Mc Groaw-Hill. BMJ Open Sport Exerc Med. Far is advised to eat one bowl of oatmeal at breakfast Mudryj et al.

Video

11 Golden Rules to Build Muscle While Losing Fat

Efficient fat utilization -

Of note, carbohydrate ingestion attenuates muscle and plasma NH 3 accumulation during exercise , another potential mechanism through which carbohydrate ingestion exerts its ergogenic effect. Enhanced exercise performance has also been observed from simply having carbohydrate in the mouth, an effect that has been linked to activation of brain centres involved in motor control Increased plasma fatty acid availability decreases muscle glycogen utilization and carbohydrate oxidation during exercise , , High-fat diets have also been proposed as a strategy to decrease reliance on carbohydrate and improve endurance performance.

Other studies have demonstrated increased fat oxidation and lower rates of muscle glycogen use and carbohydrate oxidation after adaptation to a short-term high-fat diet, even with restoration of muscle glycogen levels, but no effect on endurance exercise performance , If anything, high-intensity exercise performance is impaired on the high-fat diet , apparently as a result of an inability to fully activate glycogenolysis and PDH during intense exercise Furthermore, a high-fat diet has been shown to impair exercise economy and performance in elite race walkers A related issue with high-fat, low carbohydrate diets is the induction of nutritional ketosis after 2—3 weeks.

However, when this diet is adhered to for 3 weeks, and the concentrations of ketone bodies are elevated, a decrease in performance has been observed in elite race walkers The rationale for following this dietary approach to optimize performance has been called into question Although training on a high-fat diet appears to result in suboptimal adaptations in previously untrained participants , some studies have reported enhanced responses to training with low carbohydrate availability in well-trained participants , Over the years, endurance athletes have commonly undertaken some of their training in a relatively low-carbohydrate state.

However, maintaining an intense training program is difficult without adequate dietary carbohydrate intake Furthermore, given the heavy dependence on carbohydrate during many of the events at the Olympics 9 , the most effective strategy for competition would appear to be one that maximizes carbohydrate availability and utilization.

Nutritional ketosis can also be induced by the acute ingestion of ketone esters, which has been suggested to alter fuel preference and enhance performance The metabolic state induced is different from diet-induced ketosis and has the potential to alter the use of fat and carbohydrate as fuels during exercise.

However, published studies on trained male athletes from at least four independent laboratories to date do not support an increase in performance. Acute ingestion of ketone esters has been found to have no effect on 5-km and km trial performance , , or performance during an incremental cycling ergometer test A further study has reported that ketone ester ingestion decreases performance during a The rate of ketone provision and metabolism in skeletal muscle during high-intensity exercise appears likely to be insufficient to substitute for the rate at which carbohydrate can provide energy.

Early work on the ingestion of high doses of caffeine 6—9 mg caffeine per kg body mass 60 min before exercise has indicated enhanced lipolysis and fat oxidation during exercise, decreased muscle glycogen use and increased endurance performance in some individuals , , These effects appear to be a result of caffeine-induced increases in catecholamines, which increase lipolysis and consequently fatty acid concentrations during the rest period before exercise.

After exercise onset, these circulating fatty acids are quickly taken up by the tissues of the body 10—15 min , fatty acid concentrations return to normal, and no increases in fat oxidation are apparent. Importantly, the ergogenic effects of caffeine have also been reported at lower caffeine doses ~3 mg per kg body mass during exercise and are not associated with increased catecholamine and fatty acid concentrations and other physiological alterations during exercise , This observation suggests that the ergogenic effects are mediated not through metabolic events but through binding to adenosine receptors in the central and peripheral nervous systems.

Caffeine has been proposed to increase self-sustained firing, as well as voluntary activation and maximal force in the central nervous system, and to decrease the sensations associated with force, pain and perceived exertion or effort during exercise in the peripheral nervous system , The ingestion of low doses of caffeine is also associated with fewer or none of the adverse effects reported with high caffeine doses anxiety, jitters, insomnia, inability to focus, gastrointestinal unrest or irritability.

Contemporary caffeine research is focusing on the ergogenic effects of low doses of caffeine ingested before and during exercise in many forms coffee, capsules, gum, bars or gels , and a dose of ~ mg caffeine has been argued to be optimal for exercise performance , The potential of supplementation with l -carnitine has received much interest, because this compound has a major role in moving fatty acids across the mitochondrial membrane and regulating the amount of acetyl-CoA in the mitochondria.

The need for supplemental carnitine assumes that a shortage occurs during exercise, during which fat is used as a fuel. Although this outcome does not appear to occur during low-intensity and moderate-intensity exercise, free carnitine levels are low in high-intensity exercise and may contribute to the downregulation of fat oxidation at these intensities.

However, oral supplementation with carnitine alone leads to only small increases in plasma carnitine levels and does not increase the muscle carnitine content An insulin level of ~70 mU l —1 is required to promote carnitine uptake by the muscle However, to date, there is no evidence that carnitine supplementation can improve performance during the higher exercise intensities common to endurance sports.

NO is an important bioactive molecule with multiple physiological roles within the body. It is produced from l -arginine via the action of nitric oxide synthase and can also be formed by the nonenzymatic reduction of nitrate and nitrite.

The observation that dietary nitrate decreases the oxygen cost of exercise has stimulated interest in the potential of nitrate, often ingested in the form of beetroot juice, as an ergogenic aid during exercise. Indeed, several studies have observed enhanced exercise performance associated with lower oxygen cost and increased muscle efficiency after beetroot-juice ingestion , , The effect of nitrate supplementation appears to be less apparent in well-trained athletes , , although results in the literature are varied Dietary nitrate supplementation may have beneficial effects through an improvement in excitation—contraction coupling , , because supplementation with beetroot juice does not alter mitochondrial efficiency in human skeletal muscle , and the results with inorganic nitrate supplementation have been equivocal , Lactate is not thought to have a major negative effect on force and power generation and, as mentioned earlier, is an important metabolic intermediate and signalling molecule.

Of greater importance is the acidosis arising from increased muscle metabolism and strong ion fluxes. In humans, acidosis does not appear to impair maximal isometric-force production, but it does limit the ability to maintain submaximal force output , thus suggesting an effect on energy metabolism and ATP generation Ingestion of oral alkalizers, such as bicarbonate, is often associated with increased high-intensity exercise performance , , partly because of improved energy metabolism and ionic regulation , As previously mentioned, high-intensity exercise training increases muscle buffer capacity 74 , A major determinant of the muscle buffering capacity is carnosine content, which is higher in sprinters and rowers than in marathon runners or untrained individuals Ingestion of β-alanine increases muscle carnosine content and enhances high-intensity exercise performance , During exercise, ROS, such as superoxide anions, hydrogen peroxide and hydroxyl radicals, are produced and have important roles as signalling molecules mediating the acute and chronic responses to exercise However, ROS accumulation at higher levels can negatively affect muscle force and power production and induce fatigue 68 , Exercise training increases the levels of key antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase , and non-enzymatic antioxidants reduced glutathione, β-carotene, and vitamins C and E can counteract the negative effects of ROS.

Whether dietary antioxidant supplementation can improve exercise performance is equivocal , although ingestion of N -acetylcysteine enhances muscle oxidant capacity and attenuates muscle fatigue during prolonged exercise Some reports have suggested that antioxidant supplementation may potentially attenuate skeletal muscle adaptation to regular exercise , , Overall, ROS may have a key role in mediating adaptations to acute and chronic exercise but, when they accumulate during strenuous exercise, may exert fatigue effects that limit exercise performance.

The negative effects of hyperthermia are potentiated by sweating-induced fluid losses and dehydration , particularly decreased skeletal muscle blood flow and increased muscle glycogen utilization during exercise in heat Increased plasma catecholamines and elevated muscle temperatures also accelerate muscle glycogenolysis during exercise in heat , , Strategies to minimize the negative effects of hyperthermia on muscle metabolism and performance include acclimation, pre-exercise cooling and fluid ingestion , , , To meet the increased energy needs of exercise, skeletal muscle has a variety of metabolic pathways that produce ATP both anaerobically requiring no oxygen and aerobically.

These pathways are activated simultaneously from the onset of exercise to precisely meet the demands of a given exercise situation. Although the aerobic pathways are the default, dominant energy-producing pathways during endurance exercise, they require time seconds to minutes to fully activate, and the anaerobic systems rapidly in milliseconds to seconds provide energy to cover what the aerobic system cannot provide.

Anaerobic energy provision is also important in situations of high-intensity exercise, such as sprinting, in which the requirement for energy far exceeds the rate that the aerobic systems can provide.

This situation is common in stop-and-go sports, in which transitions from lower-energy to higher-energy needs are numerous, and provision of both aerobic and anaerobic energy contributes energy for athletic success.

Together, the aerobic energy production using fat and carbohydrate as fuels and the anaerobic energy provision from PCr breakdown and carbohydrate use in the glycolytic pathway permit Olympic athletes to meet the high energy needs of particular events or sports.

The various metabolic pathways are regulated by a range of intramuscular and hormonal signals that influence enzyme activation and substrate availability, thus ensuring that the rate of ATP resynthesis is closely matched to the ATP demands of exercise.

Regular training and various nutritional interventions have been used to enhance fatigue resistance via modulation of substrate availability and the effects of metabolic end products.

The understanding of exercise energy provision, the regulation of metabolism and the use of fat and carbohydrate fuels during exercise has increased over more than years, on the basis of studies using various methods including indirect calorimetry, tissue samples from contracting skeletal muscle, metabolic-tracer sampling, isolated skeletal muscle preparations, and analysis of whole-body and regional arteriovenous blood samples.

However, in virtually all areas of the regulation of fat and carbohydrate metabolism, much remains unknown. The introduction of molecular biology techniques has provided opportunities for further insights into the acute and chronic responses to exercise and their regulation, but even those studies are limited by the ability to repeatedly sample muscle in human participants to fully examine the varied time courses of key events.

The ability to fully translate findings from in vitro experiments and animal studies to exercising humans in competitive settings remains limited. The field also continues to struggle with measures specific to the various compartments that exist in the cell, and knowledge remains lacking regarding the physical structures and scaffolding inside these compartments, and the communication between proteins and metabolic pathways within compartments.

A clear example of these issues is in studying the events that occur in the mitochondria during exercise. One area that has not advanced as rapidly as needed is the ability to non-invasively measure the fuels, metabolites and proteins in the various important muscle cell compartments that are involved in regulating metabolism during exercise.

Although magnetic resonance spectroscopy has been able to measure certain compounds non-invasively, measuring changes that occur with exercise at the molecular and cellular levels is generally not possible.

Some researchers are investigating exercise metabolism at the whole-body level through a physiological approach, and others are examining the intricacies of cell signalling and molecular changes through a reductionist approach. New opportunities exist for the integrated use of genomics, proteomics, metabolomics and systems biology approaches in data analyses, which should provide new insights into the molecular regulation of exercise metabolism.

Many questions remain in every area of energy metabolism, the regulation of fat and carbohydrate metabolism during exercise, optimal training interventions and the potential for manipulation of metabolic responses for ergogenic benefits.

Exercise biology will thus continue to be a fruitful research area for many years as researchers seek a greater understanding of the metabolic bases for the athletic successes that will be enjoyed and celebrated during the quadrennial Olympic festival of sport.

Hawley, J. Integrative biology of exercise. Cell , — Article CAS PubMed Google Scholar. Sahlin, K. Energy supply and muscle fatigue in humans. Acta Physiol. Medbø, J. Anaerobic energy release in working muscle during 30 s to 3 min of exhausting bicycling. Article PubMed Google Scholar.

Parolin, M. et al. Regulation of skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exercise. CAS PubMed Google Scholar. Greenhaff, P. The metabolic responses of human type I and II muscle fibres during maximal treadmill sprinting.

Article Google Scholar. Relative importance of aerobic and anaerobic energy release during short-lasting exhausting bicycle exercise. Tesch, P. Muscle metabolism during intense, heavy-resistance exercise.

Koopman, R. Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males. Carbohydrate dependence during prolonged, intense endurance exercise. Sports Med. Carbohydrate dependence during marathon running.

Sports Exerc. PubMed Google Scholar. Romijn, J. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration.

van Loon, L. The effects of increasing exercise intensity on muscle fuel utilisation in humans. Bergström, J. A study of the glycogen metabolism during exercise in man. Wahren, J. Glucose metabolism during leg exercise in man.

Article CAS PubMed PubMed Central Google Scholar. Ahlborg, G. Substrate turnover during prolonged exercise in man.

Watt, M. Intramuscular triacylglycerol, glycogen and acetyl group metabolism during 4 h of moderate exercise in man. Article CAS Google Scholar. Inhibition of adipose tissue lipolysis increases intramuscular lipid and glycogen use in vivo in humans.

Article PubMed CAS Google Scholar. Wasserman, D. Four grams of glucose. Coggan, A. Effect of endurance training on hepatic glycogenolysis and gluconeogenesis during prolonged exercise in men.

Coyle, E. Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. Horowitz, J. Lipid metabolism during endurance exercise.

Kiens, B. Skeletal muscle lipid metabolism in exercise and insulin resistance. Stellingwerff, T. Significant intramyocellular lipid use during prolonged cycling in endurance-trained males as assessed by three different methodologies.

Spriet, L. An enzymatic approach to lactate production in human skeletal muscle during exercise. Brooks, G. The lactate shuttle during exercise and recovery. Miller, B. Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion. Lactate elimination and glycogen resynthesis after intense bicycling.

Hashimoto, T. Lactate sensitive transcription factor network in L6 cells: activation of MCT1 and mitochondrial biogenesis. FASEB J. Takahashi, H. TGF-β2 is an exercise-induced adipokine that regulates glucose and fatty acid metabolism.

Metab 1 , — Scheiman, J. Meta-omics analysis of elite athletes identifies a performance-enhancing microbe that functions via lactate metabolism. Rennie, M. Effect of exercise on protein turnover in man. Wagenmakers, A. Carbohydrate supplementation, glycogen depletion, and amino acid metabolism during exercise.

Howarth, K. Effect of glycogen availability on human skeletal muscle protein turnover during exercise and recovery. McKenzie, S. Endurance exercise training attenuates leucine oxidation and BCOAD activation during exercise in humans.

Wilkinson, S. Differential effects of resistance and endurance exercise in the fed state on signalling molecule phosphorylation and protein synthesis in human muscle.

Egan, B. Exercise metabolism and the molecular regulation of skeletal muscle adaptation. Cell Metab. New insights into the interaction of carbohydrate and fat metabolism during exercise. Hargreaves, M. Exercise metabolism: fuels for the fire. Cold Spring Harb. Article PubMed PubMed Central CAS Google Scholar.

Richter, E. Muscle glycogenolysis during exercise: dual control by epinephrine and contractions. Gaitanos, G. Human muscle metabolism during intermittent maximal exercise. Kowalchuk, J. Factors influencing hydrogen ion concentration in muscle after intense exercise.

Howlett, R. Regulation of skeletal muscle glycogen phosphorylase and PDH at varying exercise power outputs. Wojtaszewski, J. Chen, Z. AMPK signaling in contracting human skeletal muscle: acetyl-CoA carboxylase and NO synthase phosphorylation. Stephens, T.

Progressive increase in human skeletal muscle AMPKα2 activity and ACC phosphorylation during exercise. Yu, M. Metabolic and mitogenic signal transduction in human skeletal muscle after intense cycling exercise. Rose, A. McConell, G. Hoffman, N. Global phosphoproteomic analysis of human skeletal muscle reveals a network of exercise-regulated kinases and AMPK substrates.

Nelson, M. Phosphoproteomics reveals conserved exercise-stimulated signaling and AMPK regulation of store-operated calcium entry. EMBO J. Needham, E.

Phosphoproteomics of acute cell stressors targeting exercise signaling networks reveal drug interactions regulating protein secretion.

Cell Rep. e6 Perry, C. Mitochondrial creatine kinase activity and phosphate shuttling are acutely regulated by exercise in human skeletal muscle. Miotto, P. In the absence of phosphate shuttling, exercise reveals the in vivo importance of creatine-independent mitochondrial ADP transport.

Holloway, G. Nutrition and training influences on the regulation of mitochondrial adenosine diphosphate sensitivity and bioenergetics. Suppl 1. Article PubMed PubMed Central Google Scholar.

Effects of dynamic exercise intensity on the activation of hormone-sensitive lipase in human skeletal muscle. Talanian, J. Beta-adrenergic regulation of human skeletal muscle hormone sensitive lipase activity during exercise onset.

CAS Google Scholar. Exercise, GLUT4, and skeletal muscle glucose uptake. Sylow, L. Exercise-stimulated glucose uptake: regulation and implications for glycaemic control.

Bradley, N. Acute endurance exercise increases plasma membrane fatty acid transport proteins in rat and human skeletal muscle. Smith, B. Sport Sci.

Petrick, H. High intensity exercise inhibits carnitine palmitoyltransferase-I sensitivity to L-carnitine. Krustrup, P. Muscle and blood metabolites during a soccer game: implications for sprint performance. Achten, J. Maximal fat oxidation during exercise in trained men. Harris, R.

The time course of phosphorylcreatine resynthesis during recovery of the quadriceps muscle in man. Pflugers Arch. Taylor, J. Neural contributions to muscle fatigue: from the brain to the muscle and back again.

Allen, D. Skeletal muscle fatigue: cellular mechanisms. Amann, M. Central and peripheral fatigue: interaction during cycling exercise in humans. Burke, L. Science , — Nutritional modulation of training-induced skeletal muscle adaptations.

Maughan, R. IOC consensus statement: dietary supplements and the high-performance athlete. Roberts, A. Anaerobic muscle enzyme changes after interval training. Sharp, R. Effects of eight weeks of bicycle ergometer sprint training on human muscle buffer capacity.

Weston, A. Skeletal muscle buffering capacity and endurance performance after high-intensity interval training by well-trained cyclists. McKenna, M. Sprint training enhances ionic regulation during intense exercise in men. Gibala, M. Physiological adaptations to low-volume, high-intensity interval training in health and disease.

Lundby, C. Biology of VO 2 max: looking under the physiology lamp. Convective oxygen transport and fatigue. Holloszy, J. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences.

Chesley, A. Regulation of muscle glycogen phosphorylase activity following short-term endurance training. Leblanc, P. Effects of 7 wk of endurance training on human skeletal muscle metabolism during submaximal exercise. Determinants of endurance in well-trained cyclists.

Westgarth-Taylor, C. Metabolic and performance adaptations to interval training in endurance-trained cyclists. Seynnes, O. Early skeletal muscle hypertrophy and architectural changes in response to high-intensity resistance training.

Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Hultman, E. Muscle creatine loading in men. Influence of oral creatine supplementation of muscle torque during repeated bouts of maximal voluntary exercise in man.

Casey, A. Creatine ingestion favorably affects performance and muscle metabolism during maximal exercise in humans. Vandenberghe, K. Long-term creatine intake is beneficial to muscle performance during resistance training. Hermansen, L. Muscle glycogen during prolonged severe exercise.

Ørtenblad, N. Muscle glycogen stores and fatigue. Matsui, T. Brain glycogen decreases during prolonged exercise. Diet, muscle glycogen and physical performance.

Carbohydrate-loading and exercise performance: an update. Balsom, P. High-intensity exercise and muscle glycogen availability in humans.

Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate. Reversal of fatigue during prolonged exercise by carbohydrate infusion or ingestion. Effect of carbohydrate ingestion on exercise metabolism. Jeukendrup, A. Carbohydrate ingestion can completely suppress endogenous glucose production during exercise.

Effect of carbohydrate ingestion on glucose kinetics during exercise. Nybo, L. CNS fatigue and prolonged exercise: effect of glucose supplementation. Snow, R. PubMed PubMed Central Google Scholar. Billat VL, Hill DW, Pinoteau J, Petit B, Koralsztein JP.

Effect of protocol on determination of velocity at VO 2max and on its time to exhaustion. Arch Physiol Biochem. Coyle EF, Coggan AR, Hopper MK, Walters TJ. Determinants of endurance in well-trained cyclists.

J Appl Physiol. Dyck DJ, Peters SA, Wendling PS, Chesley A, Hultman E, Spriet LL. Regulation of muscle glycogen phosphorylase activity during intense aerobic cycling with elevated FFA. Am J Physiol.

Google Scholar. Dyck DJ, Putman CT, Hegenhauser GJF, Hultman E, Spriet LL. Regulation of fat-carbohydrate interaction in skeletal muscle during intense aerobic cycling.

Elia M, Livesey G. Energy expenditure and fuel selection in biological systems: the theory and practice of calculations based on indirect calorimetry and tracer methods. World Rev Nutr Diet. Goedecke JH, St Clair GA, Grobler L, Collins M, Noakes TD, Lambert EV.

Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. Am J Physiol Endocrinol Metab. Ghosh AK. Anaerobic threshold: its concept and role in endurance sport. Malays J Med Sci. Hetlelid KJ, Plews DJ, Herold E, Laursen PB, Seiler S.

Rethinking the role of fat oxidation: substrate utilization during high-intensity interval training in well-trained and recreationally trained runners. BMJ Open Sport Exerc Med. doi: Horowitz FJ, Klein S. Lipid metabolism during endurance exercise.

Am J Clin Nutr. Howley ET, Bassett DR, Welch HG. Criteria for maximal oxygen uptake: review and commentary. Article CAS Google Scholar. Jeukendrup AE.

Modulation of carbohydrate and fat utilization by diet, exercise and environment. Biochem Soc Trans. Regulation of fat metabolism in skeletal muscle. Ann N Y Acad Sci. Jones AM, Doust JH.

J Sport Sci. Maughan JR, Gleeson M. The biochemical basis of sports performance. Oxford University Press; Mickelson TC, Hagerman FC. Anaerobic threshold measurements of elite oarsmen.

Meyer T, Lucia A, Earnest CO, Kindermann W. A conceptual framework for performance diagnosis and training prescription from submaximal gas exchange parameters—theory and application.

Mooses M, Tippi B, Mooses K, Durussel J, Mäestu J. Better economy in field running than on the treadmill: evidence from high-level distance runners. Biol Sport. Article CAS PubMed PubMed Central Google Scholar. Pierce S, Hahn A, Davie A, Lawton E.

Prolonged incremental tests do not necessarily compromise VO 2max in well-trained athletes. J Sci Med Sports. Rehrer NJ, Wagenmakers AJM, Beckers EJ, Halliday D, Leiper JB, Brouns F, Maughan RJ, Westerterp K, Saris WHM.

Gastric emptying, absorption and carbohydrate oxidation during prolonged exercise. Romijn JA, Coyle EF, Sidossis LS, Zhang XJ, Wolfe RR. Regulation between fatty acid delivery and fatty acid oxidation during strenuous exercise.

Rapoport BI. Metabolic factors limiting performance in marathon runners. PLoS Comput Biol. Article PubMed PubMed Central Google Scholar. Sidossis LS, Gastaldelli A, Klein S, Wolfe RR. Regulation of plasma fatty acid oxidation during low- and high-intensity exercise. Stepto NK, Martin DT, Fallon KE, Hawley JA.

Metabolic demands of intense aerobic interval training in competitive cyclists. Van Loon LJC, Paul LG, Constantin TD, Saris WHM, Wagenmakers AJM. The effects of increasing exercise intensity on muscle fuel utilization in humans. J Physiol. Download references. The study authors would like to thank Pitre Bourdon and Scott Collier for technical and language editing support.

RP contributed to the study design, data collection and analysis, and manuscript drafting. MM and ZN contributed to the study design and manuscript drafting.

All authors read and approved the final manuscript. Ratko Peric, Marco Meucci, and Zoran Nikolovski declare that they have no conflict of interest, and no financial support was received for the conduct of this study or preparation of this manuscript.

Institute for Sport and Occupational Medicine Banja Luka, Zdrave Korde 4, , Banja Luka, Bosnia and Herzegovina. Department of Health and Exercise Science, Appalachian State University, Boone, NC, USA.

Department of Biochemistry, Aspire Academy, Doha, Qatar. You can also search for this author in PubMed Google Scholar. Correspondence to Ratko Peric. Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Peric, R. Fat Utilization During High-Intensity Exercise: When Does It End?.

Sports Med - Open 2 , 35 Download citation. Received : 26 April Accepted : 22 August Published : 31 August Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.

Skip to main content. The reason for the increased acidity during high intensity exercise is not because of lactic acid formation as once thought. Instead, acidosis increases because the muscle is using more ATP at the contracting muscle fibers just outside of the mitochondria , and the splitting of ATP releases many hydrogen ions into the cellular fluid sarcoplasm leading to the acidosis in the cell Robergs, Ghiasvand and Parker, Too much emphasis is often placed on percent of fatty acid contribution of Calories burned during a single bout of exercise.

Recovery from a bout of exercise as well as training adaptations to repeated bouts are important to consider when working with clients with fat loss goals. Focus Paragraph. The Splitting of Adenosine Triphosphate ATP ATP is split by water called hydrolysis with the aid of the ATPase enzyme.

During intense exercise there is a high level of hydrolysis of ATP by the muscles fibers. Each ATP molecule that is split releases a hydrogen ion, which is the cause of acidosis in the cell Robergs, Ghiasvand and Parker, This acidosis can slow the carnitine shuttle that moves fatty acids into the mitochondria for oxidation.

This elevated metabolic rate is termed excess post exercise oxygen consumption EPOC. EPOC appears to be greatest when exercise intensity is high Sedlock, Fissinger and Melby, For example, EPOC is higher after high intensity interval training HIIT compared to exercise for a longer duration at lower intensity Zuhl and Kravitz, EPOC is also notably observed after resistance training Ormsbee et al.

EPOC is particularly elevated for a longer period of time after eccentric exercise due to additional cellular repair and protein synthesis needs of the muscle cells Hackney, Engels, and Gretebeck, Many studies also show that during the period of EPOC, fat oxidation rates are increased Achten and Jeukendrup, , Jamurtas et al.

Comparatively, fatty acid use during high intensity bouts of exercise such as HIIT and resistance training may be lower as compared to moderate intensity endurance training; however, high intensity exercise and weight training may make up for this deficit with the increased fatty acid oxidation through EPOC.

Comparison of Effect of Light Exercise versus Heavy Exercise on EPOC Some key factors that contribute to the elevated post-exercise oxygen consumption during high intensity exercise include the replenishment of creatine phosphate, the metabolism of lactate, temperature recovery, heart rate recovery, ventilation recovery, and hormones recovery Sedlock, Fissinger and Melby, Interestingly, lipolysis breakdown of fats to release fatty acids and fat release from adipocytes is not different between untrained and trained people Horowitz and Klein, This suggests that the improved ability to burn fat in trained people is attributed to differences in the muscle's ability to take up and use fatty acids and not the adipocyte's ability to release fatty acids.

The adaptations that enhance fat usage in trained muscle can be divided into two categories: 1 those that improve fatty acid availability to the muscle and mitochondria and 2 those that improve the ability to oxidize fatty acids. Fatty acid availability One way exercise can improve fatty acid availability is by increasing fatty acid transport into the muscle and mitochondria.

As mentioned above, specific proteins mediate transport of fatty acids into the muscle and mitochondria. Together these proteins will improve fat transport into the muscle and mitochondria to be used for energy.

Exercise may also cause changes in the intramuscular lipid droplet that contains IMTAGs. The intramuscular lipid droplet is mostly found in close proximity to the mitochondria Shaw, Clark and Wagenmakers, Having IMTAGs close to the mitochondria makes sense for efficient IMTAG usage so that fatty acids released from the lipid droplet do not have to travel far to reach the mitochondria.

Exercise training can further increase IMTAG availability to the mitochondria by causing the lipid droplet to conform more closely to the mitochondria. This increases surface area for more rapid fatty acid transport from the lipid droplet into the mitochondria Shaw, Clark and Wagenmakers, Exercise training may also increase the total IMTAG stores Shaw, Clark and Wagenmakers, Another training adaptation that may improve fatty acid availability is increased number of small blood vessels within the muscle Horowitz and Klein, Remember, fatty acids can enter the muscle through the very small blood vessels.

Increasing the number of capillaries around the muscle will allow for increased fatty acid delivery into the muscle.

Fatty acid breakdown IMTAGs are a readily available substrate for energy during exercise because they are already located in the muscle. Trained athletes have an increased ability to use IMTAG efficiently during exercise Shaw, Clark and Wagenmakers, Athletes also tend to have larger IMTAG stores than lean sedentary individuals.

Overweight and obese individuals, interestingly, also have high levels of IMTAG but are not able to use IMTAGs during exercise like athletic individuals can Shaw, Clark and Wagenmakers, So what causes the reduced ability to use IMTAGs in obese individuals? A logical guess would be that they have dysfunctional mitochondria that cannot use fatty acid properly.

Research has shown however, that the mitochondria from muscles of obese individuals are not dysfunctional Holloway et al. Instead, the number of mitochondria per unit of muscle mitochondrial density is reduced in an obese population Holloway et al.

Reduced mitochondrial density is a more likely explanation for reduced ability to use fat for energy in obese individuals. An important adaptation to exercise training is increased mitochondrial density Horowitz and Klein ; Zuhl and Kravitz, Increasing mitochondrial density would improve the ability to use fat and benefit individuals with fat loss goals.

Endurance exercise training is an effective way to improve the body's fatty acid usage abilities by improving the availability of fatty acids to the muscle and mitochondria and by increasing fatty acid oxidation Horowitz and Klein, HIIT training has also been shown to result in similar fat burning adaptations while requiring fewer workouts and less total time commitment Zuhl and Kravitz, Practical application Rather than trying to maximize fat oxidation in a single bout of exercise, it is recommended that the personal trainer design a workout program aimed at causing muscle adaptations described above to improve fatty acid oxidation ability.

The exercise professional should include interval and endurance training programs as these have been shown to improve mitochondrial density and fat oxidation Zuhl and Kravitz, In addition, regular progressively increasing programs of resistance training are encouraged as this training will enhance EPOC and post-workout fat oxidation.

Also, the personal trainer should encourage the client to engage in low to moderate intensity exercise such as walking and cycling on “off hard workout days” in order to enhance caloric deficit and support muscle adaptions between training days.

Workout examples High intensity interval training HIT with variable recovery modified from Seiler and Hetlelid, High intensity interval training uses exercise intensity that corresponds to the individual's VO2max.

Seiler and Hetlelid exercised subjects at their highest running speeds for 4 minutes with 1, 2 or 4 minutes of recovery and repeated this interval 6 times. The idea of a systematic variation of the recovery is a very novel approach to interval training and certainly warrants more research.

The workout Have the client complete up to 6 sets of 4-minute bouts at a maximal sustained workout effort and vary each recovery period to be 1 min, 2 min or 4 minutes at a light intensity client's self-selected intensity.

Sprint interval training SIT Modified from Burgomaster et al. The maximal effort generated in SIT necessitates a small work to larger rest ratio.

That is, SIT is often done with a second all-out effort followed by a 4. The trainer can do SIT with clients using a variety of different modes of exercise including the stationary bike, elliptical cross-trainer and rowing machine. The resistance on the chosen mode of exercise should be relatively challenging during the work bout.

During the sprint interval the trainer should verbally encourage the client to maintain maximal effort throughout the bout. During the recovery phase between bouts the client is encouraged to continue “moving” on the exercise machine at a very low self-selected “light” effort.

The workout Have the client complete 3 to 4 bouts of second all-out bouts bout with 4. Special Comments This is a very challenging workout.

Modifications may be required to match the individual's fitness level needs. Resistance Training RT modified form Melby et al. This is total body weight lifting workout that uses 10 exercises. The exercises are arranged in 5 pairs so that each pair of exercise is completed before resting and moving on to the next pair.

The whole circuit of exercise should be completed up to 6 times. The rest interval between pairs should be no longer than 2 minutes. The resistance used on each exercise should allow the client to lift 8 to 12 repetitions. The Workout- o Pair 1 o Bench press o Bent over row o Pair 2 o Split squat Right leg forward o Split squat Left leg forward o Pair 3 o Military press o Crunches o Pair 4 o Biceps curls o Triceps extensions o Pair 5 o Half squat o Lateral raises Special Comments As with any workout, exercise modifications or substitutions may be necessary to fit individual's fitness needs and abilities.

Tabata-inspired interval training modified form Tabata et al.

Urilization you for visiting nature. You are using a browser version with limited Finger-prick glucose monitor for Diabetes diet and lifestyle. Utilizatino obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. An Author Correction to this article was published on 10 September Independent of total body aft mass, jtilization upper ugilization Efficient fat utilization mass distribution is strongly Micronutrient-rich nuts with cardio-metabolic comorbidities. However, utilizatioon mechanisms Ffat fat mass localization utilizatioj Diabetes diet and lifestyle fully understood. Although a large utilizatjon of evidence indicates sex-specific fat mass Efficeint, women are still excluded from many physiological Nutritional tips for weightlifters and Diabetes diet and lifestyle specific utiliaation 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. Despite a relatively limited level of evidence, the analyzed studies indicate that fat oxidation during endurance exercise is higher in women with lower upper-to-lower-body fat mass ratio than in women with higher upper-to-lower-body fat mass ratio.