What is the primary energy source in ultra short-term performances

Running is simple, we put one foot in front of the other, and allow it to happen naturally.

That is how we start, but once we get into running a little more, we want to learn more about how to improve our speed by increasing our step frequency and step length, we want to know which foods will give us the most energy on our runs, and we want to understand which energy systems we use in a 400m sprint.

There are so many questions, and there is so much to learn about running. If you want to be the best runner you can be, these are areas you probably want to start paying attention to.

If you want to increase your running speed, you probably already know that it is actually not your speed holding you back, but your aerobic endurance, and while knowing what to eat before, during, and after each type of training run is very important, I should firstly introduce the physiology of energy metabolism during different levels of exercise.

If you need the aerobic energy system explained, you are in the right place. Today we we break the three energy systems down, so you can learn how you have the energy to sprint as fast as you can, how the anaerobic energy system works, and what the aerobic energy system is.

Each of these play a role in us being able to run faster, so let’s learn more about them:

What is the primary energy source in ultra short-term performances

Why do I need to know about energy metabolism?

Knowing the predominant energy system you are using during your workouts will help you determine your recovery needs for nutrition and rest.

Energy is stored in the body in various forms of carbohydrates, fats, and proteins as well as in the molecule creatine phosphate.

Carbohydrate and fat are the primary sources of energy, with protein contributing a minimal amount under normal conditions.

Adenosine triphospate (ATP) is the body’s usable form of energy. The body uses 3 different systems of metabolism to transfer stored energy to form ATP.

What is the primary energy source in ultra short-term performances

What are the 3 Energy Systems?

The Phosphagen System

The phosphagen system of energy transfer does not require oxygen (anaerobic) and is called upon when there is a sudden increase in energy demand such as starting a workout, starting explosive hill sprints, or throwing a discus.

It is the most direct and quickest form of energy production but can only supply enough energy for a short burst intense activity like a maximum weight lift or a 5 second sprint.

This system relies on the availability of creatine phosphate, which is in limited supply and is depleted quickly.

When creatine phosphate is used up, the body must call on other systems of energy transfer to sustain continued activity.

Glycolysis (anaerobic) System

Another system that doesn’t require oxygen is glycolysis, also known as the lactate system.

This system provides enough ATP to fuel 1 to 3 minutes of intense activity when adequate oxygen isn’t available for aerobic metabolism.

Lactate or lactic acid is something that most runners have heard of and may even fear because of its connection with sore muscles and fatigue.

Hopefully the following explanation of glycolysis will help you picture what is going on.

Glucose is the only fuel that can be used during glycolysis, which literally means the breakdown of glucose.

This breakdown creates ATP as glucose is converted into 2 molecules of pyruvate.

Now:

Hydrogen is also produced during this process and if oxygen is present, the aerobic system (explained next) can use hydrogen and pyruvate to produce more ATP.

However, often times the aerobic system cannot keep up with the excess hydrogen being produced so instead the hydrogen combines with pyruvate to form lactic acid.

Lactic acid then enters the bloodstream and is cleared by the liver.

The point at which the production of lactate is faster than lactate clearance is called the lactate threshold, also referred to as the anaerobic threshold, when lactic acid begins to accumulate in the blood.

The increased acidity of the blood inhibits the use of fatty acids for energy production through aerobic metabolism and thus increases the body’s reliance on carbohydrate and glycolysis.

As blood lactate levels continue to rise and carbohydrate stores become depleted, the muscles begin to fatigue and performance is diminished.

An athlete can increase their lactate threshold through adaptations made during proper endurance training.

This is where my knowledge of the lactate threshold ends and I leave it to the expert coaches to figure out the best way to do that!

I will say though that one of those adaptations is the increasing the efficiency of the aerobic system.

The Aerobic System

The aerobic system can use carbohydrates, fats, or proteins to produce energy.

Energy production is slower, but more efficient than the other two systems.

As you can tell by the name, the aerobic system requires that there be adequate oxygen available to the working muscles.

Therefore this system is used more heavily during low-intensity activity, but actually, most of our races, even a 5k mostly use the aerobic system.

One key highlight of aerobic metabolism is the ability to burn fat as fuel.

Our bodies have a seemingly unlimited capacity for storing fat and fat provides over twice as much energy per gram than protein or carbohydrate, making it a very attractive choice for energy production.

In prolonged activities where intensity is low, the body will use fat as a main energy source and spare the use of muscle glycogen and blood glucose so that it is available for use if exercise intensity increases and oxygen availability is decreased.

Keep in mind that aerobic metabolism doesn’t use one substrate exclusively.

Although you may be burning mostly fat, a steady supply of carbohydrate is still necessary for the breakdown of fat into an energy source.

What’s the bottom line?

Just like the aerobic system isn’t exclusive to one substrate, energy metabolism isn’t exclusive to one system.

All 3 systems are working simultaneously to fuel the body during exercise.

Remember this:

However, certain characteristics such as exercise duration and intensity will determine the predominate system and thus how long the activity can be performed at that level.

Other factors that influence what substrates and systems are being used include the fuels that are available, the fitness level of the athlete, and the nutritional status of the athlete.

These factors may change over time and through training so just like overall nutrition, energy metabolism is very individualized and dynamic.

What Should I Eat Before Running Workouts?

If you are still wondering about eating before a run or workout, make sure you go back and read more about when you should and should not eat before.

One big reason for having adequate fuel before a workout, as well as on a daily basis, is to prevent the use of protein as a fuel source.

Protein is usually spared from being used as an energy source and is used predominately by the body for tissue maintenance, growth, and repair.

However, when glycogen stores are depleted, amino acids from muscle protein can be used to produce glucose.

As we learned before, glycogen stores can be depleted through intense and prolonged exercise, a chronic low carbohydrate diet, or an overall low-energy diet that cannot keep up with the body’s demands.

This is important:

If the body consistently relies on protein for fuel, muscle protein stores will begin to decrease along with lean body mass, which can be detrimental to performance.

This highlights the importance of fully replenishing glycogen stores after intense workouts, as well as on a daily basis.

1. Glaister M. Multiple sprint work: physiological responses, mechanisms of fatigue and the influence of aerobic fitness. Sports Medicine. 2005;35(9):757–777. [PubMed] [Google Scholar]

2. Spriet LL. Anaerobic metabolism in human skeletal muscle during short-term, intense activity. Canadian Journal of Physiology and Pharmacology. 1992;70(1):157–165. [PubMed] [Google Scholar]

3. Bigland-Ritchie B, Woods JJ. Changes in muscle contractile properties and neural control during human muscular fatigue. Muscle and Nerve. 1984;7(9):691–699. [PubMed] [Google Scholar]

4. Søgaard K, Gandevia SC, Todd G, Petersen NT, Taylor JL. The effect of sustained low-intensity contractions on supraspinal fatigue in human elbow flexor muscles. Journal of Physiology. 2006;573(2):511–523. [PMC free article] [PubMed] [Google Scholar]

5. Bogdanis GC, Nevill ME, Boobis LH, Lakomy HKA, Nevill AM. Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man. Journal of Physiology. 1995;482(2):467–480. [PMC free article] [PubMed] [Google Scholar]

6. Bogdanis GC, Nevill ME, Boobis LH, Lakomy HKA. Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise. Journal of Applied Physiology. 1996;80(3):876–884. [PubMed] [Google Scholar]

7. Bogdanis GC, Nevill ME, Lakomy HKA, Boobis LH. Power output and muscle metabolism during and following recovery from 10 and 20 s of maximal sprint exercise in humans. Acta Physiologica Scandinavica. 1998;163(3):261–272. [PubMed] [Google Scholar]

8. Jacobs I, Bar Or O, Karlsson J, et al. Changes in muscle metabolites in females with 30-s exhaustive exercise. Medicine and Science in Sports and Exercise. 1982;14(6):457–460. [PubMed] [Google Scholar]

9. Vollestad NK, Sejersted OM. Biochemical correlates of fatigue. A brief review. European Journal of Applied Physiology and Occupational Physiology. 1988;57(3):336–347. [PubMed] [Google Scholar]

10. Atkinson DE. Cellular Energy Metabolism and Its Regulation. 1st edition. New York, NY, USA: Academic Press; 1977. [Google Scholar]

11. Norman B, Glenmark B, Jansson E. Muscle AMP deaminase deficiency in 2% of a healthy population. Muscle and Nerve. 1995;18(2):239–241. [PubMed] [Google Scholar]

12. Norman B, Sabina RL, Jansson E. Regulation of skeletal muscle ATP catabolism by AMPD1 genotype during sprint exercise in asymptomatic subjects. Journal of Applied Physiology. 2001;91(1):258–264. [PubMed] [Google Scholar]

13. Verzijl HTFM, Van Engelen BGM, Luyten JAFM, et al. Genetic characteristics of myoadenylate deaminase deficiency. Annals of Neurology. 1998;44(1):140–143. [PubMed] [Google Scholar]

14. Fischer H, Esbjörnsson M, Sabina RL, Strömberg A, Peyrard-Janvid M, Norman B. AMP deaminase deficiency is associated with lower sprint cycling performance in healthy subjects. Journal of Applied Physiology. 2007;103(1):315–322. [PubMed] [Google Scholar]

15. Bassini-Cameron A, Monteiro A, Gomes A, Werneck-de-Castro JPS, Cameron L. Glutamine protects against increases in blood ammonia in football players in an exercise intensity-dependent way. British Journal of Sports Medicine. 2008;42(4):260–266. [PubMed] [Google Scholar]

16. Casas H, Murtra B, Casas M, et al. Increased blood ammonia in hypoxia during exercise in humans. Journal of Physiology and Biochemistry. 2001;57(4):303–312. [PubMed] [Google Scholar]

17. Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York, NY, USA: W. H. Freeman; 2002. [Google Scholar]

18. Medbø JI, Burgers S. Effect of training on the anaerobic capacity. Medicine and Science in Sports and Exercise. 1990;22(4):501–507. [PubMed] [Google Scholar]

19. Kemp GJ, Roussel M, Bendahan D, Le Fur Y, Cozzone PJ. Interrelations of ATP synthesis and proton handling in ischaemically exercising human forearm muscle studied by 31P magnetic resonance spectroscopy. Journal of Physiology. 2001;535(3):901–928. [PMC free article] [PubMed] [Google Scholar]

20. Casey A, Constantin-Teodosiu D, Howell S, Hultman E, Greenhaff PL. Metabolic response of type I and II muscle fibers during repeated bouts of maximal exercise in humans. American Journal of Physiology. 1996;271(1):E38–E43. [PubMed] [Google Scholar]

21. Åstrand PO, Rodahl K. Textbook of Work Physiology. 3rd edition. New York, NY, USA: McGraw-Hill; 1986. [Google Scholar]

22. Greenhaff PL, Nevill ME, Soderlund K, et al. The metabolic responses of human type I and II muscle fibres during maximal treadmill sprinting. Journal of Physiology. 1994;478(1):149–155. [PMC free article] [PubMed] [Google Scholar]

23. Greenhaff PL, Timmons JA. Interaction between aerobic and anaerobic metabolism during intense muscle contraction. Exercise and Sport Sciences Reviews. 1998;26:1–36. [PubMed] [Google Scholar]

24. Maughan RJ, Gleeson M, Greenhaff PL. Biochemistry of Exercise and Training. New York, NY, USA: Oxford University Press; 1997. [Google Scholar]

25. Sahlin K, Harris RC, Hultman E. Resynthesis of creatine phosphate in human muscle after exercise in relation to intramuscular pH and availability of oxygen. Scandinavian Journal of Clinical and Laboratory Investigation. 1979;39(6):551–558. [PubMed] [Google Scholar]

26. Withers RT, Sherman WM, Clark DG, et al. Muscle metabolism during 30, 60 and 90 s of maximal cycling on an air-braked ergometer. European Journal of Applied Physiology and Occupational Physiology. 1991;63(5):354–362. [PubMed] [Google Scholar]

27. Walter G, Vandenborne K, McCully KK, Leigh JS. Noninvasive measurement of phosphocreatine recovery kinetics in single human muscles. American Journal of Physiology. 1997;272(2):C525–C534. [PubMed] [Google Scholar]

28. Siegler JC, Bell-Wilson J, Mermier C, Faria E, Robergs RA. Active and passive recovery and acid-base kinetics following multiple bouts of intense exercise to exhaustion. International Journal of Sport Nutrition and Exercise Metabolism. 2006;16(1):92–107. [PubMed] [Google Scholar]

29. McMahon S, Jenkins D. Factors affecting the rate of phosphocreatine resynthesis following intense exercise. Sports Medicine. 2002;32(12):761–784. [PubMed] [Google Scholar]

30. Harris RC, Edwards RHT, Hultman E. The time course of phosphorylcreatine resynthesis during recovery of the quadriceps muscle in man. Pflugers Archiv European Journal of Physiology. 1976;367(2):137–142. [PubMed] [Google Scholar]

31. Forbes SC, Paganini AT, Slade JM, Towse TF, Meyer RA. Phosphocreatine recovery kinetics following low- and high-intensity exercise in human triceps surae and rat posterior hindlimb muscles. American Journal of Physiology. 2009;296(1):R161–R170. [PMC free article] [PubMed] [Google Scholar]

32. Newcomer BR, Boska MD, Hetherington HP. Non-P(i) buffer capacity and initial phosphocreatine breakdown and resynthesis kinetics of human gastrocnemius/soleus muscle groups using 0.5 s time-resolved 31P MRS at 4.1 T. NMR in Biomedicine. 1999;12(8):545–551. [PubMed] [Google Scholar]

33. Quistorff B, Johansen L, Sahlin K. Absence of phosphocreatine resynthesis in human calf muscle during ischaemic recovery. Biochemical Journal. 1992;291(3):681–686. [PMC free article] [PubMed] [Google Scholar]

34. Taylor DJ, Bore PJ, Styles P. Bioenergetics of intact human muscle. A 31P nuclear magnetic resonance study. Molecular Biology and Medicine. 1983;1(1):77–94. [PubMed] [Google Scholar]

35. Crowther GJ, Kemper WF, Carey MF, Conley KE. Control of glycolysis in contracting skeletal muscle. II. Turning it off. American Journal of Physiology. 2002;282(1):E74–E79. [PubMed] [Google Scholar]

36. Pilegaard H, Domino K, Noland T, et al. Effect of high-intensity exercise training on lactate/H+ transport capacity in human skeletal muscle. American Journal of Physiology. 1999;276(2):E255–E261. [PubMed] [Google Scholar]

37. Jones NL, McCartney N, Graham T, et al. Muscle performance and metabolism in maximal isokinetic cycling at slow and fast speeds. Journal of Applied Physiology. 1985;59(1):132–136. [PubMed] [Google Scholar]

38. Jones NL, McCartney N. Influence of muscle power on aerobic performance and the effects of training. Acta Medica Scandinavica. 1986;220(711):115–122. [PubMed] [Google Scholar]

39. Beneke R, Pollmann C, Bleif I, Leithäuser RM, Hütler H. How anaerobic is the wingate anaerobic test for humans? European Journal of Applied Physiology. 2002;87(4-5):388–392. [PubMed] [Google Scholar]

40. Ren J-M, Hultman E. Regulation of glycogenolysis in human skeletal muscle. Journal of Applied Physiology. 1989;67(6):2243–2248. [PubMed] [Google Scholar]

41. Serresse O, Lortie G, Bouchard C, Boulay MR. Estimation of the contribution of the various energy systems during maximal work of short duration. International Journal of Sports Medicine. 1988;9(6):456–460. [PubMed] [Google Scholar]

42. Smith JC, Hill DW. Contribution of energy systems during a Wingate power test. British Journal of Sports Medicine. 1991;25(4):196–199. [PMC free article] [PubMed] [Google Scholar]

43. Van Someron K. The physiology of anaerobic training. In: Whyte G, editor. The Physiology of Training. Oxford, UK: Elsevier; 2006. pp. 85–115. [Google Scholar]

44. Medbø JI, Tabata I. Relative importance of aerobic and anaerobic energy release during short-lasting exhausting bicycle exercise. Journal of Applied Physiology. 1989;67(5):1881–1886. [PubMed] [Google Scholar]

45. Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology. 2004;287(3):R502–R516. [PubMed] [Google Scholar]

46. Balsom PD, Gaitanos GC, Ekblom B, Sjodin B. Reduced oxygen availability during high intensity intermittent exercise impairs performance. Acta Physiologica Scandinavica. 1994;152(3):279–285. [PubMed] [Google Scholar]

47. Gladden LB. Lactate metabolism: a new paradigm for the third millennium. Journal of Physiology. 2004;558(1):5–30. [PMC free article] [PubMed] [Google Scholar]

48. Fletcher WM, Hopkins FG. Lactic acid in amphibian muscle. The Journal of Physiology. 1907;35:247–309. [PMC free article] [PubMed] [Google Scholar]

49. Hill AV, Lupton H. Muscular exercise, lactic acid and the supply and utilization of oxygen. The Quarterly Journal of Medicine. 1923;16:135–171. [Google Scholar]

50. Margaria R, Edwards HT, Dill DB. The possible mechanism of contracting and paying the oxygen debt and the role of lactic acid in muscular contraction. American Journal of Physiology. 1933;106:689–714. [Google Scholar]

51. Hermansen L. Human Muscle Fatigue: Physiological Mechanisms. London, UK: Pittman Medical; 1981. Glycolitic and oxidative energy metabolism and contraction characteristics of intact human muscle; pp. 75–88. (Ciba Found Symposium, no. 82). [Google Scholar]

52. Gevers W. Generation of protons by metabolic processes other than glycolysis in muscle cells: a critical view. Journal of Molecular and Cellular Cardiology. 1979;11(3):325–330. [PubMed] [Google Scholar]

53. Robergs RA. Exercise-induced metabolic acidosis: where do the protons come from? Sportscience. 2001;5(2) [Google Scholar]


Page 2

What is the primary energy source in ultra short-term performances

Stack plots of the change in (a) ATP turnover and key phosphagen system metabolites during 3 minutes of intense exercise to volitional exhaustion. (b) Creatine phosphate, (c) inorganic phosphate, and (d) ATP.  Note the well maintained preservation of muscle ATP for most of the duration of the exercise bout.

  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances
  • What is the primary energy source in ultra short-term performances

Click on the image to see a larger version.