Fat oxidation training -
The molecular adaptation of skeletal muscle to low-intensity endurance training is largely unknown. GLUT4, the major glucose transporter in skeletal muscle, and hexokinase II, which catalyzes the phosphorylation of glucose to glucosephosphate, are two key genes involved in glucose utilization.
LPL is responsible for hydrolysis of plasma triglycerides and directs the released free fatty acids FFAs into the tissue Inside the muscle cell, ACC2 has recently been suggested to control the rate of fatty acid oxidation and triglyceride storage Finally, the skeletal muscle-specific uncoupling protein-3 UCP3 has also been suggested to be involved in fatty acid metabolism, but the exact function is still under debate Therefore, the third aim of the present study was to examine the effect of low-intensity endurance training on the expression of the above-mentioned genes.
The characteristics of the six healthy nonobese male volunteers are presented in Table 1. The nature and risks of the experimental procedure were explained to the subjects, and all subjects gave written informed consent.
The study was approved by the Medical-Ethical Committee of Maastricht University. Subjects participated in two stable isotope experiments, separated by 1 week, to measure total and plasma-derived fatty acid oxidation in random order. In these tests, an infusion of either [U- 13 C]palmitate or [1,2- 13 C]acetate was given for 2 h at rest and 1 h during exercise.
Acetate is directly converted to acetyl-CoA, and the recovery of acetate can be used to correct [ 13 C]palmitate oxidation for loss of label in the tricarboxylic acid TCA cycle, as previously described 19 , On a separate day, a muscle biopsy was taken after an overnight fast. Immediately after the last stable isotope experiment, the training period was started.
After the week training program, a second muscle biopsy was taken 6—7 days after the last training session. The two stable isotopes experiments were repeated 7—8 and 14—15 days after the end of the week training program in random order.
In this way, it was prevented that the last training session could influence the measurements. Three days before the first stable isotope experiment, subjects were asked to write down their food intake and to consume the same food items before every other stable isotope experiment.
Subjects were asked not to consume any products with a high abundance of 13 C carbohydrates derived from C4 plants such as maize and sugar cane 1 week before and during the entire experimental period.
Subjects were asked to refrain from physical activity 2 days before the sampling of the muscle biopsy and before the stable isotope experiments. Subjects trained three times per week for 12 weeks.
Training duration for subjects per session was Heart rate was monitored continuously during the training sessions Polar Electro, Oy, Finland. After 4 and 8 weeks of exercise training, a maximal aerobic exercise test was performed, and the training workload and duration were adjusted if necessary.
All training sessions took place at the university under the supervision of a professional trainer. One week before and after the training program, body density was determined by underwater weighing in the fasted state. Body weight was measured with a digital balance, accurate to 0.
Lung volume was measured simultaneously with the helium dilution technique using a spirometer Volugraph ; Mijnhardt. Body fat percentage was calculated using the equations of Siri Fat-free mass, in kilograms, was calculated by subtracting fat mass from total body mass.
One week before and after the training program, each subject performed an incremental exercise test on an electronically braked cycle ergometer Lode Excalibur to determine maximal oxygen consumption V o 2max and maximal power output W max.
Subjects started cycling at 75 W for 5 min. Thereafter, workload was increased by 50 W every 2. When subjects were approaching exhaustion, as indicated by heart rate and subjective scoring, the increment was reduced to 25 W. Heart rate was registered continuously using a Polar Sport tester Kempele, Finland.
Oxygen consumption and carbon dioxide production were measured using open circuit spirometry Oxycon-β; Mijnhardt.
At a. after an overnight fast, subjects underwent an isotope infusion test. Teflon catheters were inserted in an antecubital vein for isotope infusion and retrogradely into a contralateral dorsal hand vein for sampling of arterialized venous blood.
After placement of the catheters, subjects rested on a bed, and the cannulated hand was placed in a hotbox, in which air was circulated at 60°C to obtain arterialized venous blood.
After 30 min, baseline oxygen consumption and carbon dioxide production was measured, and breath and blood samples were collected. Immediately thereafter, subjects were given an intravenous dose of 0. Then, at time zero, a constant intravenous infusion of either [U- 13 C]palmitate 0.
With these infusion rates, the amount of 13 C infused during palmitate and acetate infusion are similar. Blood samples and breath samples were taken at 0, , , and min at rest and , , and min during exercise.
At rest, V o 2 and V CO 2 were measured continuously during the first 90 min using open circuit spirometry Oxycon-β. During exercise, V o 2 and V CO 2 were measured immediately before the measurement of breath 13 CO 2 enrichment.
To determine the exact infusion rate, the concentration of palmitate in the infusate was measured for each experiment using analytical gas chromatography GC using heptadecanoic acid as internal standard see sample analysis. The acetate concentration was measured in each infusate with an enzymatic method Boehringer Mannheim, Mannheim, Germany.
Muscle biopsies were taken from the mid-thigh region from M. vastus lateralis according to the technique of Bergstrom et al.
The subjects were required to abstain from training or vigorous exercise 48 h before the biopsy. The biopsy was used for isolation of total RNA using the acid phenol method of Chomozynski and Sacchi 28 , with an additional DNAse digestion step with concomitant acid phenol extraction and ethanol precipitation.
The mRNA levels of LPL, hexokinase II, GLUT4, ACC2, and UCP3 were quantified by RT-competitive PCR For the assays, the RT reaction was performed from 0. The competitive PCR assays were performed as previously described 30 — To improve the quantification of the amplified products, fluorescent dye-labeled sense oligonucleotides were used.
The PCR products were separated and analyzed on an ALFexpress DNA sequencer Pharmacia with the Fragment Manager Software.
Total RNA preparations and RT-competitive PCR assays of the two skeletal muscle samples from the same individual before and after weight loss were performed simultaneously. Oxygen saturation Hemoximeter OSM2; Radiometer, Copenhagen, Denmark was determined immediately after sampling in heparinized blood and used to check arterialization.
Fifteen milliliters of arterialized venous blood was sampled in tubes containing EDTA to prevent clotting and immediately centrifuged at 3, rpm 1, g for 10 min at 4°C. Plasma substrates were determined using the hexokinase method Roche, Basel for glucose, the Wako NEFA nonesterified fatty acid C test kit Wako Chemicals, Neuss, Germany for FFAs, and the glycerolkinase-lipase method Boehringer Mannheim for glycerol and triglycerides.
For determination of plasma palmitate, FFAs were extracted from plasma, isolated by thin-layer chromatography, and derivated to their methyl esters. From palmitate oxidation, plasma-derived fatty acid oxidation was then calculated by dividing palmitate oxidation rate by the fractional contribution of palmitate to the total FFA concentration.
Differences in measured variables before and after training were tested using paired t tests. Repeated measures one-way ANOVA were used to detect differences in variables in time. For testing differences in blood parameters between treatments, areas under the concentration versus time curve where calculated for 0— min at rest and — during exercise.
On average, subjects completed a total of 31 ± 1. Therefore, the average exercise duration per week was 2. The week training program had no influence on percentage body fat or V o 2max Table 1. At rest, total fat oxidation was not significantly influenced by the week training program ± 18 vs.
Similarly, plasma-derived fatty acid oxidation was not significantly influenced by the week training program ± 24 vs. Plasma-derived fatty acid oxidation during exercise was not significantly influenced by the training program ± 88 vs. Rate of appearance of FFA was not influenced by the training program, neither at rest ± 41 vs.
The percentage of R a that was oxidized was also not influenced by the training program, neither at rest 40 ± 4 vs. At rest, carbohydrate oxidation was not significantly affected by the training program ± 9 vs. Carbohydrate oxidation during exercise tended to be lower after training 1, ± vs.
Energy expenditure, both at rest 4. Acetate recovery, both at rest Plasma triglyceride concentrations Fig. Both at rest and during exercise, the average concentrations for plasma glucose at rest: 4. The week training program had no effect on two genes involved in the transport and oxidation of blood glucose: hexokinase II 2.
However, the expression of two genes encoding for key enzymes in fatty acid metabolism were affected by the training program: skeletal muscle ACC2 was significantly lower after training ± 24 vs. The expression of UCP3 The effect of endurance training on the contribution of different fat sources to total fat oxidation after endurance training is under debate.
Part of this controversy could be explained by the methodological difficulties in using [ 13 C]- and [ 14 C]-fatty acid tracers to estimate the oxidation of plasma fatty acids, especially in the resting state However, Sidossis et al.
We showed that this acetate recovery is reproducible 25 but has a high interindividual variation and is influenced by infusion period, metabolic rate, respiratory quotient, and body composition 21 and therefore needs to be determined in every individual under similar conditions and at similar time points as the measurement of plasma-derived fatty acid oxidation.
In the present study, we therefore measured the acetate recovery factor at all time points in each individual both before and after the training program at least 7 days separated from the last training session to exclude the influence of the last exercise bout on the measurements and were therefore able to correct plasma-derived fatty acid oxidation rate for loss of label in the TCA cycle.
With the available stable isotope tracer methodology, we cannot distinguish between IMTG- or VLDL-derived fatty acid oxidation. Fat Burning vs.
What does fat oxidation mean? What Happens during Fat Oxidation? Oxidation: Burning Fat for Fuel As the fatty acids enter the cell, they are stored in the cytoplasm of the cell, which is the thick solution that fills the inner regions of the cell. How to Increase Fat Oxidation Since most people entering the fitness space are wanting to lose fat, it would make sense to discuss what things we can do to enhance fat oxidation and accelerate fat loss.
Reduce Calories One of these ways is by reducing caloric expenditure, i. Regulate Insulin Levels Earlier in this article, we discussed the importance of hormone-sensitive lipase in the liberating of stored fatty acids from adipose tissue.
Is there anything you can do? And it comes in the form of Exercise As we stated above, increasing your calories out is one of the ways you can tip energy balance in favor of fat loss. Muscle glycogen content Your body has a finite amount of glycogen stored in the muscle.
Exercise intensity Low to moderate intensity forms of exercise primarily use fat as their source of energy. Does that mean you should only perform steady-state cardio when trying to lose body fat?
No, not at all. html Arner, P. Human fat cell lipolysis: biochemistry, regulation and clinical role. Lipolysis — A highly regulated multi-enzyme complex mediates the catabolism of cellular fat stores.
Progress in Lipid Research. Holloway, G. Acta Physiologica, , Achten, J. Optimizing fat oxidation through exercise and diet. Nutrition Burbank, Los Angeles County, Calif.
Effects of Prior Fasting on Fat Oxidation during Resistance Exercise. International Journal of Exercise Science. Achten J, Gleeson M, Jeukendrup AE.
Determination of the exercise intensity that elicits maximal fat oxidation. Med Sci Sports Exerc. Achten J, Jeukendrup A. Maximal fat oxidation during exercise in trained men.
Int J Sports Med. Venables, M. Determinants of fat oxidation during exercise in healthy men and women: a cross-sectional study. Journal of Applied Physiology, 98 1 , — Of these studies, 9 compared the effects of HIIT vs.
MICT, 7 evaluated the effects of HIIT vs. MICT, and 2 included a control group and a MICT group. The main results of this study show that IT training increases fatty acid oxidation with an average increase of 0.
These effects were significantly greater in overweight and obese individuals. Furthermore, a significant effect on FatOx can be expected after at least 4 weeks of training. The magnitude of the effect increases with the duration of the training protocol, with each additional week increasing FatOx by 0.
The effects on FatOx would appear to be very slightly greater for IT than for MICT 0. This could be explained by a higher level of intramuscular triglycerides and a higher plasma concentration of fatty acids.
This meta-analysis shows once again that there is almost no difference between interval training and classic cardio in terms of the fat oxidation process, and ultimately fat loss.
With an average FatOx of 0. Not really an exceptional result considering the investment in terms of effort. The results reflect those of various meta-analyses on the subject, which lead to the same conclusion: exercise alone, i.
without an associated and calibrated diet, which does not compensate for the caloric deficit created by the exercise, is not sufficient for effective fat loss. On average, the loss is 0. This will have very little clinical or aesthetic effect.
Periodization for sports performance SchrauwenDorien P. van Aggel-LeijssenGabby HulAnton J. Wagenmakers Natural plant extracts, Traijing Vidal oxiation, Wim Natural plant extracts. SarisMarleen A. van Baak; The Effect of a 3-Month Low-Intensity Endurance Training Program on Fat Oxidation and Acetyl-CoA Carboxylase-2 Expression. Diabetes 1 July ; 51 7 : — Endurance training has been shown to increase fat oxidation both at rest and during exercise. Independent of total body Natural plant extracts mass, odidation upper Importance of dietary flavonoids Fwt mass distribution is strongly associated Consistency through proper hydration practices cardio-metabolic comorbidities. Ooxidation, the mechanisms underlying ocidation mass oxidaton are not fully understood. Although a large body Importance of dietary flavonoids evidence Natural plant extracts sex-specific fat mass distribution, women are still excluded from many fraining studies and their specific features have been investigated only in few studies. Moreover, endurance exercise is an effective strategy for improving fat oxidation, suggesting that regular endurance exercise could contribute to the management of body composition and metabolic health. However, no firm conclusion has been reached on the effect of fat mass localization on fat oxidation during endurance exercise. By analyzing the available literature, this review wants to determine the effect of fat mass localization on fat oxidation rate during endurance exercise in women, and to identify future research directions to advance our knowledge on this topic.
0 thoughts on “Fat oxidation training”