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Results for “energy deficit”

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At least 19 recordsLinked to original sources

PubMed1998

Relation between circulating leptin concentrations and appetite during a prolonged, moderate energy deficit in women.

BACKGROUND: On the basis of observations in rodents, leptin is thought to play a key role in the regulation of energy expenditure and food intake, but less is known of its influence on ingestive behavior and energy balance in humans. OBJECTIVE: We examined the effect in women of a chronic energy deficit on plasma leptin concentrations and self-reported appetite and explored possible relations between leptin and appetite sensations. DESIGN: Twelve healthy women (body mass index, in kg/m2: 23-37) participated in a metabolic ward study in which 3 wk of neutral energy balance was followed by 12 wk of energy deficit (energy intake reduced by 2 MJ/d and energy expenditure increased by 0.8 MJ/d). Body weight and composition were monitored, fasting leptin concentrations were measured 4 times, and feelings of hunger, fullness, desire to eat, and prospective consumption were monitored hourly throughout the day on 7 selected days. RESULTS: Adiposity-adjusted leptin decreased by 54% after 1 wk of a moderate energy deficit and remained low after 6 and 12 wk. Leptin was associated with self-reported hunger, desire to eat, and prospective consumption (range of r: -0.6 to -0.7, P < 0.01). The greatest hunger increase coincided with the largest percentage drop in circulating leptin and the lowest final leptin concentration. The relation between leptin and hunger was not influenced by amount of weight or body fat loss. CONCLUSIONS: These findings support the idea that leptin is a physiologic regulator of hunger during energy deficits in humans; the role of leptin in the long-term regulation of food intake warrants further study.

Adipose Tissue↗

PubMed2000

Relationship between energy deficits and body composition in elite female gymnasts and runners.

PURPOSE: The purpose of this study was to evaluate energy balance and body composition in 42 gymnasts (mean age = 15.5 yr) and 20 runners (mean age = 26.6 yr), all of whom were on national teams or were nationally ranked. METHODS: Athletes were assessed for body composition using DEXA and skinfolds, and energy balance was determined with a Computerized Time-Line Energy Analysis (CTLEA) procedure. RESULTS: Results from the CTLEA were assessed as the number of within-day energy deficits (largest and frequency) and within-day energy surpluses (largest and frequency). There was a significant difference (P = 0.000) in the mean number of hourly energy deficits > 300 kcal experienced by gymnasts (9.45 +/- 6.00) and runners (3.70 +/- 5.34). There was also a significant difference (P = 0.001) in the mean number of hourly energy surpluses > 300 kcal experienced by gymnasts (1.40 +/- 3.04) and runners (6.20 +/- 5.50). The mean largest daily energy deficit was 743 (+/- 392) kcal for gymnasts and 435 (+/- 340) kcal for runners. The mean largest daily energy surplus was 239 (+/- 219) kcal for gymnasts, and 536 (+/- 340) kcal for runners. There was a significant relationship between the number of daily energy deficits > 300 kcal and DEXA-derived body fat percent for gymnasts (r = 0.508; P = 0.001) and for runners (r = 0.461; P = 0.041). There was also a negative relationship between the largest daily energy surplus and DEXA-derived body fat percentage for gymnasts (r = -0.418; P = 0.003). Using the energy balance variables, age, and athlete type (artistic gymnast, rhythmic gymnast, middle-distance runner, long-distance runner) as independent variables in a forward stepwise regression analysis, a small but significant amount of variance was explained in DEXA-derived (P = 0.000; R2 = 0.309) and skinfold-derived (P = 0.000; R2 = 0.298) body fat percent by the number of energy deficits > 300 kcal and age. CONCLUSIONS: These data suggest that within-day energy deficits (measured by frequency and/or magnitude of deficit) are associated with higher body fat percentage in both anaerobic and aerobic elite athletes, possibly from an adaptive reduction in the REE. These data should discourage athletes from following restrained or delayed eating patterns to achieve a desired body composition.

Adolescent↗

PubMed1999

Modeling of energy balance in early lactation and the effect of energy deficits in early lactation on first detected estrus postpartum in dairy cows.

The general pattern of energy balance in early lactation was modeled. For this purpose, several lactation curves were investigated. The best fitting curve was fit in a random regression model that provided predicted energy balance curves for all lactations. By use of these curves, total energy deficit per lactation, postpartum interval of return to positive energy balance, and nadir of energy balance was determined. In predicted energy balances, nadir of energy balance was present, but variation in postpartum interval to nadir was small. First lactation cows had a smaller energy deficit in early lactation than did older cows. Differences among cows in nadir and total energy deficits in early lactation were large. Both were related to the postpartum interval to first detected estrus with a larger energy deficit and a smaller nadir corresponding to a larger postpartum interval to first detected estrus. From this study, it can be concluded that large energy deficits in early lactation delay first detected estrus.

Animals↗

PubMed2004

Energy deficit without reducing dietary carbohydrate alters resting carbohydrate oxidation and fatty acid availability.

Reduced carbohydrate (CHO) availability after exercise has a potent influence on the regulation of substrate metabolism, but little is known about the impact of fat availability and/or energy deficit on fuel metabolism when dietary CHO availability is not reduced. The purpose of this study was to determine the influence of a postexercise energy deficit, independent of CHO availability, on plasma substrate concentrations and substrate oxidation. Seven moderately trained men (peak oxygen uptake: 56 +/- 2 ml.kg(-1).min(-1)) performed exhaustive cycling exercise on two separate occasions. The two trials differed only by the meals ingested after exercise: 1) a high-fat diet designed to maintain energy balance or 2) a low-fat diet designed to elicit energy deficit. The CHO and protein contents of the diets were identical. The next morning, we measured plasma substrate and insulin concentrations and CHO oxidation, and we obtained muscle biopsies from the vastus lateralis for measurement of pyruvate dehydrogenase kinase (PDK)-2 and PDK-4 mRNA expression by using RT-PCR. Despite identical blood glucose (5.0 +/- 0.1 and 4.9 +/- 0.1 mM) and insulin (7.9 +/- 1.1 and 8.4 +/- 0.9 microU/ml) concentrations, plasma fatty acid and glycerol concentrations were elevated three- to fourfold during energy deficit compared with energy balance and CHO oxidation was 40% lower (P < 0.01) the morning after energy deficit compared with energy balance (328 +/- 69 and 565 +/- 89 micromol/min). The lower CHO oxidation was accompanied by a 7.3 +/- 2.5-fold increase in PDK-4 mRNA expression after energy deficit (P < 0.05), whereas PDK-2 mRNA was similar between the trials. In conclusion, energy deficit increases fatty acid availability, increases PDK-4 mRNA expression, and suppresses CHO oxidation even when dietary CHO content is not reduced.

Adult↗

PubMedDate not supplied

Energy deficits associated with nasogastric feeding in patients with burns.

This study was designed to identify whether significant energy deficits occur when feedings are (1) withheld perioperatively and (2) withheld because of gastric ileus. We studied patients with more than 20% total body surface area burns, who had survived at least one surgery, and who were intubated within 3 days of admission. Energy needs and energy received from enteral feedings were summed across the period during which the patients underwent surgical procedures. The difference between energy needed and energy received was divided into that caused by feedings being withheld perioperatively and that caused by feedings being withheld because of a gastric ileus. Twenty-five patients (9 women and 16 men) were included in the study. The total energy deficit was a mean of 15,969 kcal (31.6% of 50,546 kcal needed); 58% of the energy deficit (9264 kcal of the 15,969 kcal deficit) was caused by feedings being withheld perioperatively and 42% of the energy deficit (6705 kcal of the 15,969 kcal deficit) was caused by feedings being withheld because of gastric ileus. The withholding of feedings perioperatively and because of gastric ileus were both significant contributors to energy deficits. Future studies are necessary to determine whether energy needs being more closely met would result in improved outcomes for these patients.

Adult↗

PubMed2004

Leptin, thyrotropin, and thyroid hormones in obese/overweight women before and after two levels of energy deficit.

The aim of our study was to compare serum concentration of leptin and pituitary-thyroid axis hormones in obese/overweight women before and after two levels of energy deficit with those parameters in lean women on adequate energy intake. Additionally, we attempted to elucidate if the effect of weight reduction could be related to anthropometric and hormonal parameters before treatment. Anthropometric and hormonal parameters-serum leptin, TSH, T4, fT4, T3 and leptin to fat mass (Lep/fm), T3/T4, fT4/T4, T4/TSH, fT4/TSH--were compared in two groups of women (n =18 each)--lean women (C: BMI 22.0 +/- 1.2) and overweight/obese (Ov/Ob: BMI 29.9 +/- 3.3). Ov/Ob women were subjected to weight-reducing treatment consisting of energy intake equal to 80% of calculated total energy expenditure for the first 4 wk and to 50% for subsequent 4 wk. All baseline hormone concentrations, Lep/fm, and fT4/T4 were higher in overweight/obese group. After 20% energy deficit decrease in BMI, percent body fat (fm%), leptin, T3, and TSH serum concentrations as well as in Lep/fm and T3/T4 was observed; T4/TSH increased, fT4, fT4/T4 and fT4/TSH did not change significantly. Increase in energy deficit from 20% to 50% resulted in normalization of Lep/fm, on the other hand, it provoked greater decline in thyroid hormone plasma concentration, which could hinder further mass reduction. Leptin and TSH levels were positively correlated after 50% energy deficit treatment. Changes in fm% were directly related to baseline T4/TSH, fT4/TSH, and log TSH. In conclusion, TSH serum concentration and its ratio to T4 and fT4 before weight reduction could be a good predictor of successful weight loss.

Adipose Tissue↗

PubMed2003

Influence of cortisol, gonadal steroids and an energy deficit on biochemical indicators of bone turnover in Swine.

In the pig a high growth potential seems to favour a disposition for skeletal problems. Hormones of growth hormone (GH)/insulin-like growth factor (IGF)-I axis as well as cortisol and gonadal steroids are endocrine determinants of the anabolic potential but their effects on bone turnover in pigs have not been described. Thus, key hormones were either infused for 7 days (cortisol, 5alpha-dihydrotestosterone (DHT), oestradiol) or influenced by Metyrapone (inhibition of cortisol synthesis) or energy deficit (increasing GH). Each treatment was carried out in six growing barrows/treatment. Bone turnover was characterized by daily measurements indirect parameter of osteoblastic and osteoclastic activity, osteocalcin (OC) and tartrate-resistant acid phosphatase (TRAP) respectively. All treatments except cortisol infusion seemed to favour bone formation, as they led either to a pronounced increase in OC (Metyrapone: +14%) or to significantly reduced TRAP (DHT: -9%, E2: -17%, energy deficit: -25%) followed by significantly higher OC (DHT: +9%, E2: +6%, energy deficit: +18%). Cortisol infusion affected bone loss mainly by a severe inhibition of osteoblastic activity (OC: -61%). Some reactions are explained by direct effects of the infused gonadal steroids on bone cells (inhibition of osteoclasts) or of the experimentally modified cortisol levels (inhibition of osteoblasts by cortisol). Other effects seem to be mediated by concomitant changes of IGF-I (inhibition of osteoclasts after energy deficit or cortisol) and GH-secretion (increased osteoblastic activity during energy deficit), respectively. Consequences for co-ordinated bone turnover are discussed.

Acid Phosphatase↗

PubMed1998

Uncoupling the effects of energy expenditure and energy intake: appetite response to short-term energy deficit induced by meal omission and physical activity.

The effects of two methods of inducing an acute energy deficit (exercise and a low-energy breakfast) on appetite were investigated in 11 healthy females, all of whom were regular exercisers and regular breakfast eaters. There were four experimental days: with exercise and a high-energy (500 kcal) breakfast (EHB), exercise and a low-energy (64 kcal) breakfast (ELB), no exercise and a high-energy breakfast (NEHB) and no exercise and a low-energy breakfast (NELB). Hunger and moods were monitored each hour from 8 a. m. until 5 p.m. Energy and macronutrient intake were measured during an ad libitum lunch test meal 4 h after the exercise and breakfast. Heart rate was continuously monitored using the Polar sport tester. The low-energy breakfasts (ELB and NELB) led to increased hunger during the morning and an increase in energy intake at lunch compared with the high-energy breakfasts. Subjects also experienced significantly more food cravings after LBs than after HBs. Exercise failed to have any significant effect on these variables. Thus, two methods of inducing a short-term energy deficit had markedly different effects on appetite. The low-energy breakfast presumably fails to generate the inhibitory satiety signals induced by the 500 kcal breakfast, whereas the metabolic effects of an exercise session failed to generate excitatory signals to hunger and food intake.

Adult↗

PubMed1985

Recovery from energy deficit in golden hamsters.

Hamsters feeding at greater than 2-h intermeal intervals (IMI) lose weight but recover from weight losses without hyperphagia if they are allowed to feed at 2-h IMIs (Am. J. Physiol. 236 (Endocrinol. Metab. Gastrointest. Physiol. 5): E105-E112, 1979). To determine the relative importance of changes in energy expenditure and fat synthesis in their energy regulation, measurements were made of resting metabolic rate, respiration by brown adipose tissue (BAT), locomotion, fecal energy content, and insulin and hepatic lipogenic enzyme responses to feeding in underweight hamsters allowed to feed at 2- or 5-h IMIs. Energy deficit suppressed the resting metabolic rate and general locomotor activity and increased the activity of fatty acid synthetase (FAS). Heat production by BAT increased in underweight hamsters. Increase in IMIs blocked the postprandial insulin release, reduced plasma insulin concentration and FAS activity, and increased malic enzyme activity. Thus ad libitum feeding hamsters recover from energy deficit by reducing energy expenditure, whereas failure to add additional meals and impaired insulin and changed lipogenic responses to feeding produce energy deficits in infrequently feeding hamsters.

Adipose Tissue, Brown↗

PubMed1990

The integrated analysis of seasonal energy deficits: problems and prospects.

The emergence of energy flow studies is reviewed, from their origins in ecosystem research in the 1950s, to their application to agricultural systems suffering from the 'energy crisis' of the 1970s, and the application of Optimal Foraging Theory to small-scale societies. Methodological problems are then discussed, in particular problems of measuring human and draft animal labour, ways of assessing fuel energy and the contribution of biomass to cultivation, and the need to define appropriate spatial and temporal units for analysis. Finally, the scope for studying seasonal energy deficits by means of an integrated analysis of energy flows is considered. The household unit is identified as the most promising unit for such analysis.

Adaptation, Physiological↗

PubMed2006

The effect of a medium-term activity- and diet-induced energy deficit on subjective appetite sensations in obese children.

OBJECTIVE: To assess the subjective appetite responses to an imposed activity- and diet-induced energy deficit during a residential intervention programme for obese children. DESIGN: A 6-week intervention of fixed, reduced dietary intake and 6 h/day of skill-based physical activity while resident in a weight loss camp. SUBJECTS: Thirty-eight obese (mean body mass index (BMI)=34.9 kg m(-2)) boys and girls (mean age 13.9+/-1.57). MEASUREMENTS: An electronic appetite rating system (EARS) was used to periodically measure subjective appetite sensations at the start (WK1) and at the end (WK6) of the camp. Subjective ratings of hunger and fullness were compared at the start and end of 6 weeks of an activity- and diet-induced-based weight loss intervention. RESULTS: At the end of the 6 weeks, the children had lost 8.4 kg in body mass. The diurnal profiles of subjective appetite sensations demonstrated clear oscillations in hunger and fullness. There was a significant increase in hunger (P<0.0001) and decrease in fullness (P<0.005) at the end (WK6) of the medium-term energy deficit. In WK6, morning ratings of hunger were higher than in WK1 (P<0.005) and the fixed energy evening meal induced a lower suppression of hunger (P<0.02). CONCLUSION: A programme of fixed, reduced-dietary intake combined with an activity and behavioural programme was successful at inducing a significant reduction in body mass in obese children. Subjective sensations of appetite were sensitive to a medium-term negative energy balance and weight loss. These data are essential as we continue to evolve methods of treatment for overweight and obese children.

Adolescent↗

PubMed1998

Heart failure: is there an energy deficit contributing to contractile dysfunction?

UNLABELLED: Alterations in myocardial energy metabolism have been demonstrated in both animal experiments and clinical observations. Whether these changes contribute to heart failure has been a longstanding and controversial issue. I. The creatine kinase (CK) system and the high energy phosphates under physiological conditions and in acute heart failure: 1. According to in vivo and in vitro experiments the myocardial creatine/creatine phosphate (Cr/CP) system is directly linked to mitochondrial oxidative phosphorylation via the mitochondrial CK. 2. The shift in the mass action ratio of the CK reaction with increasing myocardial oxygen consumption enables marked stimulation of mitochondrial respiratory function via the Cr/CP system with almost maintained free energy of the adenosine triphosphate/adenosine diphosphate (ATP/ADP) system. 3. In acute heart failure the depressed myocardial content mainly of CP can be considered as an adaptive mechanism related to increased oxygen demands. II. The CK system and the high energy phosphates in chronic heart failure: 1. The alterations observed in the CK system in chronic heart failure cannot be interpreted in terms of an "energy deficit" (i.e., the excess of what is spent over what is received on energy). 2. "Energy reserve" (i.e., energy kept back for future use, to fill an emergency) is markedly reduced in heart failure. 3. Under steady state conditions decreased "energy reserve" cannot be expected to contribute to heart failure. Under stress conditions, however, this mechanism is manifest by reducing contractile reserve. 4. The mechanisms by which decreased "energy reserve" induces depression of contractile reserve is not elucidated. III. Heart failure related to alterations in energy metabolism (mitochondrial diseases, stunned, and hibernating myocardium): 1. The phenotype of mitochondrial diseases is predominantly determined by neurological disorders and myopathies. Therefore, the patients are rarely referred to a cardiologist, although the cardiac involvement may ultimately determine the patients' prognosis. 2. Stunned and hibernating myocardium are characterized by prolonged contractile dysfunction in the presence of reversibly damaged myocardium. The underlying mechanisms and its triggers are unknown. INTERPRETATIONS: 1. The reduced energy reserve in heart failure may be considered to contribute to the progression of the disease. 2. As an alternative, however, it can likewise represent a mechanism to protect the endangered myocardium from overload.

Adenosine Diphosphate↗

PubMed1986

Energy deficits in hepatocytes isolated from phenobarbital-treated or fasted rats and briefly exposed to halothane and hypoxia in vitro.

Experimental factors implicated in the pathogenesis of halothane hepatotoxicity in the phenobarbital-hypoxia rat model were examined for direct effects on the energy status of isolated rat liver cells in vitro. Intact hepatocytes were isolated after collagenase perfusion of livers of adult male Fischer 344 rats previously treated with phenobarbital (0.1% in drinking water for 5-7 days) and/or deprived of food for 48 h. Cells were incubated in Krebs-Henseleit buffer + substrates for 10 min at steady states of energy metabolism, with extracellular PO2 constant at 32, 16, or 4 mmHg +/- 1% halothane. Fasting produced the largest energy deficits in incubated hepatocytes, regardless of phenobarbital treatment status, PO2 value, or presence/absence of halothane. The combination of hypoxic PO2 (4 mmHg) and 1% halothane shifted lactate metabolism toward lactate production, whereas hypoxia or halothane alone did not. Prior phenobarbital treatment plus hypoxia decreased adenosine triphosphate/adenosine diphosphate (ATP/ADP) and increased lactate production compared with drug treatment or hypoxia alone. We conclude that pathogenic factors that interact to produce halothane hepatotoxicity act directly and jointly on isolated liver cells to produce energy deficits within 10 min. Differences in the relative importance of pathogenic factors in vitro and in vivo suggest that short-term, direct effects on hepatocellular energy status are not solely responsible for halothane hepatotoxicity.

Adenosine Diphosphate↗

PubMed1991

Short-term energy deficit causes net accumulation of linoleoyl-enriched triacylglycerols in rat liver.

Energy depletion by reduced food intake over 4 days resulted in a 73% reduction in total rat liver triacylglycerols (TG). In liver TG of energy-depleted rats, dilinoleoyl oleoyl glycerol (OLL) and trilinoleoyl glycerol (LLL) were quantitatively increased by 85% and 147%, respectively. The net increase in linoleoyl-enriched species could be quantitatively accounted for by the release of linoleate from monolinoleoyl species and its subsequent reacylation into dilinoleoyl species and trilinolein during energy depletion. Hence while palmitate, oleate and some linoleate are being hydrolyzed, presumably for oxidation, some linoleate is retained and contributes to the remodelling of hepatic triacylglycerols during energy deficit.

Animals↗

PubMed2002

The effect of an acute energy deficit on the hormone profile of dominant follicles in dairy cows.

The effect of an acute energy deficit on the hormone balance of dominant follicles was studied in six normally-cycling, high-yielding Italian Friesian cows at 60 and 90 days after calving. At 60 days after calving, the cows, which had been fed according to their maintenance and production requirements, were synchronized and follicular fluid was collected from the dominant follicles under ultrasound guidance. At 90 days after calving, the same protocol was used on the same cows, which had been subjected to an acute dietary restriction since the day of the second prostaglandin treatment for synchronization. At the follicular level, the dietary restriction caused a significant reduction (P < 0.05) in the concentration of estradiol-17beta and a significant increase (P < 0.05) in NEFA. There were no significant differences in follicular diameter, follicular concentrations of progesterone, and Insulin-like Growth Factor-I (IGF-I). The amount of IGFBP2 and IGFBP3 in follicular fluid increased. The results suggest that an acute dietary restriction induces substantial changes at the dominant follicle level, despite the fact that the recruitment and selection phase occurred before the cows' diet was restricted.

Animals↗

PubMed2003

Precursor-protein convertase 1 gene expression in the mouse hypothalamus: differential regulation by ob gene mutation, energy deficit and administration of leptin, and coexpression with prepro-orexin.

The expression of precursor-protein convertase (PC)1, PC2 and paired basic amino acid cleaving enzyme four mRNA was studied by in situ hybridisation in regions of the hypothalamus involved in energy regulation in relation to obese (ob) gene mutation and energy deficit. PC1 gene was differentially expressed in hypothalamic nuclei of mice from different genetic backgrounds or energetic status, whereas no differences in expression were observed for either the PC2 or paired basic amino acid cleaving enzyme four genes. In obese ob/ob mice, PC1 mRNA levels were increased in the paraventricular nucleus, decreased in the lateral hypothalamus and unchanged in the ventromedial nucleus and arcuate nucleus relative to lean controls. In response to intraperitoneal injection of murine leptin, PC1 mRNA levels in obese ob/ob mice decreased in the arcuate nucleus, increased in the lateral hypothalamus and were unchanged in both the paraventricular nucleus and ventromedial nucleus. In mice deprived of food for 24 h, PC1 mRNA levels were reduced in the ventromedial nucleus, increased in the lateral hypothalamus and unchanged in the paraventricular nucleus and arcuate nucleus relative to ad libitum-fed controls. Overall, whilst the data show effects related to leptin and energetic status, they do not support a strong and consistent link between PC1 gene expression and energy balance. This suggests that if PC1 is important to the control of energy balance then protein expression and activity, rather than gene expression may be the more critical parameters of regulation. The relationship between PC1 and candidate energy balance-related genes in the lateral hypothalamus was investigated by dual in situ hybridisation. PC1 mRNA was localised in prepro-orexin mRNA expressing neurons in the lateral hypothalamus, which suggests a functional relationship.

Animals↗

PubMed1986

Influence of aerobic energy deficit, ouabain and harmaline on the phenylalanine and galactose active transport by snail intestine.

The effect of anaerobiosis (N2 bubbling of the medium) or 10(-4) M dinitrophenol on the penetration of 0.5 mM Phe in snail and rat everted intestine, in 2 min and 30 min incubation periods, has been studied. The aerobic energy deficit inhibits the amino acid net entry in both species, but whereas the active transport is annulled in rat, snail intestine is capable of continuing to accumulate Phe against a gradient. The prolonged action (30 min of preincubation) of 1 mM ouabain inhibits 0.1 mM Phe and 0.1 mM galactose entry in snail intestine. Amino acid uptake is far higher than the one obtained in the absence of Na+, in which condition Phe keeps accumulating against a gradient in the tissue water. Galactose active transport, instead, becomes null in the presence of the glucoside or in the absence of Na+. One mM harmaline is able to inhibit the initial entry of galactose into the tissue, while higher than 5 mM concentrations are required to inhibit that of Phe. Results confirm that snail intestine is capable of easily carrying out active transport processes with energy from anaerobic origin. On the other hand Phe transport is less sensitive to the absence of Na+, presence of ouabain or harmaline than that of galactose, so that contrary to what has been observed for the sugar, the active transport of the amino acid is not annulled in any of the three conditions.

Anaerobiosis↗

PubMed1997

Physical performance and metabolic recovery among lean, healthy men following a prolonged energy deficit.

Previous studies have demonstrated that full recovery from weight loss may take months or years. The present investigation examined short-term recovery (5 wks "post") of physical performance (muscular strength, muscular power, vertical jump), body composition, metabolic hormones (testosterone, luteinizing hormone, sex hormone binding globulin, insulin-like growth factor-1, triiodothyronine, thyroxine, thyroid binding globulin, and thyroid-stimulating hormone) and metabolic markers (transferrin, ferritin, prealbumin, glycerol, nonesterified fatty acids, high-density lipoproteins, and lactate) in 10 healthy young men after an 8-week Army course with an energy deficit (1000 kcal/d) and loss of body mass (-12%). Subjects ate ad libitum after the course ended ("post"). Body composition was determined by dual-energy X-ray absorptiometry; strength from a simulated power clean, power from body mass and jump height, and metabolic hormones were measured in morning-fasted blood by radioimmunoassay. With the exception of transferrin and glycerol, all study parameters were significantly (p<.05) altered by the training course. At 5 weeks post fat-free mass along with all physical performance measures returned to initial levels; however, fat mass had significantly (p<.05) increased over initial levels. Also, with the exception of lactate, all measured hormones and markers were close to initial levels and within normal ranges. Reported complications during recovery included sleep irregularities, diarrhea, loss of motivation and feelings of fatigue. While the long range effect of this energy deprivation experience is uncertain, these data do suggest that severe weight loss does not result in lasting alterations of the contractile and metabolic properties of skeletal muscle in young, lean, healthy men.

Adult↗