Increase In Basal Metabolic Rate Research Articles

Thermoregulatory and metabolic phenotypes of mice lacking noradrenaline and adrenaline.

Adrenaline and noradrenaline, the main effectors of the sympathetic nervous system and adrenal medulla, respectively, are thought to control adiposity and energy balance through several mechanisms. They promote catabolism of triglycerides and glycogen, stimulate food intake when injected into the central nervous system, activate thermogenesis in brown adipose tissue, and regulate heat loss through modulation of peripheral vasoconstriction and piloerection. Thermogenesis in brown adipose tissue occurs in response to cold and overeating (diet induced), and there is an inverse relationship between diet-induced thermogenesis and obesity both in humans and in animal models. As a potential model for obesity, we generated mice that cannot synthesize noradrenaline or adrenaline by inactivating the gene that encodes dopamine beta-hydroxylase. These mice are cold intolerant because they have impaired peripheral vasoconstriction and are unable to induce thermogenesis in brown adipose tissue through uncoupling protein (UCP1). The mutants have increased food intake but do not become obese because their basal metabolic rate is also elevated. The unexpected increase in basal metabolic rate is not due to hyperthyroidism, compensation by the widely expressed uncoupling protein UCP2, or shivering.

Limits to Sustained Metabolic Rate: The Link between Food Intake, Basal Metabolic Rate, and Morphology in Reproducing Mice, Mus musculus

Thirty virgin female white (MF1) mice (Mus musculus) were divided into three groups: an unmated control group; a second, mated group, allowed to proceed to peak gestation; and a third, mated group, allowed to proceed to peak lactation. Nine unmated animals and eight of each of the two mated groups had their basal metabolism (oxygen consumption at 28° C) measured and were then killed by means of a CO₂ overdose, and the wet masses of 14 different body components measured. Body mass of the control animals averaged 26.5 g, not significantly different from animals in the other two groups immediately postmating. At peak gestation body mass averaged 50.5 g, immediate postpartum mass was 35.5 g, and by the end of lactation it was 38. 4 g. Basal metabolic rate (BMR) of the control animals (0.313 W) was significantly lower than the BMR of both pregnant (0.78 W) and lactating (0.95 W) animals. Food intake of controls was 97.9 kJ d⁻¹ (3.6 X BMR). At peak gestation food intake was 119.3 kJ d⁻¹ (2.4 X BMR), and at peak lactation it was 405.5 kJ d⁻¹ (5.96 X BMR). If BMR had not increased throughout reproduction, the peak food intake would have represented 12.2 times BMR. Morphological changes associated with the reproductive cycle mainly included increases in the masses of the alimentary tract, liver, kidneys, heart, and lungs. A principal components analysis revealed four major dominant axes of variability in the morphology. The first principal component was dominated by the combined alimentary effects and explained 71.8% of the variation in BMR. These data are consistent with the hypotheses that maximal sustainable metabolic rate reflects a link between structure of the alimentary tract, maximal daily food assimilation, and BMR. That is, as mice progressed through reproduction, their increasing food requirements were beyond the capacity of their guts to supply them. This led to hypertrophy of the alimentary tract and associated organs, with a consequent increase in BMR.

A SINGLE BOUT OF RESISTANCE EXERCISE INCREASES BASAL METABOLIC RATE IN HEALTHY 60-70 YEAR OLD MEN 251

The extent to which there is a prolonged elevation in metabolic rate, after resistance exercise, is unclear. The purpose of this study was to assess whether a single bout of resistance exercise can alter basal metabolic rate(BMR) in healthy older men with normal glucose tolerance (n=6; age 66±5 yr; weight 80.4±8.8 kg; BMI 26.2±1.4 kg·m-2; body fat 23.4±3.0%). BMR was measured on two separate occasions, once after a non-exercise control period and again 48 hours after a bout of resistance exercise. The exercise bout consisted of single-leg knee extensions (right and left leg) and chest press (16 sets, 10 repetitions/set) at 75% of the individual's 3 repetition maximum. Subjects only performed the concentric phase of the lift. To control diet and activity subjects resided in the General Clinical Research Center for a 3 day period during each measurement. The subjects were provided a eucaloric diet (15% protein, 60% carbohydrate, 25% fat) and did not exercise prior to the control measurement, or during the 48 hours after the resistance exercise bout. BMR was measured 12 hours post-absorptive. Subjects were awakened, voided, were weighed and then reclined in bed for a continuous 30 min breath collection using a flow through hood system (Hartmann and Braun O2 and CO2 analyzers). VO2;L/min) was higher (p<0.05) 48 hours after the exercise bout(.242±0.03) compared to the control measure (.235±0.03). Extrapolated over a 24-hour periód, thé energy expenditure corresponded to 1789±36 and 1692±77 kcals for the exercise and control measures, respectively. We conclude that an acute bout of resistance exercise causes an increase in BMR in healthy older males for up to 48 hours after exercise.

Observations on the patterns of 24-hour energy expenditure changes in body composition and gastric emptying in head-injured patients receiving nasogastric tube feeding.

Although intolerance to nasogastric feeding is commonly observed after head injury, quantitative measurements of gastric emptying are lacking. Concepts about energy requirements are limited by the lack of long-term measurements of total energy expenditure. Six male subjects with severe head injury had their gastric emptying measured by the phenol red technique. N and energy balances were measured by classic balance techniques, which included continuous indirect calorimetry for up to 24 hours (days 3 to 5). Measurements of body composition were made on days 3 to 5 and 12 to 19 (4 subjects only). The subjects lost a mean of 9.8 kg of which 2.3 kg was estimated to be due to fat (equivalent to -14 g N/d and -1690 kcal/d). On days 3 to 5, basal metabolic rate (BMR) was 130% to 135% of predicted. The low dietary intake (650 kcal and 4.2g N/d) was associated with negative energy (-1710 +/- 520 kcal/d) and N balances (-19 +/- 5 g N/d). Gastric emptying was delayed twofold (days 3 to 5) compared with controls (p < .001) and was associated with significant regurgitation of feed into the mouth (16 of 31 saliva samples contained glucose at a concentration of > 0.5 mmol/L compared with control values of < 0.2 mmol/L. The large negative energy balance in the subjects studied was largely due to the inadequate nasogastric feeding, which was associated with a twofold reduction in the rate of gastric emptying and frequent regurgitation of feed. The large negative N balance and the high contribution of protein oxidation to total energy expenditure (25% to 28%) was predominantly due to the injury sustained and immobility. An increase in BMR is not necessarily associated with increased total energy expenditure or energy requirements.

Macronutrients and energy balance in obesity

Energy balance is the difference between metabolizable energy intake and total energy expenditure. Energy intake is difficult to measure accurately; changes in body weight, for example, are not a good measure of the adequacy of energy intake, because fluctuations in body weight are common even if the overall trend is toward weight loss. It is now customary to assess energy requirements indirectly from total energy expenditure. Total energy expenditure consists of basal metabolism, postprandial thermogenesis, and physical activity. Energy expenditure is related to both body weight and body composition. A reduction in total energy expenditure accompanies weight loss, because basal metabolic rate decreases with the loss of lean tissue mass. Similarly, with weight gain, there is an increase in basal metabolic rate, because lean tissue mass grows to support the increase in fat tissue mass. Excess energy intake over energy expenditure causes weight gain and an accompanying increase in total energy expenditure. Following a period of adaptation, total energy expenditure will match energy intake and body weight will stabilize at a higher level. This same relationship holds for weight loss. Respiratory quotient (measured in steady state) is an indication of the proportion of energy expenditure derived from fat and carbohydrate oxidation. Over long periods of time, fat balance is equivalent to energy balance, as an excess of fat intake over fat oxidation causes fat storage.

Effects of recombinant human growth hormone on basal metabolic rate in adults with pituitary deficiency

The effect of recombinant human growth hormone (rhGH) on basal metabolic rate (BMR) was studied in a placebo-controlled, double-blind, crossover trial. Ten patients with a history of complete pituitary insufficiency were randomized for 26 weeks in each period. Three patients were excluded due to withdrawal, fever, and claustrophobia, respectively. All patients had received adrenal, thyroid, and gonadal substitution therapy for at least 1 year before the study. The dose of rhGH was 0.25 to 0.5 U/kg/wk, administered subcutaneously once a day in the evening. BMR was determined by indirect calorimetry in a computerized ventilated open-hood system. Body composition was examined using four different methods—computed tomography (CT), tritium dilution, 40K determinations, and total body nitrogen (TBN) measured with neutron activation. The body composition data have previously been reported. Fat-free mass (FFM) increased and body fat (BF) decreased during the first 6 weeks of rhGH treatment, but no further changes in body composition occurred between 6 and 26 weeks. Baseline BMRs in GH-deficient (GHD) patients were in the lower part of the reference range, but BMR and the ratio between BMR and FFM (BMR/FFM) were not significantly lower than in a carefully selected control group. BMR increased between 0 and 6 weeks (mean ± SD: from 6.68 ± 1.55 to 7.75 ± 1.35 MJ/24 h, P < .001) and then remained unchanged between 6 and 26 weeks. The increase in BMR was closely related to the increase in FFM ( r = .91, P < .01). However, the increase in BMR was not solely related to changes in FFM, since there was a significant increase in BMR/FFM at 6 weeks that was maintained at 26 weeks. Pearson correlation analysis also revealed a close association between the increase in BMR after 6 weeks of rhGH treatment and increases in a number of metabolic variables, including total 3,5,3′-triiodothyronine ([T 3] r = .84, P < 0.05), procollagen III peptide ([pIIIp] r = .85, P < .05), and free fatty acids ([FFA] r = .95, P < .01). Therefore, the increase in BMR after rhGH treatment is not simply a reflection of altered body composition, but may also involve other mechanisms including lipolysis, increased thyroxine (T 4) deiodination resulting in increased circulating T 3 concentrations, and/or increased protein synthesis as demonstrated by increased circulating pIIIp levels.

Nutrition and Energetics of Exercise at Altitude

Altitude exposure may lead to considerable weight loss. Most reports, showing weight losses of 3% in 8 days at 4300m and up to 15% after 3 months at 5300 to 8000m, appear to indicate that this weight loss is a function of both absolute altitude and the duration of exposure. Based on the available scientific evidence to date, it is concluded that altitude weight loss is because of an initial loss of water and subsequent loss of fat and muscle mass due to malnutrition. Up to 5500m, malabsorption of macronutrients does not occur. Up to altitudes around 5000m, weight loss from a reduction of fat and muscle appears to be avoidable by maintaining adequate dietary intake. Primary anorexia, lack of comfort and palatable food, detraining, and possibly direct effects of hypoxia on protein metabolism seem inevitably to lead to weight loss during longer exposures at higher altitudes. To minimise losses, it is advisable to acclimatise properly, reduce the length of stay at extreme altitude as much as possible and maintain a high and varied nutrient intake. With sojourns at intermediate altitude for training purposes, adequate energy intake should be maintained taking into account the decrease in aerobic training intensity and the increase in basal metabolic rate that ensue from the hypoxic environment.

β-Adrenoceptor Subtypes Mediating the Metabolic Effects of BRL 35135 in Man

1. The aim of the present study was to evaluate the metabolic responses produced in man by the beta 3-adrenoceptor agonist BRL 35135, and to determine which of these responses are beta 3-, rather than beta 1- or beta 2-, mediated. 2. Eight normal male subjects received single oral doses of BRL 35135 (8 mg) or the selective beta 2-adrenoceptor agonist salbutamol (8 mg) after pretreatment with placebo, bisoprolol (5 mg) as a selective beta 1-antagonist or nadolol (20 mg) to block beta 1- and beta 2-, but not beta 3-adrenoceptors. 3. BRL 35135 and salbutamol produced a significant fall in serum potassium concentration compared with placebo, in keeping with beta 2-adrenoceptor stimulation. Both drugs also produced a significant increase in serum glucose, insulin and lactate concentrations, which mirrored the hypokalaemic response, being unaffected by selective beta 1-blockade (bisoprolol), but completely blocked by nadolol. BRL 35135 (but not salbutamol) also produced a significant rise in serum free fatty acid and glycerol concentrations, which appeared to be beta 2-mediated. 4. A significant increase in basal metabolic rate occurred with both BRL 35135 and salbutamol. In the case of salbutamol, this effect appeared to be mediated solely by beta 2-adrenoceptors, whereas BRL 35135 produced a thermogenic response which could only be partially accounted for by a combination of beta 1- and beta 2-adrenoceptor stimulation. 5. These results infer the possibility of thermogenic beta 3-adrenoceptors in man, although these do not appear to be involved in the control of carbohydrate or fat metabolism.

Measurement of Oxygen Consumption After Uncomplicated Acute Myocardial Infarction

Oxygen consumption (VO2) has been shown to be decreased after acute myocardial infarction (AMI) complicated by cardiogenic shock. To evaluate early measurement of VO2 by indirect calorimetry after an uncomplicated AMI (UAMI). Prospective nonrandomized case study. Emergency department of a large urban hospital. Twenty-six consecutive patients presenting with confirmed UAMI. VO2 was measured by indirect calorimetry (Deletrac, Datex Ins,) which is noninvasive. All patients received buccal or intravenous nitroglycerin and thrombolytic therapy, and none received opiates before VO2 measurement. Two groups of patients were identified by subsequent development of cardiogenic shock. Group 1 did not develop cardiogenic shock, and group 2 developed shock within 24 h of admission. Group 1 (n = 22) had a significantly higher VO2 compared to group 2 (n = 4), mean 154(SD 25) vs mean 100(SD 13) ml/min.m2, p < 0.002. Group 1 had a significantly higher increase in basal metabolic rate than group 2, mean 30 percent (SD 11) vs mean 10(SD 15) percent, p < 0.007. There was no significant difference in age, heart rate (HR), shock index (SI), or rate-pressure product (RPP) between groups 1 and 2. All patients in group 2 developed cardiogenic shock despite thrombolytic therapy, and two died within 24 h of admission. VO2 is increased in UAMI and represents increased metabolic demands of peripheral tissues and not cardiac oxygen uptake. A reduction in VO2 (< 100 ml/min.m2) after AMI may be an early predictor of subsequent development of cardiogenic shock. Measurement of VO2 in UAMI by indirect calorimetry in the emergency department may be of value to identify patients at high risk and could influence their management.

Do β&lt;sub&gt;3&lt;/sub&gt;-adrenoceptors mediate metabolic responses to isoprenaline

We investigated whether the putative beta 3-adrenoceptors mediated metabolic responses to isoprenaline. Seven normal volunteers received infusions of isoprenaline, a (beta 1, beta 2 and beta 3-agonist), at 0.5-3.0 micrograms/min. They were pretreated with either placebo, 25 mg atenolol (a selective beta 1 antagonist), or 5, 20 and 80 mg nadolol (which blocks beta 1 and beta 2 but not beta 3-adrenoceptors). Isoprenaline markedly (30.6%) increased basal metabolic rate (BMR): this increase was significantly reduced by 25 mg atenolol but not by 5 mg nadolol. Significant beta 2-blockade (from tremor data) occurred with 5 mg nadolol but not with 25 mg atenolol. This suggests that beta 1 but not beta 2-adrenoceptors are involved in the mediating thermogenic effects of isoprenaline. However, the rise in BMR was not totally blocked even by 80 mg nadolol (9.5%), which produced complete beta 1/beta 2 blockade, as evidenced by the elimination of the chronotropic effect of isoprenaline. This implies that the thermogenic response has a non-beta 1/beta 2-mediated component. There were also significant increases in plasma free fatty acids, glycerol, glucose, insulin and lactate, but these were completely abolished by beta 1/beta 2 blockade. Overall, isoprenaline produced an increase in BMR which is only partly due to stimulation of beta 1-adrenoceptors, and which is not associated with beta 1/beta 2-mediated effects on carbohydrate and fat metabolism. This suggests the possibility of thermogenic beta 3-adrenoceptors in man, although their location and role remain unknown.

Effect of testosterone on metabolic rate and body composition in normal men and men with muscular dystrophy.

We have examined the effect of testosterone enanthate injections (3 mg/kg.week, im) on the basal metabolic rate (BMR) estimated by indirect calorimetry and on lean body mass (LBM) estimated by 40K counting in four normal men and nine men with muscular dystrophy. Testosterone treatment increased plasma testosterone levels in all subjects (3-fold mean elevation). BMR increased significantly after 3 months of testosterone treatment (mean, 10%; P less than 0.01; 13% mean increase in the men with muscular dystrophy and 7% mean increase in the normal subjects). BMR remained elevated (mean increase, 9%) after 12 months of testosterone treatment in four men with muscular dystrophy. LBM also was significantly higher after 3 months of treatment (mean, 10%; P less than 0.01) and remained elevated at 12 months. The percent increase in LBM was similar in men with muscular dystrophy (+10%) and normal men (+11%). When BMR was adjusted for the increase in LBM by linear regression, the men with muscular dystrophy had an increase in adjusted BMR after 3 months of testosterone treatment (mean increase, 7%), but not after 12 months. The normal men did not have an increase in adjusted BMR. Testosterone treatment for 12 months slightly reduced body fat, whereas there was an increase in body fat in subjects with muscular dystrophy who were treated with placebo for 12 months. We conclude that there is a significant increase in BMR associated with pharmacological testosterone treatment, which for the most part is explained by the increase in LBM. However, in men with muscular dystrophy, there is a small hypermetabolic effect of testosterone beyond that explained by increased LBM.

Energy expenditure under free-living conditions in normal-weight and overweight women

Total energy expenditure under free-living conditions of 12 normal-weight and 26 overweight women was determined with the 2H2(18)O method. Overweight women tended to expend more energy (mean +/- SD, 11.20 +/- 1.79 MJ/d) than normal-weight women (9.46 +/- 0.87 MJ/d, P less than 0.005). Approximately half of this effect was explained by an increase in basal metabolic rate (BMR) in the overweight group compared with the normal-weight group (6.47 +/- 0.74 vs 5.68 +/- 0.39 MJ/d, respectively, P less than 0.005) and the other half by an increase in above-basal energy expenditure (4.73 +/- 1.49 vs 3.78 +/- 0.94 MJ/d, P less than 0.05). Total energy expenditure was approximately 1.7 times the BMR in both groups. After adjusting energy expenditure for weight or lean body mass by analysis of covariance, there was no significant difference between normal-weight and overweight groups. We conclude that most overweight subjects must consume more energy than lean subjects to maintain their excess weight, although some could maintain their obesity without eating more than lean subjects.

Energy Requirements of Pregnancy

The energy requirements of pregnancy is a topic of considerable uncertainty because the apparent energy costs--to supply the energy required for the changes in maternal and fetal tissues and to cover the increase in basal metabolic rate (BMR), amounting to the equivalent of an extra 250-300 kcal/day--are rarely paralleled by actual findings. However, few studies have investigated this problem in a controlled longitudinal and statistically acceptable fashion. In this study, measurements of energy intake, BMR, body weight and fatness, physical activity, and mechanical efficiency of movement were made on 162 women in Scotland at 2- to 4-wk intervals throughout pregnancy, and data from 98 of these women were also obtained in the prepregnant state. Data from a parallel study in the Netherlands are also given. The gains in body weight, fatness, the fetal and placental weights, and the increase in BMR were all at the normal expected values. However, increases in energy intake were on the order of only 100 kcal/day during the second and third trimesters. Comparatively small reductions in physical activity, which would be difficult to measure precisely, are described that could account for the difference between actual energy intake and the energy costs of pregnancy.

Energy Requirements of Pregnancy

The energy requirements of pregnancy is a topic of considerable uncertainty because the apparent energy costs--to supply the energy required for the changes in maternal and fetal tissues and to cover the increase in BMR (basal metabolic rate), amounting to the equivalent of an extra 250-300 kcal/d--are rarely paralleled by actual findings. However few studies have investigated this problem in a controlled, longitudinal, and statistically acceptable fashion. In the present study, measurements of energy intake, BMR, body weight and fatness, physical activity, and mechanical efficiency of movement, were made on 162 women in Scotland at 2 to 4 weekly intervals throughout pregnancy and data from 98 of these women were also obtained in the pre-pregnant state. Data from a parallel study in Holland are also given. The gains in body weight, fatness, the fetal and placental weights, and the increase in BMR were all at the normal expected values. However, increases in energy intake were of the order of only 100 kcal/d during the second and third trimesters. Comparatively small reductions in physical activity, which would be very difficult to measure precisely, are described which could account for the difference between actual energy intakes and the energy costs of pregnancy.

The effect of exercise and improved physical fitness on basal metabolic rate

1. The suggestion that there is a sustained enhancement in metabolic rate after exercise was investigated during the course of a study in which six normal-weight volunteers (three men, three women) took part in a 9-week training programme. Baseline values were assessed in a 3-5 week control period of minimal activity before training. At the end of the study the subjects were capable of running for 1 h/d, 5 d/week. 2. Throughout the entire study the subjects were maintained on a constant diet. Measurement of energy expenditure by the doubly-labelled water (2H2(18)O) method showed that the subjects had an energy imbalance of +3% in the control and -20% at the end of the training period. The subjects were in positive (1.1 (SE 0.2) g) nitrogen balance in the second week of the control, and in negative (-0.6 (SE 0.3) g) N balance in the last week of the exercise period. 3. Over the course of the study maximum oxygen consumption (VO2max) and high-density-lipoprotein-cholesterol levels increased by 30%. Heart rate at rest and when performing a standard step test fell significantly. 4. Body composition was assessed weekly by 40K counting and skinfold thickness measurements, in addition to 2H2 dilution at the beginning and end of the study. Fat-free mass was apparently gained in the early phases of the study, but there was lack of agreement between the different methods of assessing body composition. Changes in body-weight were not significant. 5. Basal metabolic rate (BMR), overnight metabolic rate (OMR) and sleeping metabolic rate (SMR) were measured on three occasions: in the control period, and the beginning and end of the training periods. Average BMR in the control period was 5.91 (SE 0.39) MJ/24 h and was not changed with activity. There were no changes in OMR (5.71 (SE 0.27) MJ/24 h in the control) nor in SMR (5.18 (SE 0.27) MJ/24 h in the control), nor in BMR, OMR or SMR when expressed per kg body-weight, or per kg fat-free mass. 6. These results do not support the suggestions that there is a sustained increase in BMR following exercise that can usefully assist in weight-loss programmes.

Thyroid hormone metabolism in hypermetabolic patients with haematological disorders.

Turnover tracer studies of T4 and T3 using the single injection, noncompartmental approach were performed in 6 hypermetabolic patients with haematological disorders (HHD) (basal metabolic rate (BMR): median 141%, range 122-166%), in 10 controls with stable, nonthyroidal illness (NTIC), and in 14 healthy controls (HC). The main finding was an increase of approximately 30% of the production rate (PR) of both T4 and T3 in patients with HHD. Median PR of T4 was 134 nmol/day x 70 kg in HHD, compared to 78 nmol/day x 70 kg in NTIC (P less than 0.05) and 98 nmol/day X 70 kg in HC (p less than 0.1), whereas median PR of T3 was 40.3 nmol/day x 70 kg in HHD, compared to 25.6 nmol/day x 70 kg in NTIC (P less than 0.01) and 31.1 nmol/day x 70 kg in HC (P less than 0.1). An increase of similar magnitude was found for the apparent distribution volume and the pool size of both T4 and T3. In contrast, the mean transit times of the hormones were similar in the 3 groups. Patients with HHD had normal levels of basal serum TSH as well as of the TSH response to TRH. Only PR of T3 correlated to the BMR (R = 1.00, P less than 0.02). The data are compatible with an increased consumption of thyroid hormones by malignant haematologic cells, and the increase of BMR seems to be dependent on the production of T3.

High intensity interval training program in the aquatic environment (HIITAQ) in obese teens

The increased prevalence of obesity has compromised the health of Brazilian adolescents. Regular exercise and lifestyle changes are recommended as prevention and treatment. However, there is no consensus on the dose-response of exercise programs. This study aims to verify the effectiveness of a high-intensity interval training program in the aquatic environment (HIITAQ) on physical fitness and cardiometabolic risk factors in obese adolescents. The sample consisted of 18 adolescents of both sexes, aged 12 to 17 years, diagnosed with obesity. Anthropometric variables, physical fitness, blood glucose, and lipid profile were evaluated before and after 12 weeks of training. The program consisted of two sets of 4-8 repetitions lasting 30 seconds (85% -95% of maximum heart rate) for 60 seconds of the active rest interval. After the exercise program, there was a reduction in body mass index z-score, BMIz (p &lt;0.01), reduction of Total Cholesterol, TC (p &lt;0.01), and LDL (p &lt;0.01). There was an increase in basal metabolic rate (p &lt;0.01) and peak VO2 (p &lt;0.01). No differences were observed after training in the percentage of fat, body mass index, BMI, waist/height ratio WHtR, fasting blood glucose, insulin, and HDL-c (p&gt;0,05). The high-intensity training program in the aquatic environment was effective in reducing cardiometabolic risk factors.

ENERGY REQUIREMENTS OF PREGNANCY IN RURAL THAILAND

The energy cost of pregnancy was measured in rural Thai women between 10 wk gestation and term. The energy cost of pregnancy, which includes the increase in basal metabolic rate (BMR), the energy equivalent of maternal fat laid down, and the assumed energy equivalent of fetal fat and fetal and maternal protein, was 202 MJ (1 MJ = 239 kcal). BMR increased by 100 MJ overall and maternal fat gain averaged about 1·3 kg, equivalent to 60 MJ. The energy cost was more than covered by an overall increase in food intake of 238 MJ with little evidence of any complementary reduction in total energy expenditure by reduced physical activity.

Injury severity, whole body protein turnover, and energy expenditure in pediatric trauma

The purpose of this study was to quantify the changes in energy expenditure and protein turnover imposed by blunt trauma in children and to correlate them with the Injury Severity Score (ISS). We studied 19 children (mean age 10 +/- 1 year, mean ISS 20 +/- 2). Basal metabolic rate (BMR) was measured in the postabsorptive state by open-circuit indirect calorimetry. Whole body protein turnover (Q) and synthesis (S) were determined by the 15N enrichment of urinary ammonia in a 12-hour collection following a single dose of 15N glycine. Twelve-hour total urinary nitrogen excretion (E) was also determined. Because nitrogen intake was 0 during the study period, Q was equivalent to protein breakdown (B). Eleven patients were restudied at 3- to 5-day intervals during hospitalization and eight were restudied after discharge (mean 34 +/- 6 days post injury). There was a significant increase in BMR, Q, S, and E following injury, when compared with post injury baseline values. However, while BMR increased by 14%, there were 93% and 82% increases in Q (B) and S, respectively. Negative nitrogen balance resulted from the fact that protein breakdown increased more than protein synthesis. The initial increase in BMR varied directly with the severity of injury, as reflected in the ISS (r = 0.56, P less than .02). There was no significant correlation between ISS and any of the parameters of protein metabolism. These results suggest that the metabolic response of pediatric patients to multiple trauma may differ from that of adults. In addition, they imply that the ISS may not be a reliable indicator of the severity of tissue injury.

Catabolic effects of thyroid hormone excess: The contribution of adrenergic activity to hypermetabolism and protein breakdown

Although patients with thyrotoxicosis improve clinically after treatment with beta-adrenergic blocking drugs, it has never been established whether the hypermetabolism and body protein wasting caused by thyroid hormone excess are actually mediated by adrenergic mechanisms. To evaluate this issue, we measured basal energy expenditure, epinephrine-stimulated calorigenesis, and leucine kinetics (an index of body protein catabolism) in six normal volunteers before and after triiodothyronine (T 3) administration (150 μg/d for 1 week). Serum T 3 rose nearly threefold ( P < 0.001) during T 3 administration, producing significant increases in basal metabolic rate (21%, P < 0.001), nitrogen excretion (45%, P < 0.001), and leucine flux (45%, P < 0.01). In response to epinephrine infusion, the absolute rise in metabolic rate above basal was 57% greater in the thyrotoxic condition ( P < 0.02). Although beta-adrenergic blockade with intravenous propranolol totally abolished the calorigenic response to epinephrine, it had no detectable effect on either the accelerated basal metabolic rate or the augmented body protein catabolism caused by thyroid hormone excess. Our data suggest that in the basal, resting state, the increased metabolic rate and accelerated protein breakdown caused by thyroid hormone are not adrenergically mediated. However, under nonbasal conditions (when sympathetic activity is stimulated), enhanced responsiveness to catecholamine calorigenesis may exaggerate the hypermetabolic state and thereby contribute to weight loss and other clinical manifestations of thyrotoxicosis. This mechanism may explain the clinical efficacy of beta-adrenergic blocking agents in the treatment of thyrotoxicosis.