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Biomedical subjects

J Calles-Escandon

Publications and source records attributed to J Calles-Escandon.

At least 19 recordsLinked to original sources

Diabetes and endothelial dysfunction: a clinical perspective.

The main etiology for mortality and a great percent of morbidity in patients with diabetes mellitus is atherosclerosis. A hypothesis for the initial lesion of atherosclerosis is endothelial dysfunction, defined pragmatically as changes in the concentration of the chemical messengers produced by the endothelial cell and/or by blunting of the nitric oxide-dependent vasodilatory response to acetylcholine or hyperemia. Endothelial dysfunction has been documented in patients with diabetes and in individuals with insulin resistance or at high risk for developing type 2 diabetes. Factors associated with endothelial dysfunction in diabetes include activation of protein kinase C, overexpression of growth factors and/or cytokines, and oxidative stress. Several therapeutic interventions have been tested in clinical trials aimed at improving endothelial function in patients with diabetes. Insulin sensitizers may have a beneficial effect in the short term, but the virtual absence of trials with cardiovascular end-points preclude any definitive conclusion. Two trials offer optimism that treatment with ACE inhibitors may have a positive impact on the progression of atherosclerosis. Although widely used, the effect of hypolipidemic agents on endothelial function in diabetes is not clear. The role of antioxidant therapy is controversial. No data have been published regarding the effects of hormonal replacement therapy on endothelial dysfunction in postmenopausal women with type 2 diabetes.

Angiotensin-Converting Enzyme Inhibitors↗

Type 2 diabetes: one disease, multiple cardiovascular risk factors.

Type 2 diabetes mellitus is a major independent risk factor for coronary artery disease. Atherosclerosis accounts for about 80% of all deaths from type 2 diabetes, of which roughly 75% are attributable to coronary artery disease and the remainder to cerebrovascular or peripheral vascular events [1]. The earlier onset and accelerated course of atherosclerosis in individuals with type 2 diabetes mellitus is multifactorial. Type 2 diabetes is associated with abnormalities in lipoprotein metabolism and increased propensity for oxidative damage. The hyperglycemia of patients with type 2 diabetes, in itself, may accelerate vascular damage. Type 2 diabetes is a hypercoagulable state attributable to enhanced coagulation and decreased fibrinolysis, as well as platelet hyperaggregability and endothelial dysfunction. Hypertension is common in individuals with type 2 diabetes and has a major impact in the accelerated atherosclerosis of this disease. This review provides an overview of selected aspects of these alterations.

Arteriosclerosis↗

Menopause, central body fatness, and insulin resistance: effects of hormone-replacement therapy.

In addition to being associated with termination of reproductive life in women, the menopause coincides with an increase in several comorbidities including cardiovascular disease. This increase in the prevalence of cardiovascular disease in the postmenopausal years has been partially attributed to adverse effects of estrogen deficiency on plasma lipid-lipoprotein levels and on the cardiovascular system, although other factors are contributing. Central body fatness and insulin resistance are components of a cluster of metabolic abnormalities which also increases the risk of cardiovascular disease. This review summarizes studies that have examined the effects of the menopause transition and of estrogen-replacement therapy on central body fatness and insulin resistance. Review of cross-sectional studies suggests that the menopause transition is associated with an increase in abdominal and visceral adipose tissue accumulation, as measured either with dual X-ray absorptiometry or computed tomography. These results appear to be independent of the aging process and total body fatness. In general, cross-sectional studies using circumference measurements did not find any significant effect of the menopause. Longitudinal studies also support that accumulation of central body fatness accelerates with menopause. The effects of the menopause on insulin resistance appear to be moderate, if any, although available studies are clearly insufficient to draw firm conclusions. The majority of interventional studies support the notion that hormone-replacement therapy attenuates the accumulation of central fat in postmenopausal women, compared with control or placebo-treated women. Retrospective comparisons of hormone users and nonusers also support a protective effect of hormone replacement on fat distribution. Moderate effects of estrogen therapy were found on insulin resistance in postmenopausal women, although long-term, controlled trials using accurate measurements of insulin sensitivity are lacking. Treatment with progestins exerts moderate deleterious effects on insulin sensitivity, which may be attributable to the partial androgenicity of progestins used. It is concluded that part of the increased incidence of cardiovascular disease in postmenopausal women may be attributable to increased central body fatness. Therapies aiming at preventing these changes in fat distribution such as hormone-replacement therapy, diet or exercise are likely to provide long-term cardiovascular and metabolic benefits for women's health.

Abdomen↗

Total daily energy expenditure in free-living older African-Americans and Caucasians.

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.

Aged↗

Effects of short-term inactivity on glucose tolerance, energy expenditure, and blood flow in trained subjects.

The purpose of this investigation was to examine the effects of 7-10 days of inactivity (IA) on glucose tolerance (GT), resting metabolic rate (RMR), thermic effect of a meal (TEM), and limb blood flow in endurance-trained men. Eight highly trained (peak O2 consumption 64 +/- 2 ml . kg-1 . min-1) endurance athletes participated in this study involving two identical test days, one approximately 24 h after a normal training bout (Tr) and the second after 7-10 days of IA. The following tests were conducted at each visit: 75-g oral glucose tolerance test (OGTT), RMR, and TEM and measurements of calf and forearm blood flow (BF) by using venous occlusive plethysmography. Body weight remained unchanged during this short period of IA (Tr, 78.5 +/- 1 kg; IA, 78.7 +/- 1 kg). The area under the glucose and insulin curves increased 65% (Tr, 3,375 +/- 877 vs. IA, 5,559.4 +/- 621 mg . dl-1 . 180 min-1) and 73% (Tr, 2,182.5 +/- 270 vs. IA, 3,793.1 +/- 739 microU . ml-1 . 180 min-1) after IA, respectively (P < 0.01). RMR decreased significantly (4%; 1.5 +/- 0. 02 vs. 1.44 +/- 0.02 kcal/min; P < 0.05) and respiratory exchange ratio during the OGTT increased (4%, 0.812 +/- 0.011 vs. 0.842 +/- 0. 009; P < 0.05) after IA, whereas TEM increased similarly in the Tr and IA states. In the Tr state, mean calf BF increased by 22% (3.17 +/- 0.22 vs. 3.87 +/- 0.38 ml . 100 ml-1 . min-1; P < 0.05) during the OGTT but remained unchanged after IA, whereas no differences at rest or during OGTTs existed between the two conditions for forearm BF. Incremental insulin area above fasting during the OGTT was correlated with mean calf BF in the Tr (r = 0.76, P < 0.05) and IA (r = 0.72, P < 0.05) states. In conclusion, 7-10 days of IA results in a deterioration in GT and a reduction in RMR. After glucose ingestion, calf BF was elevated compared with resting levels in the Tr state but was unchanged in the IA state; however, limb BF was not related to GT or RMR. Thus our findings raise questions regarding the relative contribution of BF in modulating glucose tolerance and energy expenditure in endurance athletes in their habitual Tr or IA state.

Adult↗

Induction of hyperinsulinemia combined with hyperglycemia and hypertriglyceridemia increases plasminogen activator inhibitor 1 in blood in normal human subjects.

Hypofibrinolysis caused by increased plasminogen activator inhibitor 1 (PAI-1) has been implicated in the vasculopathy of type 2 diabetes, typified by increased insulin, glucose, and triglycerides. However, short-term infusions of insulin have not increased PAI-1 in normal subjects. We hypothesized that induction of increased insulin accompanied by increased glucose and triglycerides would increase PAI-1. Accordingly, 30% glucose and 10% Intralipid were infused for 6 h in ten normal lean individuals (54 +/- 3 years) resulting in increased insulin (42 +/- 5 microU/dl), glucose (200 +/- 24 mg/dl), and triglycerides (425 +/- 45 mg/dl), simulating changes in type 2 diabetes. In contrast to results with infusion of saline alone (n = 16) and euglycemic-hyperinsulinemic clamps (n = 10, serum insulin = 89 +/- 7 microU/dl), PAI-1 in blood increased significantly 6 h after the onset of infusion (15 +/- 5 ng/ml, P < 0.05 vs. baseline = 7.4 +/- 1.1, saline 6 h = 3.4 +/- 1.1, and insulin alone 6 h = 3.7 +/- 0.8) and remained elevated for an additional 6 h (combined infusion = 13.8 +/- 3.8 ng/ml, saline = 6.7 +/- 2 ng/ml, insulin alone = 7.8 +/- 1.7 ng/ml, P = 0.06). Our data suggest that combined hyperinsulinemia, hypertriglyceridemia, and hyperglycemia are likely to contribute to hypofibrinolysis of type 2 diabetes by increasing the blood levels of PAI-1. Moreover, these results underscore the potential importance of modifying insulin resistance as well as achieving glycemic and lipidemic control in individuals with type 2 diabetes.

Adult↗

Gender differences in fat oxidation and sympathetic nervous system activity at rest and during submaximal exercise in older individuals.

1. Gender differences in fat oxidation at rest and during exercise may contribute to higher body fat in women. We examined gender differences in fat oxidation at rest and during submaximal exercise and their relationship to sympathetic nervous system activity, free fatty acid availability, body composition and aerobic capacity in older volunteers. 2. We measured free fatty acid kinetics using [14C]palmitate, absolute (micromol/min) and relative (respiratory quotient) rates of fat oxidation by indirect calorimetry and sympathetic nervous system activity from noradrenaline kinetics using [3H]noradrenaline in 12 older men (70+/-4 years) and 12 older women (66+/-4 years) at rest and during 30 min of submaximal exercise (45% of peak oxygen consumption). 3. At rest, men oxidized more fat than women on both an absolute (88+/-19 versus 51+/-15 micromol/min; P<0.01) and relative (respiratory quotient: 0.80+/-0. 04 versus 0.85+/-0.04; P<0.01) basis. These differences were not related to noradrenaline appearance rate, free fatty acid concentration, body composition or aerobic capacity. During exercise, fat oxidation was higher (P<0.05 to P<0.01) in men on an absolute level, but respiratory quotient did not differ. Higher absolute fat oxidation in men during exercise was explained by their higher absolute workload. Plasma free fatty acids and free fatty acid rate of appearance did not differ between men and women during exercise despite higher (P<0.05 to P<0.01) plasma noradrenaline concentrations in men. 4. We conclude that: (i) resting fat oxidation is higher in older men compared with older women independent of differences in noradrenaline appearance rate, free fatty acid availability, body composition or aerobic capacity, and (ii) despite higher plasma noradrenaline concentrations during submaximal exercise, no gender differences in free fatty acid appearance rate or fat oxidation were found. These results suggest a sex dimorphism in post-absorptive fat metabolism in the elderly.

Aged↗

Gender differences in resting metabolic rate and noradrenaline kinetics in older individuals.

The physiological factors mediating gender differences in resting metabolic rate (RMR) in older individuals are presently unclear. We examined the contribution of sympathetic nervous system activity to gender differences in resting metabolic rate in older men and women and its relation to body fat distribution. We performed measurements of noradrenaline (NA) kinetics from infusions of [3H]-NA, RMR, body fat distribution, body composition, peak Vo2 and dietary intake in 29 older men (69 +/- 6 years) and 26 older women (65 +/- 5 years). Older men weighed more (P < 0.01) and had a greater fat-free mass (P < 0.01) and a larger waist circumference (P < 0.01) than older women. Older men had a higher RMR (P < 0.05) than older women, which persisted after controlling for differences in fat-free mass and fat mass. Older men also showed a greater NA appearance rate (P < 0.01) at rest than older women. The higher NA appearance rate in older men was partly related to their greater waist circumference (r = 0.50, P < 0.01). We explored the sympathetic contribution to gender differences in RMR by statistically controlling for differences in body composition and NA appearance rate. After this procedure, we found no gender differences in adjusted RMR between older men (4.3 +/- 0.5 kJ min(-1)) and older women (4.3 +/- 0.4 kJ min(-1)). Our results suggest that: (a) older men have a higher RMR than older women independent of differences in body composition; (b) the higher RMR in older men may be partly due to higher levels of sympathetic nervous system activity; (c) the higher sympathetic nervous system activity in older men is partly related to their greater waist circumference, a proxy measure of central body fatness.

Aged↗

Relationship between physical activity and HDL-cholesterol in healthy older men and women: a cross-sectional and exercise intervention study.

We used cross-sectional and exercise intervention studies to examine whether physical activity levels or increases in peak aerobic capacity (peak VO2) explain variation in high density lipoprotein cholesterol (HDL-C) levels in older men and women. In the cross-sectional study, 307 older individuals (169 men; 138 women; 67 +/- 7 years) were characterized for HDL-C, leisure time physical activity, peak VO2, body composition, body fat distribution and dietary intake. HDL-C was 19% higher (P < 0.001) in women (57 +/- 14 mg/dl) versus men (48 +/- 14 mg/dl). Thirty-two percent of the variation in HDL-C in older men was explained by the waist circumference (r2 = 16%), percent dietary intake of alcohol (r2 = 11%), and carbohydrate (r2 = 6%). Waist circumference was also the best predictor of HDL-C in older women, (r2 = 7%); with percent dietary intake of carbohydrate adding an additional 6% to the model. Neither peak VO2 nor leisure time physical activity were independent predictors of HDL-C. Statistical control for the aforementioned variables diminished, but did not abolish gender differences in HDL-C. Thirty-seven older individuals (23 men; 14 women) participated in a 2-month exercise program in which individuals by week eight were expending approximately 900 kcal per week in exercise energy expenditure. Subjects were maintained in energy balance throughout the exercise program. Endurance training significantly increased peak VO2 by 15% in both men and women, and by design, body composition and body fat distribution did not change. No changes in HDL-C levels were noted. In conclusion, variations in leisure time physical activity or increases in peak VO2 are not independent predictors of HDL-C levels in healthy older men and women. Instead, central adiposity, as estimated by the waist circumference, and to a lesser extent, dietary intake of carbohydrate and alcohol, are significant predictors of variation in plasma HDL-C levels. Furthermore, short-term exercise training, generating less than 900 kcal per week in exercise energy expenditure, in the absence of weight loss, fails to influence HDL-C levels.

Aged↗

The membrane-associated 40 KD fatty acid binding protein (Berk's protein), a putative fatty acid transporter is present in human skeletal muscle.

Muscle tissue (1.1 +/- 0.1 grams) was obtained from seven healthy individuals (3 males, 4 females) using an open incision approach before and after ingestion of either 75 grams of dextrose (N=5) or water (N=2). Purified sarcolemmal membranes from the muscle were prepared using a sucrose step gradient. A polyclonal antibody raised against the purified (99%) rat hepatocyte 40 KD membrane fatty acid binding protein (mFABP-L) was used to probe for this putative transporter in the muscle membranes using Western blot. A single band at the 40 KD MW band was identified which reacted antigenically with the protein purified from rat livers. These response of Berk's protein 60-75 minutes after dextrose ingestion (or water) was erratic and no specific trend could be identified. Our data demonstrate that the 40 KD mFABP-L originally isolated from rat liver is also present in human skeletal muscle membrane. This protein may be involved in transport of fatty acids across the membrane of skeletal muscle, however its physiological role in human fatty acid metabolism remains to be established.

Adult↗

Decrease in fat oxidation following a meal in weight-reduced individuals: a possible mechanism for weight recidivism.

This study examined the effect that dietary-induced weight loss has on body composition, energy metabolism, and substrate oxidation at rest and during the 5-hour period following a meal. Twenty older (age:mean +/- SE, 61 +/- 1 years; range, 56 to 70 y) obese (body mass index > 32 kg/m2) subjects (12 women, eight men) completed an 11-week dietary restriction program in which they lost 9 +/- l kg. Fat and fat-free mass were reduced (P < .05) by 15% and 5%, respectively. Resting metabolic rate decreased by 15% (P < .05). Overall, weight loss did not alter the percentage of energy derived from fat sources (approximately 47% of energy) under resting conditions. In contrast, the percentage of calories derived from fat during the 5-hour postmeal period decreased from baseline to post-weight loss from 38% +/- 3% to 26% +/- 4% (P < .05) of total calories expended. The reduction in fat oxidation subsequent to a meal may facilitate fat storage, and may be one mechanism by which one regains weight following weight loss.

Aged↗

Contrasting effects of resistance and aerobic training on body composition and metabolism after diet-induced weight loss.

This study examined whether exercise training facilitates maintenance of body weight at reduced levels following weight loss by attenuating weight loss-induced reductions in resting metabolism and fat oxidation. The effects of 12 weeks (three times per week) of either aerobic or weight training exercise on body weight, body composition, and energy metabolism during rest and following a meal in 18 older (mean +/- SE, 61 +/- 1 years; range, 56 to 70) subjects who had recently lost a mean of 9 +/- 1 kg were studied. During the exercise training period, the aerobic training group (five women, four men) had a significant (P < .05) reduction in body weight (-2.5 +/- 0.6 kg) as compared with the weight training group (five women, four men) (0.4 +/- 0.9 kg). Eight of nine aerobic training subjects lost additional weight, while six of nine weight training subjects gained weight. Neither type of training reversed the depressions in resting metabolism or fat oxidation rates (ie, resting or postprandial) that had occurred as a consequence of the prior weight loss. Thus, alterations in resting metabolism or fat oxidation (resting or postprandial) do not appear to be the mechanism(s) by which exercise training facilitates maintenance of diet-induced weight loss.

Aged↗

Amelioration of the inhibition of fibrinolysis in elderly, obese subjects by moderate energy intake restriction.

A possible cause of accelerated atherothrombosis in the syndrome of insulin resistance appears to be an elevated blood concentration of plasminogen activator inhibitor type-1 (PAI-1). Insulin resistance occurs with aging, attributable partly to increased adiposity. Scarce information exists regarding the effects of weight loss in elderly, obese individuals on PAI-1 concentrations. Consequently, weight loss (9 +/- 1 kg) was induced by energy intake restriction in 19 elderly, obese individuals, and its effect on fibrinolytic system peptides was measured. Initially elevated PAI-1 concentrations decreased by 50%, with a simultaneous decrease in the concentration of tissue-type plasminogen activator (t-PA)/PAI-1 complexes but no significant change in t-PA suggested a decrease in inhibition of the fibrinolytic system. The concentration of plasmin/antiplasmin complexes (PAP complex) increased by approximately 20%, indicating augmented fibrinolytic system activity. The decline in PAI-1 correlated with that of the decrease in body weight (r = 0.5, P < 0.05) and fat mass losses (r = 0.46, P < 0.05). The increase in PAP complexes correlated with weight and fat mass losses (r = 0.4 and r = 0.46, respectively; P < 0.05 for both). No correlation was seen between fibrinolytic system variables and baseline concentrations of substrates or insulin, but the change in PAI-1 correlated with the change in plasma triacylglycerols (r = 0.58, P < 0.05). Results indicate that energy restriction sufficient to induce moderate weight loss leads to diminution of elevated plasma PAI-1 and relief of inhibition of the fibrinolytic system in elderly, obese subjects. To the extent that these changes are associated with a decrease in the progression of vasculopathy, weight loss in elderly, obese individuals may be a useful means to reduce cardiovascular morbidity and mortality.

Aged↗

Rates of free fatty acid appearance and fat oxidation in healthy younger and older men.

Alterations in the mobilization and oxidation of fat may partially account for age-related alterations in body composition. To investigate age-related alterations in fat metabolism, we compared basal rate of appearance of free fatty acids (FFAapp) and total body fat oxidation as measured by infusions of [14C] palmitate and indirect calorimetry, respectively, in 18 younger (23 +/- 1 yr) and 30 older (69 +/- 1 yr) men. We also examined whether age-related differences in body composition, body fat distribution, peak oxygen consumption, dietary intake, and/or fasting insulin levels may explain age-related variation in FFAapp and total body fat oxidation. The FFAapp showed a tendency to be higher in older compared with younger men (1,134 +/- 184 vs. 680 +/- 105 mu mol/min; P = 0.07), whereas total body fat oxidation was similar between groups (257 +/- 25 vs. 222 +/- 9 mu mol/min). The estimated rate of nonoxidative disposal of free fatty acids showed a tendency to be higher in the older (913 +/- 182 mu mol/min) than in younger men (423 +/- 103 mu mol/min; P = 0.06). Fat-free mass was the most significant predictor of FFAapp in younger (r = 0.63; P < 0.01) and older (r = 0.41; P < 0.05) men. These results suggest that older men recruit fatty acids from adipose tissue stores in excess of the energy needs of respiring tissue. However, variation in FFAapp between the age groups could not be explained by differences in body habitus or fasting insulin levels.

Adult↗

Effects of caffeine ingestion on NE kinetics, fat oxidation, and energy expenditure in younger and older men.

Age-related differences in energy expenditure, fat oxidation, and norepinephrine (NE) kinetics after caffeine ingestion were examined using a placebo-controlled double-blind study in 10 older (O, 65-80 yr) and 10 younger (Y, 19-26 yr) men who were moderate consumers of caffeine. Caffeine ingestion resulted in similar increases in Y and O men for plasma caffeine levels (Y = 89 +/- 100 to 6,340 +/- 1,938 ng/ml, P < 0.05; O = 124 +/- 38 to 7,066 +/- 2,366 ng/ml, P < 0.05) and energy expenditure (Y = 11%, 1.38 +/- 0.15 to 1.52 +/- 0.22 kcal/min, P < 0.05; O = 9.5%, 1.15 +/- 0.13 to 1.26 +/- 0.20 kcal/min, P < 0.05). However, caffeine ingestion increased fatty acid concentrations (362 +/- 159 to 803 +/- 253 mumol/l, P < 0.05) and tended to increase rate of appearance of fatty acids (624 +/- 376 to 1,394 +/- 1,331 mumol/l, P = 0.07) in younger but not older men. Rates of fat oxidation and NE appearance and clearance did not significantly differ from baseline values in either group. In conclusion, older and younger men show a similar thermogenic response to caffeine ingestion, whereas older men show a smaller increase in fatty acid availability after a caffeine challenge. These metabolic differences are not related to alterations in NE kinetics or fat oxidation.

Administration, Oral↗

Sympathetic nervous system activity, body fatness, and body fat distribution in younger and older males.

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.

Adipose Tissue↗

Effects of endurance training on total fat oxidation in elderly persons.

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.

Aged↗

Effects of increased energy intake and/or physical activity on energy expenditure in young healthy men.

This study was designed to examine effects of alterations in energy balance on adaptive changes in components of total energy expenditure (TEE). Nineteen young healthy males were studied during a 10-day sedentary energy balance baseline period and then randomly assigned to one of four 10-day treatment groups: 1) no change in energy intake (EI) or physical activity (PA; energy balance at low energy flux), 2) EI increased by 50% with no change in PA (positive energy balance), 3) TEE increased by 50% by increasing PA, matched by a 50% increase in EI (energy balance at high energy flux), and 4) TEE increased by 50% by increasing PA with no change in EI (negative energy balance). TEE was measured with doubly labeled water, resting metabolic rate (RMR) by indirect calorimetry, and thermic response to feeding (TEF) by indirect calorimetry; energy expenditure of physical activity (EEPA) was estimated by subtracting RMR, TEF, and prescribed PA from TEE. TEE was significantly increased by PA (by design) but not EI. There was a significant main effect of intake and a significant intake-by-activity interaction for changes in RMR. In post hoc analysis, RMR was significantly increased during positive energy balance and energy balance at high energy flux relative to change in RMR when energy balance was maintained at low energy flux. A significant increase in RMR was also noted during negative energy balance after adjustment for change in fat-free mass. There was no significant difference in change in RMR among the three treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗