Fat Metabolism During Low Intensity Exercise In Endurance Trained And Untrained Men PdfBy Kari L. In and pdf 27.03.2021 at 04:54 9 min read
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- Hormonal and metabolic substrate status in response to exercise in men of different phenotype
- Fat Metabolism in Exercise
- Associations of Aerobic Fitness and Maximal Muscular Strength With Metabolites in Young Men
Not only but particularly due to their time efficiency, High-Intensity Interval Training HIIT is becoming increasingly popular in fitness-oriented endurance sports. HIIT and MICE protocols, when adjusted for total workload, similarly increased running performance in untrained male subjects; however, the underlying mechanisms differ fundamentally. Due to its effects on aerobic and anaerobic performance improvement, HIIT can be recommended for untrained individuals as a time-efficient alternative or complementary training method to MICE.
Exercise is a powerful and effective preventive measure against chronic diseases by increasing energy expenditure and substrate mobilization. Long-duration acute exercise favors lipid mobilization from adipose tissue, i. Several hormones and factors have been shown to stimulate lipolysis in vitro in isolated adipocytes.
Hormonal and metabolic substrate status in response to exercise in men of different phenotype
Adult 4-month-old male Wistar rats were assigned to a training group rats trained on a treadmill for 8 weeks or a sedentary control group. Moreover, endurance training increased mitochondrial capacity to oxidize the lipid-derived fuels at all studied temperatures. We conclude that hyperthermia enhances but hypothermia attenuates the rate of the oxidation of fatty acids and glycerolphosphate in rat skeletal muscle mitochondria isolated from both untrained and trained rats.
This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability: All relevant data are within the paper and in the Supporting Information. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist. Fatty acids are a vital source of energy for mammalian skeletal muscles both when they are at rest and particularly during sustained physical exercise [ 1 — 3 ].
It is well established that the maximal rate of fatty acid oxidation is higher in endurance-trained muscles than in untrained muscles [ 4 — 6 ]. However, the underlying mechanism controlling the maximal rate of fatty acid oxidation in the working muscle remains unclear for a review, see [ 3 , 6 — 8 ]. Endurance training-induced enhancement of the maximal rate of fatty acid oxidation increases exercise tolerance by slowing the depletion of muscle carbohydrates [ 4 , 9 ].
It has been postulated that training-induced increases in the oxidation of fatty acids by skeletal muscles are caused by the intensification of mitochondrial biogenesis and the resulting increase in the level of fatty acid oxidation enzymes for a review, see [ 6 , 9 , 10 ]. However, there is a growing body of evidence that the training-induced enhancement of the maximal rate of fatty acid oxidation in skeletal muscles is governed by the up-regulation of fatty acid transporters [ 7 , 8 , 11 ].
It has been proposed that CD36, a fatty acid transporter, may play a key role in the control of the transport of fatty acids into muscle cells and their oxidation at rest and during exercise, as well as in muscle fuel selection and endurance exercise performance [ 10 , 12 ].
Surprisingly, little attention has been paid to the role of muscle temperature as a potential factor in the regulation of the rate of fatty acid oxidation in skeletal muscles. It is well established that thermal stress can change the proportion of fatty acids and carbohydrates oxidized during exercise, as originally shown by Fink et al. Namely, it has been reported that exercise in heat seems to increase carbohydrate utilization.
However, to the best of our knowledge, no study has been conducted to determine the effect of various temperatures on skeletal muscle mitochondria capacity to oxidize fatty acids. Moreover, no study has been conducted to evaluate the effect of endurance training on the mammalian mitochondrial capacity to oxidize fatty acids under various survivable thermal conditions such as hypothermia, normothermia and hyperthermia for ref.
The study was performed on 24 adult 4-month-old male Wistar rats. All rats had unrestricted access to standard rat feed and tap water. Animals were sacrificed, and all efforts were made to minimize suffering. In the first week of the training, the rats were familiarized with running on the treadmill at various velocities 20—30 m x min -1 during 20—30 min running sessions.
At the end of the first week, the duration of a training session was increased to approximately 40 min. In the first two weeks of training, the basal running velocity was set at 30 m x min -1 , but every 10 min it was increased to 40 m x min -1 for approximately 20 s.
From the fifth week of training, the duration of the training sessions was extended to approximately 60 min. The basal running velocity at this stage of training was set to 30 m x min -1 , and approximately every 10 min the running velocity was increased up to 40 m x min The duration of the higher speed was gradually increased from 20 s in the 6th week to approximately 40 s in the final week of training. At the end of the training period, 22—24 h after completing the last training session, exercising and sedentary rats were sacrificed by decapitation.
All efforts were made to minimize suffering. Immediately after decapitation of the animals both control and trained rats hind limbs were rapidly removed at the level of the hip joints in order to dissect all major hind limb locomotor muscles the gastrocnemius, soleus, and quadriceps muscles.
In order to obtain sufficient mass of muscle tissue to collect adequate amount of mitochondrial fraction the obtained muscles from shank and thigh were used as a mixed muscle sample to obtain muscle homogenates and mitochondria fractions for further measurements as previously described [ 15 , 17 ]. We have assessed purity of mitochondrial fractions by detection of peroxisome contamination S1 Fig. In contrast to muscle homogenates, mitochondrial fractions probed with antibody to peroxisome membrane marker PMP70 displayed no signal, indicating the absence of peroxisome membrane contamination in mitochondrial preparations.
Muscle homogenate and mitochondrial protein concentration was determined using the Bradford method with BSA as a standard. Similar values of the highest and the lowest survivable core temperatures have been reported for humans [ 23 , 24 ]. Oxygen uptake was determined polarographically using a Hansatech oxygen electrode in 0. To chelate the endogenous free fatty acids in mitochondrial preparations especially in mitochondria from trained rats , 0.
Mitochondrial oxidation of palmitoylcarnitine and glycerolphosphate were measured with 0. The muscle homogenates and mitochondrial fractions were isolated in the presence of protease inhibitors.
Appropriate horseradish peroxidase-conjugated secondary antibodies were used. Each isolation was performed from one control or trained animal. Functional measurements and immunodetections were performed in triplicate. Differences in reactions to training, measured at different temperatures, would result in a non-zero interaction between the factors. Both univariate and multivariate tests for repeated measures in all studied variables resulted in non-significant interactions, however.
The significance of differences between the levels of the studied variables three training-control comparisons at various temperatures for each variable were examined using planned comparisons. The obtained P values were corrected using the Holm—Bonferroni method. The effect of endurance training on the expression level of muscle proteins was analyzed using unpaired t- test. For each assay temperature, the oxidation of the lipid-derived fuels was significantly higher in skeletal muscle mitochondria isolated from endurance-trained rats compared to that isolated from control animals.
The non-phosphorylating respiration in the absence of ADP and respiratory control ratio were studied for the three tested temperatures in mitochondria isolated from the skeletal muscles of trained and control rats using glycerolphosphate as a respiratory substrate Table 1. In both types of mitochondria, beside the increase in phosphorylating respiration state 3 , an elevation of non-phosphorylating respiration state 4 was observed with increasing temperature.
For a given assay temperature, a significant increase in phosphorylating respiration was accompanied by a significant decrease in non-phosphorylating respiration in muscle mitochondria from trained rats compared to those of the controls.
In both types of mitochondria, the respiratory control ratio decreased significantly with the increasing assay temperature, indicating a temperature-induced mitochondrial uncoupling. Independent of temperature, the respiratory control ratio was considerably higher in mitochondria from the muscles of trained rats than from the muscles of control rats, indicating that endurance training leads to less uncoupling in muscle mitochondria.
The eight-week endurance training program applied in this study resulted in a significant increase in mitochondrial biogenesis in the locomotor hind limb muscles of trained rats. Determination of protein levels in skeletal muscle homogenates A and mitochondria B from control c and trained t rats.
Moreover, significantly increased levels of other mitochondrial proteins involved in fatty acid metabolism, i. Therefore, we cannot directly relate our results to previous studies. Therefore, the present study is the first to show that hyperthermia is not a limiting factor for mitochondrial capacity to oxidize fatty acids and that endurance training performed at room temperature i.
Our findings concerning the impact of assay temperature on the mitochondrial capacity for fatty acid oxidation are in accordance with the early study by Brooks et al.
We consider that the temperature-induced increase in mitochondrial fatty acid oxidation observed in our study represents qualitative temperature-induced changes in the muscle mitochondria resulting mainly from the temperature-related enhancement of mitochondrial enzyme activities.
Our results obtained under in vitro conditions cannot be simply transferred into in vivo conditions, in which the regulation of fatty acid transport into mitochondria is much more complex and involves several possible limiting steps for an overview see, e. Nevertheless, our study suggests that the exercise-induced hyperthermia that occurs during high-intensity sustained exercise [ 19 ] could not limit and even could potentiate muscle mitochondrial capacity for fatty acid oxidation. Whereas hypothermia that can be induced for example by body exposure to low ambient temperatures could decrease the maximal rate of muscle mitochondrial fatty acid oxidation.
It could be one of the factors that limits exercise performance at very low ambient temperatures. However, the extent to which our in vitro results relate to mitochondrial function in vivo remains to be determined. Our results show that oxidation of reducing substrates originating from lipid catabolism, i. This observation is in agreement with previous studies showing that endurance training increases the rate of mitochondrial fatty acid oxidation in skeletal muscles [ 12 , 27 , 28 ].
This observation indicates that the mechanism responsible for the training-induced enhancement of mitochondrial capacity for fatty acid oxidation is temperature-independent. This property might explain the beneficial effect of endurance training performed under thermoneutral conditions for enhancement of physical performance at high and low temperatures. The results of other groups also show that prolonged endurance training increases muscle mitochondrial biogenesis [ 31 — 34 ].
In the present study, the endurance training-induced increase in OXPHOS activity was directly confirmed by a significant increase in oxidation of palmitoylcarnitine and glycerolphosphate in skeletal muscle mitochondria from trained rats compared to control animals Fig 1. The increase in OXPHOS activity leads to the improvement of muscle metabolic stability during exercise of given power output, resulting in increased resistance to muscle fatigue [ 30 , 33 , 35 , 36 ].
However, in mitochondria from both control and trained rats, the resulting respiratory control ratio decreased significantly with the increasing assay temperature, indicating a temperature-induced mitochondrial uncoupling.
Independent of temperature, the respiratory control ratio was considerably higher in mitochondria from the muscles of trained rats than from the muscles of control rats, indicating that endurance training attenuates high temperature-elevated mitochondrial uncoupling. These results are consistent with our previous measurements performed with substrates of the Krebs cycle succinate and malate in rat skeletal muscle mitochondria isolated from control and trained rats [ 17 ].
Our results indicate that under phosphorylating conditions, endurance training may augment the temperature-induced increase in maximal oxidation of reducing substrates originating from lipid catabolism. The underlying physiological mechanism responsible for the endurance training-induced increase in fatty acid oxidation is not completely understood.
Two factors are currently considered to explain this muscle adaptive response: i the training-induced enhancement of mitochondrial oxidative capacity [ 6 , 9 , 10 ], and ii the training-induced enhancement of fatty acid transporters, especially CD36 [ 10 , 12 , 37 ] and CPT1-dependent mitochondrial transport [ 6 ]. In our study, the training-induced increase in mitochondrial fatty acid oxidation was accompanied by an increase in expression level of and proteins considered to determine the rate of mitochondrial fatty acid oxidation, i.
For a long time, mitochondrial biogenesis and the resulting increase in the level of enzymes catalyzing fatty acid oxidation was considered as the main mechanism of training-induced enhancement of fatty acid oxidation [ 6 , 9 , 10 ]. However, this concept has been challenged by recent studies performed with the CD36 knockout mice model, which show that the selective training-induced enhancement of fatty acid transporters, especially the CD36, and not the increase of mitochondrial oxidative capacity is the key factor responsible for the training-induced enhancement of fatty acid oxidation in the endurance trained skeletal muscles [ 10 , 12 ].
Our finding of the training-induced increase in CD36 in the trained skeletal muscles Fig 2A is in agreement with a previous studies showing a similar muscle response to training [ 10 , 12 , 38 ]. Moreover, in our study, in mitochondria isolated from the skeletal muscles of trained rats, the expression level of CD36 was enhanced significantly Fig 2B.
Recently, it has been reported that in skeletal muscle, CD36 is located on the outer mitochondrial membrane, upstream of long-chain acyl-CoA synthetase, and regulates palmitate oxidation [ 39 ]. Thus, endurance training enhanced the CPT1 system, which controls the entry of long-chain fatty acid acyl-CoA into mitochondria and mitochondrial long-chain fatty acid oxidation.
Our results show that the training-induced intensification of mitochondrial biogenesis is accompanied by the increase in expression levels of fatty acid transporter CD36 and other mitochondrial proteins involved in fatty acid metabolism, such as CPT1A and ACADS. This suggests that under physiological conditions, endurance training up-regulates both the fatty acid transporter and muscle mitochondrial oxidative capacity.
It has also been reported that Nrf2 is responsible for regulating the expression of proteins of the mitochondrial electron transport chain [ 40 ] and also involved in the regulation of the rate of fatty acid oxidation [ 25 ]. This muscle adaptive response might play a key role in the mechanism of the training-induced increase of endurance exercise performance via an enhancement of ATP supply from fatty acid oxidation allowing for slowing-down the rate of muscle glycogen depletion, considered as a core factor of muscle fatigue [ 9 , 36 , 42 , 43 ].
In this study, we have demonstrated for the first time that hyperthermia enhances but hypothermia attenuates the oxidation rate of fatty acids and glycerolphosphate in rat skeletal muscle mitochondria isolated from both untrained and trained rats. We postulate that this effect is caused by the temperature-related enhancement of mitochondrial enzyme activities. A representative immunodection is shown.
Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Introduction Fatty acids are a vital source of energy for mammalian skeletal muscles both when they are at rest and particularly during sustained physical exercise [ 1 — 3 ]. Materials and methods Animals The study was performed on 24 adult 4-month-old male Wistar rats.
Skeletal muscle homogenate and mitochondria preparation Immediately after decapitation of the animals both control and trained rats hind limbs were rapidly removed at the level of the hip joints in order to dissect all major hind limb locomotor muscles the gastrocnemius, soleus, and quadriceps muscles. Protein concentration determination Muscle homogenate and mitochondrial protein concentration was determined using the Bradford method with BSA as a standard.
Fat Metabolism in Exercise
Irisin is produced by a proteolytic cleavage of fibronectin type III domain-containing protein 5 FNDC5 and has emerged as a potential mediator of exercise-induced energy metabolism. The purpose of this study was to review the results of studies that investigated irisin responses to acute and chronic exercise and provide an update. The focus of the analysis was on data concerning FNDC5 mRNA expression in skeletal muscle and circulating irisin concentration relatively to exercise mode, intensity, frequency and duration and the characteristics of the sample used. Circulating irisin levels may either not relate to FNDC5 transcription or expression of the later precedes irisin rise in the blood. There are no reports regarding irisin responses to field sport activities. Although animal studies suggest that irisin may also respond to systematic exercise training, the majority of human studies has produced contradictory results.
Request PDF | Fat metabolism during high-intensity exercise in six endurance-trained men and six untrained men were studied during 30 in plasma insulin concentration suppresses fat oxidation during low ( % V O.
Associations of Aerobic Fitness and Maximal Muscular Strength With Metabolites in Young Men
Whole-body lipolytic rates and the rate of triglyceride-fatty acid cycling reesterification of fatty acids released during lipolysis were measured with stable isotopic tracers in the basal state and during beta-adrenergic blockade with propranolol infusion in five cachectic patients with squamous cell carcinoma of the esophagus, five cachectic cancer-free, nutritionally-matched control patients, and 10 healthy volunteers. Resting energy expenditure and plasma catecholamines were normal in all three groups. The basal rate of glycerol appearance in blood in the patients with cancer 2. We conclude that the increase in lipolysis and triglyceride-fatty acid cycling in "unstressed" cachectic patients with esophageal cancer is due to alterations in their nutritional status rather than the presence of tumor itself. Increased beta-adrenergic activity may be an important contributor to the stimulation of lipolysis.
Fatty acids are the most abundant source of endogenous energy substrate. They can be mobilized from peripheral adipose tissue and transported via the blood to active muscle. During higher intensity exercise, triglyceride within the muscle can also be hydrolyzed to release fatty acids for subsequent direct oxidation. Control of fatty acid oxidation in exercise can potentially occur via changes in availability, or via changes in the ability of the muscle to oxidize fatty acids.
Somatotypes, which to some extent express genetic determinism, are significantly associated with the level of physical fitness 1 , 2 , and as a consequence with the content of adipose tissue 1. Adipocytes are highly metabolically active cells releasing adipokines and adipocytokines which affect the processes in neighboring and distant cells by autocrine, paracrine and endocrine fashion 3.
Is irisin the new player in exercise-induced adaptations or not? A 2017 update
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During recovery, glycerol and FFA R, values decreased more rapidly in trained than in untrained subjects. We conclude that highly trained male endurance runners use more fat as a fuel during low-intensity exercise than do untrained healthy men despite similar rates of lipoly- sis and FFA uptake from plasma.