Fat Oxidation Rate Research Articles

MAXIMAL FAT OXIDATION DURING AEROBIC EXERCISE IN ADOLESCENTS WITH TYPE 1 DIABETES

ABSTRACT Objective: To compare maximal fat oxidation rates (FATMAX) and analyze their association with cardiorespiratory fitness in adolescents with type 1 diabetes mellitus (T1DM). Methods: Twenty-two male and female adolescents aged between 11 to 17 years, following clinical and anthropometric evaluations, were assigned to the diabetic group (DG; n = 10) or control group (CG; n = 12). Cardiorespiratory fitness was determined by maximal oxygen uptake (VO2max) during a maximal aerobic test on a cycle ergometer using the Balke protocol. Maximal fat oxidation (FATMAX) was determined by the respiratory exchange ratio proposed in the Lusk table. Results: Adolescents in the DG had lower mean FATMAX (p<0.01) and %VO2FATMAX (p=0.001) values when compared with those in the CG. FATMAX values were inversely correlated with serum glycosylated hemoglobin (HbA1c) levels (r= −0.77) and directly correlated with BMI z-scores (r=0.76), while %VO2FATMAX results were correlated with age (r=0.81), BMI z-scores (r=0.65), and VO2max values (r=0.81). On multiple linear regression, HbA1c values explained 54% (adjusted r²=0.54, p=0.009) and BMI z-scores explained 3.1% (adjusted r²=-0.031, p=0.009) of the variation in FATMAX in the DG. Adolescents with T1DM had similar cardiorespiratory fitness and lower FATMAX rates (35±11 VO2max) when compared with controls (60±12 VO2max). Conclusion: These results suggest lower fat oxidation rates and greater use of glucose as an energy substrate during exercise and worse control in T1DM. Therefore, results may contribute to appropriate exercise prescription in T1DM, after verifying exercise intensity to reduce hypoglycemia risk. Level of evidence III; Case-control study.

Determination and validation of peak fat oxidation in endurance-trained men using an upper body graded exercise test.

Peak fat oxidation rate (PFO) and the intensity that elicits PFO (Fatmax ) are commonly determined by a validated graded exercise test (GE) on a cycling ergometer with indirect calorimetry. However, for upper body exercise fat oxidation rates are not well elucidated and no protocol has been validated. Thus, our aim was to test validity and inter-method reliability for determination of PFO and Fatmax in trained men using a GE protocol applying double poling on a ski-ergometer. PFO and Fatmax were assessed during two identical GE tests (GE1 and GE2) and validated against separated short continuous exercise bouts (SCE) at 35%, 50%, and 65% of V̇O2peak on the ski-ergometer in 10 endurance-trained men (V̇O2peak : 65.1±1.0mL·min-1 ·kg-1 , mean±SEM). Between GE tests no differences were found in PFO (GE1: 0.42±0.03; GE2: 0.45±0.03g·min-1 , P=.256) or Fatmax (GE1: 41±2%; GE2: 43±3% of V̇O2peak , P=.457) and the intra-individual coefficient of variation (CV) was 8±2% and 11±2% for PFO and Fatmax , respectively. Between GE and SCE tests, PFO (GEavg : 0.44±0.03; SCE; 0.47±0.06g·min-1 , P=.510) was not different, whereas a difference in Fatmax (GEavg : 42±2%; SCE: 52±4% of V̇O2peak , P=.030) was observed with a CV of 17±4% and 15±4% for PFO and Fatmax , respectively. In conclusion, GE has a high day-to-day reliability in determination of PFO and Fatmax in trained men, whereas it is unclear if PFO and Fatmax determined by GE reflect continuous exercise in general.

Higher dietary protein intake preserves lean body mass, lowers liver lipid deposition, and maintains metabolic control in participants with long-chain fatty acid oxidation disorders.

Medical nutrition therapy for long-chain fatty acid oxidation disorders (LC-FAODs) currently emphasizes fasting avoidance, restricted dietary long-chain fatty acid intake, supplementation with medium chain triglycerides, and increased carbohydrate intake. We hypothesize that increasing dietary protein intake relative to carbohydrate intake would preserve metabolic control yet induce physical benefits including reduced hepatic lipogenesis. Therefore, we compared two dietary approaches with similar fat intake but different carbohydrate to protein ratios in participants diagnosed with LC-FAODs. Thirteen participants were enrolled and randomized into either a high-protein (PRO) or a high-carbohydrate (CHO) diet for 4 months. Baseline and 4-month assessments included body composition, ectopic lipid deposition, and resting energy expenditure. End of study assessments also included total energy expenditure, metabolic responses to oral feedings, and whole-body fatty acid oxidation capacity. At the end of the dietary intervention, both groups had similar energy expenditure, fat and glucose oxidation rates, and glucolipid responses to mixed meal and oral glucose loads. Neither dietary group experienced worsening symptoms related to their LC-FAOD. Compared to the CHO group, the PRO group exhibited increased blood levels of short-chain acylcarnitines, reduced intrahepatic lipid content, and maintained lean body mass while the CHO group lost lean mass. In patients with LC-FAODs, increasing protein intake maintained metabolic control, reduced liver fat without risk of metabolic decompensation, and helped preserve lean body mass. We propose that a modest increase in dietary protein along with fasting avoidance and fat restriction may improve body composition and energy expenditure in patients with LC-FAODs.

TNF blockade contributes to restore lipid oxidation during exercise in children with juvenile idiopathic arthritis

BackgroundChildren with juvenile idiopathic arthritis (JIA) have impaired physical abilities. TNF-α plays a crucial role in this pathogenesis, but it is also involved in the use of lipids and muscle health. Objective of this study was to explore substrate oxidation and impact of TNF blockade on energy metabolism in children with JIA as compared to healthy children.MethodsFifteen non-TNF-blockaded and 15 TNF-blockaded children with JIA and 15 healthy controls were matched by sex, age, and Tanner stage. Participants completed a submaximal incremental exercise test on ergocycle to determine fat and carbohydrate oxidation rates by indirect calorimetry.ResultsThe maximal fat oxidation rate during exercise was lower in JIA children untreated by TNF blockade (134.3 ± 45.2 mg.min− 1) when compared to the controls (225.3 ± 92.9 mg.min− 1, p = 0.007); but was higher in JIA children under TNF blockade (163.2 ± 59.0 mg.min− 1, p = 0.31) when compared to JIA children untreated by TNF blockade. At the same relative exercise intensities, there was no difference in carbohydrate oxidation rate between three groups.ConclusionsLipid metabolism during exercise was found to be impaired in children with JIA. However, TNF treatment seems to improve the fat oxidation rate in this population.Trial registrationIn ClinicalTrials.gov, reference number NCT02977416, registered on 30 November 2016.

Primary defects in lipid handling and resistance to exercise in myotubes from obese donors with and without type 2 diabetes

Several studies have shown that human primary myotubes retain the metabolic characteristic of their donors in vitro. We have demonstrated, along with other researchers, a reduced lipid turnover and fat oxidation rate in myotubes derived from obese donors with and without type 2 diabetes (T2D). Because exercise is known to increase fat oxidative capacity in skeletal muscle, we investigated if in vitro exercise could restore primary defects in lipid handling in myotubes of obese individuals with and without T2D compared with lean nondiabetic donors. Primary myotubes cultures were derived from biopsies of lean, obese, and T2D subjects. One single bout of long-duration exercise was mimicked in vitro by electrical pulse stimulation (EPS) for 24 h. Lipid handling was measured using radiolabeled palmitate, metabolic gene expression by real-time qPCR, and proteins by Western blot. We first showed that myotubes from obese and T2D donors had increased uptake and incomplete oxidation of palmitate. This was associated with reduced mitochondrial respiratory chain complex II, III, and IV protein expression in myotubes from obese and T2D subjects. EPS stimulated palmitate oxidation in lean donors, while myotubes from obese and T2D donors were refractory to this effect. Interestingly, EPS increased total palmitate uptake in myotubes from lean donors while myotubes from T2D donors had a reduced rate of palmitate uptake into complex lipids and triacylglycerols. Novelty Myotubes from obese and T2D donors are characterized by primary defects in palmitic acid handling. Both obese and T2D myotubes are partially refractory to the beneficial effect of exercise on lipid handling.

Effect Of Ethnicity On Change In Vo2max And Substrate Oxidation In Response To HIIT

INTRODUCTION: About 20% of adults meet the 2008 Physical Activity Guidelines and this lack of physical activity increases individuals' risk of heart disease, stroke, type-2 diabetes, and certain cancers which increases morbidity and all-cause mortality. Typically, moderate intensity continuous training (MICT) is prescribed to clients to improve overall fitness and health status, although a primary barrier to regular physical activity among sedentary individuals is lack of time. An alternative to MICT is high intensity interval training (HIIT) which significantly increases VO2max and fat oxidation, in turn improving exercise capacity and reducing health risks. One widely ignored aspect of individual response to exercise training is ethnicity, as there are minimal data examining the effect of ethnicity on responses to exercise training. PURPOSE: To determine if ethnicity alters adaptation to low volume HIIT in sedentary women. METHODS: Inactive, non-obese women (age and VO2max = 24.3 ± 4.1 yr and 29.1 ± 2.1 mL/kg/min) participated in 9 sessions over a 3-week period of cycling-based HIIT (8-10 1-minute bouts at 85% PPO interspersed with 75-sec recovery at 10% PPO). Participants were Caucasian (C) (n=6) or Hispanic (H) (n=4). To assess VO2max, the initial work rate began at 30 or 40 W for 2-min followed by a 15 or 20 W/min increase in power output until volitional exhaustion. To assess substrate oxidation, a 6-min warm up began at 10% PPO and subsequently work rate increased by 10% PPO every 5-min during 4 remaining stages. These variables were measured pre- and post-training. RESULTS: Training elicited a HR equal to 88-94% HRmax. Data showed an increase (p=0.016) in VO2max in C (30.5 ± 1.3 vs 32.6 ± 3.9 mL/kg/min, +7%) and H (27.7 ± 2.8 vs 31.7 ± 2.6 mL/kg/min, +14%) with no significant groupXtime interaction (p=0.35). There was a significant trainingXboutXgroup interaction for fat oxidation (p=0.005), carbohydrate oxidation (p=0.009), and RER (p=0.000). Data showed an increase in the rate of fat oxidation and a reduction in carbohydrate oxidation in response to training which differed based on ethnicity. CONCLUSION: These data show HIIT induces significant increases in VO2max which are slightly higher in H vs C. In addition, ethnicity seems to mediate changes in substrate metabolism after interval-based exercise.

Relationship Of Leptin,Body Composition And Resting Metabolic Rate In Chinese Overweight And Obese Adults

PURPOSE: Resting metabolic rate (RMR) and substrate utilization are important factors in maintaining energy balance and leptin is postulated to be involved in the regulation of body weight. However, in overweight and obese individuals, excess fat mass has a significant impact on metabolic function both directly through altered metabolic rate and substrate oxidation, and indirectly, through chronic changes in hormonal concentrations. This study determined the relationship of body composition and leptin with RMR and substrate utilization (carbohydrate, fat and protein oxidation rates) in Chinese overweight and obese adults. METHODS: The subjects were 33 women (age = 44.0±12.1 years; BMI =27.9±3.2 kg/m2; percent body fat (%fat) = 38.7 ± 4.0%) and 34 men (age= 30.0±9.7years; BMI=27.4±1.7 kg/m2; percent body fat (%fat) = 27.5 ± 4.3%). RMR and substrate utilization were measured by indirect calorimetry (Metamax 3B® Metabolic Measurement system, German) and body composition by the bioelectrical impedance method. Serum leptin levels were determined by radioimmunoassay. RESULTS: In men and women, RMR significantly correlated with Skeletal Muscle Mass (Men: R=0.556, p=0.001; Women: R=0.493, p=0.004), but both not significantly correlated with leptin(both p>0.05). In stepwise multiple regression analysis, SMM was the main predictor of RMR, explaining 42.5% and 28.5% of the variance of RMR in men and women respectively. In women, but not men, leptin significantly correlated with RER (R=-0.581, p=0.029) and carbohydrate, fat, and protein oxidation rates respectively (R=-0.558, 0.689, 0.690; all p<0.01).Furthermore,in stepwise multiple regression analysis, leptin explaining 33.7% of the variance of RER in women. CONCLUSIONS: Skeletal Muscle Mass is a significant predictor of RMR in Chinese overweight and obese adults, evaluation of body composition may be an effective and efficient way to evaluate metabolic status. Serum leptin concentrations in female subjects showed a negative association with respiratory quotient and carbohydrate oxidation rate and positive association with fat and protein oxidation rates. We suggest that sex-specifc evaluations are also necessary. Acknowledgements: This work was supported by National science and technology program of China (Grants No.2013FY114700)

Effects of Moderate versus Variable High Intensity Cycling on Metabolic Responses During Recovery.

PURPOSE: Examine oxygen consumption (VO2), energy expenditure and respiratory exchange ratio (RER) during recovery following moderate-intensity exercise (MIE) and variable high-intensity exercise (VIE) in healthy adults (n=5; age = 20.2 ± 5.7 yrs). METHODS: Two experimental conditions (MIE and VIE) were randomized and performed on separate days in the fasted state. Both conditions commenced with a 15-min seated rest, followed by the assigned exercise. MIE consisted of continuous moderate-intensity exercise at 40% of WRmax. VIE consisted of sixteen 10-sec supramaximal sprints (120% WRmax), sixteen 20-sec high intensity bouts (60% WRmax) and low-intensity recovery (20% WRmax) interspersed throughout the exercise. Total duration and total work were matched between conditions. Following exercise, there was 75 minutes of seated recovery. Resting VO2 was averaged over the final 10 min of rest. VO2 and respiratory exchange ratio (RER) were recorded during exercise and every 15-minutes of recovery. NetVO2 was calculated as the VO2 above resting VO2. Energy expenditure (EE) and fat oxidation rate (FatOx) were calculated. VO2 and RER responses between conditions were compared using a 2-way repeated measure ANOVAs and EE and FatOx between conditions were compared using paired t-tests. Significance was established if p≤0.05. RESULTS: During recovery, net VO2 decreased in both conditions from exercise (VIE = 1184.2 ± 247.0 ml·min-1; MIE = 1005.8 ± 222.1 ml·min-1) to 75 minutes (VIE = 40.3 ml·min-1 ± 23.6; MIE = 16.1 ± 10.2 ml·min-1). There were no differences in net VO2 between conditions during recovery. Net EE during recovery from VIE and MIE were 10.8 ± 6.7 kcals and 5.5 ± 3.9 kcals, respectively (p =0.13). During VIE and MIE, RER was 1.02 ± 0.4 and 0.96 ± 0.06, respectively (P=0.06). During recovery, RER was lower in VIE compared to MIE at 30 (0.81 ± 0.07 vs. 0.89 ± 0.07) and 45 minutes (0.85 ± 0.11 vs. 0.95 ± 0.09) but was similar at 15 and 60 minutes. At the end of recovery, RER for VIE and MIE were 0.89 ± 0.08 and 0.95 ± 0.09, respectively (p = 0.08). FatOx at the end of recovery was significantly greater in VIE (0.05 ± 0.04 g·min-1) than MIE (0.01 ± 0.03 g·min-1). CONCLUSION: Although, NetVO2 and EE were similar during recovery, VIE appears to alter fuel utilization patterns during recovery towards a lower RER and greater fat oxidation.

Acute Hypoxia Suppresses Exogenous Glucose Oxidation, Lowers Fat Oxidation, and Increases Muscle Glycogenolysis During Steady-state Aerobic Exercise (P08-084-19)

ObjectivesLowlanders performing steady-state aerobic exercise during high-altitude (HA) sojourns, hypoxia mediates increased endogenous carbohydrate oxidation compared to sea level (SL). At SL, ingesting carbohydrate during exercise spares endogenous carbohydrate stores and improves endurance. However, it is unclear whether that strategy is effective at HA, as data from a recent study suggests exogenous glucose oxidation is suppressed during aerobic exercise performed 5 hr after arriving at HA. This observation has not been replicated. The objective of this study was to determine substrate oxidative responses to exogenous carbohydrate ingestion during steady-state aerobic exercise at SL and HA. MethodsUsing a randomized, crossover design, native lowlanders (n = 8 males, mean ± SD, age: 23 ± 2 yr, body mass: 87 ± 10 kg, and VO2peak: SL 4.3 ± 0.2 L/min and HA 2.9 ± 0.2 L/min) consumed 145 g (1.8 g/min) of glucose while performing 80 min of metabolically-matched (SL: 1.66 ± 0.14 L/min 347 ± 29 kcal, HA: 1.59 ± 0.10 L/min, 369 ± 39 kcal) treadmill exercise at SL (757 mmHg) and HA (460 mmHg) conditions after a 5 hr exposure. Total carbohydrate and fat oxidation rates (g/min) during exercise were determined by indirect calorimetry, and exogenous, muscle- and hepatic-derived glucose oxidation by tracer technique using breath and blood measurements of 13C-glucose. ResultsTotal carbohydrate oxidation was higher (P < 0.05) at HA (2.15 ± 0.32) compared to SL (1.39 ± 0.14). Exogenous glucose oxidation was lower (P < 0.05) at HA (0.35 ± 0.07) than SL (0.44 ± 0.05). Muscle glycogen oxidation was higher at HA (1.67 ± 0.26) compared to SL (0.83 ± 0.13). There was no difference in hepatic glycogen oxidation between SL (0.13 ± 0.03) and HA (0.13 ± 0.04). Fat oxidation was lower at HA (0.05 ± 0.07) than SL (0.31 ± 0.08). ConclusionsThese data confirm that acute hypoxic exposure suppresses exogenous carbohydrate oxidation during steady-state exercise. Coupled with observations that fat oxidation was reduced and muscle glycogenolysis accelerated in hypoxia, these findings suggest that ingesting carbohydrate during exercise upon acute hypoxia exposure is not an effective strategy for attenuating oxidation of endogenous carbohydrate stores. Funding SourcesViews expressed are the authors and do not reflect the official policy of the Army, DoD, or the U.S. Government. Supported by USAMRMC.

Short-Term Back Squat Protocol Effect on 5km Run Performance

PURPOSE: Previous research indicates conflicting data on concurrent training. For instance, high intensity strength training, an uncommon training method for runners, has the potential to be beneficial as studies show it allows for enhanced fatigue resistance during high intensity endurance performance. Conversely, some evidence suggests high intensity strength training is harmful for endurance running performance and may alter fuel substrate utilization. Therefore, this study sought to determine the effects of a short-term, high repetition back squat training protocol on 5km run performance as well as on carbohydrate and fat oxidation rates. METHODS: Fifteen runners [4 men, 11 women; 150+ minutes of endurance exercise per week; age = 22 + 5.1y; 20.4 + 5.2 body mass index] completed two weeks of a high repetition back squat training protocol consisting of three sets of 15-24 repetitions at 60% of one-repetition max (1RM), three times per week. Pre- and post-tests included a 5km timed run on an outdoor track, respiratory exchange ratio (RER) through indirect calorimetry during two different intensities of steady-state treadmill exercise (60% and 70% heart rate max (HRmax)), and 1RM for back squats. RESULTS: Back squat 1RM significantly increased by 15% with training (48.0+27.9 to 56.7+30 kg, P = <0.001). However, no statistically significant differences were found in 5km times adjusted for heat-stress of outdoor conditions (Pre: 21.6+8.3 vs. Post: 21.1+8.0 minutes, P = 0.20), which potentially had a significant confounding effect on post-training outcomes. RER at 60% HRmax (Pre: 0.81+0.04 vs. Post: 0.79+0.05, P = 0.45) and 70% HRmax (Pre: 0.84+0.04 vs. 0.85+0.04, P = 0.85) was unchanged. CONCLUSIONS: Performing a high repetition back squat protocol for two weeks does not appear to impact 5km running time or alter the body’s fuel utilization during exercise but is an effective way to improve lower body strength. Further studies are necessary in a temperature-regulated testing environment to determine whether high repetition strength training alters 5km running performance and fuel utilization.

19-OR: Controlled-Release Mitochondrial Protonophore (CRMP) Reverses Hypertriglyceridemia and Hepatic Steatosis in Dysmetabolic Nonhuman Primates

NAFLD is estimated to affect up to one third of the general population and is a major predisposing factor in the pathogenesis of hepatic insulin resistance, NASH, and T2D. While weight loss is highly effective at reversing NAFLD, insulin resistance and T2D, it is difficult to sustain and new therapies are required. Our lab has recently developed a controlled-release mitochondrial protonophore (CRMP) that is functionally liver-targeted and promotes oxidation of hepatic triglycerides by promoting a subtle sustained increase in hepatic mitochondrial inefficiency. While we have previously demonstrated that CRMP safely reverses hypertriglyceridemia, fatty liver, and hepatic inflammation/fibrosis in diet-induced rodent models of obesity, there remains a critical need to assess the safety and efficacy in a model highly relevant to humans. Here, we evaluated the impact of CRMP treatment on hepatic mitochondrial oxidation and the reversal of hypertriglyceridemia, NAFLD, and insulin resistance in a spontaneous nonhuman primate model of NAFLD and the metabolic syndrome. Using Positional Isotopomer NMR Tracer Analysis (PINTA), we demonstrate that acute CRMP treatment (single dose of 5 mg/kg) significantly increases rates of hepatic mitochondrial fat oxidation by 40% (P&amp;lt;0.05). Importantly, CRMP treatment (5 mg/kg/day x 6 weeks) reduced hepatic and plasma triglycerides by 20% (both P=0.05) independently of changes in body weight, food intake, body temperature or adverse reactions. Furthermore, administration of CRMP significantly reduced endogenous glucose production by 18% (P&amp;lt;0.05), which could be attributed to a ~20% reduction in hepatic acetyl-CoA content (as assessed by whole-body βOHB turnover) and pyruvate carboxylase flux. Conclusion: These studies provide important proof-of-concept data to support the development of novel liver-targeted mitochondrial uncouplers for the treatment of NAFLD/NASH and T2D in humans. Disclosure L. Goedeke: None. V. Montalvo Romeral: None. G. Butrico: None. M. Kahn: None. S. Dufour: None. X. Zhang: None. G. Cline: None. K. Petersen: Advisory Panel; Spouse/Partner; Aegerion Pharmaceuticals, AstraZeneca, AstraZeneca, Janssen Research &amp; Development, Merck &amp; Co., Inc., Novo Nordisk A/S. Consultant; Spouse/Partner; Gilead Sciences, Inc. Consultant; Self; Merck &amp; Co., Inc. Consultant; Spouse/Partner; Nimbus Discoverey. Consultant; Self; Novo Nordisk A/S. K. Chng: None. G.I. Shulman: Advisory Panel; Self; AstraZeneca, Janssen Research &amp; Development, Merck &amp; Co., Inc. Advisory Panel; Spouse/Partner; Merck &amp; Co., Inc. Board Member; Self; Novo Nordisk A/S. Consultant; Self; Aegerion Pharmaceuticals, IMetabolic BioPharma Corporation, Longitude Capital, Nimbus Discovery, Inc., Staten Biotechnology B.V. Funding National Institutes of Health

Myokine/Adipokine Response to "Aerobic" Exercise: Is It Just a Matter of Exercise Load?

PurposeExercise health benefits are partly mediated by exertional changes in several myokines/adipokines. This study aimed to compare the acute response of some of these biomarkers to aerobic exercise performed at the intensity corresponding to the maximum fat oxidation rate (FATmax) or the “anaerobic” threshold (AT).MethodsFollowing a cross-over, counterbalanced design, 14 healthy untrained men (23 ± 1 years) performed a 45-min exercise bout at their FATmax or AT intensity (been previously determined through incremental exercise tests). The concentration of interleukin (IL)-15, follistatin, myostatin, fibroblast-growth factor (FGF)-21, irisin, resistin, and omentin was measured at baseline and 0, 1, 3, 24, 48, and 72 h post-exercise.ResultsAT exercise was performed at a higher intensity (85 ± 8 vs. 52 ± 14% of maximal oxygen uptake [VO2 max], p < 0.001) and induced a higher energy expenditure (p < 0.001) than FATmax, whereas a greater fat oxidation was observed in the latter (p < 0.001). A higher peak response of FGF-21 (+90%, p < 0.01) and follistatin (+49%, p < 0.05) was found after AT-exercise, as well as a trend toward a higher peak level of omentin (+13%, p = 0.071) and a greater decrease in resistin (−16%, p = 0.073).ConclusionIncreasing exercise load (from FATmax to AT) results in a higher response of FGF-21, follistatin and omentin to aerobic exercise, with the subsequent potential cardiometabolic benefits. No effects were, however, observed on the remainder of biomarkers. Future research should address if manipulating other exercise variables (e.g., type, frequency) can promote a higher myokine/adipokine response.

Ambient temperature influences metabolic substrate oxidation curves during running and cycling in healthy men

Fat oxidation in cold environments and carbohydrate (CHO) use in hot environments are increased during exercise at steady-state submaximal workloads. However, the influence of cold and heat on fat and CHO oxidation curves remain unknown. We therefore examined the influence of a cold and warm ambient temperature on fat and CHO oxidation across a wide range of exercise intensities during treadmill and cycle ergometer exercise. Nine, young, healthy, male subjects completed four trials, during which they performed an incremental peak oxygen consumption (⩒O2peak) test on a cycle ergometer or treadmill in a 4.6°C or 34.1°C environment. Substrate oxidation, maximal fat oxidation rate (MFO), and exercise intensity where MFO occurs (Fatmax) were assessed via indirect calorimetry. MFO was significantly greater in the cold vs. warm during the treadmill exercise (0.66 ± 0.31 vs. 0.43 ± 0.23 g min−1; p = 0.02) but not during cycling (0.45 ± 0.24 vs. 0.29 ± 0.11 g min−1; p = 0.076). MFO was also greater during treadmill vs. cycling exercise, irrespective of ambient temperature (0.57 g min−1 vs. 0.37 g min−1; p = 0.04). Fatmax was greater in the cold vs. warm for both treadmill (57 ± 20 vs. 37 ± 17%⩒O2peak; p = 0.025) and cycling (62 ± 28 vs. 36 ± 13%⩒O2peak; p = 0.003). Multiple, linear, mixed-effects regressions revealed a strong influence of ambient temperature on substrate oxidation. We demonstrated that exercising in a cold environment increases MFO and Fatmax, predominantly during treadmill exercise. These results validate the implication of ambient temperature on energy metabolism over a wide range of exercise intensities.

Impaired Muscular Fat Metabolism in Juvenile Idiopathic Arthritis in Inactive Disease.

Objectives: The objective of this study was to evaluate muscular metabolic function in children with inactive juvenile idiopathic arthritis (JIA).Methods: Fifteen children with inactive JIA and fifteen healthy controls were matched by sex, biological age, and Tanner stage. Participants completed a submaximal incremental exercise test to determine their fat and carbohydrate oxidation rates.Results: Between the two groups, heart rate values and carbohydrate oxidation rates were the same, regardless of the relative intensity of exercise. Lipid oxidation rates were lower in JIA patients, regardless of the percentage of VO2 peak (p < 0.05). Respiratory exchange ratios beyond 50% of VO2 peak were higher in patients with JIA (p < 0.05). Respective maximal fat oxidation rates (MFO) for controls and children with JIA were 218.7 ± 92.2 vs. 157.5 ± 65.9 mg ⋅ min-1 (p = 0.03) and 4.9 ± 1.9 vs. 3.4 ± 1.2 mg ⋅ min-1 ⋅ kg-1 (p = 0.04). There was no difference between the two groups in heart rate, percentage of VO2 peak, or power of exercise to achieve MFO. Controls reached their MFO at an exercise power significantly higher than did JIA subjects (42.8 ± 16.8 and 31.9 ± 9.8 W, p = 0.004).Conclusion: Children with JIA show metabolic disturbance during exercise, even when the disease is considered inactive. This disturbance is seen in a lower lipid oxidation rate during submaximal exercise.

Liver function and energy metabolism in hepatocellular carcinoma developed in patients with hepatitis B-related cirrhosis

Energy metabolism in patients with Hepatocellular carcinoma (HCC) accompanying by hepatitis B cirrhosis is unknown.To compare the differences in liver functions and energy metabolism between patients with hepatitis B-related cirrhosis and patients with HCC.This was a retrospective study of patients with hepatitis B-related cirrhosis (LC group, n = 75) and patients with HCC accompanying by hepatitis B cirrhosis (HCC group, n = 80) treated in Beijing You’an Hospital between January 2013 and June 2017. The resting energy expenditure (REE), respiratory quotient (RQ), carbohydrate oxidation rate (CHO%), fat oxidation rate (FAT%), and protein oxidation rate (PRO%) were measured using a metabolic cart. Liver function, renal function, blood coagulation, etc. were collected.Compared to the LC group, patients with HCC had normal metabolism, but RQ (0.83 ± 0.07 vs 0.85 ± 0.08, P = .073) and CHO% (35.5% vs 49%, P = .013) were lower and FAT% was higher (41% vs 33%, P = .030). Compared with patients with LC group, albumin (ALB), γ-glutamyltranspeptadase (GGT), alkaline phosphatase (AKP), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and prothrombin time activity (PTA) were elevated in the HCC group, while total bilirubin (TB), total bile acid (TBA), and international normalized ratio (INR) were reduced (P < .05). Cholinesterase (CHE) was positively correlated with RQ, CHO, and CHO% (P < .05), while negatively correlated with FAT and FAT% (P < .05). AKP was negatively correlated with RQ, CHO, and CHO% (P < .05), while positively correlated with FAT and FAT% (P < .05). TBA was negatively correlated with RQ and CHO (P < .05), while positively correlated with FAT (P < .05).HCC leads to increased liver synthetic function and improve the liver functions of patients with LC, at least to some extent, but the nutritional metabolism was poor.

Improvement of energy substrate metabolism by late evening snack supplementation in patients with liver cirrhosis: a meta-analysis.

Aim: Malnutrition is one of the most common complications in patients with liver cirrhosis. Abnormal energy substrate metabolism may contribute to aggravation of malnutrition. Late evening snack (LESs) supplementation has been recommended as an intervention to reduce starvation time and improve nutritional status. Published studies have analyzed the effect of LESs on the branched-chain amino acid (BCAA)/tyrosine ratio (BTR) and oxidation rate of fat and carbohydrate in patients with liver cirrhosis.Methods: We searched PubMed, Cochrane Library, Web of Science and Embase for relevant research from January 2000 to October 2018. The primary outcome for this analysis was changes in BTR and fat and carbohydrate oxidation in patients with liver cirrhosis.Results: A total of 9 articles, containing 211 patients, were included in this analysis. The results supported that supplementation with BCAA-enriched LESs improved BTR, and long-term supplementation with BCAAs (>1 month) may be more beneficial than short-term supplementation (<1 month) in patients with liver cirrhosis. In addition, supplementation with BCAAs may increase the oxidation rate of carbohydrates and decrease the oxidation rate of fat. Furthermore, compared with liquid-enriched LESs, BCAA was a better choice for increasing the oxidation of carbohydrates and decreasing the rate of fat oxidation.Conclusion: BCAA-enriched LES supplementation is an appropriate nutritional intervention to improve abnormal energy substrate metabolism, which may improve malnutrition in patients with liver cirrhosis. Further research is needed on the long-term benefit and improved survival in patients with liver cirrhosis.

Effects of Exercise With and Without Energy Replacement on Substrate Utilization in the Fasting State

Objective: The present study aimed to examine the interactive effect of exercise and energy balance on energy expenditure and substrate utilization.Method: Seven men and 7 women underwent three 2-day experimental protocols in a random order. Each protocol consisted of no exercise (NE), exercise only (EO), or exercise with a matched energy replacement (ER) on day 1 followed by metabolic testing that occurred after a 12-hour overnight fasting on day 2. Both EO and ER involved treadmill running at 60% maximal oxygen uptake (VO2max) that induced an energy expenditure of ∼ 500 kcal. The replacement meal used in ER contained ∼ 500 kcal made up of 45% carbohydrate, 30% fat, and 25% protein. During metabolic testing, oxygen uptake (VO2), heart rate (HR), respiratory exchange ratio (RER), and rates of carbohydrate (COX) and fat oxidation (FOX) were determined in three successive 15-minute periods including rest and exercise at 50% and 70% VO2max.Results: No differences in VO2 and HR were found at rest among NE, EO, and ER. However, RER was lower in EO than NE (0.840 ± 0.014 vs 0.889 ± 0.012, p < 0.05), COX (g·min−1) was lower in ER than NE (0.144 ± 0.016 vs 0.197 ± 0.019, p < 0.05), and FOX (g·min−1) was higher in EO or ER than NE (0.054 ± 0.010 or 0.057 ± 0.009 vs 0.034 ± 0.007, p < 0.05). No treatment effects were observed for all variables at either intensity.Conclusions: This study demonstrates that an exercise of moderate intensity can increase resting fat oxidation even when the exercise-induced energy expenditure is balanced by energy intake. This finding suggests that muscle action is vital in augmenting fat utilization.

Blunted fat oxidation upon submaximal exercise is partially compensated by enhanced glucose metabolism in children, adolescents, and young adults with Barth syndrome.

Barth syndrome (BTHS) is a rare X-linked condition resulting in abnormal mitochondria, cardioskeletal myopathy, and growth delay; however, the effects of BTHS on substrate metabolism regulation and their relationships with tissue function in humans are unknown. We sought to characterize glucose and fat metabolism during rest, submaximal exercise, and postexercise rest in children, adolescents, and young adults with BTHS and unaffected controls and examine their relationships with cardioskeletal energetics and function. Children/adolescents and young adults with BTHS (n = 29) and children/adolescent and young adult control participants (n = 28, total n = 57) underwent an infusion of 6'6'H2 glucose and U-13 C palmitate and indirect calorimetry during rest, 30-minutes of moderate exercise (50% ), and recovery. Cardiac function, cardioskeletal mitochondrial energetics, and exercise capacity were examined via echocardiography, 31 P magnetic resonance spectroscopy, and peak exercise testing, respectively. The glucose turnover rate was significantly higher in individuals with BTHS during rest (33.2 ± 9.8 vs 27.2 ± 8.1 μmol/kgFFM/min, P < .01) and exercise (34.7 ± 11.2 vs 29.5 ± 8.8 μmol/kgFFM/min, P < .05) and tended to be higher postexercise (33.7 ± 10.2 vs 28.8 ± 8.0 μmol/kgFFM/min, P < .06) compared to controls. Increases in total fat (-3.9 ± 7.5 vs 10.5 ± 8.4 μmol/kgFFM/min, P < .0001) and plasma fatty acid oxidation rates (0.0 ± 1.8 vs 5.1 ± 3.9 μmol/kgFFM/min, P < .0001) from rest to exercise were severely blunted in BTHS compared to controls. Conclusion: An inability to upregulate fat metabolism during moderate intensity exercise appears to be partially compensated by elevations in glucose metabolism. Derangements in fat and glucose metabolism are characteristic of the pathophysiology of BTHS. A severely blunted ability to upregulate fat metabolism during a modest level of physical activity is a defining pathophysiologic characteristic in children, adolescents, and young adults with BTHS.

Relationship between individual ventilatory threshold and maximal fat oxidation (MFO) over different obesity classes in women.

ObjectiveThe use of the Individual Ventilatory Threshold (IVT), as parameter to prescribe exercise intensity in individuals with obesity, has become more frequent during the last years. This study aimed to evaluate the relationship between IVT and Maximal Fat Oxidation (MFO) in women with obesity.MethodsFifty-two obese female adults (age = 43.6±10.9 years; BMI = 38.5±5.2 kg/m2) were included in this study. According to the BMI classification, subjects were divided into three groups: Obese Class I (OBI, n = 16); Obese Class II (OBII, n = 20) and Obese Class III (OBIII, n = 16). All subjects performed an incremental graded exercise test to evaluate peak oxygen uptake (VO2peak), IVT and MFO. MFO was evaluated using a stoichiometric equation. Fat max zone was determined for each subject within 10% of fat oxidation rates at MFO. For each HR, %HRmax, VO2 and %VO2peak variable, Pearson’s correlation test was done between IVT and MFO exercise intensity. When statistical correlation was found we used a comparative statistical analysis to assess differences between IVT and MFO. Statistical significance was set at P ≤ 0.05.ResultsFor each HR, %HRmax, VO2 and %VO2peak variable there was a positive significant correlation (P<0.01) between IVT and MFO. No significant differences were found for HR, %HRmax, and VO2 between IVT and MFO. %VO2peak was significantly higher at IVT than at MFO (P = 0.03).MFO rates were significantly higher in OBIII women than in women of the other two classes. In all subjects, IVT was within the fat max zone.ConclusionThe use of HR and VO2 corresponding to IVT could be a useful parameter not only to improve cardiorespiratory fitness but also to prescribe physical activity that maximize fat oxidation in obese subjects.

Plasma free fatty acid concentration is closely tied to whole body peak fat oxidation rate during repeated exercise

Plasma free fatty acids (FFA) are a major contributor to whole body fat oxidation during exercise. However, the extent to which manipulating plasma FFA concentrations will influence whole body peak fat oxidation rate (PFO) during exercise remains elusive. In this study we aimed to increase plasma FFA concentrations through a combination of fasting and repeated exercise bouts. We hypothesized that an increase in plasma FFA concentration would increase PFO in a dose-dependent manner. Ten healthy young (31 ± 6 yr) (mean ± SD) well-trained (maximal oxygen uptake 65.9 ± 6.1 ml·min-1·kg-1) men performed four graded exercise tests (GXTs) on 1 day. The GXTs were interspersed by 4 h of bed rest. This was conducted either in a fasted state or with the consumption of a standardized carbohydrate-rich meal 3.5 h before each GXT. Fasting and previous GXTs resulted in a gradual increase in PFO from 0.63 ± 0.18 g/min after an overnight fast (10 h) to 0.93 ± 0.17 g/min after ∼22 h of fasting and three previous GXTs. This increase in PFO coincided with an increase in plasma FFA concentrations (r2 = 0.73, P < 0.0001). Ingestion of a carbohydrate-rich meal 3.5 h before each GXT resulted in unaltered PFO. This was also reflected in unchanged plasma FFA, glucose, and insulin concentrations. In this study we show that plasma FFA availability is closely tied to whole body PFO and that the length of fasting combined with previous exercise are robust stimuli toward increasing plasma FFA concentration, highlighting the importance for preexercise standardization when conducting GXTs measuring substrate oxidation. NEW & NOTEWORTHY We show that peak fat oxidation is increased in close relationship with plasma free fatty acid availability after combined fasting and repeated incremental exercise tests in healthy highly trained men. Therefore it may be argued that whole body fat oxidation rate measured in most cases after an overnight fast indeed does not represent whole body maximal fat oxidation rate but a whole body peak fat oxidation rate within the context of the preexercise standardization obtained in the study design.