A Ketogenic Diet

https://www.mdpi.com/2218-273X/11/3/402

The potential benefits of the ketogenic diet for exercise performance are thought to be related to the increased availability of ketones, which can provide an alternative fuel source for the body during exercise. Additionally, the ketogenic diet has been shown to reduce inflammation and oxidative stress, which may benefit exercise recovery and reduce the risk of overtraining.

However, there are also potential drawbacks to the ketogenic diet for exercise performance. One major concern is the reduction in carbohydrate availability, which may limit high-intensity exercise performance, particularly during longer-duration activities. Additionally, the ketogenic diet may result in a reduction in muscle glycogen stores, which can also limit exercise performance.

Research on the ketogenic diet and exercise performance is still limited, and much of the existing evidence is limited to animal studies or small-scale human trials. Some studies have reported improvements in endurance exercise performance with the ketogenic diet, while others have found no significant differences compared to a higher-carbohydrate diet.

It is important to note that the effects of the ketogenic diet on exercise performance may be highly individual, depending on factors such as the type and duration of exercise, as well as an individual's baseline diet and metabolic state. Athletes who are considering adopting a ketogenic diet for performance purposes should consult with a qualified nutritionist or sports medicine professional to ensure that the diet is appropriate for their needs and goals.

In summary, while there is some evidence to suggest that the ketogenic diet may have potential benefits for exercise performance, more research is needed to fully understand its effects on various types of exercise and athletic performance. As with any dietary intervention, it is important to weigh the potential benefits and drawbacks and make informed decisions based on individual needs and goals.

References:

1. Burke LM. Re-Examining High-Fat Diets for Sports Performance: Did We Call the 'Nail in the Coffin' Too Soon? Sports Med. 2015 Nov;45 Suppl 1:S33-49. 2. Volek JS, Noakes T, Phinney SD. Rethinking fat as a fuel for endurance exercise. Eur J Sport Sci. 2015;15(1):13-20. 3. McSwiney FT, Wardrop B, Hyde PN, Lafountain RA, Volek JS, Doyle L. Keto-adaptation enhances exercise performance and body composition responses to training in endurance athletes. Metabolism. 2018;81:25-34. 4. Shaw DM, Merien F, Braakhuis A, et al. Effect of a ketogenic diet on submaximal exercise capacity and efficiency in runners. Med Sci Sports Exerc. 2019;51(10):2135-2146. 5. Burke LM, Hawley JA, Wong SHS, Jeukendrup AE. Carbohydrates for training and competition. J Sports Sci. 2011;29 Suppl 1:S17-27.

What is Fat Oxidation in the Muscle?

Fat oxidation is a biological process by which fatty acids are broken down and converted into energy in the form of adenosine triphosphate (ATP). This process occurs predominantly in the mitochondria of muscle cells, where fatty acids are transported and metabolized. The capacity for fat oxidation in the muscle is influenced by factors such as genetics, physical activity level, diet, and overall metabolic health.

Factors Influencing Metabolic Flexibility

Several factors can impact metabolic flexibility, including:

1. Genetics: Genetic factors can influence an individual's inherent capacity for fat oxidation and metabolic flexibility.

2. Diet: Dietary composition, particularly the balance between carbohydrate and fat intake, can affect the body's ability to switch between glucose and fat oxidation.

3. Physical Activity: Aerobic exercise has been shown to enhance metabolic flexibility by increasing the muscle's capacity for fat oxidation and insulin-mediated glucose uptake.

4. Weight Loss: Moderate weight loss combined with improved aerobic fitness has been shown to restore metabolic flexibility in overweight and obese individuals.

Summary of Fuel Metabolism Changes within Skeletal Muscle and Adipose Tissue during Periods of Sleeping, Fasting, Feeding, Rest, and Exercise

The Role of Fat Oxidation in Energy Metabolism

During periods of fasting or prolonged exercise, the body relies on fat oxidation as its primary energy source. This transition to a higher reliance on fat oxidation helps to spare the utilization of plasma glucose and delay the consumption of muscle glycogen, essential adaptations for maintaining energy homeostasis in the body. In healthy individuals, the muscle can efficiently switch between glucose and fat oxidation in response to various physiological conditions.

Insulin Sensitivity and Fat Oxidation

Research has shown that the capacity for fat oxidation in skeletal muscle is related to insulin sensitivity. Insulin is a hormone that helps regulate blood sugar levels by promoting glucose uptake by muscle cells. In individuals with high insulin sensitivity, the muscle demonstrates a higher capacity for fat oxidation. Conversely, impaired fat oxidation in the muscle has been associated with insulin resistance, a condition that can lead to type 2 diabetes and obesity.

The Concept of Metabolic Flexibility

Metabolic flexibility refers to the ability of an organism to efficiently switch between glucose and fat oxidation in response to changes in nutrient availability and energy demands. This trait is crucial for maintaining energy balance and overall metabolic health. Metabolic flexibility is influenced by a variety of factors, including genetics, diet, and physical activity levels.

Metabolic Inflexibility and Insulin Resistance

Individuals with obesity or type 2 diabetes often exhibit metabolic inflexibility, characterized by a reduced ability to switch between glucose and fat oxidation. This inflexibility may contribute to the development of insulin resistance, as impaired fat oxidation can lead to the accumulation of toxic fatty acid metabolites in the muscle, disrupting insulin signaling pathways. As a result, glucose uptake and utilization are impaired, leading to elevated blood sugar levels and, eventually, insulin resistance.

The flexibility of skeletal muscle to switch between oxidizing fat and glucose is related to insulin sensitivity, percentage of body fat, and fitness. Differences in the patterns of glucose and fat oxidation in skeletal muscle during fasting conditions are shown in a lean, aerobically fit individual (A), in whom there is a high reliance upon fat oxidation during fasting conditions, and in an obese, sedentary individual (B), in whom there is less reliance on fat and a greater reliance on glucose oxidation.

Cellular Mechanisms Underlying Fat Oxidation and Metabolic Flexibility

The cellular mechanisms responsible for metabolic flexibility in fat oxidation are not fully understood, but mitochondria are believed to play a crucial role. Mitochondria are the energy-producing powerhouses of the cell and are responsible for both glucose and fat metabolism.

Competition between Glucose and Fat Oxidation

Competition between glucose and fat oxidation can occur at several locations within the mitochondria. One such juncture is the mitochondrial outer membrane, where the relative activities of pyruvate dehydrogenase (PDH) and carnitine palmitoyltransferase (CPT) complexes determine the balance between glucose and fat oxidation. Additionally, competition may occur within the mitochondrial matrix, involving interactions between the β-oxidation and tricarboxylic acid (TCA) cycles and the delivery of FADH2 and NADH to different loci within the electron transport chain.

Mitochondrial Indecision Results in Metabolic Inflexibility

Nutrient Sensing and Signaling Regulate Substrate Selection during Fasting and Feeding

Mitochondrial Dysfunction and Insulin Resistance

Emerging research suggests that mitochondrial dysfunction may contribute to the development of insulin resistance and the reduced capacity for fat oxidation observed in individuals with metabolic inflexibility. Studies have shown that muscle cells from patients with type 2 diabetes exhibit reduced oxidative enzyme activity and impaired mitochondrial metabolism. Further research is needed to elucidate the precise mechanisms by which mitochondrial dysfunction contributes to insulin resistance and metabolic inflexibility.

Nutrient Overload Leads to Mitochondrial Gridlock and Cellular Dysfunction

Aerobic Exercise and Fat Oxidation

Aerobic exercise, such as running or cycling, has been shown to improve fat oxidation capacity in the muscle and enhance metabolic flexibility. Regular aerobic exercise promotes several beneficial adaptations in the muscle, including increased mitochondrial density, improved oxidative enzyme activity, and enhanced insulin sensitivity.

Skeletal muscle adaptations to aerobic and resistance exercise

The Role of Intramyocellular Lipid Content

Intramyocellular lipid (IMCL) content refers to the amount of fat stored within muscle cells. While increased IMCL content has been associated with insulin resistance, research has demonstrated that endurance-trained athletes, who are typically lean and insulin-sensitive, also exhibit relatively high IMCL content. This paradox suggests that the relationship between IMCL content and insulin sensitivity may be more complex than previously thought.

It has been proposed that in endurance-trained athletes, a high content of muscle triglyceride provides a reservoir for high rates of fat oxidation, and that the pool of intramyocellular triglyceride undergoes exercise-induced depletion and postprandial repletion. In contrast, sedentary or overweight individuals may experience slower fractional turnover of triglycerides and a relative impairment in fat oxidation.

Diet and Fat Oxidation

Dietary composition can influence the balance between glucose and fat oxidation in the muscle. Diets high in carbohydrates can promote glucose oxidation, while diets high in fat can increase reliance on fat oxidation. However, it is important to note that excessive fat intake can also contribute to the development of insulin resistance, as elevated plasma fatty acid levels have been shown to impair insulin-stimulated glucose uptake and disposal in the muscle.

Based on J. P. Flatt's theory, the main regulator of lipid oxidation, and hence balance, is carbohydrate availability and oxidation. While an increase in carbohydrate intake leads to an increase in carbohydrate oxidation, an increase in fat intake does not trigger fat oxidation and results in fat storage. By utilizing glycogen stores, exercise increases fat oxidation.

Weight Loss and Metabolic Flexibility

Moderate weight loss combined with improved aerobic fitness has been shown to restore metabolic flexibility in overweight and obese individuals. This improvement in metabolic flexibility is associated with enhanced insulin-stimulated glucose disposal and suppression of fat oxidation during insulin-stimulated conditions. However, weight loss achieved without a concurrent increase in aerobic fitness does not appear to improve the capacity for fat oxidation, highlighting the importance of exercise in promoting metabolic flexibility.

Summary

Fat oxidation in the muscle is a critical factor in energy metabolism and overall metabolic health. The ability of the muscle to efficiently switch between glucose and fat oxidation, known as metabolic flexibility, is essential for maintaining energy balance and preventing the development of insulin resistance.

Aerobic exercise and dietary modifications can enhance metabolic flexibility and improve overall health outcomes. Further research is needed to elucidate the cellular mechanisms underlying these processes and develop novel interventions for individuals with metabolic inflexibility and insulin resistance.

References

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1159159/

2. https://pubmed.ncbi.nlm.nih.gov/28467922/

3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4765362/

4. https://pubmed.ncbi.nlm.nih.gov/28543022/

5. https://pubmed.ncbi.nlm.nih.gov/32963340/

6. https://pubmed.ncbi.nlm.nih.gov/35578962/

The study aimed to determine whether exercise prescribed relative to physiological thresholds results in lower variability in exercise tolerance and physiological responses compared to traditional intensity anchors.

The researchers used critical power (CP) and maximum oxygen uptake (VO2max) as physiological thresholds, and fixed percentages of VO2max or heart rate as traditional intensity anchors.

Physiological thresholds are points during exercise where specific physiological changes occur and can be tested for, for example, lactate thresholds LT1 and LT2.

Blood lactate concentration rises exponentially during graded exercise when muscles produce more lactate than the body can remove, and the blood lactate-related thresholds are parameters based on this curve used to evaluate performance level and help athletes optimize training. Check that out here: https://pubmed.ncbi.nlm.nih.gov/30427900/

Traditional intensity anchors are fixed percentages of VO2max or heart rate that are used to prescribe exercise intensity. For example, exercising at 60% of VO2max or 80% of maximum heart rate, and may be common tools to follow for lots of available training plan.

The study found that prescribing exercise using physiological thresholds reduced the variability in exercise tolerance and acute metabolic responses compared to using traditional intensity anchors. At higher intensities approaching or exceeding the transition from heavy to severe-intensity exercise, the imprecision of using fixed percentages of VO2max as an intensity anchor becomes amplified.

By getting tested to measure your individual physiological thresholds, you can likely plan a more effective training program, while probably improving the effectiveness of exercise interventions themselves. Because we are adaptive organisms, fitness will change all of the time depending on the current environment and lifestyle, and we will probably respond slightly differently, so an off the shelf, one-size-fits-all training plan is unlikely to be well suited to an individual who is gearing more towards a more specific performance goal.

So if you're moderately serious about training towards a goal, getting tested and coached, could go a long way rather than following a textbook off-the-shelf training plan.

Nice one!

Malonyl-CoA is a metabolic intermediate that serves as a fuel sensor for the body. During high energy demand, the levels of malonyl-CoA decrease, allowing the transport of fatty acids into the mitochondria for oxidation, leading to increased energy production. This process is an example of metabolic flexibility, allowing the body to switch between different fuel sources to meet the energy demands of the body.

The utilization of ketone bodies and glucose as primary fuels, the crossover point, malonyl-CoA as the fuel sensor, lactate, and exercise are all important factors that contribute to metabolic flexibility.

In some circles there is a downward pressure on dietary carbohydrate, particularly refined carbohydrate, including from this account, because the carb-rich dietary guidelines and environment are worth questioning in the context of a sedentary general population, and their chronic effects on metabolism - a big topic for another day, and is generally what my thesis is about. So this post is about metabolic flexibility, and generally viewed from a health perspective rather than one for optimal exercise performance.

Carbohydrate habituation is a phenomenon that occurs when the body becomes less responsive to dietary carbohydrates over time. This can happen when an individual consumes a relatively high-carbohydrate diet over a prolonged period, combined with inactivity. Carbohydrate habituation can lead to negative health outcomes, including insulin resistance, impaired glucose metabolism, and a reduced ability to oxidise fat.

Several studies have investigated the impact of carbohydrate habituation on insulin sensitivity. For example, in a study by Volek et al., healthy adults were fed either a low-carbohydrate or high-carbohydrate diet for six days. The high-carbohydrate group showed a significant decrease in insulin sensitivity, while the low-carbohydrate group did not. There are obviously other factors at play - these were not individuals cycling all day with HC climbs in a stage at the TDF.

The mechanism behind carbohydrate habituation is not fully understood, but it is thought to involve changes in insulin receptor signaling and glucose transporter expression. The reduced insulin sensitivity associated with carbohydrate habituation can lead to high blood glucose levels for many people, which can contribute to the development of type 2 diabetes and other metabolic disorders. The fate of dietary glucose is individual, and depends a lot on the sensitivity of muscle to the hormone insulin to oxidise it for energy.

The crossover point

The crossover point describes when the contribution of carbohydrate sources of substrate oxidation supersedes that of fat oxidation. Under most conditions, carbohydrate intake decreases fat oxidation, and visa versa, known as the Randle Cycle. When carbohydrate is consumed, large increases in insulin are seen, which affect the rate of lipolysis, thereby decreasing the availability of fat for oxidation https://pubmed.ncbi.nlm.nih.gov/15212756/.

The crossover point increases the requirement for dietary carbohydrates to meet the energy demands of the body during exercise.

The ability to switch between different fuel sources, including glucose and fatty acids, is crucial for metabolic flexibility in health, and optimal performance during exercise. Dietary carbohydrate manipulation can delay the crossover point toward higher intensities and maximise preservation of endogenous carbohydrate stores.

Recently, it was shown here https://www.frontiersin.org/articles/10.3389/fphys.2023.1150265/abstract

that "adaptation to the LCHF diet shifts the crossover point to a higher %VO2max (>80%VO2max) than previously reported. Second, substantially higher FATMAX values (>1.5g/min) can be measured in athletes adapted to the LCHF diet. Third, endurance athletes exercising at >85%VO2max, whilst performing 6x800m running intervals, measured the highest rates of fat oxidation yet reported in humans. Peak fat oxidation rates measured at 86.4±6.2%VO2max were 1.58±0.33g/min with 30% of subjects achieving >1.85g/min".

The Crossover Point (Adapted from Brooks and Mercier, 1994)

Fuel sources

For simplicity, the two main energy substrates in a healthy individual are fatty acids and carbohydrate sources of energy; glucose and lactate. So a metabolically flexible state exists, when there is a rapid switch between fatty acids and carbohydrates during the transition between a fed and fasting state. Lactate is also a fuel - there are different enantiomers so this refers to the L(-) enantiomer of lactic acid. It is not a binary point, and is individual.

Ketone bodies are produced in the liver and serve as a fuel source for the body. The utilization of ketone bodies as primary fuels is an example of metabolic flexibility, allowing the body to adapt to periods of low glucose availability. The body must balance the utilization of both fuel sources to maintain energy homeostasis.

Regulation of a co-enzyme called malonyl-CoA determines the switch between fatty acid synthesis and oxidation, however malonyl-CoA content does not increase during exercise at 90% VO2 max and does not contribute to the lower rate of fat oxidation in skeletal muscle, maybe because lactate acts as a signaling molecule. https://pubmed.ncbi.nlm.nih.gov/9575949/.

Metabolic Flexibility - glucose, lactic acid, and ketone bodies https://pubmed.ncbi.nlm.nih.gov/22162139/

Carbohydrate and Exercise

It's quite clear from the literature that for optimal exercise performance, especially in the Heavy and Severe domains, dietary carbohydrates and a high-carbohydrate diet are king, and as you go up the performance ladder in terms of athletic ability, to maximise glycogen stores, maintain power, and optimal exercise performance.

There is research showing long-term adaptation to a LCHF diet showing no difference in performance level, however it is often quite individual and perhaps has better application further down the performance spectrum, or in slow, low-intensity events, but do often show improvements in overall metabolic health.

There are great bits of recent research from Tim Podlogar and Gareth Wallis which you can read here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9734239/.

Also from the table below, you can see that if someone is a serious athlete, there is a lot of benefit to having lactate testing to identify zones, (LT1/LT2/MLSS etc.) because like everything in biology, they are not fixed, and change a lot depending on your lifestyle, e.g., with health status, fitness level, diet, and can be tracked to monitor training effectiveness, but it helps to identify optimal nutrition strategies for exercise performance for an individual.

Asker Jeukendrup has done maybe the most work in this area, and you can calculate nutritional requirements for proteins, fats and carbohydrate using stoichiometry formulas and gas exchange.

Summary

Humans have all retained an innate ability to oxidise fat at a high rate, and are 'ketogenic'. However, we can use a range of different fuels depending on energy expenditure. At rest and at low-intensities, fat sources of energy are the predominant fuels. While exercising at higher intensities, glucose and lactate become dominant sources of energy, and for someone who is on a long-term 'ketogenic' diet, they oxidise more fat at higher intensities, delaying the crossover point.

Maintaining good metabolic flexibility is great for long term health, so think of fueling for exercise as being individual - Dr. Dan Plews has a good way of saying it - "Right Fuel, Right Time" https://www.endureiq.com/ and you can get tested to measure your carbohydrate requirements during rest and exercise.

Other References:

1. Volek, J. S., Sharman, M. J., Love, D. M., Avery, N. G., Gomez, A. L., Scheett, T. P., & Kraemer, W. J. (2002). Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism, 51(7), 864-870.

2. Buettner, R., Schölmerich, J., & Bollheimer, L. C. (2007). High-fat diets: modeling the metabolic disorders of human obesity in rodents. Obesity, 15(4), 798-808.

3. McDevitt, R. M., Bott, S. J., Harding, M., Coward, W. A., & Bluck, L. J. (2001). De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. The American journal of clinical nutrition, 74(6), 737-746.

4. Burke, L. M., Angus, D. J., Cox, G. R., Cummings, N. K., Febbraio, M. A., Gawthorn, K., ... & Hargreaves, M. (2000). Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling. Journal of applied physiology, 89(6), 2413-2421.

5. American Diabetes Association. (2019). Standards of medical care in diabetes-2019 abridged for primary care providers. Clinical diabetes, 37(1), 11-34.

The randle cycle, "The glucose-fatty acids cycle" a homeostatic mechanism to control concentrations of glucose and fatty acids. LCFA, long-chain fatty acids;TAG, triacylglycerol; Pyr, pyruvate (Hue and Taegtmeyer, 2009).

The Randle cycle is based on the observation that glucose and fatty acid metabolism are mutually inhibitory. When glucose is abundant, its uptake by cells inhibits the oxidation of fatty acids, whereas when fatty acids are abundant, they inhibit the uptake and oxidation of glucose. This reciprocal relationship is mediated by a number of metabolic and signaling pathways.

Metabolism is like a see-saw

The Randle cycle has been implicated in a number of physiological and pathological processes, including insulin resistance, diabetes, and obesity. Studies have shown that alterations in the Randle cycle can lead to metabolic dysfunction and contribute to the development of these conditions. For example, impaired fatty acid oxidation and increased glucose utilization have been observed in insulin-resistant individuals, suggesting that dysregulation of the Randle cycle may play a role in the pathogenesis of insulin resistance.

Summary

the Randle cycle is a key metabolic pathway that regulates the balance between glucose and fatty acid metabolism in mammals. The reciprocal relationship between these two fuels is mediated by a number of metabolic and signaling pathways, including insulin. Dysregulation of the Randle cycle has been implicated in a number of metabolic disorders and may represent a promising avenue for future development of metabolic therapies.

References:

1. Randle, P. J., Garland, P. B., & Hales, C. N. (1963). The glucose fatty-acid cycle: its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. The Lancet, 281(7285), 785-789.

2. Muoio, D. M., & Newgard, C. B. (2008). Mechanisms of disease: molecular and metabolic mechanisms of insulin resistance and beta-cell failure in type 2 diabetes. Nature Reviews Molecular Cell Biology, 9(3), 193-205.

3. Kim, J. Y., & Hickner, R. C. (2018). The Randle cycle revisited: a new head for an old hat. American Journal of Physiology-Endocrinology and Metabolism, 315(4), E582-E591.

4. Dobbins, R. L., Szczepaniak, L. S., Myhill, J., Tamura, Y., Uchino, H., Giacca, A., & McGarry, J. D. (2002). The composition of dietary fat directly influences glucose-stimulated insulin secretion in rats. Diabetes, 51(7), 1825-1833.

5. van den Brom, Charissa & Bulte, Carolien & Loer, Stephan & Bouwman, R. Arthur & Boer, Christa. (2013). Diabetes, perioperative ischaemia and volatile anaesthetics: Consequences of derangements in myocardial substrate metabolism. Cardiovascular diabetology. 12. 42. 10.1186/1475-2840-12-42.

Macros for a ketogenic diet:

https://www.mdpi.com/2072-6643/9/5/517

The potential benefits of the ketogenic diet for exercise performance are thought to be related to the increased availability of ketones, which can provide an alternative fuel source for the body during exercise, and act as a signaling molecule. Additionally, the ketogenic diet has been shown to reduce inflammation and oxidative stress, which may benefit exercise recovery and reduce the risk of overtraining.

However, there are also potential drawbacks to the ketogenic diet for exercise performance. One major concern is the reduction in carbohydrate availability, which may limit high-intensity exercise performance, particularly during longer-duration activities. Additionally, the ketogenic diet may result in a reduction in muscle glycogen stores, which can also limit high-intensity exercise performance.

Research on the ketogenic diet and exercise performance is not new, but has experienced a revival in recent years. Much of the existing evidence is limited to animal studies or small-scale human trials, generally in sport and exercise science. Some studies have reported improvements in endurance exercise performance with the ketogenic diet, while others have found no significant differences compared to a higher-carbohydrate diet.

Generally, in my view, the use of a ketogenic diet is more suited to ultra-endurance, low-intensity exercise, or rapid fat reduction and improvements in body composition. It's use may also be dependent on athletic ability, as part of a performance spectrum and metabolic health spectrum. For example, individuals racing or lifting high-intensity, world-class performance will have different fueling requirements by comparison to an everyday athlete, who will have different requirements to someone with metabolic disorders such as Type-2 Diabetes.

Therefore, it is important to note that the effects of the ketogenic diet on exercise performance may be highly individual, depending on factors such as the type and duration of exercise, as well as an individual's baseline diet and metabolic state.

Athletes who are considering adopting a ketogenic diet for performance purposes should consult with a qualified nutritionist or sports medicine professional to ensure that the diet is appropriate for their needs and goals.

Summary In summary, while there is some evidence to suggest that the ketogenic diet may have potential benefits for some types of exercise performance, more research is needed to fully understand its effects on various types of exercise and athletic performance. As with any dietary intervention, it is important to weigh the potential benefits and drawbacks and make informed decisions based on individual needs and goals.

References:

1. Burke LM. Re-Examining High-Fat Diets for Sports Performance: Did We Call the 'Nail in the Coffin' Too Soon? Sports Med. 2015 Nov;45 Suppl 1:S33-49. 2. Volek JS, Noakes T, Phinney SD. Rethinking fat as a fuel for endurance exercise. Eur J Sport Sci. 2015;15(1):13-20. 3. McSwiney FT, Wardrop B, Hyde PN, Lafountain RA, Volek JS, Doyle L. Keto-adaptation enhances exercise performance and body composition responses to training in endurance athletes. Metabolism. 2018;81:25-34. 4. Shaw DM, Merien F, Braakhuis A, et al. Effect of a ketogenic diet on submaximal exercise capacity and efficiency in runners. Med Sci Sports Exerc. 2019;51(10):2135-2146. 5. Burke LM, Hawley JA, Wong SHS, Jeukendrup AE. Carbohydrates for training and competition. J Sports Sci. 2011;29 Suppl 1:S17-27.

For endurance exercise, much of the benefit comes from training at low intensities with high volume. While HIT and high intensity exercise has it's place in a well-rounded training program, everyday training for health should incorporate low-intensity, stress-busting exercise.

Zone 1 Training: An Overview

Zone 1 training is a form of aerobic exercise that aims to improve cardiovascular endurance, increase the body's ability to transport and utilize oxygen, and enhance the endurance of the muscles used in physical activity. This type of training is characterized by low-intensity exercise that is performed at a heart rate between 60-70% of maximum. In this article, we will examine the benefits, methods, and best practices for zone 1 training.

All training is good: https://www.mdpi.com/2073-4409/10/10/2639

Benefits of Zone 1 Training

1. Improving Cardiovascular Endurance: Zone 1 training has been shown to improve cardiovascular endurance by increasing the efficiency of the cardiovascular system. This type of exercise stimulates the growth of new blood vessels, which results in improved oxygen delivery to the muscles and a decrease in fatigue. 2. Enhancing the Body's Ability to Utilize Oxygen: Zone 1 training also leads to an increase in the number and size of mitochondria in the muscle cells, which are responsible for producing energy in the form of ATP. The increased number and size of mitochondria means that the body is better able to produce energy, more efficiently, and at a lower intensity. 3. Reducing the Risk of Cardiovascular Disease: By increasing cardiovascular endurance and improving cardiovascular health, zone 1 training can also reduce the risk of cardiovascular disease. Regular aerobic exercise has been shown to lower blood pressure, reduce cholesterol levels, and improve overall cardiovascular function. 4. Minimizing the Risk of Injury: Zone 1 training is less intense than higher-intensity exercise, making it less stressful on the body and reducing the risk of injury. This makes it an ideal form of exercise for individuals who are looking to improve their health and fitness, without putting unnecessary stress on their muscles, bones, and joints.

Three intensity zones defined by physiological determination of the first and second ventilatory turnpoints using ventilatory equivalents for O 2 (VT 1 ) and CO 2 (VT 2).

Methods of Zone 1 Training There are several methods that can be used to perform zone 1 training, including steady-state exercise, interval training, and strength training.

1. Steady-State Exercise: This type of training involves performing low-intensity exercise at a consistent pace for an extended period of time. Examples of steady-state exercise include running, cycling, or swimming. 2. Interval Training: Interval training involves alternating between periods of high-intensity and low-intensity exercise. This type of training can be performed with a variety of exercises, including running, cycling, or swimming. 3. Strength Training: Strength training involves the use of resistance to challenge the muscles and improve muscular strength and endurance. This can be performed with weight lifting, bodyweight exercises, or resistance band exercises.

Best Practices for Zone 1 Training

1. Start Slow: When starting zone 1 training, it is important to start slow and gradually increase the intensity and duration of the exercise over time. This will help the body to adapt to the new demands placed on it and reduce the risk of injury. 2. Monitor Heart Rate: To ensure that you are performing zone 1 training at the correct intensity, it is important to monitor your heart rate using a heart rate monitor or a fitness tracker. This will help you to stay within the recommended heart rate range for zone 1 training. There are several formulas that can be used, but a popular formula can be 220-AGE, multiplied by 0.6 and 0.7. For example, 220-33 = 187. 187 x 0.6 = 112 and 187 x 0.7 = 130. This is an indication that Zone 1 is between 112 and 130 beats per minute. 3. Follow a Structured Training Plan: To get the most out of zone 1 training, it is important to follow a structured training plan that is designed specifically for your individual needs and goals. This may involve a combination of steady-state exercise, interval training, and strength training. 4. Monitor Progress: It is also important to monitor your progress and make adjustments to your training plan as necessary, in order to ensure that you are making progress and meeting your goals.

Training Models and How They Fit The Individual

Read More: https://kids.frontiersin.org/articles/10.3389/frym.2018.00017

Summary

In conclusion, zone 1 training is a form of aerobic exercise that aims to improve cardiovascular endurance, and enhances mitochondrial capacity, size and function, with reduced risk of injury. While simple formula can help identify your zones, it's common that we are all a little bit different, our environment interacts with us all a little bit differently, so testing can refine your zones. This is important across the health and performance spectrum, including training and racing.

Exercise Easy, Train, Repeat #EASYREP

It shows substrate availability in the plasma (blood) either as glucose or long-chain-fatty acids. A dominant hormone involved in regulating glucose homeostasis, is insulin. Carbohydrate has a dominant effect on insulin response, of the three macronutrients: proteins, fats, and carbohydrates. Of these three, carbohydrates are non-essential, due to the process of gluconeogenesis. Elevated insulin inhibits the release of long chain fatty acids into the plasma, inhibiting oxidation.

Indeed, post-prandial hypoglycaemia, in the time after a meal, is most pronounced following ingestion of carbohydrate, leading to a sensation of hunger and stress hormones, due the corresponding insulin response, often stimulating an intake of excess calories, rather than returning to and remaining in the post-prandial state (Chandler-Laney, 2014, Wyatt et al., 2021). Hyperinsulinism in response to ingested nutrients is wide-ranging and individual; it occurs most commonly with refined sugars, grains, and starches (Brand-Miller et al., 2009, Coulston et al., 1983, Galgani et al., 2006, Hertzler and Kim, 2003, Mayer, 1953, Nilsson et al., 2008, Reynolds et al., 2009, Wolever et al., 2006).

The capacity across a population to oxidise carbohydrate in the muscle tissue is wide-ranging, individual, and changes over time, depending on whether the cell is 'insulin resistant', and overall sensitivity to insulin, a signal a bit like a knock at the door.

Insulin Resistance Syndrome

In insulin resistance, the capacity of glucose to be oxidised in the muscle tissue is impaired, leading to a downstream effect of reduced energy production and regulation within the tissue and cell; 'the door', being the cell, is ignoring the signal of insulin, 'the knock'. This can lead to sensations of tiredness and fatigue after mealtimes, particularly after an energetically mixed or 'balanced' meals, containing both carbohydrate and fat together.

It has been suggested that the prevalence of insulin resistance in the general population is driven in part by our evolution (Brand-Miller et al., 2011, Ségurel et al., 2013) due to an extended period of low carbohydrate conditions, in our evolution where there was a near-exclusive reliance on animal products for approximately two million years (Ben-Dor et al., 2021).

Pathological insulin resistance differs from peripheral resistance, and develops in some individuals because of excess carbohydrate rather than total energy intake (Hussein et al., 2009) but the consumption of industrially processed and refined ‘hyper-palatable food’ (Monteiro et al., 2019) containing added sugars, refined flours and industrialised fats compounds the issue of insulin resistance, substantially increasing risk of all-cause mortality (Rauber et al., 2018, Marti, 2019) and certain types of cancer (Fiolet et al., 2018).

Both low carbohydrate intake and high energy expenditure improves insulin sensitivity (Volek et al., 2016) and historically, treatments to restrict CHO on a ‘protein diet’ for Obesity and Type 2 Diabetes were common and with good evidence base, hence the reason for their frequent reappearance in the literature and public view (Bistrian et al., 1977, Yang 1980, Feinman et al., 2015) an approach consistent with our evolution in a low CHO environment (Ben-Dor et al., 2021).

Lipid oxidation

Fritzen et al., 2020 have recently released a paper 'Tuning fatty acid oxidation in skeletal muscle with dietary fat and exercise' and state: both the consumption of a diet rich in fatty acids and exercise training result in similar adaptations in several skeletal muscle proteins. These adaptations are involved in fatty acid uptake and activation within the myocyte, the mitochondrial import of fatty acids and further metabolism of fatty acids by β-oxidation. Fatty acid availability is repeatedly increased postprandially during the day, particularly during high dietary fat intake and also increases during, and after, aerobic exercise.

Lipid and Glucose Oxidative Pathways

What this means is that the body will adjust, often in as little as 3-4 days, to increase the capability of the muscle tissue for lipid oxidation, and that a low-carbohydrate, high-fat diet is complimentary to energetic regulation in the tissue, cell, aerobic activity and exercise.

Further: both the consumption of a diet rich in fatty acids and exercise training result in similar adaptations in several skeletal muscle proteins. These adaptations are involved in fatty acid uptake and activation within the myocyte, the mitochondrial import of fatty acids and further metabolism of fatty acids by β-oxidation. Fatty acid availability is repeatedly increased postprandially during the day, particularly during high dietary fat intake and also increases during, and after, aerobic exercise (Fritzen et al., 2020).

Summarised:

• Both high fat intake and aerobic exercise training increase the abundance and activity of several lipid metabolic proteins in skeletal muscle related to fatty acid uptake, handling and mitochondrial import.

• Mitochondrial biogenesis is induced primarily by aerobic exercise training and not by high fat intake in humans, probably due to increased ATP turnover occurring only during exercise.

• Fatty acid availability seems to be a key signal for adaptations in muscle proteins involved in lipid metabolism as fatty acids act as ligands for peroxisome proliferator-activated receptors and through β-oxidation-driven sirtuin 1 signalling.

• Obesity is characterized by impairments in fatty acid oxidation capacity, but aerobic exercise training is a potent tool to restore such impairments by induction of lipid metabolic proteins in muscle.

• An efficient capacity to handle and oxidize fatty acids, and the ability to adapt fatty acid utilization to fatty acid availability, seem to be of great importance for both lipid and glucose homeostasis and insulin action.

Evolutionary Perspectives:

Prior to the introduction of agriculture, humans were near exclusive carnivores in low carbohydrate conditions for two million years during the Pleistocene Epoch (Ben-Dor et al., 2021) and the inclusion of nutrient-dense animal products provided the energy and nutrition necessary for extensive brain development and growth; development which has since been declining or showing no subsequent increase since the Holocene (Henneberg, 1988).

Easy to dismiss as a fad, simplistic. But, true. Difficult to replicate..

Our genome has not changed significantly since modern humans first emerged from East Africa between 50 – 100ka and we are best adapted for foods consumed then (Eaton, 2007). This is evidenced by a stomach that has adjusted to lower pH levels than obligate carnivores, such as cats (Widdowson, 1985). It is suggested that the strong stomach acidity enabled our survival as a scavenger rather than a forager to increase the tolerance for pathogen exposure (Ben-Dor et al., 2021).

Diets lower in animal products, and higher in plant and carbohydrate content contain anti-nutrients limiting full use by the brain and body for energy (Hervik & Svihus, 2019; Schnorr et al., 2015). Long-term exposure to higher carbohydrate conditions can lead to chronic high plasma fasting and post-prandial glucose levels, promote atrophy of the hippocampus and amygdala, even with blood glucose (BG) values within the normal range and in the absence of diabetes (Cherbuin, 2012).

It should not be surprising however, that some people may be better suited towards vegetarianism and plant-based diets and experience negligeable developmental issues of the brain (Crozier et al., 2019) and that some people may retain insulin sensitivity with dietary CHO and be better adapted toward starch-based diets, given the exposure to agricultural practice after the Pleistocene Epoch and into the Holocene (Ben-Dor et al., 2021). This exposure allows a hypothesis for the subsequent development and appearance of the AMY1 gene for starch digestion, although this is not conclusive (Fernández and Wiley, 2017).

It is clear that a good proportion of the population has higher tolerance to carbohydrate, and experiences no symptoms of insulin resistance across the lifespan. What is applicable to some, however, is not applicable to all, all of the time.

So What?

Research indicates we were scavenger apex predators for a period of nearly two million years, and adaptations to this period remains embedded in modern humans' biology, in the form of genetics, metabolism, and morphology.

Take Home:

The capacity across a population to oxidise carbohydrate in the muscle tissue is wide-ranging, individual, and changes over time. Insulin resistance syndrome manifests itself as glucose intolerance. A low-carbohydrate, higher fat diet is complimentary both to the understanding of energy regulation, evolution and the ability to improve aerobic function.

References:

Ben-Dor, M, Sirtoli, R, Barkai, R. The evolution of the human trophic level during the Pleistocene. Yearbook Phys Anthropol. 2021; 1– 30. https://doi.org/10.1002/ajpa.24247

Bistrian, D. R., Winterer, J., Blackburn, G. L., Young, V., & Sherman, M. (1977). Effect of a protein-sparing diet and brief fast on nitrogen metabolism in mildly obese subjects. The Journal of laboratory and clinical medicine, 89(5), 1030–1035.

Brand-Miller, J. C., Stockmann, K., Atkinson, F., Petocz, P., & Denyer, G. (2009). Glycemic index, postprandial glycemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1,000 foods. The American journal of clinical nutrition, 89(1), 97–105. https://doi.org/10.3945/ajcn.2008.26354

Brand-Miller, J. C., Griffin, H. J., & Colagiuri, S. (2012). The carnivore connection hypothesis: revisited. Journal of obesity, 2012, 258624. https://doi.org/10.1155/2012/258624.

Chandler-Laney, P. C., Morrison, S. A., Goree, L. L., Ellis, A. C., Casazza, K., Desmond, R., & Gower, B. A. (2014). Return of hunger following a relatively high carbohydrate breakfast is associated with earlier recorded glucose peak and nadir. Appetite, 80, 236–241. https://doi.org/10.1016/j.appet.2014.04.031

Coulston, A. M., Liu, G. C., & Reaven, G. M. (1983). Plasma glucose, insulin and lipid responses to high-carbohydrate low-fat diets in normal humans. Metabolism: clinical and experimental, 32(1), 52–56. https://doi.org/10.1016/0026-0495(83)90155-5

FioletT, SrourB, SellemL, Kesse-GuyotE, AllèsB, MéjeanC et al. Consumption of ultra-processed foods and cancer risk: results from NutriNet-Santé prospective cohortBMJ 2018; 360 :k322 doi:10.1136/bmj.k322

Fritzen, A.M., Lundsgaard, AM. & Kiens, B. Tuning fatty acid oxidation in skeletal muscle with dietary fat and exercise. Nat Rev Endocrinol16, 683–696 (2020). https://doi.org/10.1038/s41574-020-0405-1.

Galgani, J., Aguirre, C., & Díaz, E. (2006). Acute effect of meal glycemic index and glycemic load on blood glucose and insulin responses in humans. Nutrition journal, 5, 22. https://doi.org/10.1186/1475-2891-5-22

Hue, L., & Taegtmeyer, H. (2009). The Randle cycle revisited: a new head for an old hat. American journal of physiology. Endocrinology and metabolism, 297(3), E578–E591.

Hennenberg, M. (1988). Decrease of Human Skull Size in the Holocene. Human Biology,60(3), 395-405. Retrieved July 16, 2021, from http://www.jstor.org/stable/41464021

Hertzler, S. R., & Kim, Y. (2003). Glycemic and insulinemic responses to energy bars of differing macronutrient composition in healthy adults. Medical science monitor : international medical journal of experimental and clinical research, 9(2), CR84–CR90.

Mayer, J., Bates, M. W., and Van Itallie, T. B. (1952). Blood sugar and food intake in rats with lesions of anterior hypothalamus. Metabolism. 1:340-348.

Nilsson, A. C., Ostman, E. M., Holst, J. J., & Björck, I. M. (2008). Including indigestible carbohydrates in the evening meal of healthy subjects improves glucose tolerance, lowers inflammatory markers, and increases satiety after a subsequent standardized breakfast. The Journal of nutrition, 138(4), 732–739. https://doi.org/10.1093/jn/138.4.732

Randle PJ, Garland PB, Hales CN, Newsholme EA. (1963). The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet1: 785–789.

Rauber F, da Costa Louzada ML, Steele EM, Millett C, Monteiro CA, Levy RB. Ultra-Processed Food Consumption and Chronic Non-Communicable Diseases-Related Dietary Nutrient Profile in the UK. (2018) Nutrients. 10(5):587.

Reynolds, A., Mann, J., Cummings, J., Winter, N., Mete, E., & Te Morenga, L. (2019). Carbohydrate quality and human health: a series of systematic reviews and meta-analyses. Lancet (London, England), 393(10170), 434–445. https://doi.org/10.1016/S0140-6736(18)31809-9.

Ségurel, L., Austerlitz, F., Toupance, B. et al. Positive selection of protective variants for type 2 diabetes from the Neolithic onward: a case study in Central Asia. Eur J Hum Genet21, 1146–1151 (2013). https://doi.org/10.1038/ejhg.2012.295

Wolever, T. M., Yang, M., Zeng, X. Y., Atkinson, F., & Brand-Miller, J. C. (2006). Food glycemic index, as given in glycemic index tables, is a significant determinant of glycemic responses elicited by composite breakfast meals. The American journal of clinical nutrition, 83(6), 1306–1312. https://doi.org/10.1093/ajcn/83.6.1306

(Widdowson, 1985)

Wyatt P, Berry S, Finlayson G, O’Driscoll R, Hadjigeorgiou G, Drew D, Khatib H, L, Linenberg I, Chan A, Spector T, Pranks P, Wolf J, Blundell J, Valdes A (2021) Nature Metabolism doi.org/10.1038/s42255-021-00383-x

Yang SP, Martin LJ, Schneider G. Weight reduction utilizing a protein-sparing modified fast. (1980). J Am Diet Assoc. Apr;76(4):343-6.

A recreationally active individual typical of the general population engaged in health and fitness, defined as 'participating less than or equal to twice a week in aerobic activity for a total of 80 minutes at moderate intensity' (ACSM, 2006) can make larger performance gains with simple lifestyle interventions that improve underlying metabolic health, by reducing carbohydrate intake to increase fat oxidation rates (Volek et al., 2016). The basis to training for many, should be an individual focus on metabolic health, which drives energy production, to later improve aerobic function, strength, performance, recovery and adherence with improved overall health.

Unless eking out the final performance improvements, for most, expensive equipment is nice, probably not required.

Technology

Training by heart rate became a popular method for training when the heart rate monitor was first developed (Säynäjäkangas, 1977), which has since been superseded as technological developments have allowed increased access to collection of complex physiological performance metrics. These are useful when used appropriately for peak performance at an elite or sub-elite level. However, for most, understanding the physiological processes that occur with activity, and the adaptations to exercise, will mean heart rate training is of greater benefit in the longer term, to reduce injury risk, maintain engagement and improve performance.

Heart Rate Training: Finding Your 'Gears'

Heart rate training is underrated, and, particularly for endurance sports, should be the basis to training. By training to heart rate you can find the underlying aerobic condition of the body for that mode of exercise, and develop it appropriately by using the MAF formula: 180-AGE (Maffetone and Laursen, 2020) most importantly, with the lowest risk of injury and greatest rate of recovery to allow for an increase in volume. Increasing the time at a lower heart rate improves aerobic capacity and mitochondrial function.

Training by heart rate is individual, and tells you more accurately than pace or power metrics, which substrate you are predominantly oxidising for energy. Once these gears, or zones, are identified, you can fuel workouts appropriately, develop the aerobic 'engine' and consider applications of HIIT for performance. Heart Rate Variance can also monitor underlying 'stress' from all areas of life, such as alcohol, illness, injury and disease.

Keep it simple: Train by Feel, Track Heart Rate, Heart Rate Variance (HRV) and Time.

Proprioception: Feel and Focus

This is the ability of the brain to detect the body's position in space, much like an intrinsic awareness system. Proprioception relies on populations of mechanosensory neurons distributed throughout the body, which are collectively referred to as proprioceptors (Tuthill et al., 2018) and was traditionally thought of as a 'muscle sense' for the body to control motor commands. It is a vital aspect of motor control for everyday activities, and when degraded or lost, can have a profound impact on function in diverse clinical populations (Hillier et al., 2015). Proprioception can also be impaired in gradual-onset musculoskeletal pain disorders and following trauma (Clark et al., 2015).

Training by Feel

Being aware of the body and how it responds to physical activity and training can be individual, and this requires proprioception. The great Arnold Schwarzenegger was an advocate of 'putting the brain in the muscle' to recognise muscle failure when bodybuilding. Other techniques can include closing eyes to enhance awareness during a 'stork stand' for balance, and kinesthetic tape following injury. Exercise enhances proprioception and the ability of the body to send messages to the brain. By focusing on developing proprioception rather than a specific pace or time, you can individualise your training.

How it was done for a very long time, in different and harsh environments, for survival.

So what?

If you are currently always training to a fixed performance metric such as pace or power, make a change by tracking heart rate to find your 'gears' you are training in, train those gears for your specific goal. Heart rate variability (HRV) to measure cumulative recovery, and train by time to observe how the body feels.

Take home:

Developing proprioception, or the ability to 'put the brain in the muscle' develops the mind-muscle connection, and improves awareness of one's body in space, important as we age and for injury recovery and prevention, but also for pushing the envelope. This is useful in developing feel, to reduce risk of injury and increase performance.

Check out the great MAF: https://philmaffetone.com/

References

Clark, N. C., Röijezon, U., & Treleaven, J. (2015). Proprioception in musculoskeletal rehabilitation. Part 2: Clinical assessment and intervention. Manual Therapy, 20(3), 378–387.

Hillier, S., Immink, M., & Thewlis, D. (2015). Assessing Proprioception: A Systematic Review of Possibilities. Neurorehabilitation and neural repair, 29(10), 933–949.

Maffetone, P., Laursen, P.B. (2020). Maximum Aerobic Function: Clinical Relevance, Physiological Underpinnings, and Practical Application. Front. Physiol, 11, 296.

Tuthill, J. C., & Azim, E. (2018). Proprioception. Current biology : CB, 28(5), R194–R203.

Volek, J. S., Freidenreich, D. J., Saenz, C., Kunces, L. J., Creighton, B. C., Bartley, J. M., Davitt, P. M., Munoz, C. X., Anderson, J. M., Maresh, C. M., Lee, E. C., Schuenke, M. D., Aerni, G., Kraemer, W. J., & Phinney, S. D. (2016). Metabolic characteristics of keto-adapted ultra-endurance runners. Metabolism: clinical and experimental, 65(3), 100–110.

Whaley, M. H., Brubaker, P. H., Otto, R. M., & Armstrong, L. E. (2006). ACSM's guidelines for exercise testing and prescription. Philadelphia, Pa: Lippincott Williams & Wilkins.

Mitochondrial function is essential to health and performance.

Carbohydrate and fat metabolism

The main function of adipose tissue (body fat) is to provide energy to the body, which is sufficient even for glycolytic-dependent tissues (Cahill, 1970). Adipose tissue is the largest endocrine organ in the body and exerts an impact on whole body metabolism, regulating appetite and fat mass through the hormones Leptin and Adiponectin among others; dysfunctional or ‘overfat’ (Maffetone and Laursen, 2016) adipose tissues are implicated in the development of inflammatory diseases, insulin resistance and cardiometabolic disorders (Coelho, 2013, Maffetone and Laursen, 2016, 2020).

Fight-or-Flight: Stress

Elevated blood glucose, or hyperglycemia, is a response to stress. Mitochondrial dysfunction is attributed to many chronic disease states. With high blood sugar levels, most mitochondrial Acetyl-CoA will be derived from glucose, and after a meal or in a ‘fasted’ state, once blood sugar levels return to normal, Acetyl-CoA is produced via β-oxidation of fatty acids (Alabduladhem and Bordoni, 2021). In the time after a meal, glycogen stores are spared for energy and are not used as the primary source of energy, unless for an acute emergency, such as high-intensity exercise, our in-built fight or flight response (Cahill, 1970).

Metabolic Switch

(Purdom et al., 2018) The crossover concept. The relative decrease in energy derived from lipid (fat) as exercise intensity increases, our fight-or-flight response, corresponds with an increase in carbohydrate (CHO). The crossover point describes when the CHO contribution to substrate oxidation supersedes that of fat. MFO: maximal fat oxidation. Adapted from Brooks and Mercier, 1994.

Maximising MFO:

Strategies to improve fat oxidation rates include training with low carbohydrate stores, modifying carbohydrate intake depending on the session, and training in the heat, which all improve cellular adaptations toward increased oxidation of lipid sources. (Maunder et al., 2021).

What are you burning?

Respiratory quotient (RQ) is a measure of gasses, oxygen and carbon dioxide absorbed and released during respiration. It can measure whether metabolism is predominantly burning fat, the normal resting and low intensity state, or more sugar. Predominantly burning fat throughout the day leads to improved energy levels.

Children are better fat-burners than adults (Kostyak et al., 2007).

So what?

Reducing overall carbohydrate intake in conjunction with an increase in calories from fat can improve fat oxidation rates. This can improve low-intensity, steady state, sustained aerobic performance.

Take home:

Take the test: hand-held respirometers are available to monitor fuel use in the body, whether you are predominantly burning fat or carbohydrate: Lumen: https://www.lumen.com/en-us/home.html.

Healthful carbohydrate metabolism is individual, and changes through lifespan.

Carbohydrate intake for performance is specific to the exercise context.

References:

Alabduladhem T.O., Bordoni B. (2021). Physiology, Krebs Cycle. Feb 7. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.

Cahill GF Jr. (1970). Starvation in man. N Engl J Med. 19;282(12).

Coelho M, Oliveira T, Fernandes R. (2013). Biochemistry of adipose tissue: an endocrine organ. Arch Med Sci. Apr 20;9(2):191-200.

Kostyak JC, Kris-Etherton P, Bagshaw D, DeLany JP, Farrell PA. Relative fat oxidation is higher in children than adults. Nutr J. 2007 Aug 16;6:19. doi: 10.1186/1475-2891-6-19. PMID: 17705825; PMCID: PMC2014754.

Maffetone PB, Rivera-Dominguez I, Laursen PB. Overfat and underfat: new terms and definitions long overdue. Front Public Health. (2016) 4:279.

Maffetone Philip B., Laursen Paul B. (2020). The Perfect Storm: Coronavirus (Covid-19) Pandemic Meets Overfat Pandemic. Frontiers in Public Health 8, 135.

Maunder, E., Plews, D.J., Wallis, G.A., Brick, M.J., Leigh, W.B., Chang, W.-L., Watkins, C.M. and Kilding, A.E. (2021), Temperate performance and metabolic adaptations following endurance training performed under environmental heat stress. Physiol Rep, 9: e14849.

Purdom, T., Kravitz, L., Dokladny, K. et al. Understanding the factors that effect maximal fat oxidation. J Int Soc Sports Nutr 15, 3 (2018). https://doi.org/10.1186/s12970-018-0207-1.

Sugar addiction is a behavioural and physiological response to excessive sugar intake (Avena et al., 2007). Animal data shows dependence to sugar and signs of Dopamine habituation, opioid dependence, when given intermittent access to sugar (Rada et al., 2005). Sugar addiction seems to be characterised by a dependence to the natural endogenous opioids that get released with sugar intake (DiNicolantonio, J.J et al., 2017). These behaviors are then related to neurochemical changes in the brain that also occur with addictive drugs (Avena et al., 2007). In a subset of vulnerable individuals, high-glycemic-index carbohydrates trigger addiction-like neurochemical and behavioral responses (Lennerz, B., Lennerz, J.K, 2017).

Hyperglycemia, or substantial blood glucose rises, have been observed to increase the contractile response in vascular smooth muscle causing vasoconstriction, a stress response, even after typical carbohydrate-rich meals (Jackson et al., 2016). Additionally, hyperglycemia has been observed to bleed the brain and cause intracerebral hemorrhage, in rats and mice (Nieswandt and Stoll, 2011).

Dietary carbohydrate is mostly digested to sugar

Stored fat, not stored carbohydrate, provides energy at rest, and during most activity

There are only two major energy stores in the body: adipose tissue (fat) and muscle tissue. This is in the form of fatty acids and protein. Carbohydrate stores are limited, and are maintained by gluconeogenesis; the making of new sugar. Muscle tissue serves as a starvation reserve, once adipose tissues have been exhausted. Muscle tissue also undergoes a process of constant recycling and remodeling, highlighting the importance of sufficient daily intake. The main function of adipose tissue is to provide energy to the body, which is sufficient even for sugar-dependent tissues (Cahill, 1970).

With high blood sugar levels, most energy will be derived from glucose, and in the post-prandial or ‘fasted’ state, once blood sugar levels return to normal, most energy is produced from fatty acids (Alabduladhem and Bordoni, 2021).

Fight-or-flight, stress response

Glycogen stores are spared for energy and are not used as the primary source of energy, unless for an acute emergency, such as high-intensity exercise, our in-built fight-or-flight mechanism (Cahill, 1970). When we are 'stressed' our liver naturally increases the blood sugar concentration to prepare for high-intensity exercise. Repeated high-intensity exercise efforts can be maintained for exercise performance with carbohydrate intake, and is nuanced.

So what?

Focusing on nutrient-dense foods sourced from complete proteins, is a simple and effective strategy for a healthy diet. Tolerance to carbohydrate-rich foods, while maintaining a high rate of fat oxidation is individual, and can change over time. Refined carbohydrates can have addictive qualities, cause vascular dysfunction and ingestion can simulate the fight-or-flight response.

Take Home:

Take the test: do you crave sugar and rewards shortly after ingestion of sugar-rich foods? If so, take a 7 day no-sugar challenge.

Nutrient-density promotes health and performance

References:

Ahmed SH, et al. Sugar addiction: pushing the drug-sugar analogy to the limit. Curr Opin Clin Nutr Metab Care. 2013;16(4). doi: 10.1097/MCO.0b013e328361c8b8.

Avena NM, et al. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008; 32(1). doi: 10.1016/j.neubiorev.2007.04.019.

DiNicolantonio JJ, O'Keefe JH, Wilson WL. Sugar addiction: is it real? A narrative review. Br J Sports Med. 2018;52(14):910-913. doi:10.1136/bjsports-2017-097971

Hasin DS, et al. DSM-5 Criteria for Substance Use Disorders: Recommendations and Rationale. Am J Psychiatry. 2013; 170(8). doi: 10.1176/appi.ajp.2013.12060782.

Kalon E, et al. Psychological and Neurobiological Correlates of Food Addiction. Int Rev Neurobiol. 2016; 129. doi: 10.1016/bs.irn.2016.06.003.

Kolarzyk E, et al. Assessment of daily nutrition ratios of opiate-dependent persons before and after 4 years of methadone maintenance treatment. Przegl Lek. 2005;62(6).

Lennerz B, Lennerz JK. Food Addiction, High-Glycemic-Index Carbohydrates, and Obesity. Clin Chem. 2018;64(1):64-71. doi:10.1373/clinchem.2017.273532

Lundqvist MH, et al. Is the Brain a Key Player in Glucose Regulation and Development of Type 2 Diabetes? Front Physiol. 2019; 10. doi: 10.3389/fphys.2019.00457.

Lu H, et al. Abstinence from Cocaine and Sucrose Self-Administration Reveals Altered Mesocorticolimbic Circuit Connectivity by Resting State MRI. Brain Connect. 2014; 4(7). doi: 10.1089/brain.2014.0264.

Mysels DJ, Sullivan MA. The relationship between opioid and sugar intake: Review of evidence and clinical applications. J Opioid Manag. 2010; 6(6).

Nieswandt, B., Stoll, G. Sugar rush bleeds the brain. Nat Med17, 161–162 (2011). https://doi.org/10.1038/nm0211-161

Saha TD, et al. Analyses Related to the Development of DSM-5 Criteria for Substance Use Related Disorders: Toward Amphetamine, Cocaine and Prescription Drug Use Disorder Continua Using Item Response Theory. Drug Alcohol Depend. 2012; 122(1-2). doi: 10.1016/j.drugalcdep.2011.09.004.

Veldhuizen MG, et al. Integration of sweet taste and metabolism determines carbohydrate reward. Curr Biol. 2017; 27(16). doi: 10.1016/j.cub.2017.07.018.

Detecting Stress

When the brain detects a perceived threat from the environment, the sympathetic response becomes elevated, resulting in a stress response such as increased breathing rate, increased heart rate and increasing blood glucose output in preparation for the 'fight-or-flight' response. This is a beneficial process to ensure survival. Over time, the brain can become sensitised to stress signals and the response becomes habituated, or to an extent, learned. This can come through exposure and practice, so we don't get overloaded by the same stimulus. However, a dysregulation of the sympathetic system is associated with increased risk of poor hormonal, metabolic and cardiovascular health (Mastorakos et al., 2005). Moderating and keeping the two systems in balance, so we are not always in 'fight-or-flight' mode, is a key skill to develop for health and performance. Regular physical activity of the right kind, and cognitive behavioral techniques like mindfulness and meditation can help keep these systems in balance (Mc Wewen, B.S., 2017).

Stressed

There are many signals in our environment that can contribute to the sympathetic response, such as email notifications, sleep disturbances, drug and alcohol abuse, and overall work-life balance. Stress is cumulative, so if there is a lot going on, that one extra stress might be too much to handle. It is difficult. Particularly if we have disrupted sleep, this can impair the balance and over time, contribute to impaired glucose tolerance, systemic inflammation and increase chronic disease risk.

Training: Needing, Wanting, or Feeling?

Needing to train is very different from wanting to train, which again is different from feeling like training. Add poor sympathetic regulation to the stress of 'needing' to train, especially to a performance metric in competitive session or group, added anxiety and stress to each session will keep the systems out of balance, and substantially increase risk of injury. This could be further compounded by an external or internal pressure to 'perform better' in the next session.

Destressing

Attempting to destress via an exercise that activates the 'fight or flight' response, such as High-Intensity Interval Training, can cause further stress, elevate blood glucose particularly if untrained, and cause hormonal dysfunction. Even in recreationally active individuals 'over reaching', in as little as three weeks, increases in muscle sympathetic activity decreased performance (Coates et al., 2018).

So What?

Across a competitive season, or in life, ignoring the underlying condition of the body is a recipe for poor health and performance in the long term. Stress is cumulative, and by practicing regulating the parasympathetic and sympathetic systems, through techniques such as breathing, and mindset, low-intensity exercise, can help to reduce overall stress, improve blood flow, focus the mind and improve performance in the long term.

Go slow, especially if you're untrained, for better parasympathetic regulation.

Take home: Track Heart Rate Variance (HRV) over time to monitor the balance of the parasympathetic and sympathetic systems. Salivary Cortisol Tests have recently been developed to easily check stress hormones. Know when you're in balance, and when you're not. Training when you are out of balance will reduce health and performance.

Listen to the body, train by feel, and have fun!

References:

1. Coates, A., INCOGNITO, A., SEED, J., DOHERTY, C., MILLAR, P. and BURR, J., 2021. Three Weeks of Overload Training Increases Resting Muscle Sympathetic Activity.

2. G, M., M, P., E, D. and GP, C., 2021. Exercise and the stress system. [online] PubMed. Available at: <https://pubmed.ncbi.nlm.nih.gov/16613809/> [Accessed 3 May 2021].

3. McEwen, B., Nasca, C. and Gray, J., 2021. Stress Effects on Neuronal Structure: Hippocampus, Amygdala, and Prefrontal Cortex.