Combining metformin and aerobic exercise training in the treatment of type 2 diabetes and NAFLD in OLETF rats.

Here, we sought to compare the efficacy of combining exercise and metformin for the treatment of type 2 diabetes and nonalcoholic fatty liver disease (NAFLD) in hyperphagic, obese, type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. OLETF rats (age: 20 wk, hyperglycemic and hyperinsulinemic; n = 10/group) were randomly assigned to sedentary (O-SED), SED plus metformin (O-SED + M; 300 mg·kg(-1)·day(-1)), moderate-intensity exercise training (O-EndEx; 20 m/min, 60 min/day, 5 days/wk treadmill running), or O-EndEx + M groups for 12 wk. Long-Evans Tokushima Otsuka (L-SED) rats served as nonhyperphagic controls. O-SED + M, O-EndEx, and O-EndEx + M were effective in the management of type 2 diabetes, and all three treatments lowered hepatic steatosis and serum markers of liver injury; however, O-EndEx lowered liver triglyceride content and fasting hyperglycemia more than O-SED + M. In addition, exercise elicited greater improvements compared with metformin alone on postchallenge glycemic control, liver diacylglycerol content, hepatic mitochondrial palmitate oxidation, citrate synthase, and ß-HAD activities and in the attenuation of markers of hepatic fatty acid uptake and de novo fatty acid synthesis. Surprisingly, combining metformin and aerobic exercise training offered little added benefit to these outcomes, and in fact, metformin actually blunted exercise-induced increases in complete mitochondrial palmitate oxidation and ß-HAD activity. In conclusion, aerobic exercise training was more effective than metformin administration in the management of type 2 diabetes and NAFLD outcomes in obese hyperphagic OLETF rats. Combining therapies offered little additional benefit beyond exercise alone, and findings suggest that metformin potentially impairs exercise-induced hepatic mitochondrial adaptations.

Intrinsic aerobic capacity impacts susceptibility to acute high-fat diet-induced hepatic steatosis.

Aerobic capacity/fitness significantly impacts susceptibility for fatty liver and diabetes, but the mechanisms remain unknown. Herein, we utilized rats selectively bred for high (HCR) and low (LCR) intrinsic aerobic capacity to examine the mechanisms by which aerobic capacity impacts metabolic vulnerability for fatty liver following a 3-day high-fat diet (HFD). Indirect calorimetry assessment of energy metabolism combined with radiolabeled dietary food was employed to examine systemic metabolism in combination with ex vivo measurements of hepatic lipid oxidation. The LCR, but not HCR, displayed increased hepatic lipid accumulation in response to the HFD despite both groups increasing energy intake. However, LCR rats had a greater increase in energy intake and demonstrated greater daily weight gain and percent body fat due to HFD compared with HCR. Additionally, total energy expenditure was higher in the larger LCR. However, controlling for the difference in body weight, the LCR has lower resting energy expenditure compared with HCR. Importantly, respiratory quotient was significantly higher during the HFD in the LCR compared with HCR, suggesting reduced whole body lipid utilization in the LCR. This was confirmed by the observed lower whole body dietary fatty acid oxidation in LCR compared with HCR. Furthermore, LCR liver homogenate and isolated mitochondria showed lower complete fatty acid oxidation compared with HCR. We conclude that rats bred for low intrinsic aerobic capacity show greater susceptibility for dietary-induced hepatic steatosis, which is associated with a lower energy expenditure and reduced whole body and hepatic mitochondrial lipid oxidation.

Accuracy of field methods in assessing body fat in collegiate baseball players.

When assessing the fitness levels of athletes, body composition is usually estimated, as it may play a role in athletic performance. Therefore, the purpose of this study was to determine the validity of bioelectrical impedance analysis (BIA) and skinfold (SKF) methods compared with dual-energy X-ray absorptiometry (DXA) for estimating percent body fat (%BF) in Division 1 collegiate baseball players (n = 35). The results of this study indicate that the field methods investigated were not valid compared with DXA for estimating %BF. In conclusion, this study does not support the use of the TBF-350, HBF-306, HBF-500, or SKF thickness for estimating %BF in collegiate baseball players. The reliability of these BIA devices remains unknown; therefore, it is currently uncertain if they may be used to track changes over time.

Short-term removal of exercise impairs glycemic control in older adults: A randomized trial.

Postprandial glycemia (PPG) predicts cardiovascular disease, and short-term physical inactivity increases PPG in young, active adults. Whether this occurs in older, active adults who may be more prone to bouts of inactivity is unknown. This study determined if postprandial interstitial glucose (PPIG) was impaired in active older adults following the removal of exercise for 3 days (NOEX) compared to active young adults. In this randomized, crossover study, 11 older (69.1 ± 1.9 years) and 9 young (32.8 ± 1.8 years) habitually active (≥90 min/week of exercise) adults completed 3-days of NOEX and 3-days of normal habitual exercise (EX), separated by ≥1 week. Diet was standardized across phases. Glycemic control (3-day average) was assessed via continuous glucose monitoring during both phases. Significant main effects of age and phase were detected (p < 0.05), but no interaction was found for steps/day (p > 0.05) (old EX: 6283 ± 607, old NOEX: 2380 ± 382 and young EX: 8798 ± 623, young NOEX: 4075 ± 516 steps/day). Significant main effects of age (p = 0.002) and time (p < 0.001) existed for 1-h PPIG, but no effect of phase or interactions was found (p > 0.05). Significant main effects (p < 0.05) of age (old: 114 ± 1 mg/dl, young: 106 ± 1 mg/dl), phase (NOEX: 112 ± 1 mg/dl, EX: 108 ± 1 mg/dl), and time (0 min: 100 ± 2, 30 min: 118 ± 2, 60 min: 116 ± 2, 90 min: 111 ± 2, 120 min: 108 ± 2 mg/dl) in 2-h PPIG were detected, but no interaction was found (p > 0.05). However, only significant main effects of phase (NOEX: 14 ± 1 and EX:12 ± 1, p > 0.05) were found for 24-h blood glucose standard deviation. Older adults appear to have impaired glycemic control compared to young adults and exercise removal impairs glycemic control in both populations. Yet, the impairment in glycemic control with exercise removal is not different between old and young adults.

Dietary weight loss-induced improvements in metabolic function are enhanced by exercise in people with obesity and prediabetes.

The additional therapeutic effects of regular exercise during a dietary weight loss program in people with obesity and prediabetes are unclear. Here, we show that whole-body (primarily muscle) insulin sensitivity (primary outcome) was 2-fold greater (P = 0.006) after 10% weight loss induced by calorie restriction plus exercise training (Diet+EX; n = 8, 6 women) than 10% weight loss induced by calorie restriction alone (Diet-ONLY; n = 8, 4 women) in participants in two concurrent studies. The greater improvement in insulin sensitivity was accompanied by increased muscle expression of genes involved in mitochondrial biogenesis, energy metabolism and angiogenesis (secondary outcomes) in the Diet+EX group. There were no differences between groups in plasma branched-chain amino acids or markers of inflammation, and both interventions caused similar changes in the gut microbiome. Few adverse events were reported. These results demonstrate that regular exercise during a diet-induced weight loss program has profound additional metabolic benefits in people with obesity and prediabetes.Trial Registration: ClinicalTrials.gov (NCT02706262 and NCT02706288).

The acute response of practical occlusion in the knee extensors.

Training at low intensities with moderate vascular occlusion results in increased muscle hypertrophy, strength, and endurance. Elastic knee wraps, applied to the proximal portion of the target muscle, might elicit a stimulus similar to the KAATSU Master Apparatus. The purpose of this study was to test the hypothesis that intermittently occluding the leg extensors with elastic knee wraps would increase whole-blood lactate (WBL) over control (CON). Twelve healthy men and women participated in this study (age 21.2 ± 0.35 years, height 168.9 ± 2.60 cm, and body mass 71.2 ± 4.16 kg). One repetition maximum (1RM) testing for the leg extensors was performed on a leg extension machine for the first trial, followed by occlusion (OCC) and CON trials. Four sets of leg extension exercise (30-15-15-15) were completed with 150-second rest between sets at 30% 1RM. Whole-blood lactate, heart rate (HR), and ratings of perceived exertion (RPEs) were measured after every set of exercise and 3 minutes postexercise. Data were analyzed using repeated-measures analysis of variance with statistical significance set at p ≤ 0.05. Whole-blood lactate increased in response to exercise (p = 0.01) but was not different between groups (OCC 6.28 ± 0.66 vs. CON 5.35 ± 0.36 mmol·L, p = 0.051). Heart rate (OCC 128.86 ± 4.37 vs. CON 119.72 ± 4.10 b·min⁻¹) was higher with OCC from sets 2-4 (p ≤ 0.03), with no difference 3 minutes postexercise (p = 0.29). Rating of perceived exertion was higher with OCC after every set (OCC 15.10 ± 0.31 vs. CON 12.16 ± 0.50, p = 0.01). In conclusion, no differences exist for WBL between groups, although there was a trend for higher levels with OCC. The current protocol for practical occlusion did not significantly increase metabolic stress more than normal low-intensity exercise. This study does not support the use of knee wraps as a mode of blood-flow restriction.

Influence of adiposity, insulin resistance, and intrahepatic triglyceride content on insulin kinetics.

BACKGROUNDInsulin is a key regulator of metabolic function. The effects of excess adiposity, insulin resistance, and hepatic steatosis on the complex integration of insulin secretion and hepatic and extrahepatic tissue extraction are not clear.METHODSA hyperinsulinemic-euglycemic clamp and a 3-hour oral glucose tolerance test were performed to evaluate insulin sensitivity and insulin kinetics after glucose ingestion in 3 groups: (a) lean subjects with normal intrahepatic triglyceride (IHTG) and glucose tolerance (lean-NL; n = 14), (b) obese subjects with normal IHTG and glucose tolerance (obese-NL; n = 24), and (c) obese subjects with nonalcoholic fatty liver disease (NAFLD) and prediabetes (obese-NAFLD; n = 22).RESULTSInsulin sensitivity progressively decreased and insulin secretion progressively increased from the lean-NL to the obese-NL to the obese-NAFLD groups. Fractional hepatic insulin extraction progressively decreased from the lean-NL to the obese-NL to the obese-NAFLD groups, whereas total hepatic insulin extraction (molar amount removed) was greater in the obese-NL and obese-NAFLD subjects than in the lean-NL subjects. Insulin appearance in the systemic circulation and extrahepatic insulin extraction progressively increased from the lean-NL to the obese-NL to the obese-NAFLD groups. Total hepatic insulin extraction plateaued at high rates of insulin delivery, whereas the relationship between systemic insulin appearance and total extrahepatic extraction was linear.CONCLUSIONHyperinsulinemia after glucose ingestion in obese-NL and obese-NAFLD is due to an increase in insulin secretion, without a decrease in total hepatic or extrahepatic insulin extraction. However, the liver's maximum capacity to remove insulin is limited because of a saturable extraction process. The increase in insulin delivery to the liver and extrahepatic tissues in obese-NAFLD is unable to compensate for the increase in insulin resistance, resulting in impaired glucose homeostasis.TRIAL REGISTRATIONClinicalTrials.gov NCT02706262.FUNDINGNIH grants DK56341 (Nutrition Obesity Research Center), DK052574 (Digestive Disease Research Center), RR024992 (Clinical and Translational Science Award), and T32 DK007120 (a T32 Ruth L. Kirschstein National Research Service Award); the American Diabetes Foundation (1-18-ICTS-119); Janssen Research & Development; and the Pershing Square Foundation.

Exercise and Postprandial Glycemic Control in Type 2 Diabetes.

Individuals with type 2 diabetes (T2D) have poor glycemic control which contributes to cardiovascular disease and other diabetic comorbidities. The often relied upon measures of fasting glucose and glycosylated hemoglobin (HbA1c) do not accurately represent glycemic control because they do not reflect what occurs after meals and throughout the day in the free-living condition. An accumulating body of evidence now suggests that postprandial glucose fluctuations are more tightly correlated with microvascular and macrovascular morbidities and cardiovascular mortality than HbA1c or fasting glucose, stagnant measure of glycemia. Thus, effective therapies are needed which will improve not only HbA1c and fasting glucose, but also regulation of postprandial glycemia. Further, testing for glycemic control should employ a challenge that simulates the free-living condition to best determine how glucose is regulated after meals and throughout the day. Unlike medications, which generally have a poor effect at improving postprandial glucose, exercise is effective in reducing postprandial glycemic excursions in as little as a few days. However, how this is accomplished and the optimal prescription for reducing postprandial glycemic excursions and maintaining improvements in postprandial glycemic control have yet to be elucidated. Still further, the utility of a mixed meal test in providing the optimal challenge for detecting exercise-induced changes in postprandial glycemic control has value that warrants further investigation. Thus, the purpose of this review is to summarize the literature regarding exercise in treating postprandial glycemia in T2D and to review strengths and weaknesses in the current methodology for assessing changes in glycemic control.

Red wine enhances glucose-dependent insulinotropic peptide (GIP) and insulin responses in type 2 diabetes during an oral glucose tolerance test.

BACKGROUND: Ingestion of ethanol before a glucose challenge enhances the insulin response by an unknown mechanism. In addition, epidemiological studies consistently indicate that moderate alcohol consumption reduces the risk of developing type 2 diabetes (T2D). The purposes of this study were to evaluate the potential involvement of glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) in alcohol-induced augmentation of the insulin response and to determine if red wine acutely improves glucose tolerance during an oral glucose tolerance test (OGTT). METHODS: Nine subjects (eight T2D and one pre-diabetes) completed two OGTT 30 min after consumption of 263 ml water or red wine (28 g ethanol). Blood samples were obtained for 3 h and analyzed for glucose, insulin, C-peptide, GIP, and GLP-1. RESULTS: Compared with water, consumption of red wine increased the incremental area under the curve (iAUC) for insulin by 50 % (14,837 ± 4759 vs. 9885 ± 2686 µU/ml × min; p < 0.05) and for GIP by 25 % (7729 ± 1548 vs. 6191 ± 1049 pmol/l × min; p < 0.05). Glucose and GLP-1 responses were not affected by red wine. CONCLUSION: Wine consumption before an OGTT augments the insulin response, which may be partially driven by a greater GIP response. Because glucose levels were not reduced, acute wine consumption may not be effective treatment for enhancing glycemic control or may need to be combined with therapy that improves insulin sensitivity.

Inverse association between carbohydrate consumption and plasma adropin concentrations in humans.

OBJECTIVE: The role of metabolic condition and diet in regulating circulating levels of adropin, a peptide hormone linked to cardiometabolic control, is not well understood. In this study, weight loss and diet effects on plasma adropin concentrations were examined. METHODS: This report includes data from (1) a weight loss trial, (2) an evaluation of acute exercise effects on mixed-meal (60% kcal from carbohydrates) tolerance test responses, and (3) a meta-analysis to determine normal fasting adropin concentrations. RESULTS: Distribution of plasma adropin concentrations exhibited positive skew and kurtosis. The effect of weight loss on plasma adropin concentrations was dependent on baseline plasma adropin concentrations, with an inverse association between baseline and a decline in concentrations after weight loss (Spearman's ρ = -0.575; P < 0.001). When ranked by baseline plasma adropin concentrations, only values in the upper quartile declined with weight loss. Plasma adropin concentrations under the main area of the bell curve correlated negatively with habitual carbohydrate intake and plasma lipids. There was a negative correlation between baseline values and a transient decline in plasma adropin during the mixed-meal tolerance test. CONCLUSIONS: Plasma adropin concentrations in humans are sensitive to dietary macronutrients, perhaps due to habitual consumption of carbohydrate-rich diets suppressing circulating levels. Very high adropin levels may indicate cardiometabolic conditions sensitive to weight loss.

Weight classification does not influence the short-term endocrine or metabolic effects of high-fructose corn syrup-sweetened beverages.

Obesity and high-fructose corn syrup (HFCS)-sweetened beverages are associated with an increased risk of chronic disease, but it is not clear whether obese (Ob) individuals are more susceptible to the detrimental effects of HFCS-sweetened beverages. The purpose of this study was to examine the endocrine and metabolic effects of consuming HFCS-sweetened beverages, and whether weight classification (normal weight (NW) vs. Ob) influences these effects. Ten NW and 10 Ob men and women who habitually consumed ≤355 mL per day of sugar-sweetened beverages were included in this study. Initially, the participants underwent a 4-h mixed-meal test after a 12-h overnight fast to assess insulin sensitivity, pancreatic and gut endocrine responses, insulin secretion and clearance, and glucose, triacylglycerol, and cholesterol responses. Next, the participants consumed their normal diet ad libitum, with 1065 mL per day (117 g·day(-1)) of HFCS-sweetened beverages added for 2 weeks. After the intervention, the participants repeated the mixed-meal test. HFCS-sweetened beverages did not significantly alter body weight, insulin sensitivity, insulin secretion or clearance, or endocrine, glucose, lipid, or cholesterol responses in either NW or Ob individuals. Regardless of previous diet, Ob individuals, compared with NW individuals, had ∼28% lower physical activity levels, 6%-9% lower insulin sensitivity, 12%-16% lower fasting high-density-lipoprotein cholesterol concentrations, 84%-144% greater postprandial triacylglycerol concentrations, and 46%-79% greater postprandial insulin concentrations. Greater insulin responses were associated with reduced insulin clearance, and there were no differences in insulin secretion. These findings suggest that weight classification does not influence the short-term endocrine and metabolic effects of HFCS-sweetened beverages.

Impact of various exercise modalities on hepatic mitochondrial function.

PURPOSE: Hepatic mitochondrial adaptations to exercise are largely unknown. In this study, we sought to determine the effects of various exercise modalities on measures of hepatic mitochondrial function and metabolism. METHODS: Male Sprague-Dawley rats were randomly assigned (n = 8-10 per group) into sedentary (SED), voluntary wheel running (VWR), VWR with food pulled during the dark cycle (VMR-OF), treadmill endurance exercise (TM-END; 30 m·min, 12% gradient, 60 min·d, 5 d·wk), or treadmill interval sprint training (TM-IST; 50 m·min, 12% gradient, 6 × 2.5 min bouts, 5 d·wk) groups for a 4-wk intervention. RESULTS: Hepatic mitochondrial state 3 and maximal uncoupled respiration were significantly (P < 0.05) increased in all four exercise groups compared with SED animals. In addition, hepatic mitochondrial [1-C] pyruvate oxidation to CO2, an index of pyruvate dehydrogenase (PDH) activity, was significantly increased in VWR-OF, TM-END, and TM-IST rats (P < 0.05), whereas exercise-induced increases in [2-C] pyruvate oxidation and [1-C] palmitate oxidation to CO2 did not reach statistical significance. Hepatic mitochondrial sirtuin 3 protein content, which putatively increases activity of mitochondrial proteins, was elevated in the VWR, VWR-OF, and TM-END groups (P < 0.05). In addition, only VWR-OF animals experienced increases in hepatic cytochrome c protein content and phosphoenolpyruvate carboxykinase mRNA, whereas PGC-1α mRNA expression and phospho-CREB protein content was increased in VWR-OF and TM-END groups. CONCLUSION: Four weeks of exercise training, regardless of exercise modality, significantly increased hepatic mitochondrial respiration and evoked other unique improvements in mitochondrial metabolism that do not appear to be dependent on increases in mitochondrial content.

Differential effects of low-fat and high-fat diets on fed-state hepatic triacylglycerol secretion, hepatic fatty acid profiles, and DGAT-1 protein expression in obese-prone Sprague-Dawley rats.

The purpose of this study was to compare the effects of short-term low-fat (LF) and high-fat (HF) diets on fed-state hepatic triacylglycerol (TAG) secretion, the content of proteins involved in TAG assembly and secretion, fatty acid oxidation (FAO), and the fatty acid profile of stored TAG. Using selectively bred obese-prone Sprague-Dawley rats, we directly measured fed-state hepatic TAG secretion, using Tyloxapol (a lipoprotein lipase inhibitor) and a standardized oral mixed meal (45% carbohydrate, 40% fat, 15% protein) bolus in animals fed a HF or LF diet for 2 weeks, after which the rats were maintained on their respective diet for 1 week (washout) prior to the liver being excised to measure protein content, FAO, and TAG fatty acid profiles. Hepatic DGAT-1 protein expression was ∼27% lower in HF- than in LF-fed animals (p < 0.05); the protein expression of all other molecules was similar in the 2 diets. The fed-state hepatic TAG secretion rate was ∼39% lower (p < 0.05) in HF- (4.62 ± 0.18 mmol·h(-1)) than in LF- (7.60 ± 0.57 mmol·h(-1)) fed animals. Hepatic TAG content was ∼2-fold higher (p < 0.05) in HF- (1.07 ± 0.15 nmol·g(-1) tissue) than in LF- (0.50 ± 0.16 nmol·g(-1) tissue) fed animals. In addition, the fatty acid profile of liver TAG in HF-fed animals closely resembled the diet, whereas in LF-fed animals, the fatty acid profile consisted of mostly de novo synthesized fatty acids. FAO was not altered by diet. LF and HF diets differentially alter fed-state hepatic TAG secretion, hepatic fatty acid profiles, and DGAT-1 protein expression.

One bout of exercise alters free-living postprandial glycemia in type 2 diabetes.

PURPOSE: Elevated postprandial glycemic (PPG) excursions are significant risk factors for cardiovascular disease in type 2 diabetes patients. In this study, we tested if and for how many meals a single bout of exercise would reduce PPG responses to subsequent meals in type 2 diabetes (T2D) patients using a continuous glucose monitor system (CGMS). METHODS: We recruited nine sedentary (<30 min·wk(-1) of exercise) individuals with T2D (mean ± SD; body mass index = 36.0 ± 1.1 kg·m(-2), age = 60.3 ± 1.0 yr, HbA1c = 6.3% ± 0.2%). The subjects consumed a eucaloric diet (51% carbohydrate, 31% fat, and 18% protein) consisting of three meals, identical in composition, for a 2-d period while wearing a continuous glucose monitor system in two different conditions (exercise [EX], one 60-min bout at 60%-75% of heart rate reserve performed before breakfast), vs a sedentary [SED] condition). We quantified 24-h average glucose, PPG area under the curve (AUC; 4-h glucose AUC after meals), and PPG-2 h (2 h postprandial glucose). RESULTS: EX significantly reduced average [glucose] during the first 24-h period (P = 0.03). EX caused a reduction in PPG-AUC (P = 0.02) for all of the meals during the 2 d (main effect between conditions). A comparison between the EX and the SED conditions at each meal revealed that EX reduced PPG-AUC after the second meal of day 1 (lunch) (P = 0.04). PPG-2 h was not significantly different between EX and SED. CONCLUSIONS: Although a single EX bout does lower 24-h average [glucose], it only significantly lowered PPG-AUC at the second meal after the bout, suggesting that daily exercise may be needed to most effectively improve PPG at the advent of exercise training in T2D patients.

Prior exercise and postprandial incretin responses in lean and obese individuals.

PURPOSE: The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) help regulate postprandial triacylglycerol (TAG) and insulin concentrations, but the effects of acute aerobic exercise on GLP-1 or GIP responses are unclear. The purpose of this study was to determine whether reductions in postprandial TAG and insulin with exercise are associated with GLP-1 and GIP responses. METHODS: Thirteen normal-weight (NW) and 13 obese (Ob) individuals participated in two, 4-d trials in random order including an exercise (EX) and a no exercise (NoEX) trial. Diet was controlled during both trials. The EX trial consisted of 1 h of treadmill walking (55%-60% of V˙O2peak) during the evening of day 3 of the trial, 12 h before a 4-h mixed meal test on day 4, during which frequent blood samples were collected to assess postprandial lipemia, glycemia, insulin, C-peptide, GIP, and GLP-1 responses. Insulin secretion was estimated using the insulinogenic index, and insulin clearance was estimated using the ratio of insulin to C-peptide. RESULTS: Postprandial TAG were 29% lower after EX in Ob individuals (P < 0.05) but were not significantly altered in NW individuals (P > 0.05). The drop in postprandial HDL cholesterol was attenuated with EX in Ob individuals (P < 0.05). Insulin responses were 14% lower after EX in Ob individuals (P < 0.05), and this was associated with reduced insulin secretion (P < 0.05), with no change in insulin clearance (P > 0.05). Glucose, C-peptide, GIP, and GLP-1 were not different between trials. CONCLUSION: A 1-h bout of moderate-intensity aerobic exercise the night before a mixed meal attenuates TAG and insulin responses in Ob but not NW individuals, an effect not associated with altered GLP-1 or GIP responses.

Liquid meal composition, postprandial satiety hormones, and perceived appetite and satiety in obese women during acute caloric restriction.

OBJECTIVE: The purpose of this study was to compare postprandial satiety regulating hormone responses (pancreatic polypeptide (PP) and peptide tyrosine tyrosine (PYY)) and visual analog scale- (VAS) assessed perceived appetite and satiety between liquid high-protein (HP) and high-carbohydrate (HC) meals in obese women during acute (24-h) caloric restriction. DESIGN: Eleven obese premenopausal women completed two conditions in random order in which they consumed 1500 calories as six 250-calorie HP meals or six 250-calorie HC meals over a 12-h period. Blood samples were taken at baseline and every 20 min thereafter and analyzed for PP and PYY concentrations. At these same points, perceived hunger and fullness were assessed with a VAS. The incremental area under the curve (iAUC) was used to compare postprandial responses. RESULTS: The 12-h PP and PYY iAUC were greater (P≤0.05) during the HP condition (PP: 4727±1306 pg/ml×12 h, PYY: 1373±357 pg/ml×12 h) compared with the HC condition (PP: 2300±528 pg/ml×12 h, PYY: 754±246 pg/ml×12 h). Perceived hunger and fullness were not different between conditions (P>0.05). The greatest changes in PYY and perceived fullness occurred after the morning meals during both conditions. CONCLUSIONS: These data suggest that in obese women during acute caloric restriction before weight loss, i) liquid HP meals, compared with HC meals, result in greater postprandial PP and PYY concentrations, an effect not associated with differential appetite or satiety responses, and ii) meal-induced changes in PYY and satiety are greatest during the morning period, regardless of dietary macronutrient composition.

The estimation of the fat free mass index in athletes.

PURPOSE: The purpose of this investigation was to compare a practical measurement of fat free mass index (FFMI) from bioelectrical impedance analysis (BIA) to the dual energy X-ray absorptiometry (DEXA) value in collegiate athletes. METHODS: Thirty-three male baseball players and 16 female gymnasts volunteered to participate in this study during their respective pre-season. Subjects visited the laboratory once and had their measurements taken in the following order: weight, height, DEXA, and Omron HBF-500. RESULTS: The BIA device investigated was not a valid estimate of FFMI when compared to the DEXA. The TE was 0.93 kg/ m(2) for males and 0.78 kg/ m(2) for females. There were also significant mean differences between the BIA prediction and the DEXA value for males (BIA=20.6 kg/m(2) vs. DEXA=21.1 kg/m(2), P=0.007) and females (BIA=16.2 kg/m(2) vs. DEXA=17.5 kg/m(2), P=0.001). CONCLUSIONS: The BIA device investigated in this study did not provide a valid estimate of FFMI in male and female collegiate athletes. Although there was a general tendency for the BIA to underestimate FFMI compared to DEXA, 98% of the estimates were within plus or minus 2 kg/ m(2). Therefore, while slightly biased, BIA may provide a reasonable (± 2 kg/ m(2)) estimate of nutritional status for practitioners who are unable able to afford more expensive equipment.