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Biomedical subjects

L S Lamont

Publications and source records attributed to L S Lamont.

At least 19 recordsLinked to original sources
PubMed2001

Relationship between leucine oxidation and oxygen consumption during steady-state exercise.

PURPOSE: The purpose of this study was to assess the relationship between whole-body leucine oxidation and oxygen consumption during steady-state exercise. Our hypothesis was that leucine oxidation will be responsive to increased whole-body energy needs. METHODS: Sixteen healthy individuals (7 women and 9 men) were infused with a stable isotope of leucine and, for comparison purposes, lysine during 60 min of moderate-intensity exercise. RESULTS: Leucine oxidation was increased (P < 0.05) and nonoxidative leucine disposal was decreased (P < 0.05), whereas leucine and lysine rate of appearance remained unchanged (P = NS) during exercise. Linear regression analysis indicated a modest relationship between leucine oxidation and steady-state oxygen consumption (R = 0.69; P < 0.003) during steady-state exercise. The coefficient of determination (R(2) = 0.49) indicates that approximately half of the variance in whole-body leucine oxidation during exercise can be explained by whole-body oxygen consumption. CONCLUSION: In a statistically appropriate sample size of humans whose dietary intake was controlled, the whole-body rate of leucine oxidation during exercise was only partially influenced by energy demands.

Adult↗
PubMed2001

Gender differences in leucine, but not lysine, kinetics.

There is a controversy in the literature as to the effects of gender on leucine kinetics. Two research groups found that men oxidize more leucine during exercise, whereas another group showed no gender effects. The purpose of our study was to examine the effects of gender on leucine and, for comparison purposes, lysine kinetics. Our subjects (n = 14) were seven matched pairs of men and women selected for their exercise habits and age. After 1 wk of a standardized diet, they exercised at 50% of maximal O(2) uptake for 1 h. There was an effect of exercise in both genders: an increased leucine oxidation and an attenuation in nonoxidative leucine disposal compared with rest (P < 0.05). Furthermore, our study confirms that there are gender differences in leucine, but not lysine, kinetics. Men had a higher rate of leucine oxidation and a lower rate of nonoxidative leucine disposal during exercise (P < 0.05). For women, a larger proportion of their exercise energy needs came from fat; for men, a greater fraction came from carbohydrate (P < 0.05). We conclude that female exercisers rely to a greater extent on fat as an energy source, thereby using less carbohydrate, amino acid, and protein as a fuel source.

Adult↗
PubMed1999

Comparison of leucine kinetics in endurance-trained and sedentary humans.

Whole body leucine kinetics was compared in endurance-trained athletes and sedentary controls matched for age, gender, and body weight. Kinetic studies were performed during 3 h of rest, 1 h of exercise (50% maximal oxygen consumption), and 2 h of recovery. When leucine kinetics were expressed both per unit of body weight and per unit of fat-free mass, both groups demonstrated an increase in leucine oxidation during exercise (P < 0.01). Trained athletes had a greater leucine rate of appearance during exercise and recovery compared with their sedentary counterparts (P < 0.05) and an increased leucine oxidation at all times on the basis of body weight (P < 0.05). However, all of these between-group differences were eliminated when leucine kinetics were corrected for fat-free tissue mass. Therefore, correction of leucine kinetics for fat-free mass may be important when cross-sectional investigations on humans are performed. Furthermore, leucine oxidation, when expressed relative to whole-body oxygen consumption during exercise, was similar between groups. It is concluded that there was no difference between endurance-trained and sedentary humans in whole body leucine kinetics during rest, exercise, or recovery when expressed per unit of fat-free tissue mass.

Adult↗
PubMed1997

Beta 1-adrenoreceptors regulate resting metabolic rate.

This was a randomized, cross-over experiment designed to determine which beta-adrenergic receptors, beta 1, beta 2, or both, regulate metabolic rate in humans. All subjects (3 women, 4 men) were administered a 7-d therapeutic dose of a selective beta 1-antagonist (atenolol 50 mg BID), a combined beta 1, beta 2-antagonist (propranolol 80 mg BID), and a placebo control (BID). Indirect calorimetry was determined before and after 1 h of submaximal exercise. Exercise was performed at 50% of the trial specific VO2peak because maximal exercise was significantly decreased in the presence of the nonselective beta 1, beta 2-antagonist (VO2peak placebo: 44.90 +/- 4.40 mL.kg-1.min-1 vs beta 1, beta 2-antagonism: 39.20 +/- 3.00 mL.kg-1.min-1; P < 0.05). Both the beta 1 and the combined beta 1, beta 2-adrenoreceptor antagonists reduced resting oxygen consumption to a similar extent (0.247 +/- 0.007 L.min-1 placebo, vs 0.218 +/- 0.007 L.min-1 beta 1-antagonism, vs 0.226 +/- 0.007 L.min-1 beta 1, beta 2-antagonism; P < 0.05). However, the 30-min and 60-min excess post-exercise oxygen consumption (mean EPOC) remained unchanged. It is concluded that the beta 1-receptors are regulating the effects of the sympathetic nervous system on resting but not exercise recovery metabolic rate. These metabolic side effects may suggest that changes need to be made in the nutritional requirements of patients using beta-adrenergic antagonists.

Adrenergic beta-Antagonists↗
PubMed1995

Beta-adrenergic blockade heightens the exercise-induced increase in leucine oxidation.

The purpose of this study was to assess the interaction between beta-blockade and exercise on amino acid kinetics. This was a three-way crossover experiment using beta 1-blockade, beta 1,beta 2-blockade, and a placebo control. Three 6-h L-[1-13C]leucine and L-[alpha-15N]lysine infusions were performed. The first 3 h established an isotopic steady state, and 1 h of exercise (approximately 50% of maximal O2 consumption) and 2 h of recovery followed. Plasma glucose decreased with exercise during all trials (P < 0.0001). During beta 1- and beta 1,beta 2-blockade, plasma free fatty acids were reduced during rest and exercise (P < 0.001). Leucine and lysine rates of appearance were unaffected by beta-blockade during rest but were decreased with placebo exercise. Leucine oxidation increased with beta-blockade (P < 0.01) and exercise (P < 0.001). There was a statistical interaction between both treatments (P < 0.004). In conclusion, leucine oxidation increased with exercise, further increased with beta 1-blockade, and was additionally heightened with beta 1,beta 2-blockade. This cumulative response indicates that leucine oxidation was regulated through beta 1- and beta 2-receptors.

Adrenergic beta-Antagonists↗
PubMed1990

Leucine kinetics in endurance-trained humans.

This study compared whole-body leucine kinetics in endurance-trained (TRN) and sedentary (SED) control subjects. Eleven men and women (6 TRN, 5 SED) underwent a 6-h primed, constant-rate infusion of L-[1-13C]leucine. Leucine turnover and oxidation were measured using tracer dilution and by measuring 13C enrichment of expired CO2 combined with respiratory calorimetry. Whole-body leucine turnover was greater in the TRN subjects (P less than 0.004; TRN 98.3 +/- 5.0, SED 75.3 +/- 4.2 mumol.kg-1.h-1; mean +/- SE), but there was no difference between groups in leucine oxidation (TRN 13.1 +/- 0.97, SED 11.5 +/- 0.48 mumol.kg-1.h-1). Thus more leucine turnover was available for nonoxidative utilization. In addition, the TRN subjects had higher resting energy expenditures compared with the SED group, and when all subjects were included in the analysis, there was a significant correlation between energy expenditure and protein turnover (n = 11, R = 0.61, P = 0.05). Therefore the heightened resting energy expenditure in the TRN subjects may be accounted for by an increased whole-body protein turnover. These results suggest that endurance training results in increased leucine and/or protein turnover, which may contribute to the increased resting energy expenditure observed in these subjects.

Adult↗
PubMed1989

Beta-adrenergic blockade alters whole-body leucine metabolism in humans.

This study examined the effects of a nonselective beta-blocking agent on whole-body leucine metabolism in humans. Five normal, healthy subjects (4 male, 1 female) underwent a 6-h primed, constant-rate infusion of L-[1-13C]leucine after 5 days of twice daily oral use of 80 mg propranolol and a placebo. Leucine turnover was determined by tracer dilution and leucine oxidation by 13C enrichment of the expired CO2. Propranolol decreased the total daily energy expenditure from 1,945 +/- 177.5 to 1,619 +/- 92.5 kcal/day (P less than 0.05). A fasting associated decrease in blood glucose and an attenuated rise in free fatty acids and ketones were observed during beta-blockade. Propranolol also increased plasma leucine concentrations (73.1 +/- 8.7 to 103.4 +/- 7.3 mumol/l; P less than 0.05) and leucine oxidation (13.2 +/- 1.2 to 17.1 +/- 1.3 mumol.kg-1.h-1; P less than 0.05), although leucine turnover was not significantly altered (100.5 +/- 7.3 vs. 126.0 +/- 12.3 mumol.kg-1.h-1). In addition, the urinary urea nitrogen-to-creatinine ratio was greater during propranolol administration (0.24 +/- 0.04 vs. 0.34 +/- 0.02 mol/g; P less than 0.05). These data suggest that the beta-adrenergic system plays a role in the modulation of whole-body leucine metabolism in humans. Whether these changes are the result of a direct effect on skeletal muscle or an indirect effect mediated by altering the fuel supply to skeletal muscle cannot be discriminated by the present study.

Adult↗
PubMed1987

Sweat lactate secretion during exercise in relation to women's aerobic capacity.

The purpose of this investigation was to determine whether sweat lactate secretion during exercise [approximately 70% maximum O2 consumption (VO2max), 60 min] differed in active vs. sedentary female subjects. Sweat rate, total sweat lactate secretion, and sweat lactate concentration were monitored in a group of sedentary (VO2max = 41.0 +/- 1.62 ml X kg-1 X min-1) and active (VO2max = 51.2 +/- 3.20 ml X kg-1 X min-1) women. Sweat rate was significantly (P less than 0.05) greater in the active subjects. There was a significant difference between groups in total amount of sweat lactate secreted (P less than 0.05), with the active group secreting less lactate (29.8 +/- 5.03 mmol, mean +/- SE) than the sedentary group (50.2 +/- 6.61 mmol). Concomitant with the lower total sweat lactate secretion in the active subjects was a significantly (P less than 0.05) more dilute sweat lactate concentration (42.6 +/- 14.08 vs. 100.4 +/- 32.37 mM). In these female subjects, sweat lactate concentration was inversely correlated (r = -0.79, P less than 0.01, n = 10) to sweat rate. It is concluded that total sweat lactate loss is significantly less in active than in sedentary women and that the active subjects secrete a greater quantity of lactate dilute sweat.

Adult↗
PubMed1987

Menstrual cycle and exercise effects on protein catabolism.

The purpose of this investigation was to determine whether exercise at different times of the menstrual cycle alters protein catabolism. Nine women exercised for 60 min at 70% VO2max when serum estradiol (E) and progesterone (P) were low (menses) and when both were high [mid-luteal (ML)]. Diet was reproduced on both occasions. Serum urea nitrogen (N), E, and P were analyzed at rest, after 15, 30, 45, and 60 min of exercise, and 15 min into recovery. Sweat urea N excretion was also determined. Urinary area N excretion was measured the day before, the day of, and 2 d following exercise. E and P were significantly greater in the ML phase, and this difference was maintained throughout exercise (P less than 0.05). No change was seen in serum urea N across exercise or between phases. Both exercise day urinary urea N excretion and total urea N excretion in sweat and urine, when added across all experimental days, were significantly greater in the ML phase compared to menses (8.5 +/- 0.96 vs 5.5 +/- 0.81 g and 24.8 +/- 2.38 vs 19.3 +/- 1.38 g, respectively, P less than 0.05). The data suggest that the greater protein use in the ML phase was due to the combined effects of exercise, a changing hormonal milieu and other unknown causes.

Adult↗
PubMedDate not supplied

Beta-blockers and their effects on protein metabolism and resting energy expenditure.

In summary, beta-adrenergic receptor blocking medications have numerous metabolic side effects. Recent evidence indicates that this class of drug acutely decreases whole-body metabolic rate and increases protein oxidation in the resting human. The result of this metabolic perturbation may be a deleterious change in body composition and perhaps a creeping increase in body weight, if no subsequent alterations are made in food consumption or activity patterns. Research indicates that long-term treatment with beta-blockade may increase body fat and decrease the fat-free tissue content of the organism. Exercise is known to favorably affect body composition by decreasing percent body fat, while increasing the fat-free body tissue. Beginning a regular, moderate exercise program may help ameliorate these deleterious nutritional side effects of long-term beta-blocker therapy. Additionally, the recommendation to engage in a moderate exercise program is further indicated because of the underlying cardiovascular pathophysiology that originally required long-term beta-adrenergic treatment.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

The major components of human energy balance during chronic beta-adrenergic blockade.

PURPOSE: The authors compare the major components of energy balance--dietary food intake, resting metabolic rate, and physical energy expenditure--in patients receiving beta-blocking medications and healthy controls. METHODS: The authors recruited subjects who were receiving beta-blocking agents (n = 22) from local hospitals and clinics. Twenty-two healthy controls were matched to each patient based on age, weight, and gender. Resting metabolic rates were determined using indirect calorimetry. Three-day dietary intakes and physical activity assessments were analyzed. RESULTS: There were no between-group differences in calories ingested or self-reported physical activity patterns. However, resting metabolic rates were lower in the beta-blocked subjects (beta-blocked = 1,541 +/- 464 kcals/day; controls = 1,817 +/- 426 kcals/day; P < 0.05). CONCLUSIONS: beta-adrenergic blockade causes a reduction in resting metabolic rate. Therefore, beta-blocked individuals should increase physical activity, decrease dietary intake, or both to maintain daily energy balance and prevent weight gain that accompanies a reduction in metabolic rate.

Adrenergic beta-Antagonists↗