The Metabolic Energy Systems for Exercise

The metabolic pathways in the human body are intertwined and efficiently breakdown substrates to produce fuel for energy demands.  The three predominant fuel systems are ATP-phosphocreatine, glycolytic, and oxidative.  Each system differs in reaction rate, duration, complexity, oxygen and substrate utilization.  The interrelated metabolism of fat and carbohydrate is dependent upon these fuel systems and these pathways are impacted by exercise intensity and duration (Meksawana, Pendergast, Vladutiuc, & Awada, 2005). 

The simplest fuel system, ATP-phosphocreatine (ATP-PCr), uses phosphocreatine (PCr) to produce powerful and quick energy at very high intensity (Pendergast, Meksawan, Limprasertkul, & Fisher, 2011).   The one step reaction anaerobically splits high-energy phosphates in the muscle to rapidly release energy in the form of adenosine diphosphate (ATP).  The ratio of split PCr is directly related to power output and oxygen deficit (Francescato, Cettolo, & Prampero, 2003).  When workload exceeds the oxygen uptake capacity, then oxygen deficit increases throughout the body and accumulated oxygen deficit (ACOD) can be used to estimate anaerobic energy contribution (Duffield, Dawson, & Goodman, 2005).  The system is limited by PCr supply ranging from 17.8-37.7 mmol/kg, and within only a few seconds (>10 seconds) it is exhausted (Francescato et al., 2003).  Other fueling systems are needed to supplement the high intensity energy demands near maximal capacity.

During slightly longer durations, the glycolytic system utilizes carbohydrates (glycogen and glucose) to provide fuel.  The more complex system provides fast fuel for moderate to high exercise intensities and the rate of glycolysis increases with workload (Kobayashi & Neely, 1979).  ATP-PCr, anaerobic, and aerobic systems overlap to sustain exercise demands that range from 40-s to 2-mins; events such as the 400 m and 800 m sprint fall within this category (Duffield, Dawson, & Goodman, 2005).    Initially in glycolysis, glucose is converted to pyruvate through a series of enzymatic reactions and depending on oxygen availability the pathways splits either aerobically or anaerobically (Kobayashi & Neely, 1979).  In aerobic glycolysis, oxidation occurs in the mitochondria and produces energy (ATP) through the electron transfer in the respiratory chain (Meksawana et al., 2005).  In contrast, without oxygen, pyruvate rapidly converts to lactate at a faster rate (Beneke et al., 2000).  To counter balance the production of this anaerobic byproduct, lactate is shuttled throughout the body to become oxidized (Coso et al., 2010; Kobayashi & Neely, 1979).  The oxidative shuttling mechanism occurs at a lower intensity with increased blood flow to tissues; this in turn restores the pH, buffers hydrogen ions, and reduces lactate concentrations.  However, when the creation of lactate and pyruvate exceeds the rate of oxidation, lactic acid accumulation occurs in the muscles and blood.  The acidic muscle environment has been linked to impaired enzymatic reactions, exhaustion of skeletal muscle contraction, and reductions in force contractility (Coso et al., 2010; Beneke et al., 2000). 

Thirdly, the oxidative system provides fuel during aerobic exercises at low to moderate intensity.  Since this reaction is slow and multifaceted, it does not provide immediate energy.  It oxidizes fuel within the mitochondria matrix to produce energy for prolonged durations (Meksawana et al., 2005).  During heavy aerobic exercise, glycogen stores are supplemented and the rate of fatigue is directly impacted by glycogen depletion.  Highly trained endurance athletes have lower respiratory exchange ratios (RER) and reduced glucose metabolism compared to fat oxidation, which delays glycogen depletion.  This in turn, blunts the increase of catecholamines and glucagon and increases insulin concentrations at a given workload (Meksawana et al., 2005; Beneke et al., 2000).    

Overall, these three systems vary depending on exercise intensity and are limited by the accumulation of different byproducts and the depletion of specific energy stores.  During high intensity exercise, the rate of fatigue has been linked to lactic acid accumulation, PCr concentrations, and detrimental decreases in the pH that accompanies glycolysis and inhibits fat oxidation (Coggan, 1997; Beneke et al., 2000).  While prolong aerobic exercises are hindered by stored energy and depletion of glycogen (Beneke et al., 2000; Meksawana et al., 2005).   After strenuous bouts of exercise, glycogen stores need up to three days to restore concentrations and carbohydrate fueling promotes resynthesis (Beneke et al., 2000).  According to a study by Howarth et al., the combination of carbohydrate (1.2 carbohydrate kg/h)  and protein (0.4 g protein kg/h) ingestion has shown to reduce the rate of protein breakdown and enhance glycogen recovery, carbohydrate alone (2009).

Fats and carbohydrates are broken down with oxygen to release energy (ATP) and these substrates shift depending on exercise.  The contribution of fat and carbohydrate oxidation during exercise can be estimated from the VO₂ and respiratory exchange ratio (RER).  As workload increases, it requires more oxygen consumption to support higher energy demands of skeletal muscles; therefore RER and VO₂ are linearly related (Pendergast et al., 2011; Beneke et al., 2000).  At maximal exercise capacity (VO₂max), oxygen is used to support working muscles and the sole contributor for fuel is readily available carbohydrate; RER is about 1.0 (Pendergast et al., 2011).  In contrast, during aerobic and low intensity exercise, more oxygen is available to breakdown fat via B-oxidation within the mitochondria (Meksawana et al., 2005).  Fat oxidation provides almost two times the amount of energy per gram compared to carbohydrate. As oxygen consumption increases due to higher exercise intensity, RER and carbohydrate oxidation rises (Pendergast et al., 2011; Meksawana et al., 2005).

Training adaptations impact the substrate balance, through lipolysis, glycolysis, and gluconeogenesis, which ultimately impacts performance (Beneke et al., 2000).  Since substrate utilization varies, untrained individuals have been linked to faster fatigue rates due to deplenished glycogen caused by carbohydrate breakdown.   While, in trained individuals, reduced RER during heavy exercise is related to slower glycogen decline, reduced glucose production, and decreases in glucose transporters.  This is linked to an increase in mitochondria size, number, and enzyme activity, which improves oxidative capacity and mobilization of fuels.  Other training adaptations that control metabolism and enhance performance include: improvements in capillary density and increases in proteins at the membrane that bind to free fatty acids (Meksawana et al., 2005). 

Overall, these three energy systems are used during exercise to efficiently sustain different exercise intensities and rates of energy demands.  Major byproducts and limiting factors released during these reactions impact performance and duration of exercise.  The oxidation of carbohydrates and fats are balanced within these systems and training adaptations improves mobilization and fueling for performance.  These macronutrients are oxidized to both provide sustained and slow energy, or quick, powerful fuel anaerobically.  The breakdown of these substrates depends on the availability of concentrations, oxidative capacity, and rate of energy demands. 

References

Beneke, R., Hutler, M., & Leithauser, R. (2000). Maximal lactate-steady-state

independent of performance. Medicine and Science in Sports and Exercise , 32, 1135-1139.

Coggan, A. (1997). Plasma glucose metabolism during exercise. MSSE , 29, 620-627.

Coso, J., Hamouti, N., Aguado-Jimenez, R., & Mora-Rodriguez, R. (2010). Restoration

of blood pH between repeated bouts of high-intensity exercise: effects of various

active-recovery protocols. Eur J Appl Physiol , 108, 523-532.

Duffield, R., Dawson, B., & Goodman, C. (2005). Energy system contribution to 400-

metre and 800-metre track running. Journal of Sports Sciences , 23, 299-307.

Francescato, M., Cettolo, V., & Prampero, P. (2003, 445). Relationships between

mechanical power, O2 consumption, O2 deficit and high-energy phosphates

during calf exercise in humans. Eur J Physiol , 622-628.

Howarth, K., Moreau, N., Phillips, S., & Gibala, M. (2009). Coingestion of protein with

carbohydrates during recovery from endurance exercise stimulates skeletal muscle protein synthesis in humans. Journal of Appl Physiology , 106, 1394-1402.

Kobayashi, K., & Neely, J. (1979). Control of Maximum Rates of Glycolysis in Rat

Cardiac Muscle. Circ Res , 44, 166-176.

Meksawana, K., Pendergast, D., Vladutiuc, G., & Awada, A. (2005). Effect of dietary fat

intake on total body and white blood cell fat oxidation in exercised sedentary

subjects. Nutrition Research , 25, 225-237.

Pendergast, D., Meksawan, K., Limprasertkul, A., & Fisher, N. (2011). Influence of

exercise on nutritional requirements. Eur J Appl Physiology , 111, 379-390.