Tamir also suggests 48 hours of recovery time after metcon workouts, unless you focus on a specific body part during those workouts; then you don't need as much rest.

For example, if you do an arms metcon workout, you're good to take less rest before tackling a leg-focused workout. Instructions: Do each move below for 30 seconds.

Rest for 60 seconds between exercises. Repeat for 4 rounds. Set 1: Do each move below for 40 seconds. Rest 20 seconds between exercises.

Repeat for 3 rounds. Instructions: Do each move below for 40 seconds. Instructions: Do 5 reps of each exercise below, no rest between.

Rest for 1 to 2 minutes after each round. Instructions: Do each exercise below, for the designated reps, no rest between. Keep that in mind if you're feel completed defeated throughout the workout, and lighten up on the intensity weight, pace, or reps if you need to.

Also, when selecting weights, make sure it's a set you can lift for a longer duration, Tamir says—and recognize when you need to go down in those weights or reps , if you feel you're sacrificing form.

Prescott suggests avoiding something super heavy. Taking time to do a warm-up before and cooling down after is also important, Prescott notes. While working at an intensity that pushes you and challenges you is key, so is taking the designated rest time to actually bring your heart rate back down.

Crouchelli suggests easing into each metcon workout—if you're doing three rounds of certain exercises, for example, start with bodyweight, slowly increase tempo, then add weight when you're ready.

Finally, always make sure you are properly fueled before and after with water and nutrients , Tamir says. And get adequate sleep, too! The most important thing about metcon workouts is focusing on the goal you want to achieve and then being consistent with the training, Prescott says.

You want these workouts to be intense—but that doesn't mean sacrificing strong form, lifting super heavy, or feeling absolutely wiped by the end. Listen to your body and you'll gain all the advantages of a metabolic conditioning workout—an efficient, effective way to train.

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What is metabolic conditioning, really? Types of energy systems. The phosphagensystem is involved in high-intensity work for a short burst of time, up to 10 seconds. This system kicks in immediately when you start moving fast and hard, using creatine phosphate to quickly produce ATP.

The glycolytic system is involved in intense work for up to a few minutes. This one uses glucose or carbs to produce energy. Like the phosphagen system, this one initially works without oxygen, making them both anaerobic systems.

The oxidative system, or aerobic system, accounts for longer, endurance events. It uses carbs and fat to produce ATP for energy and requires oxygen to do so.

Benefits of metabolic conditioning. It can improve your fitness performance. It's super time-efficient. It can help you stay motivated. Potential risks of metabolic conditioning. What a metabolic conditioning workout may look like. How often should you do metabolic conditioning workouts?

Metabolic conditioning workouts to try. To get started with some metabolic conditioning, try these workout plans:. Trainer: Liz Letchford, Ph.

Equipment: Two heavy dumbbells. Dumbbell thrusters Box jumps Renegade rows Farmer's carry. The decrease is generally greater in type II than type I muscle fibres 5. The large increases in ATP utilization and glycolysis, as well as the strong ion fluxes during such exercise, result in metabolic acidosis.

After the exercise duration extends beyond approximately 1 min for example, in an m track event , oxidative phosphorylation is the major ATP-generating pathway 6 , and intramuscular glycogen is the dominant fuel source. Although it is relatively less studied, resistance exercise, as seen during lifting events, is also associated with substantial metabolic perturbations in contracting skeletal muscle 7 , 8.

Contributions of PCr light green , glycolysis medium green and oxidative phosphorylation dark green to ATP turnover during maximal exercise. Muscle samples were obtained before and during 30 s of all-out cycling exercise. Dw, dry weight. Adapted with permission from ref. During events lasting several minutes to hours, the oxidative metabolism of carbohydrate and fat provides almost all the ATP for contracting skeletal muscle.

Even during marathon and triathlon events lasting 2—2. The major intramuscular and extramuscular substrates are muscle glycogen, blood glucose derived from liver glycogenolysis and gluconeogenesis, and from the gut when carbohydrate is ingested and fatty acids derived from both muscle intramuscular triglyceride IMTG and adipose tissue triglyceride stores.

These stores and the relative energy available from them are shown in Fig. The primary determinants of the relative contribution of these substrates to oxidative metabolism are exercise intensity and duration 11 , 12 Fig. Major sources of carbohydrate in the muscle and liver and of fat in the muscle and adipose tissue during exercise.

The estimated potential energy available from each fuel source is also provided. TG, triglyceride; FFA, free fatty acids. Trained cyclists exercised at increasing intensities, and the relative contributions of fuels for contracting skeletal muscle were measured with indirect calorimetry and tracer methods.

An increasing contribution of carbohydrate fuels, notably muscle glycogen, is observed at higher exercise intensities. FFA, free fatty acids; cal, calorie. Carbohydrate oxidation, particularly from muscle glycogen, dominates at higher exercise intensities, whereas fat oxidation is more important at lower intensities.

Oxidation of muscle glycogen and fatty acids derived from IMTG is greatest during the early stages of exercise and declines as exercise duration is extended, coinciding with progressive increases in muscle glucose and fatty acid uptake and oxidation 13 , 14 , 15 , 16 , Accompanying the increase in muscle glucose uptake is an increase in liver glucose output 15 , 18 from both liver glycogenolysis and gluconeogenesis 15 , With prolonged exercise, liver glucose output may fall below muscle glucose uptake 15 , thus resulting in hypoglycaemia that can be prevented by carbohydrate ingestion An increase in adipose tissue lipolysis supports the progressive increase in plasma fatty acid uptake and oxidation 21 , but because lipolysis exceeds uptake and oxidation, plasma fatty acid levels increase.

Inhibition of adipose tissue lipolysis increases the reliance on both muscle glycogen and IMTG but has little effect on muscle glucose uptake Nevertheless, IMTG does appear to be an important fuel source during exercise in trained individuals Despite activation of the oxidative pathways in skeletal muscle during exercise, accelerated rates of glycolysis result in the production of lactate, which accumulates in muscle and blood, particularly at higher exercise intensities Although lactate was considered simply a metabolic waste product for many years, it is now recognized as an important substrate for oxidative metabolism, gluconeogenesis and muscle glycogenesis 25 , 26 , 27 , and as a signalling molecule mediating exercise adaptations and interorgan communication 28 , 29 , Glycerol is released into the circulation from contracting skeletal muscle and adipose tissue, as is alanine from muscle, and both can serve as liver gluconeogenic precursors during exercise Exercise increases protein turnover during exercise 31 , and although amino acids, notably the branched-chain amino acids, can be oxidized by contracting skeletal muscle, the contribution to overall ATP production is low.

Under conditions of low carbohydrate availability, the contribution from amino acid metabolism is increased 32 , 33 , whereas endurance training results in decreased leucine oxidation Of greater importance are the postexercise increases in myofibrillar and mitochondrial protein synthesis that underpin the adaptations to acute and chronic endurance and resistance exercise 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.

Numerous reviews have examined the regulation of skeletal muscle energy metabolism and the adaptations that occur with physical training 1 , 36 , 37 , Here, we briefly highlight some of the factors that regulate the remarkable ability of skeletal muscle to generate ATP during strenuous physical exercise Fig.

The utilization of extramuscular and intramuscular carbohydrate and fat fuels, along with the major sites of regulation at key enzymes and transport proteins. Interactions between anaerobic and aerobic pathways, and between carbohydrate and fat, ensure the ATP supply for contracting skeletal muscle.

FFA, free fatty acids; PM, plasma membrane; FABP PM , plasma membrane fatty acid—binding protein; FATP, fatty acid transport protein; ATG, adipose triglyceride; HS, hormone sensitive; MG, monoglyceride; TG, triglyceride; FABP c , cytoplasmic fatty acid binding protein; HK, hexokinase; PFK, phosphofructokinase; LDH, lactate dehydrogenase; Cr, creatine; mtCK, mitochondrial creatine kinase; mt OM and mt IM, outer and inner mitochondrial membrane; ACT, acyl-CoA transferase; MCT, monocarboxylase transporter; ANT, adenine transport; PDH, pyruvate dehydrogenase; ETC, electron-transport chain.

When very intense short-term exercise begins, all pathways associated with both anaerobic and aerobic ATP provision are activated Box 1. However, the rates of ATP provision from the anaerobic sources, PCr and anaerobic glycolysis are much more rapid than those from aerobic pathways.

PCr is a remarkable fuel source, because only one metabolic reaction is required to provide ATP Box 1. As soon as muscle contractions begin, and ATP is broken down and the concentration of free ADP increases, this reaction moves from left to right Box 1 , and ATP is regenerated in several milliseconds.

Increases in ADP and AMP activate mainly phosphorylase a through allosteric regulation , which breaks down glycogen; the products then combine with inorganic phosphate P i , thus producing glucose 1-phosphate, glucose 6-phosphate and fructose 6-phosphate in the glycolytic pathway. The dual control by local factors associated with muscle contractions and epinephrine 39 , and the combination of covalent and allosteric regulation explain how the flux through phosphorylase can increase from very low at rest to very high during intense exercise in only milliseconds.

The increases in the allosteric regulators ADP, AMP and P i the by-products of ATP breakdown , and the substrate fructose 6-phosphate, activate the regulatory enzyme phosphofructokinase, and flux through the reactions of the glycolytic pathway continues with a net production of three ATP molecules and lactate formation Fig.

Although there are more reactions in the glycolytic pathway than in PCr hydrolysis, the production of ATP through anaerobic glycolysis is also activated in milliseconds.

Lactate accumulation can be measured in the muscle after only a 1-s contraction, and the contribution of anaerobic energy from PCr and anaerobic glycolysis is essentially equivalent after 6—10 s of intense exercise 4 , 24 , 40 Fig.

The capacity of the PCr energy store is a function of its resting content ~75 mmol per kg dry muscle and can be mostly depleted in 10—15 s of all-out exercise. The anaerobic glycolytic capacity is approximately threefold higher ~ mmol per kg dry muscle in exercise lasting 30—90 s and is limited not by glycogen availability but instead by increasing intramuscular acidity.

During the transition from rest to intense exercise, the substrate for increased aerobic ATP production is also muscle glycogen, and a small amount of the produced pyruvate is transferred into the mitochondria, where it is used to produce acetyl-CoA and the reducing equivalent NADH in the pyruvate dehydrogenase PDH reaction.

A good example is the enzyme PDH, which is kept in inactive form by resting levels of acetyl-CoA and NADH. The power of these resting regulators is weak compared with that of the heavy hitters in exercise.

Instead, AMPK activation during exercise may be functionally more important for the postexercise changes in muscle metabolism and insulin sensitivity, and for mediating some of the key adaptive responses to exercise in skeletal muscle, such as mitochondrial biogenesis and enhanced glucose transporter GLUT 4 expression.

Considerable redundancy and complex spatial and temporal interactions among multiple intramuscular signalling pathways are likely to occur during exercise. In future studies, these approaches should provide new insights into the molecular regulation of skeletal muscle energy metabolism during exercise.

In this situation, there is time to mobilize fat and carbohydrate substrates from sources in the muscle as well as from the adipose tissue and liver Fig.

The muscles still rely on anaerobic energy for the initial 1—2 min when transitioning from rest to an aerobic power output, but then aerobic metabolism dominates. To produce the required ATP, the respiratory or electron-transport chain in the mitochondria requires the following substrates: reducing equivalents in the form of NADH and FADH 2 , free ADP, P i and O 2 Fig.

The respiratory and cardiovascular systems ensure the delivery of O 2 to contracting muscles, and the by-products of ATP utilization in the cytoplasm ADP and P i are transported back into the mitochondria for ATP resynthesis.

The processes that move ATP out of the mitochondria and ADP and P i back into the mitochondria are being intensely studied and appear to be more heavily regulated than previously thought 52 , In the presence of ample O 2 and ADP and P i in the mitochondria, the increase in ADP concentration with exercise is believed to activate the respiratory chain to produce ATP In terms of the metabolic pathways, the tricarboxylic acid TCA cycle in the mitochondria specializes in producing reducing equivalents and accepts acetyl-CoA mainly from carbohydrate and fat and other fuels to do so.

Substrate accumulation and local regulators fine-tune the flux through the dehydrogenases, and a third enzyme, citrate synthase, controls TCA-cycle flux. Additional NADH is produced both in the glycolytic pathway, after which it is shuttled from the cytoplasm into the mitochondria, and in the PDH reaction, which occurs in the mitochondria.

The transport protein GLUT4 facilitates the influx of glucose into cells, and increases in glucose delivery, secondary to enhanced muscle blood flow, and intramuscular glucose metabolism ensure that the gradient for glucose diffusion is maintained during exercise Translocation of GLUT4 is a fundamental event in exercise-induced muscle glucose uptake, and its regulation has been well studied Transport proteins for fat are also translocated to the muscle membrane mainly plasma membrane fatty acid—binding protein and mitochondrial membranes mainly fatty acid translocase FAT, also known as CD36 , where they transport fatty acids into cells and mitochondria 59 , The fatty acids that are transported into the cytoplasm of the cell and released from IMTG must also be transported across the mitochondrial membranes with the help of the carnitine palmitoyl transferase CPT I system and fat-transport proteins, mainly FAT CD36 61 , Once inside the mitochondria, fat enters the β-oxidation pathway, which produces acetyl-CoA and reducing equivalents NADH and FADH 2 , and the long-chain nature of fatty acids results in generation of large amounts of aerobic ATP Box 1.

In these situations, fuel use shifts to carbohydrate, and reliance on fat is decreased Fig. However, if the endurance event is extended, the liver and skeletal muscle glycogen stores may become exhausted, thereby requiring athletes to slow down.

Researchers have now identified several sites where fat metabolism is downregulated at high aerobic exercise intensities, including decreased fatty acid release from adipose tissue and therefore less fatty acid transport into cells; decreased activation of hormone-sensitive lipase and possibly adipose triglyceride lipase; less IMTG breakdown; and inhibition of CPT I activity as a result of small decreases in muscle pH, decreased CPT I sensitivity to carnitine and possibly low levels of cytoplasmic carnitine-reducing mitochondrial-membrane transport 37 , In many team sports, a high aerobic ability is needed for players to move about the field or playing surface, whereas sprints and anaerobic ATP , as dictated by the game, are added to the contribution of aerobic ATP.

This scenario is repeated many times during a game, and carbohydrate provides most of the aerobic fuel and much of the anaerobic fuel. Unsurprisingly, almost every regulatory aspect of carbohydrate metabolism is designed for rapid provision of ATP. Carbohydrate is the only fuel that can be used for both aerobic and anaerobic ATP production, and both systems are activated very quickly during transitions from rest to exercise and from one power output to a higher power output.

In addition, the processes that provide fatty acids to the muscles and the pathways that metabolize fat and provide ATP in muscles are slower than the carbohydrate pathways.

However, in events requiring long periods of exercise at submaximal power outputs, fat can provide energy for long periods of time and has a much larger ATP-generating capacity than carbohydrate. Fat oxidation also contributes energy in recovery from exercise or rest periods between activity.

Another important aspect of metabolism in stop-and-go sports is the ability to rapidly resynthesize PCr when the exercise intensity falls to low levels or athletes rest. In these situations, continued aerobic production of ATP fuels the regeneration of PCr such that it can be completely recovered in 60— s ref.

This production is extremely important for the ability to repeatedly sprint in stop-and-go or intermittent sports. Recovery from prolonged sprinting 20—s and sustained high glycolytic flux is slower, because the associated muscle acidity requires minutes, not seconds, to recover and can limit performance 4 , Importantly, other fuels can provide aerobic energy in cells during exercise, including amino acids, acetate, medium-chain triglycerides, and the ketones β-hydroxybutyrate and acetoacetic acid.

Although these fuels can be used to spare the use of fat and carbohydrate in some moderate-intensity exercise situations, they lack the rate of energy provision needed to fuel intense aerobic exercise, because the metabolic machinery for these fuels is not designed for rapid energy provision.

Alternative fuels cannot match carbohydrate in terms of the rate of aerobic energy provision 9 , and these fuels cannot be used to produce anaerobic energy in the absence of oxygen.

Sex may have roles in the regulation of skeletal muscle metabolism. Males and females are often assumed to respond similarly to acute exercise and exercise training, but most of the work cited in this Review involved male participants.

Clear differences exist between males and females—including haemoglobin concentrations, muscle mass and reproductive-hormone levels—and have been shown to affect metabolism and exercise performance, thus making perfect comparisons between males and females very difficult.

The potential sex differences in metabolism are briefly mentioned in Box 3 , and more detailed discussion can be found in a review by Kiens 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.

Although the major principles controlling the regulation of metabolism appear to hold true for both females and males, some differences have been noted. Although one might argue that completely matching males and females is impossible when studying metabolism, early work with well-trained track athletes has reported no differences in skeletal muscle enzyme activity, fibre-type composition and fat oxidation between men and women , However, more recent work has reported that a larger percentage of whole-body fuel use is derived from fat in females exercising at the same relative submaximal intensity, and this effect is likely to be related to circulating oestrogen levels , , , , , In addition, supplementation with oestrogen in males decreases carbohydrate oxidation and increases fat oxidation during endurance exercise These results suggest that females may be better suited to endurance exercise than males.

Another area that has been investigated is the effects of menstrual phase and menstrual status on the regulation of skeletal muscle metabolism.

Generally, studies examining exercise in the luteal and follicular phases have reported only minor or no changes in fat and carbohydrate metabolism at various exercise intensities , , , Additional work examining the regulation of metabolism in well-trained female participants in both phases of the menstrual cycle, and with varied menstrual cycles, during exercise at the high aerobic and supramaximal intensities commensurate with elite sports, is warranted.

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. However, there can be a fine line between glory and catastrophe, and the same motivation that drives athletes to victory can at times push them beyond their limits.

Fatigue is the result of a complex interplay among central neural regulation, neuromuscular function and the various physiological processes that support skeletal muscle performance 1. It manifests as a decrease in the force or power-producing capacity of skeletal muscle and an inability to maintain the exercise intensity needed for ultimate success.

Over the years, considerable interest has been placed on the relative importance of central neural and peripheral muscle factors in the aetiology of fatigue. All that I am, I am because of my mind. Perhaps the two major interventions used to enhance fatigue resistance are regular training and nutrition 70 , and the interactions between them have been recognized We briefly review the effects of training and nutrition on skeletal muscle energy metabolism and exercise performance, with a focus on substrate availability and metabolic end products.

In relation to dietary supplements, we have limited our discussion to those that have been reasonably investigated for efficacy in human participants 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.

Such training is also associated with the cardiovascular and metabolic benefits often observed with traditional endurance training One hallmark adaptation to endurance exercise training is increased oxygen-transport capacity, as measured by VO 2 max 78 , thus leading to greater fatigue resistance and enhanced exercise performance The other is enhanced skeletal muscle mitochondrial density 80 , a major factor contributing to decreased carbohydrate utilization and oxidation and lactate production 81 , 82 , increased fat oxidation and enhanced endurance exercise performance The capacity for muscle carbohydrate oxidation also increases, thereby enabling maintenance of a higher power output during exercise and enhanced performance Finally, resistance training results in increased strength, neuromuscular function and muscle mass 85 , effects that can be potentiated by nutritional interventions, such as increased dietary protein intake The improved performance is believed to be due to enhanced ATP resynthesis during exercise as a result of increased PCr availability.

Some evidence also indicates that creatine supplementation may increase muscle mass and strength during resistance training No major adverse effects of creatine supplementation have been observed in the short term, but long-term studies are lacking.

Creatine remains one of the most widely used sports-related dietary supplements. 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 , Muscle glycogen is critical for ATP generation and supply to all the key ATPases involved in excitation—contraction coupling in skeletal muscle Recently, prolonged exercise has been shown to decrease glycogen in rodent brains, thus suggesting the intriguing possibility that brain glycogen depletion may contribute to central neural fatigue Muscle glycogen availability may also be important for high-intensity exercise performance Blood glucose levels decline during prolonged strenuous exercise, because the liver glycogen is depleted, and increased liver gluconeogenesis is unable to generate glucose at a rate sufficient to match skeletal muscle glucose uptake.

Maintenance of blood glucose levels at or slightly above pre-exercise levels by carbohydrate supplementation maintains carbohydrate oxidation, improves muscle energy balance at a time when muscle glycogen levels are decreased and delays fatigue 20 , 97 , Glucose ingestion during exercise has minimal effects on net muscle glycogen utilization 97 , 99 , but increases muscle glucose uptake and markedly decreases liver glucose output , , because the gut provides most glucose to the bloodstream.

Importantly, although carbohydrate ingestion delays fatigue, it does not prevent fatigue, and many factors clearly contribute to fatigue during prolonged strenuous exercise. Because glucose is the key substrate for the brain, central neural fatigue may develop during prolonged exercise as a consequence of hypoglycaemia and decreased cerebral glucose uptake Carbohydrate ingestion exerts its benefit by increasing cerebral glucose uptake and maintaining central neural drive NH 3 can cross the blood—brain barrier and has the potential to affect central neurotransmitter levels and central neural fatigue.

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.

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Additionally, exercise was standardised to the core body temperature nadir with the midpoint of exercise timed to 3 hours before, at and 2 hours after minimum core body temperature. Constant routine approaches have been implemented with varying levels of control, with some controlling for sleep-wake cycles, physical activity and nutritional intake with glucose infusion 33 or controlled mealtimes 32 , 37 and have all shown robust melatonin phase delays when exercise is completed in the evening or overnight.

The mechanism by which exercise induces these phase shifts remains unclear. Nevertheless, the fact that repeated bouts of exercise stimulus were required to induce melatonin phase shifts suggests a zeitgeber effect of exercise was present Specifically, morning exercise results in melatonin secretion phase delays whilst evening exercise-induced phase advances The counter-intuitive phase shifting reported in response to exercise relative to light exposure adds to the notion that exercise per se induced the phase shift rather than light exposure.

Furthermore, the entrainment of the biological clock may occur through exercise-induced changes in AMPK 41 , transcriptional coactivator PGC-1α 42 and the transcription factor HIF-1α 43 activities, all of which have been associated with the molecular clock. Previous work from our group has highlighted the direct effect of exercise on the biological clock in mice 24 with supporting data in humans following both endurance 44 and resistance type exercise Whilst the relationship between exercise and the biological clock is increasingly accepted, whether an optimal time exists to complete exercise remains to be resolved.

Whilst the benefits of exercise for health are beyond the scope of this review, the appreciation of physical activity as a key lifestyle factor for healthy living is well established 46 — Nevertheless, the holistic benefits of exercise and the potential to correct misaligned circadian rhythms in at-risk populations present a unique opportunity to optimise exercise prescription When discussing the impact of timed exercise on circadian clock function and health, it is essential to consider the diurnal variation in exercise capacity Improved exercise capacity coincides with several circadian-controlled biological functions collectively contributing to improved exercise capacity.

Furthermore, systemic hormone and metabolite concentrations show distinct responses to different times of exercise 24 , 52 , 53 , which may contribute to time-specific exercise outcomes 54 , The impact of exercise timing on diurnal exercise performance is a popular strategy for investigating the crosstalk between physical activity and circadian rhythms, with multiple studies utilising this approach 55 — However, it is important to note that a ubiquitous limitation of this literature is the inability to isolate the impact of timed exercise relative to other zeitgebers , such as light exposure or mealtimes.

However, regarding performance differences, several studies have also reported changes in core temperature, with no difference in the circadian oscillation of core temperature between morning and evening exercise groups 60 , Additionally, no change in testosterone or cortisol was observed following 12 weeks of morning or evening exercise 55 , raising the question of why changes in performance occur in the absence of changes in physiological markers of circadian rhythm.

Several studies highlight the interaction between exercise and the circadian system to improve health outcomes. As early as , Van Someren and Colleagues 63 reported that 3 months of routine aerobic exercise, completed 3 times weekly, counteracted age-related fragmentation of the circadian clock, resulting in improved sleep quality in otherwise healthy older men 73 ± 2 years.

Following the intervention, maximal aerobic fitness VO 2max was significantly correlated with lower intraday variability in circadian rhythm, a critical finding given the association between aerobic capacity and all-cause mortality 46 , As well as improving sleep variables in older men, individualised exercise prescription improved sleep in patients with lung cancer compared to non-exercise controls 64 , offsetting dysfunctional rest-activity rhythms pre-intervention Notably, the benefit of prescribed exercise was greatest in individuals with poorer rest-activity rhythms, suggesting that the improvements observed may have had an underlying circadian component.

Human evidence highlighting the impact of exercise timing on health outcomes remains limited, with much of our current appreciation for the role of the circadian clock function and health inferred from animal models and epidemiological studies.

However, recent evidence has provided crucial insight into the potential for timed exercise to improve metabolic health, with afternoon exercise revealing greater efficacy for improving glucose control in type 2 diabetes patients compared to morning-trained participants Further multi-omics, multi-tissue blood plasma, skeletal muscle, and adipose tissue investigations from the same research group revealed significant temporal specificity following morning and evening exercise Specifically, plasma carbohydrates were increased, with a decrease in skeletal muscle lipids following morning exercise, whereas afternoon HIT increased skeletal muscle lipids and mitochondrial protein content to a greater degree than morning training.

Whilst the clinical significance of these findings warrants further investigation, the data presented by these authors support the notion that precisely timed exercise may lead to different exercise outcomes.

Previous literature supports this notion that the timing of exercise, in addition to the quantity, duration, and type of exercise, could be one of the variables for metabolic and physiological responses to exercise 68 , However, understanding how the time of exercise rewires metabolic pathways in skeletal muscle and changes systemic metabolic adaptation remains an outstanding question.

Primarily global metabolite profiling provides a real-time fingerprint of metabolic activity and allows the identification of novel biochemicals unique to exercise timing. These may prove to be crucial diagnostic markers of metabolic disease patients and underpin differing metabolic responses to timed exercise.

Previously, our group performed high-throughput transcriptome and metabolome analyses in mouse skeletal muscle in response to a single-bout treadmill running exercise at different times of the day Significantly, many transcripts and metabolites are intensively changed only upon exercise at the early active phase biological morning rather than the early rest phase biological night , suggesting a substantial impact on skeletal muscle metabolic pathways.

Performing integrative analysis of the transcriptome and metabolome dataset, we revealed that exercise in the morning selectively rewires skeletal muscle energy metabolic pathways, including glycolytic pathways, lipid oxidation, amino acid breakdown, and ketone metabolism.

This skeletal muscle multi-omics study uncovers a functional commitment of exercise timing to determine exercise energy utilisation in skeletal muscle. The molecular circadian clock modulates the exercise timing-dependent metabolic response and exercise capacity In addition, proteomic and phosphoproteomic profiles upon acute exercise at different daily timing also point to differential biological responses in skeletal muscle unique to the exercise timing Proteins involved in energy provision and catabolic pathways are preferentially enriched after morning and evening exercise.

Lastly, skeletal muscle and multiple organ systems dependently and collectively respond to exercise unique to the time of day Our follow-up study investigated global metabolite profiles on 8 different tissues skeletal muscle, liver, heart, white adipose tissues, brown adipose tissue, hypothalamus, and blood collected from mice subjected to an acute treadmill exercise at different times of the day Figure 1A.

This allowed the detection of hundreds of different signalling molecules, of both metabolic and endocrine origin, across multiple tissues and to investigate their change in response to exercise at differing times of the day.

Comparative analyses of cross-tissue metabolite dynamics, as well as an arteriovenous sampling of hindlimb muscle and sampling across the liver, lead to a deeper understanding of time-of-day-specific tissue cross-talk following exercise Figure 1B. Finally, the study identified new exercise-induced signalling molecules exerkines in multiple tissues, which require further investigation to understand how they can individually or collectively influence health.

The most recent study unveiled a comprehensive response of multi-tissue and multi-omics to exercise training at different times of the day in men with type 2 diabetes, revealing coordinated systemic metabolic adaptation to timed exercise Thus, omics resources direct further research that can help us better understand how exercise, if timed correctly, can improve human health.

Figure 1 — Atlas of exercise metabolism unique to the time of day reveals tissue-dependent and collective metabolic responses to timed exercise A Multi-tissue metabolomics upon exercise at the early rest ZT3 versus the early active phase ZT Heatmap displaying metabolites significantly changed only in a specific tissue and only after specific timing of exercise.

B Schematic summary representing time-of-exercise-specificity of types of energy and the specific tissue of origin for energy during exercise. Exercise-induced signalling metabolites so-called exerkines act as stimuli and substrates for cellular energy sensors and signalling molecules and induce adaptive rewiring of signalling pathways and transcriptional networks in response to exercise training Novel investigations by our group have highlighted the impact of time-of-day of exercise on metabolic responses to acute exercise in skeletal muscle 24 , with more recent work providing multi-tissue metabolomic analysis in response to time-of-day specific exercise This work revealed exercise-stimulated signalling molecules capable of transducing metabolic information and mediating circadian reprogramming via energy sensors, AMP-activated protein kinase AMPK , histone modifiers, e.

Alongside mechanisms for circadian reprogramming in response to exercise timing, work from our group highlights several metabolites of interest which have demonstrated capacity for clock modification through metabolic and epigenetic mechanisms.

Whilst these metabolites have shown to be impactful in animal models, the translational applicability to humans remains to be seen. This review has discussed the bimodal impact of exercise timing on the circadian clock, including the realignment of misaligned clocks and the underpinning impact on metabolic regulation and health outcomes.

First, it is essential to consider the population groups of interest within these studies. Secondly, exercise timing may only confer a trivial benefit relative to any exercise. Whilst the timing of exercise may represent a novel strategy for optimising health outcomes and realignment of the circadian clock, it is essential to note that exercise at any time of day is of greater benefit than no exercise.

In population groups who fail to meet daily recommended physical activity targets, the timing of exercise may offer trivial differences compared to exercise at any time. SB and SS wrote the manuscript, prepared the figure, and approved the final version. All authors contributed to the article and approved the submitted version.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Demonstration of a day-night rhythm in human skeletal muscle oxidative capacity. Mol Metab 5 8 — Brown DL, Feskanich D, Sánchez BN, Rexrode KM, Schernhammer ES, Lisabeth LD.

Rotating night shift work and the risk of ischemic stroke. Am J Epidemiol 11 —7. Pan A, Schernhammer ES, Sun Q, Hu FB. Rotating night shift work and risk of type 2 diabetes: Two prospective cohort studies in women. PloS Med 8 12 :e Karlsson B, Knutsson A, Lindahl B. Is there an association between shift work and having a metabolic syndrome?

Results from a population based study of 27, people. Occup Environ Med 58 11 — Hansen AB, Stayner L, Hansen J, Andersen ZJ. Night shift work and incidence of diabetes in the Danish nurse cohort. Occup Environ Med 73 4 —8. Kervezee L, Cuesta M, Cermakian N, Boivin DB.

Simulated night shift work induces circadian misalignment of the human peripheral blood mononuclear cell transcriptome. Proc Natl Acad Sci USA 21 —5. Bescos R, Boden MJ, Jackson ML, Trewin AJ, Marin EC, Levinger I, et al. Four days of simulated shift work reduces insulin sensitivity in humans.

Acta Physiol Oxf 2 :e James FO, Cermakian N, Boivin DB. Circadian rhythms of melatonin, cortisol, and clock gene expression during simulated night shift work. Sleep 30 11 — Hampton SM, Morgan LM, Lawrence N, Anastasiadou T, Norris F, Deacon S, et al. Postprandial hormone and metabolic responses in simulated shift work.

J Endocrinol 2 — Asher G, Sassone-Corsi P. Time for food: The intimate interplay between nutrition, metabolism, and the circadian clock. Cell 1 — Panda S. Circadian physiology of metabolism. Science — A form of high-intensity interval training , metabolic conditioning a.

metcon can help you r ide longer and stronger as you tackle any kind of terrain. Here, we explain what metabolic conditioning is, its benefits for cyclists, and how to work it into your routine.

Plus, try the simple, beginner-friendly and still highly effective metcon workout you can try today. These systems help your body store and use energy efficiently so you can do a lot more in less time. Metcon is focused on short bursts of high-intensity work followed by periods of rest, making it a form of high-intensity interval training.

Some popular forms of metabolic conditioning include Tabatas , EMOMs , and AMRAPs, all of which also count at HIIT workouts.

Metabolic conditioning offers a host of benefits that can level up your riding. Think: ride longer , tackle that hill without getting so winded, and sprint to the finish line at a faster pace.

This is because it makes harder work feel easier. That means longer, steady state rides will feel easier, too.

Moreover, metabolic conditioning will increase your caloric burn during exercise as well as afterwards. One study found that resistance training significantly reduced total and LDL cholesterol and several other markers of metabolic health.

Another study found that resistance training helped increase HDL regardless of intensity, but working out three times a week led to a more significant reduction in LDL. Cardio plus resistance training may be your best bet, as health experts suggest combining the two produces optimal results for cholesterol improvement.

Triglycerides are a type of fat found in the blood. High levels of triglycerides are associated with an increased risk of heart disease.

Exercise, especially aerobic exercise, can help to reduce triglyceride levels, but the effect of strength training on triglyceride levels is less clear. The discrepancy is likely because triglyceride levels are affected by a number of different factors, including diet and genetics.

But weight loss can significantly lower triglycerides, so resistance training may indirectly reduce them by improving body composition. Waist circumference measures the widest part your stomach around your belly button and is a predictor of mortality even when BMI is considered normal. A waist circumference of 35 inches or more in women and 40 inches or more in men is considered high risk.

Exercise can help reduce waist circumference, but strength training proves to be especially effective. One study comparing the effect of aerobic exercise to resistance training found those following the resistance training program saw more significant changes in waist circumference.

Resistance exercise may be more helpful for waist circumference because of its impact on metabolism, insulin sensitivity which we will explore below , and reductions in overall fat mass. Strength training may help lower systolic and diastolic blood pressure by improving blood flow throughout the body and by supporting the structure and function of blood vessels.

One study found that ten weeks of 20 minutes of strength training plus 20 minutes of aerobic exercise led to positive blood pressure changes for people who worked out 2 or 3 sessions a week.

Your health care professional can help determine the right frequency and intensity exercise that is best for you. Resistance training provides impressive benefits for blood sugar balance, primarily by improving insulin sensitivity. Insulin is a hormone that helps to regulate blood sugar levels.

As blood sugar rises, it can increase diabetes risk and make it more challenging to lose weight. Aging is often accompanied by an increased risk of blood sugar dysregulation, so older adults may be able to reduce the impact by adding resistance training to the mix.

Resistance training can lower A1c, a measure of glycemic control, possibly even more than cardiovascular exercise. One study found that a resistance training program that included 3 sets of 7 exercises reduced A1c by 18 percent compared to aerobic training, which lowered A1c by 8 percent for previously inactive adults.

One thing to note: if you use a continuous glucose monitor CGM , you may notice that your blood sugar temporarily rises after exercise. This is a normal, short-term response related to releasing stress hormones during exercise.

Over time, strength training can help to improve blood sugar control. The intensity and duration of resistance training required for metabolic health benefits depend on your current fitness level and any health conditions you may have.

As you get used to this pace, you can being to increase intensity, duration, and frequency. For general metabolic health benefits, 2 to 3 resistance training sessions per week, each lasting at least 20 minutes, appears to be baseline beneficial according to the above research.

But they do! Starting to feel motivated? Here are a few tips to help you get started with or improve your strength training program:. Resistance training can be as hard or as easy as you make it.

You can add more weight, reps, or sets to your workouts. You can also try a different type of strength training, such as circuit or interval training. When in doubt, working with a personal trainer or signing up for group classes at a gym can be a great way to level up your training plan.

Ever felt delayed onset muscle soreness or DOMS after taking some time off? I think we all have Resistance training feels best if you are consistent. Even one extra session a week can make a difference. Slow and steady increases in training frequency and difficulty are the key to success. A personal trainer can be a great asset when starting a new exercise routine.

They can help you learn the correct form for different movements and make sure you are using the proper amount of weight. Adding strength training to your workout routine has many metabolic health benefits, including improved insulin sensitivity, blood sugar control, and lipid levels.

The intensity and duration of your workouts will depend on your current fitness level. For general metabolic health benefits, aim to do at least 2 resistance training sessions per week, each lasting at least 20 minutes.

Nutrition, stress management, and sleep are also important. Still, you can choose to focus on making resistance training a regular habit and then work on other aspects.

She has a background in acute care, integrative wellness, and clinical nutrition. Please note: The Signos team is committed to sharing insightful and actionable health articles that are backed by scientific research, supported by expert reviews, and vetted by experienced health editors.

The Signos blog is not intended to diagnose, treat, cure or prevent any disease. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider. Read more about our editorial process and content philosophy here.

Take control of your health with data-backed insights that inspire sustainable transformation. Your body is speaking; now you can listen. Interested in learning more about metabolic health and weight management?

Copyright © Signos Inc. This product is used to measure and analyze glucose readings for weight loss purposes only. It is not intended to diagnose, cure, mitigate, treat, or prevent pre-diabetes, diabetes, or any disease or condition, nor is it intended to affect the structure or any function of the body.

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