependent Ca stores.

The effect of hyperosmolality on the rate of heat production of quiescent trabeculae isolated from the rat heart.

We have measured the rate of heat production of isolated, quiescent, right ventricular trabeculae of the rat under isosmotic and hyperosmotic conditions, using a microcalorimetric technique. In parallel experiments, we measured force production and intracellular calcium concentration ([Ca2+]i). The rate of resting heat production under isosmotic conditions (mean +/- SEM, n = 32) was 100 +/- 7 mW (g dry wt)-1; it increased sigmoidally with osmolality, reaching a peak that was about four times the isosmotic value at about twice normal osmotic pressure. The hyperosmotic thermal response was: (a) abolished by anoxia, (b) attenuated by procaine, (c) insensitive to verapamil, ouabain, and external calcium concentration, and (d) absent in chemically skinned trabeculae bathed in low-Ca2+ "relaxing solution." Active force production was inhibited at all osmolalities above isosmotic. Passive (tonic) force increased to, at most, 15% of the peak active force developed under isosmotic conditions while [Ca2+]i increased, at most, 30% above its isosmotic value. We infer that hyperosmotic stimulation of resting cardiac heat production reflects, in large part, greatly increased activity of the sarcoplasmic reticular Ca2+ ATPase in the face of increased efflux via a procaine-inhibitable Ca(2+)-release channel.

Thermogenic effect of two β-adrenoceptor blocking drugs, propranolol and carvedilol, on skeletal muscle in rats. A microcalorimetric study

Abstract This study investigated the influence of the prototype β1β2-adrenoceptor antagonist propranolol and the novel carvedilol (β1β2- and α1-antagonist) on the thermogenesis of skeletal muscle ex vivo. During 1 week propranolol was given orally to 14 rats, 5 mg kg−1 once daily, and carvedilol was given to 23 rats, 3 mg kg−1 once daily; 19 rats received saline. Gastrocnemius muscle was obtained after decapitation. Carbogen-saturated Krebs—Ringer bicarbonate buffer containing glucose — insulin was pumped via heat exchangers through the microcalorimetric ampoule during the measurement procedure, starting within 50 min after the biopsies. The results showed that the mean resting heat production at 37°C was lower (p

The energy expenditure of actomyosin-ATPase, Ca(2+)-ATPase and Na+,K(+)-ATPase in guinea-pig cardiac ventricular muscle.

1. The rate of heat production (heat rate) and isometric twitch tension of ventricular trabeculae isolated from guinea-pig heart were measured at 37 degrees C in order to determine the relative contributions of actomyosin-ATPase, Ca(2+)-ATPase and Na+,K(+)-ATPase to myocardial energy metabolism. 2. The increase in heat rate recorded during isometric contractions at optimal length (contraction-related heat production) was 19.1 +/- 1.2 mW cm-3 at a stimulation rate of 2 Hz. The tension-time integral of individual contractions measured under the same conditions was 147 +/- 15 mM s cm-2. 3. The heat production of the actomyosin-ATPase was determined by inhibiting the contractile proteins with 2,3-butanedione monoxime (BDM). Contraction-related heat production was reduced by 0.219 +/- 0.010 and the isometric tension-time integral was reduced by 0.288 +/- 0.016 in the presence of 1 mM BDM. From these data an estimate of 0.76 for the relative contribution of the actomyosin-ATPase to contraction-related heat production was derived. 4. The heat production related to actomyosin-ATPase plus Ca(2+)-ATPase was studied by blocking Ca2+ influx into the myocardial cells with a solution containing 100 microM Ca2+ and 400 microM Ni2+. In this solution contraction-related heat production was reduced by 0.907 +/- 0.012. Comparison of this value with the component attributable to the actomyosin-ATPase yields an estimate of 0.15 for the relative contribution of the Ca(2+)-ATPase to contraction related heat production. 5. The heat production related to the Na+,K(+)-ATPase in resting preparations was studied by blocking the sodium pump with 400 microM dihydro-ouabain (DHO). DHO produced a transient decrease in heat rate lasting 1-2 min, which was followed by a secondary increase. From the heat transient produced by DHO the heat rate related to the Na+,K(+)-ATPase in the steady state was extrapolated. The relative contribution of the sodium pump to resting heat production was estimated to be 0.17. 6. The heat production related to the Na+,K(+)-ATPase in contracting preparations was studied by first blocking Ca2+ influx with 100 microM Ca2+ and 400 microM Ni2+, and then inhibiting the sodium pump with 400 microM dihydro-ouabain (DHO). The relative contribution of the sodium pump to contraction-related heat production extrapolated from these data was 0.10, which agreed well with the fraction of contraction-related heat production persisting after blockage of actomyosin-ATPase and Ca(2+)-ATPase (0.09).(ABSTRACT TRUNCATED AT 400 WORDS)

THE COOLING POWER OF THE PIGEON HEAD

Resting pigeons preheated to a stable core temperature of 43.2 &deg;C, which is within the range of body temperatures recorded during flight, were able to cool their body at high rates if their head and upper neck were exposed to an air stream at 23.5 &deg;C. The heat dissipation capacity of the head and neck, estimated from measurements made at a wind speed (100 km h-1) corresponding to fast flight, was 9.8 W, or 4.5 times the resting heat production. Since the greater part of this capacity, about 8 W, was attributable to the inner surfaces of the mouth, ram ventilation of the buccal cavity appears to be an important mechanism for increasing evaporative heat loss during flight. Accordingly, wind-assisted mouth cooling should be utilized by resting pigeons, since exposure to a slight breeze (approximately 10 km h-1) could augment their dissipating power by an amount equivalent to their resting metabolic rate. It is concluded that beak opening, together with a source of convection other than panting and gular flutter, is required to exploit fully the heat dissipation capacity of the buccopharyngeal mucosa of birds.

Effects of terbutaline on basal thermogenesis of human skeletal muscle and Na‐K pump after 1 week of oral use—a placebo controlled comparison with propranolol.

1. A double-blind placebo-controlled study was conducted on the effects of oral terbutaline (beta 2-adrenoceptor agonist) and propranolol (beta 1 beta 2-adrenoceptor antagonist) on basal heat production of skeletal muscle, measured ex vivo by direct microcalorimetry. Terbutaline slow-release 7.5 mg, propranolol 80 mg, and matching placebo were randomly administered twice daily for 1 week to 15 healthy males, using a cross-over design. 2. Resting heat production in biopsied vastus lateralis was lowered by median 27% (P < 0.01) after terbutaline medication as compared with placebo. The cause of this hypometabolism at the cellular level is obscure but may possibly be explained by desensitization of beta 2-receptors. 3. Propranolol decreased the metabolic rate by 17% (P > 0.3); this might imply that the sympathetic nervous system is playing only a minor role in the regulation of basal metabolic rate in muscle, or that up-regulation of beta-receptors had influenced the decline. 4. The muscle utilized about 6% of its total energy for the Na-K pump as assessed after inhibition by ouabain. 5. Serum potassium was significantly lowered by terbutaline and slightly increased by propranolol with no relationship between changes in extracellular levels and muscle content of potassium under resting conditions. Energy values for the Na-K pump in muscle after 1 week of terbutaline or propranolol medication were similar to placebo. The results are not consistent with the hypothesis that decreased serum potassium during continuous beta 2-adrenoceptor agonist treatment is due to a chronically activated Na-K pump, at least not in resting muscle.