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Physical activity energy expenditure (PAEE) is a determinant of prognosis and fitness in older patients with coronary heart disease (CHD). PAEE and total energy expenditure (TEE) are closely related to fatness, physical function, and metabolic risk in older individuals. The goal of this study was to assess effects of resistance training on PAEE, TEE, and fitness in older women with chronic CHD and physical activity limitations ( N = 51, mean age: 72 + 5 yr). The study intervention consisted of a progressive, 6-mo program of resistance training vs. a control group condition of low-intensity yoga and deep breathing. The study interventions were completed by 42 of the 51 participants. The intervention group manifested a 177 ± 213 kcal/day (+9%) increase in TEE, pre- to posttraining, measured by the doubly labeled water technique during a nonexercise 10-day period ( P < 0.03 vs. controls). This was due to a 50 ± 74 kcal/day (4%) increase in resting metabolic rate measured by indirect calorimetry ( P < 0.01, P < 0.05 vs. controls) and a 123 ± 214 kcal/day (9%) increase in PAEE ( P < 0.03, P = 0.12 vs. controls). Resistance training was associated with significant increases in upper and lower body strength, but no change in fat-free mass, measured by dual X-ray absorptiometry, or left ventricular function, measured by echocardiography and Doppler. Women in the control group showed no alterations in TEE or its determinants. There were no changes between groups in body composition, aerobic capacity, or measures of mental depression. These results demonstrate that resistance training of 6-mo duration leads to an increase in TEE and PAEE in older women with chronic CHD.

Carbon (C) in the 1-position of leucine is released as CO2with the decarboxylation of α-ketoisocaproate (KIC). Carbon in the 2-position of leucine undergoes several additional metabolic steps before entering the tricarboxylic acid (TCA) cycle in the 1-position of acetyl-CoA, where it can be released as CO2or be incorporated into other compounds. This study examined the metabolic fate of C in the 2-position of leucine. We infused 11 healthy subjects with [1-13C]leucine and [1,2-13C2]leucine for 3.5–4 h to measure leucine kinetics and the oxidation of the tracers from enrichments of13C in blood and expired CO2. The fraction of leucine infused that was oxidized (fox) was used to define the degree of recovery of the13C label(s) for each tracer. As expected, leucine appearance (means ± SE) did not differ between tracers (13C1: 92.1 ± 3.1 vs.13C2: 89.2 ± 3.2 μmol · kg−1· h−1) when calculated using plasma leucine enrichments as an index of intracellular enrichment. A small (3%) but significant ( P = 0.048) difference between tracers was found when KIC was used to calculate leucine appearance (13C1: 118.0 ± 4.1 vs.13C2: 114.4 ± 4.5 μmol · kg−1· h−1). The value of foxwas 14 ± 1% for [1,2-13C2]leucine and was lower than the foxfor [1-13C]leucine (19 ± 1%). From the foxdata, we calculated that the recovery of the 2-13C label in breath CO2was 58 ± 6% relative to the 1-13C label. These findings show that, although a majority of the 2-13C label of leucine is recovered in breath CO2, a significant percentage (∼42%) is retained in the body, presumably by transfer to other compounds, via TCA exchange reactions.

Prior studies suggest that estradiol and progesterone regulate body composition in growing female rats. Because these studies did not consider the confounding effect of changes in food intake, it remains unclear whether ovarian hormones regulate body composition independently of their effects on food intake. We utilized a pair-feeding paradigm to examine the effects of these hormones on body composition. In addition, skeletal muscle protein fractional synthesis rate and adipose tissue lipoprotein lipase activity were measured to examine pathways of substrate deposition into fat and fat-free tissue. Female Sprague-Dawley rats [pubertal: 7–8 wk old; 190 ± 0.5 (SE) g] were separated into four groups: 1) sham-operated (S; n = 8), 2) ovariectomized plus placebo (OVX; n = 8), 3) ovariectomized plus estradiol (OVX+E; n = 8), and 4) ovariectomized plus progesterone (OVX+P; n = 8). All ovariectomized groups were pair-fed to the S group. Body composition was measured using total body electrical conductivity. The relative increase in fat-free mass was greater ( P < 0.01) in the OVX group (31 ± 2%) than in the S (17 ± 2%), OVX+E (18 ± 2%), and OVX+P (22 ± 2%) groups. The fractional synthetic rates of gastrocnemius muscle protein paralleled changes in fat-free mass: OVX had a higher ( P < 0.05) synthesis rate (21 ± 3%/day) than S (12 ± 2%/day), OVX+E (11 ± 2%/day), and OVX+P (8 ± 1%/day) groups. Body fat increased in the S group (31 ± 7%; P < 0.01), whereas the OVX groups lost fat (OVX: −10 ± 7%; OVX+E: −15 ± 7%; OVX+P: −13 ± 7%). No differences in lipoprotein lipase were found. Our results suggest that estradiol and progesterone may regulate the growth of fat and fat-free tissues in female rats. Moreover, ovarian hormones may influence skeletal muscle growth through their effects on skeletal muscle protein synthesis.

Low rates of daily energy expenditure, increased energy intake, or a combination of both contribute to obesity in African-Americans. We examined whether African-Americans have lower rates of free-living daily energy expenditure than Caucasians. One hundred sixty-four (>55 yr) volunteers (37 African-American women, 52 Caucasian women, 28 African-American men, and 47 Caucasian men) were characterized for total daily energy expenditure, resting metabolic rate, and physical activity energy expenditure from the doubly labeled water method and indirect calorimetry. Absolute total daily energy expenditure was lower in women than men but was not different between African-Americans and Caucasians. However, we found race and gender differences in total daily energy expenditure after controlling for differences in fat-free mass. Total daily energy expenditure was 10% lower ( P < 0.01) in African-Americans compared with Caucasians due to a 5% lower resting metabolic rate ( P < 0.01) and 19% lower physical activity energy expenditure ( P = 0.08). Moreover, total daily energy expenditure was 16% lower ( P < 0.01) in women compared with men due to a 6% lower resting metabolic rate ( P = 0.09) and a 37% lower physical activity energy expenditure ( P = 0.06). Low rates of energy expenditure may be a predisposing factor for obesity, particularly in African-American women.

It was hypothesized that an increase in total and central body fatness is related to higher sympathetic nervous system activity (SNSA) in older men. Resting SNSA was measured from norepinephrine (NE) kinetics in 69 younger (18–36 yr) and 69 healthy older men (55–80 yr). Body fat distribution was estimated from the waist circumference, body composition from underwater weighing, peak oxygen consumption from a treadmill test to exhaustion, and dietary intake from food diaries. Plasma NE concentrations were 41% higher (P < 0.001) in older men due to a 27% increase (P < 0.001) in NE appearance rate and a tendency for a lower NE clearance rate (P = 0.08). NE appearance rate was higher in individuals of both age groups who exhibited a greater waist circumference and body fatness (range of r values 0.49–0.69; P < 0.01). The waist circumference, and not age, was the strongest predictor of the increase in NE appearance rate in older men. Statistically controlling for the waist circumference or body fatness diminished age-related differences in NE concentrations and in NE appearance rate. These findings suggest that an accumulation of total and central body fat is associated with higher levels of SNSA in older males.

We examined the contribution of variations in body composition and leisure time physical activity to the age-related decline in peak oxygen consumption (VO2) in men and women. Healthy males 17–80 yr old (n = 378) and females 18–81 yr old (n = 224) were characterized for peak VO2 from a treadmill test to exhaustion, fat-free mass and fat mass by underwater weighing, and leisure time physical activity. Peak VO2 showed a greater absolute decline (P < 0.05) with age in males (r = -0.70, slope = -0.034 l.min-1.yr-1; P < 0.01) than in females (r = -0.78, slope = -0.028 l.min-1.yr-1; P < 0.01). After statistically controlling for differences in fat-free mass and fat mass, the decline in peak VO2 was diminished in both sexes, although a greater rate of decline persisted in males (r = -0.47, slope = -0.016 l.min-1.yr-1; P < 0.01) than in females (r = -0.39, slope = -0.009 l.min-1.yr-1; P < 0.01). We found that the addition of leisure time physical activity (independent of body composition) to the regression model further attenuated the rate of decline in males (r = -0.40, slope = -0.013 l.min-1.yr-1; P < 0.01) but did not alter the age-related decline in peak VO2 in females (r = -0.39, slope = -0.009 l.min-1.yr-1; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

We examined the influence of 8 wk of endurance training on basal levels of fat oxidation and its association with changes in norepinephrine (NE) kinetics, resting metabolic rate (RMR), and body composition in 18 healthy elderly persons (66.1 +/- 1.4 yr; 10 men, 8 women). Fatty acid appearance rate and total body fat oxidation were determined from [14C]palmitate infusion and indirect calorimetry, NE kinetics were determined from infusions of [3H]NE, RMR was determined from the ventilated hood technique, and body composition was determined from underwater weighing. Endurance training increased peak oxygen consumption by 11% (1.9 +/- 0.1 to 2.1 +/- 0.1 l/min; P < 0.01) and increased RMR by 7% (1.20 +/- 0.02 to 1.28 +/- 0.02 kcal/min; P < 0.01). Endurance training increased NE appearance rate by 35% (0.51 +/- 0.04 to 0.69 +/- 0.04 micrograms/min; P < 0.01), whereas no change in NE clearance was noted. Endurance training increased fat oxidation by 22% (201.0 +/- 11.2 vs. 244.0 +/- 15.2 mumol/min; P < 0.01) but did not alter fatty acid appearance rate. Approximately two-thirds of the variation (r2 = 0.65) for the increase in fat oxidation was explained by increased NE appearance rate (r2 = 0.51; P < 0.01) and changes in fat-free weight (r2 = 0.14; P < 0.01). We conclude that 1) endurance training shifts in vivo basal substrate utilization toward greater fat oxidation in elderly individuals and 2) enhanced fat oxidation is associated with increased activity of the sympathetic nervous system and alterations in fat-free mass.

The experimental reliability of measuring CO2 production rates (rCO2) with the doubly labeled water (DLW) technique was assessed in five young healthy men (23 (DLW) technique was assessed in five young healthy men (23 +/- 4 yr; 66.1 +/- 4.6 kg). To minimize the confounding effects of fluctuations in physical activity and eating patterns on variation in energy expenditure, the subjects lived under sedentary living conditions by confinement to their own room at a Clinical Research Center and were maintained on a fixed and known level of energy intake. rCO2 was determined in duplicate over two identical 9-day study periods after separate loading doses of deuterium and oxygen-18. Turnover rates were determined from multipoint sampling to reduce error from analytical uncertainty. Dilution spaces were determined by both the intercept and plateau methods. The average experimental variation for rCO2 estimates was approximately +/- 8.5% and was not significantly different among three published calculation models that differ in their assumptions regarding the relationship between the dilution spaces of deuterium and oxygen-18. The experimental reliability of +/- 8.5% exceeds theoretical values generated from calculations based on propagation of error from analytical uncertainty. Between subjects, the experimental variation ranged from 1 to 21%, and the half-width of the 95% confidence interval for the precision of rCO2 estimates was high (+/- 12 mol/day) relative to the mean reported value of approximately 16 mol/day.(ABSTRACT TRUNCATED AT 250 WORDS)

It is currently unclear whether age-specific equations should be used for assessing body composition from bioelectrical resistance. Kushner et al. (Am. J. Clin. Nutr. 56: 835#x2013;839, 1992) showed that the relationship between height2/resistance and total body water (TBW) is robust across a wide age range, although uncertainty remained over the relationship in preschool children. We therefore cross-validated the Kushner equation for predicting total body water in 4- to 6-yr-old children in two independent laboratories. TBW was measured from H2 18O dilution, and bioelectrical resistance and reactance were measured using an RJL 101A analyzer in 31 children (15 females, 16 males; 5 +/- 0.8 yr) studied in Burlington, Vermont, and 30 children (14 females, 16 males; 5 +/- 0.2 yr) studied in Phoenix, Arizona. There was no significant difference between TBW predicted from the Kushner equation and that measured in children in Burlington (11.76 +/- 2.00 vs. 11.91 +/- 2.46 kg; r = 0.94) or in Phoenix (11.53 +/- 1.64 vs. 11.66 +/- 1.90 kg; r = 0.94). The Kushner equation for TBW can be transformed into an equation for fat-free mass (FFM) by using published age- and gender-specific constants for the hydration of FFM: hydration of FFM = 76.9 - 0.25 age (yr) - 1.9 gender where female equals 0 and male equals 1. The intraclass reliability for estimates of fat mass and FFM with the use of bioelectrical resistance in an independent group of 26 children (5.0 +/- 0.8 yr, 20.2 +/- 3.0 kg) was > 0.99 for duplicate observations performed 2 wk apart.(ABSTRACT TRUNCATED AT 250 WORDS)

We considered the association of several metabolic and lifestyle variables as modulators of the decline in resting metabolic rate (RMR) and fat-free weight (FFW) in 183 healthy females (18-81 yr). RMR showed a curvilinear decline with age, which was significant in women aged 51-81 yr but not in women aged 18-50 yr. FFW showed a curvilinear decline with age, which was significant (P < 0.01) in women 48-81 yr but not in women 18-47 yr. The decline in RMR was primarily associated with the loss of FFW (r2 = 72%), whereas the decline in FFW was explained primarily by differences in maximal O2 consumption (VO2max), age, leisure time physical activity, and dietary protein intake (total r2 = 46%). We conclude that RMR and FFW showed a curvilinear decline with age which was accelerated beyond the middle-age years. Second, the age-related decline in RMR was primarily associated with the loss of FFW. Third, the loss of FFW was partially related to a decrement in VO2max and nutritional factors. Therapeutic interventions designed to increase VO2max by elevating physical activity may preserve fat-free weight and thus offset the decline of RMR in aging women.

Physiological sources of variation in the 2H-to-18O dilution space ratio (DSR) were examined in 34 males and 20 females (4-78 yr; 14.7-143.2 kg; 1.8-61.0% body fat). Dilution spaces were obtained by time 0 extrapolation of isotope washout over 10-14 days, and body composition was obtained by underwater weight (adults) or bioelectrical impedance (children). The mean DSR was 1.050 +/- 0.015 (range 1.029-1.111), significantly higher (P < 0.001) than the traditionally assumed value of 1.029 based on exchange over 4 h. Use of the value 1.029 causes a systematic 8% overestimate of energy expenditure from doubly labeled water, relative to use of the value 1.05. The DSR was not related to body composition or age but was significantly higher (P < 0.05) in males (1.052 +/- 0.016) than in females (1.044 +/- 0.012). This gender effect was not explained by differences in the number of exchangeable hydrogens in the body. We conclude 1) variation in the 2H-to-18O DSR is not explained by body composition but is influenced by the chemical availability of exchangeable hydrogens to undergo exchange; 2) because the DSR is not easily predicted, use of the observed dilution spaces are recommended; 3) if a fixed DSR is used, values of 1.044 and 1.052 are recommended in females and males, respectively.

Physical exercise is prescribed to older individuals to increase cardiovascular fitness and improve body composition. However, there is limited information on the effect of exercise on total energy expenditure (TEE) and its components. We therefore determined the effects of short-term endurance training in 11 elderly volunteers (56–78 years) on changes in 1) TEE, from doubly labeled water; 2) resting metabolic rate (RMR), from respiratory gas analysis, 3) the energy expenditure of physical activity (EEPA), aside from that associated with the training program, and 4) body composition from a combination of body density with total body water. Endurance training increased maximum oxygen consumption (VO2max) by 9% (2.00 +/- 0.67 to 2.17 +/- 0.64 l/min; P < 0.05) and RMR by 11% (1,596 +/- 214 to 1,763 +/- 170 kcal/day; P < 0.01). There was no significant change in TEE (2,408 +/- 478 to 2,479 +/- 497 kcal/day) before and during the last 10 days of endurance training because of a 62% reduction in EEPA (571 +/- 386 to 340 +/- 452 kcal/day; P < 0.01). There was no change in body mass, but fat masxs decreased (21.6 +/- 6.6 to 20.7 +/- 6.6 kg; P < 0.05). The increase in fat-free mass (49.5 +/- 9.0 to 50.4 +/- 9.1 kg; P < 0.05) was explained by an increase in body water (35.9 +/- 6.5 to 36.8 +/- 6.3 kg; P < 0.05). We conclude that in healthy elderly persons, endurance training enhances cardiovascular fitness, but does not increase TEE because of a compensatory decline in physical activity during the remainder of the day.

We examined the effects of an 8-wk endurance training program (cycling exercise) on resting metabolic rate (RMR) and norepinephrine (NE) kinetics in 19 older persons (64 +/- 1.6 yr). Before and after training, RMR, NE kinetics, maximal O2 consumption (VO2max), body composition, supine blood pressure, estimated energy intake, and fasting levels of glucose, insulin, and thyroid hormones were measured. RMR increased 10% after training. Resting concentrations of NE increased 24% after training due to a 21% increase in NE appearance rate and no change in NE clearance. Training increased VO2max (14%; P less than 0.01) and energy intake (12%; P less than 0.01), whereas no change was noted in body composition. Supine blood pressure and plasma glucose were lower after training, whereas no change was noted in fasting levels of plasma insulin. The increase in RMR was associated with a higher rate of NE appearance (r = 0.57; P = 0.05) and with increase in energy intake (r = 0.56; P = 0.05). Together these two factors accounted for 49% (r2) of the variation of the change in RMR. Changes in blood pressure were not associated with changes in NE kinetics. We conclude that endurance training increases total energy expenditure in older individuals by the direct energy cost of physical activity and by elevating RMR. This increase is partially mediated by an increased NE appearance rate and increased food intake in healthy older individuals.

The associations among age, maximal aerobic capacity (VO2max), and body composition with resting metabolic rate (RMR), and fasting plasma hormones were examined in endurance-trained and untrained older and younger men. A higher RMR (approximately 6%; P less than 0.05), normalized per kilogram of fat-free weight (FFW), was found in endurance-trained younger and older men relative to untrained men. VO2max, independent of FFW, accounted for a significant portion of the variation in RMR. Fasting insulin and the fasting insulin-to-glucose ratio were higher in older men relative to younger men. This difference was diminished when differences in percent body fat were taken into account. Plasma thyroid hormones and glucagon were not associated with age, VO2max, or percent body fat. We conclude that endurance-trained and older men have a higher RMR than untrained younger and older men that is independent of differences in FFW. Plasma levels of thyroid hormones and glucagon are not influenced by age, VO2max, or adiposity in healthy nonobese men.

We examined the effects of age and physical activity on plasma norepinephrine (NE) kinetics in active and inactive older and younger men. NE kinetics were estimated by calculation of the rates of NE appearance and clearance during infusion of tritiated norepinephrine [( 3H]-NE). Older active men had the highest level of plasma NE (pg/ml) and NE appearance (microgram.min-1.FFW-1, where FFW is fat-free weight) relative to younger men and inactive older men. NE clearance (l.min-1.FFW-1) was not influenced by age or physical activity. No significant associations were noted between percent body fat, supine blood pressure with resting levels of NE, NE appearance, and NE clearance. We concluded that 1) chronic participation in physical activity by older men, but not younger men, is associated with higher resting levels of plasma NE and NE appearance and 2) the degree of adiposity does not influence plasma NE kinetics in healthy younger and older men. The level of physical activity is an influencing factor on plasma NE and NE appearance into circulation in healthy older men.

RE: Poehlman, Eric T., Andrew W. Gardner, Paul J. Arciero, Michael I. Goran, and Jorges Calles-Escandon. Effects of endurance training on total fat oxidation in elderly persons.

The present study investigated the interaction of genotype and short-term overfeeding on adipose tissue metabolism of six pairs of male monozygotic twins. The sedentary nonobese twins were submitted to a 22-day overfeeding period in which their normal daily intake was supplemented by an additional 1,000 kcal/day. A fat tissue biopsy was performed in the suprailiac region before and after overfeeding to determine fat cell diameter and basal and maximal stimulated epinephrine, norepinephrine, and isoproterenol lipolysis from collagenase-isolated fat cells. Fat cell basal and maximal insulin-stimulated glucose conversion into triglycerides (basal and stimulated lipogenesis) were measured using [14C]glucose. Adipose tissue heparin-releasable lipoprotein lipase activity (LPL) was also determined. A repeated measures analysis of variance revealed overfeeding induced significant elevations in basal lipogenesis (P less than 0.05) and fat cell diameter (P less than 0.05). No significant group changes were noted in basal, epinephrine-, norepinephrine-, and isoproterenol-stimulated lipolysis, insulin-stimulated lipogenesis, and LPL activity due to large individual variation in the response to overfeeding. However, significant intrapair resemblance was noted in the changes of the aforementioned variables, suggesting a coherent within-twin pair response, despite large between-pair variation in response. Less within-pair similarity was noted in changes in basal lipogenesis and fat cell diameter. The results of the present study suggest that overfeeding induced a large range of adipose tissue metabolic responses and that the genotype plays a role in determining the sensitivity of adipose tissue adaptation to caloric affluence.

The purpose of this experiment was to assess the effects of a 22-day training program on resting metabolic rate (RMR), thermic effect of a meal (TEM), and associated hormonal changes. Six pairs of male monozygotic twins were submitted to a 22-day ergocycle exercise program designed to induce a deficit in energy balance of 4.2 MJ per day. RMR and TEM after a 4.2-MJ meal challenge were measured before and after training. Results indicated that RMR and TEM did not change significantly, although a large variation in response between twin pairs was observed. Moreover, training reduced (P less than 0.05) basal and postprandial insulin response, plasma thyroid hormones triiodothyronine (T3), thyroxine (T4), and FT4 (P less than 0.05). Absolute changes in RMR and TEM exhibited significant within-pair resemblance in response, with intraclass correlations reaching r = 0.81 (P less than 0.05) and r = 0.72 (P less than 0.05), respectively. Changes in T4 and FT4 also exhibited moderate within-pair resemblance (0.42 less than or equal to r less than or equal to 0.71). These results suggest that short-term exercise training does not modify RMR and TEM but can significantly decrease plasma levels of insulin and thyroid hormones. Moreover, the similarity of response within twin pairs suggests that heredity plays a role in determining RMR, TEM, and thyroid hormone adaptation to exercise training generating a negative energy balance.