Peak Fat Oxidation Research Articles

Peak fat oxidation, peak oxygen uptake, and running performance increase during pre-season in sub-elite male football players.

In Football, the high-intensity running bouts during matches are considered decisive. Interestingly, recent studies showed that peak fat oxidation rates (PFO) are higher in football players than other athletes. This study aimed to investigate whether PFO increases following a pre-season. Secondarily, and due to COVID-19, we investigated whether PFO is related to the physical performance in a subgroup of semi-professional male football players. Before and after 8 weeks of pre-season training, 42 sub-elite male football players (18 semi-professionals and 24 non-professionals) had a dual-energy x-ray absorptiometry scan and performed a graded exercise test on a treadmill for the determination of PFO, the exercise intensity eliciting PFO (Fatmax) and peak oxygen uptake (V̇O2peak). Additionally, the semi-professional players performed a Yo-Yo Intermittent Recovery Test level 2 (YYIR2) before and after pre-season training to determine football-specific running performance. PFO increased by 11 ± 10% (mean ± 95% CI), p = 0.031, and V̇O2peak increased by 5 ± 1%, p < 0.001, whereas Fatmax was unchanged (+12 ± 9%, p = 0.057), following pre-season training. PFO increments were not associated with increments in V̇O2peak (Pearson's r2 = 0.00, p = 0.948) or fat-free mass (FFM) (r2 = 0.00, p = 0.969). Concomitantly, YYIR2 performance increased in the semi-professional players by 39 ± 17%, p < 0.001, which was associated with changes in V̇O2peak (r2 = 0.35, p = 0.034) but not PFO (r2 = 0.13, p = 0.244). PFO, V̇O2peak, and FFM increased following pre-season training in sub-elite football players. However, in a subgroup of semi-professional players, increments in PFO were not associated with improvements in YYIR2 performance nor with increments in V̇O2peak and FFM.

Association between “cluster of differentiation 36 (CD36)” and adipose tissue lipolysis during exercise training: a systematic review

Fatty acid translocase (FAT/CD36) is a transmembrane glycoprotein belonging to the scavenger class B receptor family and is encoded by the cluster of differentiation 36 (CD36) gene. This receptor has a high affinity for fatty acids and is involved in lipid metabolism. An abundance of FAT/CD36 during exercise occurs in mitochondria and solitary muscles. As such, we aimed to systematically review the evidence for the relationship FAT/CD36 and adipose tissue lipolysis during exercise training. Five electronic databases were selected for literature searches until June 2022: PubMed, Web of Science, Scopus, science direct, and Google Scholar. We combined the different synonyms and used the operators (“AND”, “OR”, “NOT”): (CD36 gene) OR (CD36 polymorphism) OR (cluster of differentiation 36) OR (FAT/CD36) OR (fatty acid translocase) OR (platelet glycoprotein IV) OR (platelet glycoprotein IIIb) AND (adipose tissue lipolysis) OR (fatty acids) OR (metabolism lipid) OR (adipocytes) AND (physical effort) OR (endurance exercise) OR (high-intensity training). All published cross-sectional, cohort, case-control, and randomized clinical trials investigating CD36 polymorphisms and adipose tissue lipolysis during exercise in subjects (elite and sub-elite athletes, non-athletes, sedentary individuals and diabetics), and using valid methods to measure FAT/CD36 expression and other biomarkers, were considered for inclusion in this review. We initially identified 476 publications according to the inclusion and exclusion criteria, and included 21 studies investigating FAT/CD36 and adipose tissue lipolysis during exercise in our systematic review after examination of titles, abstracts, full texts, and quality assessments using the PEDro scale. There were nine studies with male-only participants, three with female-only participants, and nine studies included both female and male participants. There were 859 participants in the 21 selected studies. Studies were classified as either low quality (n = 3), medium quality (n = 13), and high quality (n = 5). In general, the data suggests an association between FAT/CD36 and adipose tissue lipolysis during exercise training. Improvements in FAT/CD36 were reported during or after exercise in 6 studies, while there were no changes reported in FAT/CD36 in 4 studies. An association between fat oxidation and FAT/CD36 expression during exercise was reported in 7 studies. No agreement was reached in 5 studies on FAT/CD36 content after dietary changes and physical interventions. One study reported that FAT/CD36 protein expression in muscle was higher in women than in men, another reported that training decreased FAT/CD36 protein in insulin-resistant participants, while another study reported no differences in FAT/CD36 in young, trained individuals with type 2 diabetes. Our analysis shows an association between FAT/CD36 expression and exercise. Furthermore, an association between whole-body peak fat oxidation and FAT/CD36 expression during exercise training was demonstrated.Systematic Review Registration: [PROSPERO], identifier [CRD42022342455]

Maximal oxidative capacity during exercise is associated with muscle power output in patients with long coronavirus disease 2019 (COVID-19) syndrome. A moderation analysis

Long COVID syndrome (LCS) involves persistent symptoms experienced by many patients after recovering from coronavirus disease 2019 (COVID-19). We aimed to assess skeletal muscle energy metabolism, which is closely related to substrate oxidation rates during exercise, in patients with LCS compared with healthy controls. We also examined whether muscle power output mediates the relationship between COVID-19 and skeletal muscle energy metabolism. In this cross-sectional study, we enrolled 71 patients with LCS and 63 healthy controls. We assessed clinical characteristics such as body composition, physical activity, and muscle strength. We used cardiopulmonary exercise testing to evaluate substrate oxidation rates during graded exercise. We performed statistical analyses to compare group characteristics and peak fat oxidation differences based on power output. The two-way analysis of covariance (ANCOVA) results, adjusted for covariates, showed that the patients with LCS had lower absolute maximal fatty acid oxidation (MFO), relative MFO/fat free mass (FFM), absolute carbohydrates oxidation (CHox), relative CHox/FFM, and oxygen uptake (V˙˙O2) at maximum fat oxidation (g min-1) than the healthy controls (P<0.05). Moderation analysis indicated that muscle power output significantly influenced the relationship between LCS and reduced peak fat oxidation (interaction β=-0.105 [95% confidence interval-0.174;-0.036]; P=0.026). Therefore, when muscle power output was below 388W, the effect of the LCS on MFO was significant (62% in our study sample P=0.010). These findings suggest compromised mitochondrial bioenergetics and muscle function, represented by lower peak fat oxidation rates, in the patients with LCS compared with the healthy controls. The patients with LCS had lower peak fat oxidation during exercise compared with the healthy controls, potentially indicating impairment in skeletal muscle function. The relationship between peak fat oxidation and LCS appears to be mediated predominantly by muscle power output. Additional research should continue investigating LCS pathogenesis and the functional role of mitochondria.

The Effect of Soy and Whey Protein Supplementation on Glucose Homeostasis in Healthy Normal Weight Asian Indians.

Milk and legumes are good source of protein foods used to sustain muscle mass, but their effects on postprandial glucose homeostasis and energy metabolism may be different. This is relevant, for example, in the dietetic response to obesity or diabetes, where the intake of high-quality protein is often increased significantly. The objective of this study was to characterize the acute effect of whey and soy protein (15% vs. 30%) on glucose homeostasis, energy metabolism, and satiety. Healthy, normal body mass index (BMI) Indian adult males aged 20-35 years (n = 15) received 4 test meals (2 proteins (soy vs. whey) and 2 doses (15% vs. 30% protein: energy ratio)). Blood samples were collected serially after the meal to calculate the incremental area under the curve for plasma glucose and insulin. Energy expenditure and substrate oxidation were measured after the meal. Satiety was measured with a visual analogue scale. The insulin response, represented by the incremental area under the curve, was significantly higher for the 30% whey compared to the 30% soy protein meal (p < 0.01) but was not significantly different between the 15% protein doses. There were no differences in the plasma glucose response across protein sources or doses. The mean peak fat and carbohydrate oxidation, satiety, and energy expenditure did not differ between the protein sources and doses. In conclusion, at higher doses, whey protein has a greater insulinogenic response, compared to soy protein, and exhibits a dose-response effect. However, at lower doses, whey and soy protein elicit similar insulinogenic responses, making them equally effective protein sources in relation to glucose homoeostasis.

Substrate oxidation during exercise in childhood acute lymphoblastic leukemia survivors

Children with acute lymphoblastic leukemia (ALL) are at high risk of developing long-term cardiometabolic complications during their survivorship. Maximal fat oxidation (MFO) is a marker during exercise of cardiometabolic health, and is associated with metabolic risk factors. Our aim was to characterize the carbohydrate and fat oxidation during exercise in childhood ALL survivors. Indirect calorimetry was measured in 250 childhood ALL survivors to quantify substrate oxidation rates during a cardiopulmonary exercise test. A best-fit third-order polynomial curve was computed for fat oxidation rate (mg/min) against exercise intensity (O2peak) and was used to determine the MFO and the peak fat oxidation (Fatmax). The crossover point was also identified. Differences between prognostic risk groups were assessed (ie, standard risk [SR], high risk with and without cardio-protective agent dexrazoxane [HR + DEX and HR]). MFO, Fatmax and crossover point were not different between the groups (p = .078; p = .765; p = .726). Fatmax and crossover point were achieved at low exercise intensities. A higher MFO was achieved by men in the SR group (287.8 ± 111.2 mg/min) compared to those in HR + DEX (239.8 ± 97.0 mg/min) and HR groups (229.3 ± 98.9 mg/min) (p = .04). Childhood ALL survivors have low fat oxidation during exercise and oxidize carbohydrates at low exercise intensities, independently of the cumulative doses of doxorubicin they received. These findings alert clinicians on the long-term impact of cancer treatments on childhood ALL survivors’ substrate oxidation.

Low carbohydrate high fat ketogenic diets on the exercise crossover point and glucose homeostasis.

In exercise science, the crossover effect denotes that fat oxidation is the primary fuel at rest and during low-intensity exercise with a shift towards an increased reliance on carbohydrate oxidation at moderate to high exercise intensities. This model makes four predictions: First, >50% of energy comes from carbohydrate oxidation at ≥60% of maximum oxygen consumption (VO2max), termed the crossover point. Second, each individual has a maximum fat oxidation capacity (FATMAX) at an exercise intensity lower than the crossover point. FATMAX values are typically 0.3-0.6g/min. Third, fat oxidation is minimized during exercise ≥85%VO2max, making carbohydrates the predominant energetic substrate during high-intensity exercise, especially at >85%VO2max. Fourth, high-carbohydrate low-fat (HCLF) diets will produce superior exercise performances via maximizing pre-exercise storage of this predominant exercise substrate. In a series of recent publications evaluating the metabolic and performance effects of low-carbohydrate high-fat (LCHF/ketogenic) diet adaptations during exercise of different intensities, we provide findings that challenge this model and these four predictions. First, we show that adaptation to the LCHF diet shifts the crossover point to a higher %VO2max (>80%VO2max) than previously reported. Second, substantially higher FATMAX values (>1.5g/min) can be measured in athletes adapted to the LCHF diet. Third, endurance athletes exercising at >85%VO2max, whilst performing 6 × 800m running intervals, measured the highest rates of fat oxidation yet reported in humans. Peak fat oxidation rates measured at 86.4 ± 6.2%VO2max were 1.58 ± 0.33g/min with 30% of subjects achieving >1.85g/min. These studies challenge the prevailing doctrine that carbohydrates are the predominant oxidized fuel during high-intensity exercise. We recently found that 30% of middle-aged competitive athletes presented with pre-diabetic glycemic values while on an HCLF diet, which was reversed on LCHF. We speculate that these rapid changes between diet, insulin, glucose homeostasis, and fat oxidation might be linked by diet-induced changes in mitochondrial function and insulin action. Together, we demonstrate evidence that challenges the current crossover concept and demonstrate evidence that a LCHF diet may also reverse features of pre-diabetes and future metabolic disease risk, demonstrating the impact of dietary choice has extended beyond physical performance even in athletic populations.

Low and high carbohydrate isocaloric diets on performance, fat oxidation, glucose and cardiometabolic health in middle age males.

High carbohydrate, low fat (HCLF) diets have been the predominant nutrition strategy for athletic performance, but recent evidence following multi-week habituation has challenged the superiority of HCLF over low carbohydrate, high fat (LCHF) diets, along with growing interest in the potential health and disease implications of dietary choice. Highly trained competitive middle-aged athletes underwent two 31-day isocaloric diets (HCLF or LCHF) in a randomized, counterbalanced, and crossover design while controlling calories and training load. Performance, body composition, substrate oxidation, cardiometabolic, and 31-day minute-by-minute glucose (CGM) biomarkers were assessed. We demonstrated: (i) equivalent high-intensity performance (@∼85%VO2max), fasting insulin, hsCRP, and HbA1c without significant body composition changes across groups; (ii) record high peak fat oxidation rates (LCHF:1.58 ± 0.33g/min @ 86.40 ± 6.24%VO2max; 30% subjects > 1.85 g/min); (iii) higher total, LDL, and HDL cholesterol on LCHF; (iv) reduced glucose mean/median and variability on LCHF. We also found that the 31-day mean glucose on HCLF predicted 31-day glucose reductions on LCHF, and the 31-day glucose reduction on LCHF predicted LCHF peak fat oxidation rates. Interestingly, 30% of athletes had 31-day mean, median and fasting glucose > 100 mg/dL on HCLF (range: 111.68-115.19 mg/dL; consistent with pre-diabetes), also had the largest glycemic and fat oxidation response to carbohydrate restriction. These results: (i) challenge whether higher carbohydrate intake is superior for athletic performance, even during shorter-duration, higher-intensity exercise; (ii) demonstrate that lower carbohydrate intake may be a therapeutic strategy to independently improve glycemic control, particularly in those at risk for diabetes; (iii) demonstrate a unique relationship between continuous glycemic parameters and systemic metabolism.

Fat Oxidation during Exercise in People with Spinal Cord Injury, and Protocols Used: A Systematic Review.

The aim of this study was to summarize evidence on energy metabolism through peak fat oxidation (PFO) and maximum fat oxidation (Fatmax), as well as to analyze the protocols used in people with spinal cord injury (SCI) and to examine the main factors related to fat oxidation ability (i.e., age, sex, level of physical activity, and level and degree of injury). Studies to determine PFO and Fatmax using indirect calorimetry with an arm exercise protocol for SCI patients were included after a systematic search. Other endpoints included study design, sample size, control group, demographic data, level of injury, physical condition, protocol, outcomes measured, and statistical findings. Eight studies (n = 560) were included. The mean value of VO2peak was 1.86 L∙min-1 (range 0.75-2.60 L∙min-1) (lowest value in the tetraplegic subjects). The PFO ranged between 0.06 and 0.30 g∙min-1 (lowest rates: the non-trained subjects with cervical SCI; highest: the tetraplegic subjects). Two types of exercise protocol were found: arm cycle ergometer, and wheelchair propulsion with a computerized ergometer. Five studies used an incremental protocol (2-3 min/stage, different load increments); the rest performed tests of 20 min/stage at three intensities. There are few existing studies measuring fat oxidation in SCI, many of which used small and heterogeneous samples. PFO was lower in SCI subjects when compared with non-injured people performing lower-limb exercise; however, comparing upper-limb exercise, people with SCI showed higher values.

Exercise, aerobic fitness, and muscle strength in relation to glucose tolerance 6 to 10 years after gestational diabetes

AimsWe sought to identify self-reported exercise and objectively measured fitness variables associated with glucose tolerance and metabolic health 6–10 years after gestational diabetes (GDM) MethodsWomen (n = 84) underwent oral glucose tolerance testing (OGTT), body composition measurements, and lifestyle questionnaires 6 and 10 years after GDM. In a subset (n = 45), peak oxygen uptake (VO2peak), peak fat oxidation, and maximal isometric strength of five muscle groups were tested. ResultsAt 10 years, 41 women (49%) had impaired glucose metabolism or type 2 diabetes (T2D). VO2peak and muscle strength were lowest in the T2D group. In a regression analysis, VO2peak and all strength measurements were associated negatively with HbA1c and waist-hip ratio and positively with high-density lipoprotein cholesterol. However, only muscle strength was associated with fasting and area-under-the-curve glucose. For changes between the 6- and 10-year follow-ups, only muscle strength was associated with HbA1c change, whereas both VO2peak and strength were associated with high-density lipoprotein level and changes in waist-hip ratio. Peak fat oxidation and self-reported physical activity showed no or weak relationships with glycemic variables. ConclusionObjectively measured fitness variables, particularly muscle strength, were strongly associated with glycemic and other metabolic outcomes in a high-risk group after GDM.

Four Weeks Of A Ketogenic Diet Increases Oxygen Consumption And Fat Oxidation During Moderate-intensity Walking

PURPOSE: Establish the time-course of changes in oxygen consumption, substrate metabolism, and heart rate during treadmill walking upon commencing a ketogenic diet. METHODS: In a randomized, parallel design, 53 men and women (mean ± SD, age: 35 ± 16 years, body mass index: 24 ± 3 kg/m2) were allocated to a moderate-sugar, moderate-carbohydrate diet [MODSUG; contribution of carbohydrate (of which sugars), fat and protein to total energy intake: 50% (15%), 35%, and 15%, respectively] a low-sugar, moderate-carbohydrate diet [LOWSUG; 50% (5%), 35%, and 15%, respectively] or a low-carbohydrate, ketogenic diet [LOWCHO; 8% (2%), 77%, and 15%, respectively] for 12 weeks. Oxygen consumption and substrate metabolism were determined by Douglas bags and heart rate using electrocardiography during submaximal walking at baseline, 4-weeks and 12-weeks of the dietary intervention. The submaximal treadmill test comprised 5-minute stages at 5.2 km/h with gradients of 0%, 3%, 6% and 9%. Data were analyzed by two-way (group x time) ANOVA with post-hoc test corrected for multiple comparisons by the Bonferroni method. RESULTS: Mean oxygen consumption rates displayed a group x time interaction (P = 0.016) whereby LOWCHO increased oxygen consumption from 17.8 ± 1.8 mL/kg/min at baseline to 18.4 ± 2.1 mL/kg/min by week 4 (P = 0.02), after which levels remained elevated at 18.4 ± 2.2 at week 12 (P > 0.05). Mean heart rate during all gradients increased with LOWCHO from 115 ± 12 beats/min at baseline to 121 ± 12 beats/min by week 4 (group x time interaction, P = 0.026; post-hoc comparison, P = 0.04), reaching 120 ± 14 beats/min at week 12 (P > 0.05). Peak fat oxidation rates increased with LOWCHO from 0.37 ± 0.18 g/min at baseline to 0.58 ± 0.25 g/min at week 4 with concomitant decreases in carbohydrate oxidation rates (group x time interaction, P < 0.001; post-hoc comparison, P < 0.001) with no further increases at week 12 (0.56 ± 0.27 g/min; P > 0.05). No such increases were observed with MODSUG or LOWSUG (all P > 0.05). CONCLUSIONS: Adaptations of oxygen consumption, heart rate and fat oxidation during walking plateau by 4 weeks of commencing a low-carbohydrate ketogenic diet, suggesting 4 weeks is sufficient to maximise metabolic adaptations to exercise with ketogenic diets. Supported by The Rank Prize Funds and Kenniscentrum Suiker & Voeding.

Associations of resting and peak fat oxidation with sex hormone profile and blood glucose control in middle-aged women

Background and aimsMenopause may reduce fat oxidation. We investigated whether sex hormone profile explains resting fat oxidation (RFO) or peak fat oxidation (PFO) during incremental cycling in middle-aged women. Secondarily, we studied associations of RFO and PFO with glucose regulation. Method and resultsWe measured RFO and PFO of 42 women (age 52–58 years) with indirect calorimetry. Seven participants were pre- or perimenopausal, 26 were postmenopausal, and nine were postmenopausal hormone therapy users. Serum estradiol (E2), follicle-stimulating hormone, progesterone, and testosterone levels were quantified with immunoassays. Insulin sensitivity (Matsuda index) and glucose tolerance (area under the curve) were determined by glucose tolerance testing. Body composition was assessed with dual-energy X-ray absorptiometry; physical activity with self-report and accelerometry; and diet, with food diaries. Menopausal status or sex hormone levels were not associated with the fat oxidation outcomes. RFO determinants were fat mass (β = 0.44, P = 0.006) and preceding energy intake (β = −0.40, P = 0.019). Cardiorespiratory fitness (β = 0.59, P = 0.002), lean mass (β = 0.49, P = 0.002) and physical activity (self-reported β = 0.37, P = 0.020; accelerometer-measured β = 0.35, P = 0.024) explained PFO. RFO and PFO were not related to insulin sensitivity. Higher RFO was associated with poorer glucose tolerance (β = 0.52, P = 0.002). ConclusionAmong studied middle-aged women, sex hormone profile did not explain RFO or PFO, and higher fat oxidation capacity did not indicate better glucose control.

Increased Fat Oxidation During Arm Cycling Exercise in Adult Men With Spinal Cord Injury Compared With Noninjured Controls.

People with spinal cord injury (SCI) tend to be more sedentary and increase fat accumulation, which could have a negative influence on metabolic flexibility. The aim of this study was to investigate the capacity to oxidize fat in a homogenous sample of men with thoracic SCI compared with healthy noninjured men during an arm cycling incremental test. Forty-one men, 21 with SCI and 20 noninjured controls, performed an incremental arm cycling test to determine peak fat oxidation (PFO) and the intensity of exercise that elicits PFO (Fatmax). PFO was expressed in absolute values (g/min) and relative to whole-body and upper-body lean mass ([mg·min-1]·kg-1) through three different models (adjusting by cardiorespiratory fitness and fat mass). Gross mechanical efficiency was also calculated. PFO was higher in SCI than in noninjured men (0.27 ± 0.07 vs. 0.17 ± 0.07g/min; 5.39 ± 1.30 vs. 3.29 ± 1.31 [mg·min-1]·kg-1 whole-body lean mass; 8.28 ± 2.11 vs. 5.08 ± 2.12 [mg·min-1]·kg-1 upper-body lean mass). Fatmax was found at a significantly higher percentage of VO2peak in men with SCI (33.6% ± 8.2% vs. 23.6% ± 6.4%). Differences persisted and even increased in the fully adjustment model and at any intensity. Men with SCI showed significantly higher gross mechanical efficiency at 35 and 65W than the noninjured group. Men with SCI showed higher fat oxidation when compared with noninjured men at any intensity, even increased after full adjustment for lean mass, fat mass, and cardiorespiratory fitness. These findings suggest that SCI men could improve their metabolic flexibility and muscle mass for greater efficiency, not being affected by their fat accumulation.

Peak fat oxidation is positively associated with vastus lateralis CD36 content, fed-state exercise fat oxidation, and endurance performance in trained males.

PurposeWhole-body fat oxidation during exercise can be measured non-invasively during athlete profiling. Gaps in understanding exist in the relationships between fat oxidation during incremental fasted exercise and skeletal muscle parameters, endurance performance, and fat oxidation during prolonged fed-state exercise.MethodsSeventeen endurance-trained males underwent a (i) fasted, incremental cycling test to assess peak whole-body fat oxidation (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 30-min maximal-effort cycling time-trial preceded by 2-h of fed-state moderate-intensity cycling to assess endurance performance and fed-state metabolism on separate occasions within one week.ResultsPFO (0.58 ± 0.28 g.min−1) was associated with vastus lateralis citrate synthase activity (69.2 ± 26.0 μmol.min−1.g−1 muscle protein, r = 0.84, 95% CI 0.58, 0.95, P < 0.001), CD36 abundance (16.8 ± 12.6 μg.g−1 muscle protein, rs = 0.68, 95% CI 0.31, 1.10, P = 0.01), pre-loaded 30-min time-trial performance (251 ± 51 W, r = 0.76, 95% CI 0.40, 0.91, P = 0.001; 3.2 ± 0.6 W.kg−1, r = 0.62, 95% CI 0.16, 0.86, P = 0.01), and fat oxidation during prolonged fed-state cycling (r = 0.83, 95% CI 0.57, 0.94, P < 0.001). Addition of PFO to a traditional model of endurance (peak oxygen uptake, power at 4 mmol.L−1 blood lactate concentration, and gross efficiency) explained an additional ~ 2.6% of variation in 30-min time-trial performance (adjusted R2 = 0.903 vs. 0.877).ConclusionThese associations suggest non-invasive measures of whole-body fat oxidation during exercise may be useful in the physiological profiling of endurance athletes.

Peak Fat Oxidation Rate Is Closely Associated With Plasma Free Fatty Acid Concentrations in Women; Similar to Men.

Introduction: In men, whole body peak fat oxidation (PFO) determined by a graded exercise test is closely tied to plasma free fatty acid (FFA) availability. Men and women exhibit divergent metabolic responses to fasting and exercise, and it remains unknown how the combined fasting and exercise affect substrate utilization in women. We aimed to investigate this, hypothesizing that increased plasma FFA concentrations in women caused by fasting and repeated exercise will increase PFO during exercise. Then, that PFO would be higher in women compared with men (data from a previous study).Methods: On two separate days, 11 young endurance-trained women were investigated, either after an overnight fast (Fast) or 3.5 h after a standardized meal (Fed). On each day, a validated graded exercise protocol (GXT), used to establish PFO by indirect calorimetry, was performed four times separated by 3.5 h of bed rest both in the fasted (Fast) or fed (Fed) state.Results: Peak fat oxidation increased in the fasted state from 11 ± 3 (after an overnight fast, Fast 1) to 16 ± 3 (mean ± SD) mg/min/kg lean body mass (LBM) (after ~22 h fast, Fast 4), and this was highly associated with plasma FFA concentrations, which increased from 404 ± 203 (Fast 1) to 865 ± 210 μmol/L (Fast 4). No increase in PFO was found during the fed condition with repeated exercise. Compared with trained men from a former identical study, we found no sex differences in relative PFO (mg/min/kg LBM) between men and women, in spite of significant differences in plasma FFA concentrations during exercise after fasting.Conclusion: Peak fat oxidation increased with fasting and repeated exercise in trained women, but the relative PFO was similar in young trained men and women, despite major differences in plasma lipid concentrations during graded exercise.

Fat And Carbohydrate Oxidation During Cardiopulmonary Exercise Test In Childhood Acute Lymphoblastic Leukemia Survivors

PURPOSE: Analyses of indirect calorimetry during cardiopulmonary exercise tests (CPET) have the potential to bring new evidence about the metabolic health of childhood acute lymphoblastic leukemia (ALL) survivors. To propose a better knowledge of survivors’ metabolic health, we aimed to compare their carbohydrate and fat oxidation during a CPET. Moreover, we explored the long-term effects of doxorubicin and dexrazoxane on survivors’ metabolic health. METHODS: A total of 250 childhood ALL survivors were categorized into three groups depending on their prognostic risk (i.e., standard risk (SR), high risk with and without cardio-protective agent dexrazoxane (HR + DEX and HR)). They underwent a CPET on ergocycle to assess their oxygen consumption and their carbon dioxide production. Carbohydrate and fat oxidation rates were determined using the Peronnet and Massicotte’s equation. For each childhood ALL survivor, we produced a third-degree polynomial equation in order to obtain the best-fit curve for fat and carbohydrate oxidation rate (mg/min) against exercise intensity (%VO2peak). We also used them to compare carbohydrate and fat oxidation over a range of exercise intensities and to determine the maximal fat oxidation (MFO) rate and the peak fat oxidation (Fatmax) rate. MFO and Fatmax comparisons were made using one-way ANOVA. Multiple linear regression analysis was used to quantify each variable’s influence on the MFO and the Fatmax. RESULTS: We observed that MFO parameter was not different between the groups (p = 0.078) (SR = 273.7 ± 99.5 mg·min-1; HR + DEX = 247.3 ± 93.2 mg·min-1; and HR = 239.2 ± 86.0 mg·min-1). There was no difference between the groups for the Fatmax parameter (p = 0.865) (SR = 35.1 ± 7.4%; HR + DEX = 34.6 ± 7.5%; and HR = 35.7 ± 8.1%) and 14% of the variability was explained by the maximum oxygen uptake, sex and obesity. CONCLUSIONS: This study shows that although childhood ALL survivors have a reduced fat oxidation rates, that does not depend on the prognostic risk group. However, we observed a trend that suggests that the reduction of fat oxidation is doxorubicin dose-dependent and that the dexrazoxane treatment has the potential to limit these effects. Our study highlights that survivors’ metabolic health and substrate oxidation are compromised during a maximal cardiopulmonary exercise test.

Neither Postabsorptive Resting Nor Postprandial Fat Oxidation Are Related to Peak Fat Oxidation in Men With Chronic Paraplegia

The peak rate of fat oxidation (PFO) achieved during a graded exercise test is an important indicator of metabolic health. In healthy individuals, there is a significant positive association between PFO and total daily fat oxidation (FO). However, conditions resulting in metabolic dysfunction may cause a disconnect between PFO and non-exercise FO. Ten adult men with chronic thoracic spinal cord injury (SCI) completed a graded arm exercise test. On a separate day following an overnight fast (≥ 10 h), they rested for 60 min before ingesting a liquid mixed meal (600 kcal; 35% fat, 50% carbohydrate, 15% protein). Expired gases were collected and indirect calorimetry data used to determine FO at rest, before and after feeding, and during the graded exercise test. Participants had “good” cardiorespiratory fitness (VO2peak: 19.2 ± 5.2 ml/kg/min) based on normative reference values for SCI. There was a strong positive correlation between PFO (0.30 ± 0.08 g/min) and VO2peak (r = 0.86, p = 0.002). Additionally, postabsorptive FO at rest was significantly and positively correlated with postprandial peak FO (r = 0.77, p = 0.01). However, PFO was not significantly associated with postabsorptive FO at rest (0.08 ± 0.02 g/min; p = 0.97), postprandial peak FO (0.10 ± 0.03 g/min; p = 0.43), or incremental area under the curve postprandial FO (p = 0.22). It may be advantageous to assess both postabsorptive FO at rest and PFO in those with SCI to gain a more complete picture of their metabolic flexibility and long-term metabolic health.

Temperate performance and metabolic adaptations following endurance training performed under environmental heat stress.

Endurance athletes are frequently exposed to environmental heat stress during training. We investigated whether exposure to 33°C during training would improve endurance performance in temperate conditions and stimulate mitochondrial adaptations. Seventeen endurance‐trained males were randomly assigned to perform a 3‐week training intervention in 18°C (TEMP) or 33°C (HEAT). An incremental test and 30‐min time‐trial preceded by 2‐h low‐intensity cycling were performed in 18°C pre‐ and post‐intervention, along with a resting vastus lateralis microbiopsy. Training was matched for relative cardiovascular demand using heart rates measured at the first and second ventilatory thresholds, along with a weekly “best‐effort” interval session. Perceived training load was similar between‐groups, despite lower power outputs during training in HEAT versus TEMP (p < .05). Time‐trial performance improved to a greater extent in HEAT than TEMP (30 ± 13 vs. 16 ± 5 W, N = 7 vs. N = 6, p = .04), and citrate synthase activity increased in HEAT (fold‐change, 1.25 ± 0.25, p = .03, N = 9) but not TEMP (1.10 ± 0.22, p = .22, N = 7). Training‐induced changes in time‐trial performance and citrate synthase activity were related (r = .51, p = .04). A group × time interaction for peak fat oxidation was observed (Δ 0.05 ± 0.14 vs. −0.09 ± 0.12 g·min−1 in TEMP and HEAT, N = 9 vs. N = 8, p = .05). Our data suggest exposure to moderate environmental heat stress during endurance training may be useful for inducing adaptations relevant to performance in temperate conditions.

Effects of Two Workload-Matched High-Intensity Interval Training Protocols on Regional Body Composition and Fat Oxidation in Obese Men.

The effects of two high-intensity interval training (HIIT) protocols on regional body composition and fat oxidation in men with obesity were compared using a parallel randomized design. Sixteen inactive males (age, 38.9 ± 7.3 years; body fat, 31.8 ± 3.9%; peak oxygen uptake, VO2peak, 30.9 ± 4.1 mL/kg/min; all mean ± SD) were randomly assigned to either HIIT10 (48 × 10 s bouts at 100% of peak power [Wpeak] with 15 s of recovery) or HIIT60 group (8 × 60 s bouts at 100% Wpeak with 90 s of recovery), and subsequently completed eight weeks of training, while maintaining the same diet. Analyses of variance (ANOVA) showed only a main effect of time (p < 0.01) and no group or interaction effects (p > 0.05) in the examined parameters. Total and trunk fat mass decreased by 1.81 kg (90%CI: −2.63 to −0.99 kg; p = 0.002) and 1.45 kg (90%CI: −1.95 to −0.94 kg; p < 0.001), respectively, while leg lean mass increased by 0.86 kg (90%CI: 0.63 to 1.08 kg; p < 0.001), following both HIIT protocols. HIIT increased peak fat oxidation (PFO) (from 0.20 ± 0.05 to 0.33 ± 0.08 g/min, p = 0.001), as well as fat oxidation over a wide range of submaximal exercise intensities, and shifted PFO to higher intensity (from 33.6 ± 4.6 to 37.6 ± 6.7% VO2peak, p = 0.039). HIIT, irrespective of protocol, improved VO2peak by 20.0 ± 7.2% (p < 0.001), while blood lactate at various submaximal intensities decreased by 20.6% (p = 0.001). In conclusion, both HIIT protocols were equally effective in improving regional body composition and fat oxidation during exercise in obese men.

Resting skeletal muscle PNPLA2 (ATGL) and CPT1B are associated with peak fat oxidation rates in men and women but do not explain observed sex differences

What is the central question of this study? What is the relationship between proteins in skeletal muscle and adipose tissue determined at rest and at peak rates of fat oxidation in men and women? What is the main finding and its importance? The resting contents of proteins in skeletal muscle involved in triglyceride hydrolysis and mitochondrial lipid transport were more strongly associated with peak fat oxidation rates than proteins related to lipid transport or hydrolysis in adipose tissue. Although females displayed higher relative rates of fat oxidation than males, this was not explained by the proteins measured in this study, suggesting that other factors determine sex differences in fat metabolism. We explored key proteins involved in fat metabolism that might be associated with peak fat oxidation (PFO) and account for sexual dimorphism in fuel metabolism during exercise. Thirty-six healthy adults [15 women; 40±11years of age; peak oxygen consumption 42.5±9.5ml(kg body mass)-1 min-1 ; mean±SD] completed two exercise tests to determine PFO via indirect calorimetry. Resting adipose tissue and/or skeletal muscle biopsies were obtained to determine the adipose tissue protein content of PLIN1, ABHD5 (CGI-58), LIPE (HSL), PNPLA2 (ATGL), ACSL1, CPT1B and oestrogen receptorα (ERα) and the skeletal muscle protein content of FABP 3 (FABPpm), PNPLA2 (ATGL), ACSL1, CTP1B and ESR1 (ERα). Moderate strength correlations were found between PFO [in milligrams per kilogram of fat-free mass (FFM) per minute] and the protein content of PNPLA2 (ATGL) [rs =0.41 (0.03-0.68), P<0.05] and CPT1B [rs =0.45 (0.09-0.71), P<0.05] in skeletal muscle. No other statistically significant bivariate correlations were found consistently. Females had a greater relative PFO than males [7.1±1.9 vs. 4.5±1.3 and 7.3±1.7 vs. 4.8±1.2mg(kg FFM)-1 min-1 in the adipose tissue (n=14) and skeletal muscle (n=12) subgroups, respectively (P<0.05)]. No statistically significant sex differences were found in the content of these proteins. The regulation of PFO might involve processes relating to intramyocellular triglyceride hydrolysis and mitochondrial fatty acid transport, and adipose tissue is likely to play a more minor role than muscle. Sex differences in fat metabolism are likely to be attributable to factors other than the resting content of proteins in skeletal muscle and adipose tissue relating to triglyceride hydrolysis and fatty acid transport.

Determinants of Peak Fat Oxidation Rates During Cycling in Healthy Men and Women.

This study explored lifestyle and biological determinants of peak fat oxidation (PFO) during cycle ergometry, using duplicate measures to account for day-to-day variation. Seventy-three healthy adults (age range: 19-63 years; peak oxygen consumption [V˙O2peak]: 42.4 [10.1] ml·kg BM-1·min-1; n = 32 women]) completed trials 7-28 days apart that assessed resting metabolic rate, a resting venous blood sample, and PFO by indirect calorimetry during an incremental cycling test. Habitual physical activity (combined heart rate accelerometer) and dietary intake (weighed record) were assessed before the first trial. Body composition was assessed 2-7 days after the second identical trial by dual-energy X-ray absorptiometry scan. Multiple linear regressions were performed to identify determinants of PFO (mean of two cycle tests). A total variance of 79% in absolute PFO (g·min-1) was explained with positive coefficients for V˙O2peak (strongest predictor), FATmax (i.e the % of V˙O2peak that PFO occurred at), and resting fat oxidation rate (g·min-1), and negative coefficients for body fat mass (kg) and habitual physical activity level. When expressed relative to fat-free mass, 64% of variance in PFO was explained: positive coefficients for FATmax (strongest predictor), V˙O2peak, and resting fat oxidation rate, and negative coefficients for male sex and fat mass. This duplicate design revealed that biological and lifestyle factors explain a large proportion of variance in PFO during incremental cycling. After accounting for day-to-day variation in PFO, V˙O2peak and FATmax were strong and consistent predictors of PFO.