Choosing which of the five nutrition strategies of MET to implement will depend on a number of factors. A common strategy is to avoid overfeeding unnecessary calories for shorter and more aerobic-focused workouts, especially in base training.

Additionally, the traditional sports nutrition guidelines of feeding 60 to 90 grams of simple sugars tends to be unnecessary as metabolic efficiency improves. For example, athletes tend to see matched high performance even with 25 to 50 grams of carbohydrates per hour.

While athletes can still opt to use the traditional engineered sports nutrition, many are turning to whole food sources and novel options such as Superstarch® to meet their energy needs and support metabolic efficiency.

While the physical training component of MET is still relevant, its role in enhancing fat metabolism is not quite as profound. Interestingly, many of these benefits can also contribute to improved athletic performance! Objectively, athletes can opt to work with a professional certified in MET who can assist in the process of proper physiological testing in a performance center.

In summary, Metabolic Efficiency Training is a set of sustainable and simple nutrition and training strategies to improve fat metabolism.

Athletes can reap many potential health and performance benefits with proper implementation and monitoring. Brooks, G. Achieving or maintaining a healthy weight is a balancing act.

If we regularly eat and drink more kilojoules than we need for our metabolism, we store it mostly as fat. Most of the energy we use each day is used to keep all the systems in our body functioning properly.

This is out of our control. However, we can make metabolism work for us when we exercise. When you are active, the body burns more energy kilojoules. Our metabolism is complex — put simply it has 2 parts, which are carefully regulated by the body to make sure they remain in balance. They are:. The BMR refers to the amount of energy your body needs to maintain homeostasis.

Your BMR is largely determined by your total lean mass, especially muscle mass, because lean mass requires a lot of energy to maintain.

Anything that reduces lean mass will reduce your BMR. As your BMR accounts for so much of your total energy consumption, it is important to preserve or even increase your lean muscle mass through exercise when trying to lose weight. This means combining exercise particularly weight-bearing and resistance exercises to boost muscle mass with changes towards healthier eating patterns , rather than dietary changes alone as eating too few kilojoules encourages the body to slow the metabolism to conserve energy.

Maintaining lean muscle mass also helps reduce the chance of injury when training, and exercise increases your daily energy expenditure. An average man has a BMR of around 7, kJ per day, while an average woman has a BMR of around 5, kJ per day.

Energy expenditure is continuous, but the rate varies throughout the day. The rate of energy expenditure is usually lowest in the early morning.

Your BMR rises after you eat because you use energy to eat, digest and metabolise the food you have just eaten. The rise occurs soon after you start eating, and peaks 2 to 3 hours later. Different foods raise BMR by differing amounts. For example:. During strenuous or vigorous physical activity, our muscles may burn through as much as 3, kJ per hour.

Energy used during exercise is the only form of energy expenditure that we have any control over. However, estimating the energy spent during exercise is difficult, as the true value for each person will vary based on factors such as their weight, age, health and the intensity with which each activity is performed.

Australia has physical activity guidelines External Link that recommend the amount and intensity of activity by age and life stage. Muscle tissue has a large appetite for kilojoules. The more muscle mass you have, the more kilojoules you will burn.

People tend to put on fat as they age, partly because the body slowly loses muscle. It is not clear whether muscle loss is a result of the ageing process or because many people are less active as they age. However, it probably has more to do with becoming less active.

Research has shown that strength and resistance training can reduce or prevent this muscle loss. If you are over 40 years of age, have a pre-existing medical condition or have not exercised in some time, see your doctor before starting a new fitness program. Hormones help regulate our metabolism.

Some of the more common hormonal disorders affect the thyroid. This gland secretes hormones to regulate many metabolic processes, including energy expenditure the rate at which kilojoules are burned. Thyroid disorders include:. Our genes are the blueprints for the proteins in our body, and our proteins are responsible for the digestion and metabolism of our food.

Sometimes, a faulty gene means we produce a protein that is ineffective in dealing with our food, resulting in a metabolic disorder.

ao link. Base Endurance Training. High Intensity Training. Environmental Training. Recovery Strategies. Nutrition Supplements.

Dietary Basics. Hydration and fuelling on the move. Weight Management. Recovery Nutrition. Overuse Injuries. Psychology Coping with Emotions. Mental Drills.

Psychological Aides. Resources Issue Library. Search the site Search. My Account. My Library. Search the site. Remember Login. Register Reset Password. x You are viewing 1 of your 1 free articles. The metabolic impact of exercise - or how your body works out while you put your feet up Weight management by Andrew Hamilton.

You finished your workout a couple of hours ago and now you are relaxing as you get your regular fix of Sports Performance Bulletin. But in fact your body may not be quite as relaxed as you think. There are a number of ways in which exercise can exert lasting physiological effects that persist for long after you have showered and headed home.

And knowledge of these processes will help you to optimise your performance and recovery, as well as managing your body weight, writes John Shepherd. Weight is an important issue for sportsmen and women. Rugby or American football players, for example, need powerful lean muscle and body mass to hit their opponents hard and absorb the impacts of the game.

A top player can burn 3, calories or more on a typical training day — enough to cause a worrying loss in body weight and lean muscle if calories are not replaced consistently and appropriately.

Ronsen et al from Norway addressed this question in a study of nine elite male athletes, described in the box above.

So far, case-control studies have been mostly employed, by selecting patients with a given diagnosis of metabolic myopathy, but for whom exercise intolerance may not be the chief complaint. This shortcoming is prevented by consecutive inclusion of patients consulting for exercise intolerance and exercise-induced myalgia, in an observational study design.

The primary aim of this research was therefore to evaluate the oxygen cost during incremental exercise in different metabolic myopathies compared with patients with non-metabolic myalgia and healthy subjects, using a standardized methodology in a prospective-unselected cohort.

Table 2 summarizes the baseline characteristics and the results of exercise testing for the five subgroups of patients and the Control group.

In Glycogenoses, the average peak oxygen consumption achieved was Figure 1 displays representative oxygen uptake vs. work-rate plots for each subgroup.

Oxygen consumption plotted against power in representative patients with metabolic myopathies. Subjects performed an incremental work test on an electronically braked bicycle until exhaustion with continuous measurement of oxygen consumption.

Oxygen cost of exercise in metabolic myopathies. Lines indicate the mean values. Data were analyzed using a one-way ANOVA with post hoc Games-Howell test for intergroup analysis.

The metabolic-chronotropic relationship MCR in the MAD Absent group 0. Conversely, the MCR of Glycogenoses 1. The respiratory exchange ratio RER was similar between groups at rest, and was found to be significantly less in Glycogenoses at peak exercise 0.

Control group demonstrated a significantly higher RER at peak exercise 1. Lactate concentration at rest was significantly lower in Glycogenoses 0. At peak exercise, lactate was significantly lower in Glycogenoses 0. Ammonia concentration at peak exercise, was significantly higher in Glycogenoses This study provides evidence that patients with metabolic myopathies have an increased oxygen cost of exercise during an incremental test.

Oxygen cost of exercise has been little studied in different metabolic myopathies in the same study 12 , 22 , with exercise testing performed and reported in a standardized fashion. The present prospective methodology permits comparison both across different metabolic myopathies and with non-metabolic myalgia during incremental exercise.

Visual inspection of the plots in Fig. involving forty RCD patients. The prospective methodology we used may also account for this inconsistency, since our population of RCD patients was unselected in contrast with previous reports.

In McArdle patients, exercise-induced hyperammonemia has been proposed as a mechanism for the exaggerated ventilatory response to exercise 13 , We observed similar lactate levels at peak exercise in RCD and Control subjects, in spite of the two-fold difference in the maximal achieved power.

Increased dependence on anaerobic glycolysis, with excessive lactic acidosis for a given workload, may explain in part hyperpnoea during exercise in RCDs 3 , The heart rate increase for a given increase in oxygen consumption MCR was higher in glycogenoses, while RCDs tended to exhibit a similar pattern.

McArdle disease and mitochondrial myopathy are characterized by a hyperkinetic circulatory response to exercise 2 , 3 , 5 , 8 , i. a mismatch between oxygen utilization and delivery.

Despite a lower muscle oxygen extraction during exercise, resulting in a reduced oxygen arteriovenous difference, glycogenose and RCD patients demonstrate an exacerbated increase in cardiac output and tachycardia 2 , 3 , 5 , 8.

This excessive increase in heart rate may contribute to elevate myocardial oxygen consumption and overall oxygen uptake during exercise in RCDs and McArdle patients 13 , A common potential mechanism for hypercirculatory responses to exercise in RCD and McArdle patients is an increased sympathetic activition, as higher epinephrine and norepinephrine levels have been reported in these myopathies 13 , Due to the prospective design of our study, a single —standardized- incremental exercise protocol involving a 2-min warm-up was used in all subjects.

In contrast to glycogenoses, the MCR was decreased in MAD Absent compared with non-metabolic myalgia patients and controls, probably due to an increased adenosine formation in this enzyme defect 7. In MAD deficiency, AMP accumulation activates an alternate catabolic pathway that leads to excess production of adenosine 7 , which in turn produces negative chronotropic effect 28 , In MAD deficient subject, an elongation of muscle half-relaxation time has been reported following repetitive voluntary isometric contractions of the quadriceps During dynamic task, slowing of muscle relaxation promotes simultaneous contractions of antagonistic pairs and raises internal mechanical work, leading to increase the energy cost of exercise A metabolic impairment has been excluded in this subgroup by an exhaustive and standardized diagnostic work-up, including a muscle biopsy 15 , 16 , It has been shown that some dystrophinopathies can present with a pseudometabolic pattern 32 , 33 , i.

exercise intolerance and exercise-induced myalgia. Future utilization of whole exome sequencing in this subgroup of patients with unknown myopathy will be helpful for identifying genetic mutations that underlie exercise-induced myalgia and rhabdomyolysis From a mechanistic perspective, we acknowledge the limitation that O 2 cost of exercise was not measured during constant exercise 22 , For example, unloaded exercise is useful to determine the oxygen cost of moving the legs against zero resistance.

Moreover, epinephrine and norepinephrine levels were not measured in the present study. Additional measurement of plasma catecholamine levels in all subgroups of subjects could have provided valuable insights into the underlying mechanisms of increased oxygen cost of exercise Patients with metabolic myopathies exhibit a greater oxygen cost of exercise.

The clinical implication of this exacerbated oxygen cost of power production is that a patient with metabolic myopathy can perform less work for a given VO 2 consumption during daily life-submaximal exercises. This loss of efficiency could partially explain difficulties to maintain exercise in metabolic myopathies owing to increased perceived effort.

Written informed consent was obtained from each participant. All procedures conformed to the standards set by the Declaration of Helsinki and the protocol was approved by the institutional ethics committee of Brest Medical University Hospital Clinical Trial NCT From December 1, to November 30, , all patients undergoing exercise testing for exercise intolerance and myalgia at an academic tertiary referral center were prospectively included.

Glycogenoses subgroup was composed of 8 patients. One patient had Tarui disease GSD VII , showed severe reduction of phosphofructokinase activity in muscle biopsy 0. In this subgroup, the non-ischemic forearm exercise test showed a characteristic flat venous lactate curve with exaggerated increase in blood ammonia 1 , 5 , Myoadenylate deaminase staining was absent in seven patients and decreased in twenty-two subjects.

Seventy-three patients consecutively referred for exercise-testing to investigate exercise-induced myalgia, and with no diagnosis despite extensive diagnostic work-up including muscle biopsy 15 , 16 , 31 , 37 , 38 , were recruited as a disease-control group non-metabolic myalgia.

Participants attended the laboratory to complete an incremental step test on an electromagnetically braked cycle ergometer Ergoline GmbH, Bitz, Germany at 60 rev. The predicted peak power output for each subject predicted PPO was calculated using published formulae This theoretical maximal power was adjusted according to exercise intolerance 40 , in order to obtain an estimated peak power output estimated PPO.

The air flow was calibrated before each test using 3-liter syringes Hans Rudolph Inc. Oxygen O 2 and carbon dioxide CO 2 concentrations were analyzed via galvanic fuel cell and nondispersive infrared cell, respectively.

Before each test, the analyzers were calibrated using ambient air, and a gas of known O 2 The cycloergometer was calibrated mechanically twice a year according to the manufacturer instructions.

Calibration was further checked indirectly by annual visit of the healthy subjects for their fitness-for-work evaluation. Data from the 1 st minute of loaded exercise were discarded from analysis, owing to the initial —exponential- delay of VO 2 increase at the onset of work. Maximal heart rate HRmax was measured from continuous lead ECG and expressed as a percentage of the subject theoretical value i.

Blood sample for analysis of lactate and ammonia was drawn at rest and peak exercise from an indwelling catheter in an antecubital vein. Lactate and ammonia concentration were measured spectrophotometrically immediately following sampling All statistical analyses were conducted two-tailed with α set at 0.

Assessment of data normality was determined by Shapiro—Wilk test. Data are reported as mean ± SD. Preisler, N. Exercise in muscle glycogen storage diseases. Article CAS PubMed Google Scholar. Delaney, N. et al. Metabolic profiles of exercise in patients with McArdle disease or mitochondrial myopathy.

Taivassalo, T. The spectrum of exercise tolerance in mitochondrial myopathies: a study of 40 patients. Article PubMed Google Scholar. Tarnopolsky, M.

Exercise testing as a diagnostic entity in mitochondrial myopathies. What can metabolic myopathies teach us about exercise physiology? Dandurand, R. Mitochondrial disease. Pulmonary function, exercise performance, and blood lactate levels.

Sabina, R. Myoadenylate deaminase deficiency. Functional and metabolic abnormalities associated with disruption of the purine nucleotide cycle. Article CAS PubMed PubMed Central Google Scholar. Lewis, S. Haller, R. Myophosphorylase deficiency impairs muscle oxidative metabolism.

Porcelli, S. Riley, M. Cardiopulmonary exercise testing and metabolic myopathies. Grassi, B. Translational medicine: Exercise physiology applied to metabolic myopathies. Sports Exerc. x Rae, D. Excessive skeletal muscle recruitment during strenuous exercise in McArdle patients.

Rannou, F. Diagnostic Algorithm for glycogenoses and myoadenylate deaminase deficiency based on exercise testing parameters: A Prospective Study. Noury, J. Exercise testing-based algorithms to diagnose McArdle disease and MAD defects. Acta Neurol.

Skeletal muscle fatigue and decreased efficiency: two sides of the same coin? Sport Sci. Paridon, S.

The identification of skeletal myopathies due to defects of oxidative metabolism by analysis of oxygen utilization during exercise. Article Google Scholar. Jeppesen, T. Cycle ergometry is not a sensitive diagnostic test for mitochondrial myopathy.

Gimenes, A. Relationship between work rate and oxygen uptake in mitochondrial myopathy during ramp-incremental exercise. Article CAS Google Scholar. Heinicke, K. Exertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms.

Metabolic myopathies: Functional evaluation by analysis of oxygen uptake kinetics. Scott, C. Contribution of anaerobic energy expenditure to whole body thermogenesis. Wasserman, K. Principles of Exercise Testing and Interpretation: Including Pathophysiology and Clinical Applications.

Place, Vanuxem, D. Blood ammonia and ventilation at maximal exercise. Colin, P. Contributions of heart rate and contractility to myocardial oxygen balance during exercise. Heart Circ. Physiol , — Vissing, J. Exercise fuel mobilization in mitochondrial myopathy: A metabolic dilemma. DiMarco, J.

Adenosine: electrophysiologic effects and therapeutic use for terminating paroxysmal supraventricular tachycardia. Kalsi, K.

Decreased cardiac activity of AMP deaminase in subjects with the AMPD1 mutation - a potential mechanism of protection in heart failure. De Ruiter, C.

Muscle function during repetitive moderate-intensity muscle contractions in myoadenylate deaminase-deficient dutch subjects. Uro-Soste, E. Paris , — Figarella-Branger, D. Exertional rhabdomyolysis and exercise intolerance revealing dystrophinopathies. Acta Neuropathol. 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. Effect of carbohydrate ingestion on ammonia metabolism during exercise in humans. Chambers, E. Carbohydrate sensing in the human mouth: effects on exercise performance and brain activity.

Costill, D. Effects of elevated plasma FFA and insulin on muscle glycogen usage during exercise. Vukovich, M. Effect of fat emulsion infusion and fat feeding on muscle glycogen utilization during cycle exercise. Odland, L. Effects of increased fat availability on fat-carbohydrate interaction during prolonged exercise in men.

Phinney, S. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism 32 , — Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling.

Havemann, L. Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance. Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration.

Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers. Paoli, A. The ketogenic diet and sport: a possible marriage.

Ketogenic diets for fat loss and exercise performance: benefits and safety? Helge, J. Interaction of training and diet on metabolism and endurance during exercise in man.

Yeo, W. Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens. Hulston, C.

Training with low muscle glycogen enhances fat metabolism in well-trained cyclists. Kirwan, J. Carbohydrate balance in competitive runners during successive days of intense training.

Cox, P. Nutritional ketosis alters fuel preference and thereby endurance performance in athletes. Shaw, D. Exogenous ketone supplementation and keto-adaptation for endurance performance: disentangling the effects of two distinct metabolic states. Evans, M. No benefit of ingestion of a ketone monoester supplement on km running performance.

Prins, P. Effects of an exogenous ketone supplement on five-kilometer running performance. Dearlove, D. Nutritional ketoacidosis during incremental exercise in healthy athletes. Leckey, J. Ketone diester ingestion impairs time-trial performance in professional cyclists. Effects of caffeine ingestion on metabolism and exercise performance.

Sports 10 , — Graham, T. Performance and metabolic responses to a high caffeine dose during prolonged exercise. Caffeine ingestion and muscle metabolism during prolonged exercise in humans. Caffeine ingestion does not alter carbohydrate or fat metabolism in human skeletal muscle during exercise.

Metabolic, catecholamine, and exercise performance responses to various doses of caffeine. Desbrow, B. The effects of different doses of caffeine on endurance cycling time trial performance.

Sports Sci. Cole, K. Effect of caffeine ingestion on perception of effort and subsequent work production. Sport Nutr. Kalmar, J. Caffeine: a valuable tool to study central fatigue in humans? Exercise and sport performance with low doses of caffeine.

Suppl 2. Wickham, K. Administration of caffeine in alternate forms. Barnett, C. Effect of L-carnitine supplementation on muscle and blood carnitine content and lactate accumulation during high-intensity sprint cycling. Stephens, F. Carbohydrate ingestion augments L-carnitine retention in humans.

Wall, B. Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans. Skeletal muscle carnitine loading increases energy expenditure, modulates fuel metabolism gene networks and prevents body fat accumulation in humans.

A threshold exists for the stimulatory effect of insulin on plasma L-carnitine clearance in humans. Larsen, F. Effects of dietary nitrate on oxygen cost during exercise. Bailey, S. Dietary nitrate supplementation reduces the O 2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans.

Dietary nitrate supplementation enhances muscle contractile efficiency during knee-extensor exercise in humans. Lansley, K. Acute dietary nitrate supplementation improves cycling time trial performance.

Boorsma, R. Beetroot juice supplementation does not improve performance of elite m runners. Nyakayiru, J. No effect of acute and 6-day nitrate supplementation on VO 2 and time-trial performance in highly trained cyclists.

Jones, A. Dietary nitrate and physical performance. Whitfield, J. Dietary nitrate enhances the contractile properties of human skeletal muscle. Beetroot juice supplementation reduces whole body oxygen consumption but does not improve indices of mitochondrial efficiency in human skeletal muscle.

Dietary inorganic nitrate improves mitochondrial efficiency in humans. Ntessalen, M. Inorganic nitrate and nitrite supplementation fails to improve skeletal muscle mitochondrial efficiency in mice and humans.

Relationship of contraction capacity to metabolic changes during recovery from a fatiguing contraction. Sutton, J. Effect of pH on muscle glycolysis during exercise. Wilkes, D.

Effect of acute induced metabolic alkalosis on m racing time. Acid-base balance during repeated bouts of exercise: influence of HCO 3. Hollidge-Horvat, M. Effect of induced metabolic alkalosis on human skeletal muscle metabolism during exercise. Street, D. Metabolic alkalosis reduces exercise-induced acidosis and potassium accumulation in human skeletal muscle interstitium.

Sostaric, S. Parkhouse, W. Buffering capacity of deproteinized human vastus lateralis muscle. Derave, W. β-Alanine supplementation augments muscle carnosine content and attenuates fatigue during repeated isokinetic contraction bouts in trained sprinters.

Hill, C. Influence of β-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity. Amino Acids 32 , — Powers, S. Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production. Merry, T. Do antioxidant supplements interfere with skeletal muscle adaptation to exercise training?

Petersen, A. Infusion with the antioxidant N-acetylcysteine attenuates early adaptive responses to exercise in human skeletal muscle. Ristow, M. Antioxidants prevent health-promoting effects of physical exercise in humans. Natl Acad. USA , — Hyperthermia and fatigue. González-Alonso, J.

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise. Metabolic and thermodynamic responses to dehydration-induced reductions in muscle blood flow in exercising humans.

Fink, W. Leg muscle metabolism during exercise in the heat and cold. Febbraio, M. Muscle metabolism during exercise and heat stress in trained men: effect of acclimation.

Blunting the rise in body temperature reduces muscle glycogenolysis during exercise in humans. Influence of body temperature on the development of fatigue during prolonged exercise in the heat.

Effect of fluid ingestion on muscle metabolism during prolonged exercise. Logan-Sprenger, H. Effects of dehydration during cycling on skeletal muscle metabolism in females. Skeletal muscle enzymes and fiber composition in male and female track athletes.

Lipid metabolism in skeletal muscle of endurance-trained males and females. Horton, T. Fuel metabolism in men and women during and after long-duration exercise.

Friedlander, A. Training-induced alterations of carbohydrate metabolism in women: women respond differently from men. Tarnopolsky, L. Gender differences in substrate for endurance exercise. Carter, S. Substrate utilization during endurance exercise in men and women after endurance training.

Roepstorff, C. Gender differences in substrate utilization during submaximal exercise in endurance-trained subjects. Higher skeletal muscle α2AMPK activation and lower energy charge and fat oxidation in men than in women during submaximal exercise.

Hamadeh, M. Estrogen supplementation reduces whole body leucine and carbohydrate oxidation and increases lipid oxidation in men during endurance exercise. Hackney, A. Substrate responses to submaximal exercise in the midfollicular and midluteal phases of the menstrual cycle.

Zderic, T. Glucose kinetics and substrate oxidation during exercise in the follicular and luteal phases. Devries, M. Menstrual cycle phase and sex influence muscle glycogen utilization and glucose turnover during moderate-intensity endurance exercise.

Frandsen, J. Menstrual cycle phase does not affect whole body peak fat oxidation rate during a graded exercise test. Download references. Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia. Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.

You can also search for this author in PubMed Google Scholar. and L. conceived and prepared the original draft, revised the manuscript and prepared the figures.

Correspondence to Mark Hargreaves or Lawrence L. Reprints and permissions. Skeletal muscle energy metabolism during exercise. Nat Metab 2 , — Download citation.

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Skip to main content Thank you for visiting nature. nature nature metabolism review articles article. Download PDF. Subjects Energy metabolism Skeletal muscle. This article has been updated. Abstract The continual supply of ATP to the fundamental cellular processes that underpin skeletal muscle contraction during exercise is essential for sports performance in events lasting seconds to several hours.

Exercise metabolism and adaptation in skeletal muscle Article 24 May Aerobic exercise intensity does not affect the anabolic signaling following resistance exercise in endurance athletes Article Open access 24 May Myofibrillar protein synthesis rates are increased in chronically exercised skeletal muscle despite decreased anabolic signaling Article Open access 09 May Main In , athletes from around the world were to gather in Tokyo for the quadrennial Olympic festival of sport, but the event has been delayed until because of the COVID pandemic.

Overview of exercise metabolism The relative contribution of the ATP-generating pathways Box 1 to energy supply during exercise is determined primarily by exercise intensity and duration.

Full size image. Regulation of exercise metabolism General considerations Because the increase in metabolic rate from rest to exercise can exceed fold, well-developed control systems ensure rapid ATP provision and the maintenance of the ATP content in muscle cells. Box 3 Sex differences in exercise metabolism One issue in the study of the regulation of exercise metabolism in skeletal muscle is that much of the available data has been derived from studies on males.

Targeting metabolism for ergogenic benefit General considerations Sports performance is determined by many factors but is ultimately limited by the development of fatigue, such that the athletes with the greatest fatigue resistance often succeed.

Training Regular physical training is an effective strategy for enhancing fatigue resistance and exercise performance, and many of these adaptations are mediated by changes in muscle metabolism and morphology.

Carbohydrate loading The importance of carbohydrate for performance in strenuous exercise has been recognized since the early nineteenth century, and for more than 50 years, fatigue during prolonged strenuous exercise has been associated with muscle glycogen depletion 13 , High-fat diets Increased plasma fatty acid availability decreases muscle glycogen utilization and carbohydrate oxidation during exercise , , Ketone esters Nutritional ketosis can also be induced by the acute ingestion of ketone esters, which has been suggested to alter fuel preference and enhance performance Caffeine 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 , , Carnitine 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.

Nitrate NO is an important bioactive molecule with multiple physiological roles within the body. Antioxidants 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 Conclusion and future perspectives 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.

References Hawley, J. Article CAS PubMed Google Scholar Sahlin, K. Article CAS PubMed Google Scholar Medbø, J. Article PubMed Google Scholar Parolin, M. CAS PubMed Google Scholar Greenhaff, P. Article Google Scholar Medbø, J. Article PubMed Google Scholar Tesch, P. Article CAS PubMed Google Scholar Koopman, R.

Article CAS PubMed Google Scholar Hawley, J. PubMed Google Scholar Romijn, J. CAS PubMed Google Scholar van Loon, L. Article Google Scholar Bergström, J. Article PubMed Google Scholar Wahren, J. Article CAS PubMed PubMed Central Google Scholar Ahlborg, G.

Article CAS PubMed PubMed Central Google Scholar Watt, M. Article CAS Google Scholar van Loon, L. Article PubMed CAS Google Scholar Wasserman, D.

Article CAS PubMed Google Scholar Coggan, A. CAS PubMed Google Scholar Coyle, E. Article CAS PubMed Google Scholar Horowitz, J. Article CAS PubMed Google Scholar Kiens, B.

Article CAS PubMed Google Scholar Stellingwerff, T. Article CAS PubMed Google Scholar Spriet, L. Article CAS PubMed Google Scholar Brooks, G. Article CAS PubMed Google Scholar Miller, B. Article CAS Google Scholar Medbø, J. Article PubMed CAS Google Scholar Hashimoto, T.

Article CAS PubMed Google Scholar Takahashi, H. Article CAS PubMed PubMed Central Google Scholar Scheiman, J.

Article CAS PubMed PubMed Central Google Scholar Rennie, M. Article CAS Google Scholar Wagenmakers, A. CAS PubMed Google Scholar Howarth, K. Article CAS PubMed Google Scholar McKenzie, S. Article CAS PubMed Google Scholar Wilkinson, S. Article CAS Google Scholar Egan, B. Article PubMed Google Scholar Hargreaves, M.

Article PubMed PubMed Central CAS Google Scholar Richter, E. Article CAS PubMed Google Scholar Gaitanos, G. Article CAS PubMed Google Scholar Kowalchuk, J.

Article CAS PubMed Google Scholar Howlett, R. CAS PubMed Google Scholar Wojtaszewski, J. Article CAS Google Scholar Chen, Z. Article CAS PubMed Google Scholar Stephens, T. Article CAS PubMed Google Scholar Yu, M.

Article CAS Google Scholar Rose, A. Article CAS Google Scholar McConell, G. Article CAS PubMed Google Scholar Hoffman, N. Article CAS PubMed PubMed Central Google Scholar Nelson, M. Article CAS PubMed PubMed Central Google Scholar Needham, E.

Article CAS PubMed Google Scholar Perry, C. Article CAS Google Scholar Miotto, P. Article CAS PubMed Google Scholar Holloway, G. Article PubMed PubMed Central Google Scholar Watt, M. Article CAS Google Scholar Talanian, J. CAS Google Scholar Richter, E. Article CAS PubMed Google Scholar Sylow, L.

Article CAS Google Scholar Bradley, N. Article CAS PubMed Google Scholar Smith, B. Article PubMed Google Scholar Petrick, H. Article CAS PubMed Google Scholar Krustrup, P. Article CAS PubMed Google Scholar Achten, J.

Article CAS PubMed Google Scholar Harris, R. Article CAS PubMed Google Scholar Taylor, J. Article CAS PubMed PubMed Central Google Scholar Allen, D. Article CAS PubMed Google Scholar Amann, M. Article PubMed Google Scholar Burke, L. Article CAS PubMed Google Scholar Maughan, R. Article PubMed Google Scholar Roberts, A.

Article CAS PubMed Google Scholar Sharp, R. Article CAS PubMed Google Scholar Weston, A. Article CAS PubMed Google Scholar McKenna, M. Article CAS Google Scholar Gibala, M. Article CAS Google Scholar Lundby, C. Article CAS Google Scholar Amann, M. Article PubMed Google Scholar Holloszy, J. Article CAS PubMed Google Scholar Chesley, A.

CAS PubMed Google Scholar Leblanc, P. Article CAS PubMed Google Scholar Coyle, E. Article CAS PubMed Google Scholar Westgarth-Taylor, C. Article CAS PubMed Google Scholar Seynnes, O. Article CAS Google Scholar Hultman, E. Article CAS PubMed Google Scholar Greenhaff, P. Article CAS Google Scholar Casey, A.

CAS PubMed Google Scholar Vandenberghe, K. Article CAS PubMed Google Scholar Hermansen, L. Article CAS PubMed Google Scholar Ørtenblad, N. Article PubMed PubMed Central CAS Google Scholar Matsui, T. CAS Google Scholar Bergström, J. Article PubMed Google Scholar Hawley, J.

Article CAS PubMed Google Scholar Balsom, P. Article CAS PubMed Google Scholar Hargreaves, M. Article CAS PubMed Google Scholar Jeukendrup, A. CAS PubMed Google Scholar McConell, G. Article CAS PubMed Google Scholar Nybo, L.

Article CAS PubMed Google Scholar Snow, R. Article CAS PubMed Google Scholar Chambers, E. Article CAS Google Scholar Costill, D. Article CAS PubMed Google Scholar Vukovich, M.

Article CAS PubMed Google Scholar Odland, L. CAS PubMed Google Scholar Phinney, S. Article CAS PubMed Google Scholar Burke, L. Article CAS PubMed Google Scholar Havemann, L. Article CAS Google Scholar Paoli, A. Article PubMed Google Scholar Kiens, B. Article PubMed Google Scholar Helge, J.

Article CAS Google Scholar Yeo, W. Article CAS PubMed Google Scholar Hulston, C. Article CAS PubMed Google Scholar Kirwan, J. Article CAS PubMed Google Scholar Cox, P.

Article CAS PubMed Google Scholar Shaw, D. Article PubMed Google Scholar Evans, M. Article CAS PubMed Google Scholar Prins, P.

Article PubMed PubMed Central Google Scholar Dearlove, D. Article PubMed PubMed Central Google Scholar Leckey, J. Article PubMed PubMed Central Google Scholar Costill, D. CAS PubMed Google Scholar Graham, T. Article CAS PubMed Google Scholar Graham, T. Article CAS Google Scholar Graham, T.

Article CAS PubMed Google Scholar Desbrow, B. Article PubMed Google Scholar Cole, K. Article PubMed Google Scholar Kalmar, J. Article PubMed Google Scholar Spriet, L. Article PubMed Google Scholar Wickham, K. Article PubMed PubMed Central Google Scholar Barnett, C.

Article CAS PubMed Google Scholar Stephens, F. Article CAS PubMed Google Scholar Wall, B. Article CAS Google Scholar Stephens, F.

Andy is a sports science writer and researcher, specializing in sports nutrition and has worked in the field of fitness and sports performance for over 30 years, helping athletes to reach their true potential. He is also a contributor to our sister publication, Sports Injury Bulletin.

They use the latest research to improve performance for themselves and their clients - both athletes and sports teams - with help from global specialists in the fields of sports science, sports medicine and sports psychology.

They do this by reading Sports Performance Bulletin, an easy-to-digest but serious-minded journal dedicated to high performance sports. SPB offers a wealth of information and insight into the latest research, in an easily-accessible and understood format, along with a wealth of practical recommendations.

Sports Performance Bulletin helps dedicated endurance athletes improve their performance. Sense-checking the latest sports science research, and sourcing evidence and case studies to support findings, Sports Performance Bulletin turns proven insights into easily digestible practical advice.

Supporting athletes, coaches and professionals who wish to ensure their guidance and programmes are kept right up to date and based on credible science.

ao link. Base Endurance Training. High Intensity Training. Environmental Training. Recovery Strategies. Nutrition Supplements.

Dietary Basics. Hydration and fuelling on the move. Weight Management. Recovery Nutrition. Overuse Injuries. Psychology Coping with Emotions. Mental Drills. Psychological Aides.

Resources Issue Library. Search the site Search. My Account. My Library. Search the site. Remember Login. Register Reset Password. x You are viewing 1 of your 1 free articles. The metabolic impact of exercise - or how your body works out while you put your feet up Weight management by Andrew Hamilton.

You finished your workout a couple of hours ago and now you are relaxing as you get your regular fix of Sports Performance Bulletin. But in fact your body may not be quite as relaxed as you think.

There are a number of ways in which exercise can exert lasting physiological effects that persist for long after you have showered and headed home. And knowledge of these processes will help you to optimise your performance and recovery, as well as managing your body weight, writes John Shepherd.

Weight is an important issue for sportsmen and women. Rugby or American football players, for example, need powerful lean muscle and body mass to hit their opponents hard and absorb the impacts of the game.

A top player can burn 3, calories or more on a typical training day — enough to cause a worrying loss in body weight and lean muscle if calories are not replaced consistently and appropriately. Ronsen et al from Norway addressed this question in a study of nine elite male athletes, described in the box above.

The athletes each completed four hour trials, as follows 2 : One bout of exercise only; Two bouts of exercise separated by three hours of rest and one meal; Two bouts of exercise separated by six hours of rest and two meals; No exercise.

Increased metabolic stress — including a higher mean oxygen uptake, heart rate, rectal core temperature and EPOC and a lower respiratory exchange ratio — was observed when strenuous exercise was repeated after only three hours of recovery.

But metabolic stress was reduced when a longer recovery period, including an additional meal, was given. Andrew Hamilton Andrew Hamilton BSc Hons, MRSC, ACSM, is the editor of Sports Performance Bulletin and a member of the American College of Sports Medicine.

Register now to get a free Issue. Register now and get a free issue of Sports Performance Bulletin Get My Free Issue. Latest Issue. Our findings cement the central role of exercise in preventing cardiovascular disease.

Effect of chronic exercise in healthy young male adults: a metabolomic analysis. Cardiovasc Res. About the European Society of Cardiology. The European Society of Cardiology brings together health care professionals from more than countries, working to advance cardiovascular medicine and help people lead longer, healthier lives.

About Cardiovascular Research. Cardiovascular Research CVR is the international journal of the European Society of Cardiology ESC for basic and translational research across different disciplines and areas.

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Learn more. Show navigation Hide navigation. Sub menu. Benefits of exercise on metabolism: more profound than previously reported 02 Apr Topic s : Prevention. Disclosures : None. References 1 Koay YC, Stanton K, Kienzle V, et al.