Lactate as an End-Product and Fuel

Laktat als Endprodukt und Brennstoff


During high intensity short duration exercise, lactate (LA) accumulates at high concentrations ([LA]) because the contribution of anaerobic glycolysis to the ATP yield is large and LA clearance is much higher than LA production. Hydrolysis of glycolytic ATP releases H+ which reduces muscle and arterial pH but in this type of exercise, higher [LA] is associated with better performances. For longer exercises at lower intensity the contribution of anaerobic metabolism to ATP yield is low but [LA] also increases and, for a given workload, is higher when O2 availability and/or delivery is low and/or mitochondrial ATP production is impaired, and it has  been  suggested  that  LA  accumulation  during  prolonged  exercise  reflects  a deficit in aerobic ATP, and production of anaerobic ATP. An alternate explanation is that [LA] reflects the magnitude of homeostasis disturbances which translate into  “error  signals”  for  the  stimulation  of  mitochondrial  respiration:  increase  in redox potential and reduction in phosphate potential.This hypothesis is consistent with the observation that lower [LA] (hence smaller homeostasis disturbances) is associated with better endurance performances (although LA per se probably doesh not contribute to fatigue). LA produced in some working muscles during prolonged exercise, is released into the blood and taken up to be oxidized in other working muscles and/or other organs and tissues (lactate shuttle), thus sustaining aerobic metabolism. A portion can also be converted into glucose in the liver (Cori cycle) to sustain plasma glucose concentration. A great deal of attention has been paid  to  the  relationship  between  [LA]  and  power  output  during  ramp  exercise, and a lot of effort and ingenuity have been invested to identify anaerobic and/or lactate thresholds which remain elusive and putative.

Key words: lactate, aerobic metabolism, anaerobic metabolism, lactate shuttle, lactate threshold.


Bei hochintensiven Kurzzeitbelastungen ist der Anteil der anaeroben Glykolyse an der ATP-Gewinnung hoch und es wird mehr Laktat gebildet als eliminiert werden kann. Dementsprechend akkumuliert Laktat und die Konzentrationen steigt an.Bei der Hydrolyse des glykolytisch gewonnen ATPs wird H+ freigesetzt, das den muskulären und arteriellen pH-Wert senkt. Für diese Art von kurzzeitigen Belastungen sind höhere Laktatwerte mit größerer Leistungsfabgabe verbunden.
Bei längeren Belastungen niedrigerer Intensität ist der Beitrag des aneroben Metabolismus zur ATP-Gewinnung niedrig aber dennoch wird Laktat gebildet.
Bei  einer  bestimmten  Belastungsintensität  kann  die  Laktatkonzentration  höher  sein  wenn  die  Sauerstoffverfügbarkeit  oder  –zufuhr  niedrig  oder  und/oder die mitochondriale ATP Produktion beeinträchtigt sind. Es wird vermutet, dass die  Laktat-Akkumulation  bei  Langzeitausdauerbelastungen  ein  Defizit  in  der aeroben  und  anaeroben  ATP-Produktion  reflektiert.  Eine  alternative  Erklärung besteht  darin,  dass  die  Laktatkonzentration  das  Ausmaß  der  Störung  der  Homöostase  widerspiegelt,  welche  wiederum  zu  Fehlermeldungen  bei  der  Stimulation  der  mitochondrialen  Atmungskette  führt:  Anstieg  des  Redox-Potentials und Rückgang des Phosphat-Potentials. Diese Hypothese stimmt mit der Beobachtung  überein,  dass  geringere  Laktatkonzentrationen,  und  damit  Störungen geringeren Ausmaßes, mit einer höheren Ausdauerleistungsfähigkeit verbunden sind (auch wenn Laktat an sich nicht zur Ermüdung beiträgt). Laktat, das während Langzeitausdauerbelastungen in der Arbeitsmuskulatur gebildet wird, wird über das Blut in andere unbelastete Muskeln, Organe oder Gewebe transportiert und dort oxidiert (Laktat-Transport), wodurch der aerobe Metabolismus aufrecht erhalten werden kann. Ein gewisser Anteil an Laktat kann in der Leber zu Glukose abgebaut werden (Cori-Zyklus) um die Glukosekonzentration im Plasma zu erhalten. Großes Interesse gilt der Beziehung zwischen Laktat und der Leistung bei  rampenförmiger Belastung sowie der Identifikation von anaeroben Schwellen und Laktatschwellen, die bislang schwer fassbar scheinen.

Schlüsselwörter: Laktat,  aerober  Metabolismus,  anaerober  Metabolismus, Laktat-shuttle, Laktatschwelle.


The  characteristics  of  lactate  metabolism  and  the  significance  of plasma  lactate  concentration  ([LA])  are  different  in  response  to short duration high intensity exercise and to prolonged endurance exercise, such as the 400-m race and the Marathon race taken as extreme examples (Figure 1 and 2).


Anaerobic energy production
In response to short duration high intensity exercise the purpose of LA production is to provide a substantial portion of the energy yield: anaerobic glycolysis provides 47 kcal for each mole of  glucose  or  glycosyl  units  fermented  into  2  moles  of  LA  [1]. Plasma as well as muscle [LA] concentration are easy to measure but the amount of lactate (LA) accumulated during exercise depends on the LA-space. The distribution of LA from working muscles to the blood, and from the blood to other tissues depends on intramuscular and blood pH, and on the density of LA transporters (MCT1, MCT4 and MCT2) [2] and on blood flow in working muscles and in other tissues. Accordingly, in a given situation the LA-space could vary and it is impossible to precisely estimate the amount of LA accumulated from muscle or plasma [LA]. Direct measures in animals [3] and indirect estimates in man [4, 5] suggest that the average maximal amount of LA which can be accumulated is ~1 g/kg or about ~800 mmoles in a 70-kg subject. This amount of LA which could be accumulated in ~30 sec correspond to the release of ~18.5 kcal (~78 kJ) in a 70-kg subject (maximal accumulation rate ~2.3 g/sec).
This represents, respectively, ~55, ~50, ~40 and ~25 % of the energy yield during 200, 400, 800 and 1500-m races [6] (~3500, ~1700, ~750  and  ~350  W,  respectively).  Since  plasma  [LA]  at  the  end  of these races in actual competitions in elite athletes typically ranges between 20 and 25 mmol/L [7, 8], assuming a total amount of LA accumulated  of  ~800  mmol  (see  above),  the  LA-space  (800/20  or 25) ranges between 40 and 32 L (60-50 % body mass in a 70-kg subject).

LA production and efficiency of ATP synthesis
Based on these estimates of LA accumulation during short duration high intensity exercise it can be shown that in this situation anaerobic glycolysis is almost exclusively fuelled from muscle glycogen. Glycolysis could be fuelled either from plasma glucose which enters the  muscle  fiber  trough  facilitated  diffusion  and  GLUT4  or  from glucose-phosphate  provided  through  glycogenolysis  from  muscle glycogen. The maximal rate of plasma glucose entry into peripheral tissues observed during hyperglycemic clamp during prolonged exercise does not exceed ~2 g/min [9]. Thus, a flux through glycolysis above ~2 g/sec can only be sustained from muscle glycogen. The large increase in muscle and plasma [LA] in response to short duration high intensity exercise is indeed associated with a sharp decline in glycogen concentration in working muscles [10].
There  are  two  advantages  of  using  muscle  glycogen  and  not plasma glucose to fuel glycolysis during short duration high intensity  exercise.  The  first  advantage  is  to  conserve  plasma  glucose, which is in short supply, to other organs, mainly the brain.
The  second  advantage  is  that,  when  compared  to  glycolysis from  glucose  (which  requires  2  ATP  to  activate  one  mole  of  glucose),  glycolysis  from  glycogen  (which  only  requires  1  ATP  and  1 Pi to  activate one mole of glycosyl unit) provides more ATP (3 vs 2 moles of ATP/mole of glucose or glycosyl unit) [11] (p. 160). With 47 kcal released/mole of glucose or glycosyl unit, the efficiency of ATP resynthesis (~12 kcal/mole) by glycolysis is much higher from muscle  glycogen  (36/47  =  0.77)  than  from  glucose  (24/47  =  0.51) and  is  also  higher  than  through  aerobic  metabolism  (~0.6  for  an average P/O of 3).

LA distribution and clearance
Based on estimates of LA accumulation during short duration high intensity exercise it can also be shown that the amount of LA accumulated is equal to the amount produced (i.e., there is essentially no LA clearance during short duration high intensity exercise).
The two major pathways of LA utilization during exercise are oxidation and conversion into glucose (gluconeogenesis, GNG) in the  liver.  However,  both  processes  require  ATP  and  thus  oxygen: 0.750 L to oxidize 1 g of LA, and ~125-145 mL to convert 1 g of lactate into glucose or glycogen (6 and 7 ATP needed/mole glucose or glycosyl unit, respectively, with P/O = 3). During short duration high intensity exercise, the amount of oxygen consumed is low : e.g, < 2.5 L for a 400 m (computed from data reported by [12]).
Even  under  the  assumption  that  all  the  oxygen  available  is used to oxidize LA, this is only enough oxygen to oxidize ~3.5 g of LA (vs ~70 g produced). As for the conversion of liver GNG, first, with an hepatic blood flow during exercise < 1.5 L/min [13], only a small portion of LA produced in the working muscle can reach the liver  during  the  short  period  of  high  intensity  exercise.  Secondly, with a limited oxygen consumption in the liver (~70 mL/min) [13], which cannot possibly be entirely devoted to fuel GNG, the amount of LA which can be converted into glucose remains very low during a period of high intensity short duration exercise.

LA production/accumulation during short duration high intensity exercise
Finally, since anaerobic glycolysis with LA accumulation provides a substantial portion of the energy needed during short duration high  intensity  exercise,  the  highest  the  amount  of  LA  produced and accumulated (these are the same) the better the performance. This has been shown, for example, in a study by Lacour et al. [8] conducted in elite 400-m runners. A close positive relationship was found between the average speed sustained and plasma [LA] at the end  of  the  race  (which,  albeit  imperfect,  is  a  marker  of  LA  accumulation) (Figure 3). Two other observations can be offered as evidence that performance in short duration high intensity exercise depends on the ability to produce and accumulate large amounts of LA. The very high running speeds sustained by greyhounds during 400- and 800-m races (~25 and ~60 seconds, respectively) are not only due to their very high VO2max (~135 [14] but are also associated with very high post-race plasma [LA] (30-35 mmol/L) [15]. In contrast, patients with McArdle disease (type V  glycogenosis due a deficiency of muscle phosphorylase) are unable to produce LA from muscle glycogen and are also unable to perform any type of short duration high intensity exercise [16].


Energy metabolism is entirely aerobic
In response to prolonged endurance exercise, plasma [LA] is much lower than in response to short duration high intensity exercise :  depending  on  the  fractional  utilization  of  VO2max  sustained, training  and  nutritional  states,  and  environmental  conditions, the values range between 1.5 to 2 mmol/L [17] (i.e., only slightly above resting values) and ~10 mmol/L [18]. In addition, plasma [LA] are stable or slowly drift upwards (generally) or downwards (only at very low workloads). Under the assumption that the LAspace is stable, the slow changes in plasma LA over time, if any, suggest that the amount of LA present in the body remains fairly  constant.  As  explained  below,  this  does  not  indicate  that  LA is  not  produced,  but  that  the  rate  of  plasma  LA  disappearance closely matches its rate of appearance. Energy and ATP provided by glycolysis are only anaerobic when electrons which have been removed (along with hydrogen) when glucose or glycosyl units are oxidized in pyruvate, are accepted by pyruvate which is reduced into lactate which accumulates over time in the body. This is the case during short duration high intensity exercise (Figure 1).
However, when electrons and hydrogen which have been transiently accepted by pyruvate to produce LA are removed from LA to be finally accepted by oxygen to produce water, the energy and ATP provided by glycolysis are aerobic. The stability or near stability of plasma  [LA]  during  prolonged  endurance  exercise  (whatever  the total amount of LA present and the level of plasma [LA]) indicates that the energy needed for this type of exercise is entirely provided by aerobic metabolism.
Indeed, indirect estimates of the percent contribution of anaerobic metabolism to the energy yield indicate that it is negligible for endurance exercise [5] except at the onset of exercise when plasma [LA] rises quickly (e.g., [18]), or during transient changes in pace for tactical reasons, such as the final sprint.

Plasma [LA] and endurance performance
The higher the plasma [LA], the better the performance during short  duration  high  intensity  exercise  (see  above).  In  contrast, for a given fractional utilization of VO2max, exercise time to exhaustion is longer (i.e., endurance capability is higher) in subjects with the lower plasma [LA]. This is well exemplified in the study by Coyle et al. [19] summarized in table 1: the subjects with lower plasma [LA] during a simulated bike race at 88%VO2max were able to sustained this workload almost twice longer than those with the highest plasma [LA]. When compared to the subjects with the lowest endurance capability, the LA curve (i.e., plasma [LA] plotted against %VO2max) during incremental exercise to VO2max, was shifted to the right in subjects with the highest endurance capability. The « LA threshold » (LT) defined in this particular study as the %VO2max when plasma [LA] was 1 mmol/L above the basal value, was observed at 65.8%VO2max in subjects with  the  lowest  endurance  capability  vs  81.5%VO2max  in  subjects with the highest endurance capability.

LT and endurance performance
Based on this observation, which has been repeatedly confirmed, it is generally accepted that the LT identified during incremental exercise or during prolonged exercises at constant workload (maximal  lactate  steady  state  or  MLSS),  is  a  valid  index  of  endurance capability [20]. Although this observation is interesting and can have practical applications, it should be recognized that the term LT is a misnomer since there is obviously no threshold in the LA curve. This is precisely the reason why more than twenty different LTs have been suggested all of them based on purely geometric analysis of the LA curve without any physiological justification and significance. In addition, in almost all the studies showing good correlations between performance and a particular LT, the LT was expressed in running speed, VO2 or power output (i.e., absolute LT).
However,  the  absolute  LT  depends  in  a  large  extent  on VO2max, which is itself a major determinant of performance for events  lasting  longer  than  about  60  seconds  [21].  Thus,  in  any relationship between absolute LTs and performance, VO2max is a confounding factor which has seldom been controlled. This is probably why the absolute LTs are not selective determinants of performance  in  endurance  events  but  also  of  performance  for shorter distances such as the 800-m running and the 4-km cycling [20].

The LA shuttle
During  prolonged  endurance  exercise,  although  plasma  [LA]  is stable or almost stable, measurements of plasma LA kinetics show that LA is continuously produced in some tissues and utilized in others, but that the rate of plasma LA appearance and disappearance are similar or very close. The flux of plasma LA from the sites of production to the sites of disposal has been described as the cellto-cell LA shuttle [22-25]. Studies of LA release and uptake across various  vascular  beds  using  selective  catheterisation  techniques, coupled or not with tracer techniques, have shown that the sources of plasma LA during prolonged exercise are the working muscles but also the non-working muscles, and that these tissues along with the heart, the brain and the liver are also the sites of plasma LA removal. In the liver, LA can be converted into glucose which can be released into the blood to sustained glycaemia in a situation where plasma glucose utilization is increased. Thus, the LA shuttle, coupled with liver GNG, is a way to maintain plasma glucose concentration at the expense of muscle glycogen (it should be remembered that glucose cannot be directly released into the blood from muscle glycogen, due to the absence of glucose 6-phosphatase).
In the heart and brain, the LA removed from the blood is oxidized  and  the  LA  shuttle,  thus,  could  be  seen  as  the  way  to  fuel aerobic  metabolism  in  these  organs  also  at  the  expense  of  the large stores of muscle glycogen, thus sparing plasma glucose and the much smaller liver glycogen stores. Finally, the LA shuttle from non-working to working muscles can also be seen as way to sustain aerobic  metabolism  in  working  muscles  at  the  expense  of  glycogen stores in non-working muscles, glycogenolysis in non-working muscles being probably stimulated by the increase in plasma epinephrine concentration [24]. The significance of the shuttle of LA from working muscles, where it is produced, back to the same working muscles, where it is oxidized, is less obvious: the same result could be obtained with the lactate directly oxidized in the muscle fibers where it is produced, or in adjacent fibers, i.e, through an intramuscular  shuttle  [26-28].  There  are  two  reasons  for  the  shuttle  of  LA from  the  working  muscles  back  to  the  working  muscles  through the  circulation.  The  second  reason  is  described  in  the  following section which explains why muscle and plasma LA concentrations during prolonged exercise are higher than at rest, although the entire organism is aerobic. The first reason is that this shuttle allows the LA which is probably mainly produced in glycolytic fibers to be taken up by oxidative fibers.


Anaerobic threshold ?
During prolonged exercise the energy is entirely produced through aerobic metabolism. However, plasma [LA], which is stable or almost stable is higher than at rest and can reach values as high as 10 mmol/L [18]. Furthermore, for a given workload, plasma [LA] is stable but at a higher value in all situations where the availability of oxygen (normobaric or hypobaric hyoxia), oxygen transport (impairement in alveolar ventilation, in oxygen diffusion, in oxygen carrying capacity of the blood, in cardiac output, etc.), and oxygen utilization  (mitochondrial  disease,  detraining)  are  impaired,  and conversely [29]. Under the well entrenched theory of the anaerobic threshold, these observations are offered as the best experimental support showing that above a certain workload and VO2, anaerobic metabolism (with LA accumulation) has to be involved in ATP generation because aerobic energy supply becomes insufficient. This theory and explanation, however, cannot account for the facts
1) that there is actually no anaerobic energy provided when plasma [LA] is stable, whatever plasma [LA] (a good example is rest, a  situation  where  nobody  will  seriously  claim  that  a  portion  of the energy derives from anaerobic metabolism, but where plasma [LA] is about 1 mmol/L but stable); and 2) that a decrease in oxygen availability, or impairment in oxygen transport and utilization (although they can reduce VO2max) do not modify VO2 for a given submaximal workload.

Marker of the error signals for mitochondrial respiration
The  best  (and  simpler)  explanation  for  the  fact  that  plasma  [LA] is  stable  or  almost  stable  but  higher  than  at  rest  during  prolonged exercise is that it is a marker of error signals needed to stimulate  mitochondrial  respiration  and  production  of  aerobic  energy and  ATP  [24, 30].  The  two  factors  which  stimulate  mitochondrial respiration  are  an  increase  in  redox  potential  and  a  decrease  in phosphate potential [31, 32]. In situations where aerobic ATP production is compromised (decrease in oxygen availability, or impairment in oxygen transport and utilization) but where there is room for compensation, mitochondrial VO2 and aerobic ATP production are  maintained  at  the  cost  of  a  lower  phosphate  potential  and  a higher redox potential (the latter being due for a large part to the reduction in phosphate potential). In other words, the cost to pay for a similar VO2 and aerobic energy production is a larger disturbance  in  cell  homeostasis  and  larger  error  signals  which  control mitochondrial  respiration.  In  the  cytosol,  the  lower  phosphate potential stimulates glycolysis, increasing redox potential (NDH2/NAD) and, as consequence, the LA/pyruvate ratio, and muscle and plasma [LA].
The  significance  of  plasma  [LA]  as  a  marker  of  the  error signal  which  stimulate  mitochondrial  VO2 explains  that  reliable hallmarks of a high endurance ability are a lower plasma [LA] at any submaximal level of exercise and VO2, a right shift of the LA curve and a higher LT (which does not exist [33] but is a marker of the position of the LA curve, whatever the particular criterion chosen for “LT”).

Competing interests: none


  1. Brooks GA, Fahey DH, Baldwin KM Exercise physiology. Human bioenergetics and its applications, 4th edition. Boston: McGraw-Hill; 2005.
  2. Bonen A The expression of lactate transporters (MCT1 and MCT4) in heart and muscle. Eur J Appl Physiol 86 (2001) 6-11.
  3. Bennett AF, Licht P Anaerobic metabolism during activity in amphibians. Comparative Biochemistry and Physiology 48A (1974) 8.
  4. di Pamprero PE Energetics of muscular exercise. Rev Physiol Biochem Pharmacol 89 (1981) 144-222.
  5. Peronnet F, Thibault G Mathematical analysis of running performance and world running records. J Appl Physiol 67 (1989) 453-465.
  6. Gastin PB Energy system interaction and relative contribution during maximal exercise. Sports Med 31 (2001) 725-741.
  7. Kinderman W, Keul J Lactate acidosis with different forms of sports activity. Canadian Journal of Applied Sports Sciences 2 (1977) 177.
  8. Lacour JR, Bouvat E, Barthelemy JC Post-competition blood lactate concentrations as indicators of anaerobic energy expenditure during 400-m and 800-m races. Eur J Appl Physiol Occup Physiol 61 (1990) 172-176.
  9. Hawley JA, Bosch AN, Weltan SM, Dennis SC, Noakes TD Glucose kinetics during prolonged exercise in euglycaemic and hyperglycaemic subjects. Pflugers Arch 426 (1994) 378-386.
  10. Medbo JI, Jebens E, Noddeland H, Hanem S, Toska K Lactate elimination and glycogen resynthesis after intense bicycling. Scand J Clin Lab Invest 66 (2006) 211-226.
  11. Mayes PA Glycolysis and the oxidation of pyruvate, in: Murray RK, Granner DK, Mayes PA, Rodwell VW (Eds): Harper's biochemistry. Norwalk, Connecticut: Lange, 1988, 158-164.
  12. Duffield R, Dawson B, Goodman C Energy system contribution to 400-metre and 800-metre track running. J Sports Sci 23 (2005) 299-307.
  13. Nielsen HB, Febbraio MA, Ott P, Krustrup P, Secher NH Hepatic lactate uptake versus leg lactate output during exercise in humans. J Appl Physiol 103 (2007) 1227-1233.
  14. Weibel ER, Taylor CR, Hoppeler H The concept of symmorphosis: a testable hypothesis of structure-function relationship. Proc Natl Acad Sci U S A 88 (1991) 10357-10361.
  15. Pieschl RL, Toll PW, Leith DE, Peterson LJ, Fedde MR Acidbase changes in the running greyhound: contributing variables. J Appl Physiol 73 (1992) 2297-2304.
  16. Lewis SF, Haller RG The pathophysiology of McArdle's disease: clues to regulation in exercise and fatigue. J Appl Physiol 61 (1986) 391-401.
  17. O'Brien MJ, Viguie CA, Mazzeo RS, Brooks GA Carbohydrate dependence during marathon running. Med Sci Sports Exerc 25 (1993) 1009-1017.
  18. Kenefick RW, Mattern CO, Mahood NV, Quinn TJ Physiological variables at lactate threshold under-represent cycling time-trial intensity. J Sports Med Phys Fitness 42 (2002) 396-402.
  19. Coyle EF, Coggan AR, Hopper MK, Walters TJ Determinants of endurance in well-trained cyclists. J Appl Physiol 64 (1988) 2622-2630.
  20. Faude O, Kindermann W, Meyer T Lactate threshold concepts: how valid are they? Sports Med 39 (2009) 469-490.
  21. Levine BD VO2max: what do we know, and what do we still need to know? J Physiol 586 (2008) 25-34.
  22. Brooks GA Lactate production under fully aerobic conditions: the lactate shuttle during rest and exercise. Fed Proc 45 (1986) 2924-2929.
  23. Brooks GA The lactate shuttle during exercise and recovery. Med Sci Sports Exerc 18 (1986) 360-368.
  24. Gladden LB Lactate metabolism: a new paradigm for the third millennium. J Physiol 558 (2004) 5-30.
  25. Gladden LB Is there an intracellular lactate shuttle in skeletal muscle? J Physiol 582 (2007) 899.
  26. Baldwin KM, Campbell PJ, Cooke DA Glycogen, lactate, and alanine changes in muscle fiber types during graded exercise. J Appl Physiol 43 (1977) 288-291.
  27. Brooks GA Intra- and extra-cellular lactate shuttles. Med Sci Sports Exerc 32 (2000) 790-799.
  28. Stanley WC, Gertz EW, Wisneski JA, Neese RA, Morris DL, Brooks GA Lactate extraction during net lactate release in legs of humans during exercise. J Appl Physiol 60 (1986) 1116-1120.
  29. Wasserman K, Koike A Is the anaerobic threshold truly anaerobic? Chest 101 (1992) 211S-218S.
  30. Connett RJ, Honig CR, Gayeski TE, Brooks GA Defining hypoxia: a systems view of VO2, glycolysis, energetics, and intracellular PO2. J Appl Physiol 68 (1990) 833-842.
  31. Chance B, Williams GR The respiratory chain and oxidative phosphorylation. Adv Enzymol Relat Subj Biochem 1956;17:65-134.
  32. Wilson DF Factors affecting the rate and energetics of mitochondrial oxidative phosphorylation. Med Sci Sports Exerc 26 (1994) 37-43.
  33. Röcker K Argument about the Emperor Beard: which lactate threshold is the best. Deutsche Zeitscrift für Sportzmedizin 59 (2008) 303-304.
  34. Hirvonen J, Nummela A, Rusko H, Rehunen S, Härkönen M Fatigue and changes of ATP, creatine phosphate and lactate during the 400-m sprint. Canadian J Sport Sci 17 (1992) 141-144.
Corresponding Address:
François Péronnet
Emeritus professor
Département de kinésiologie, Université de Montréal
CP 6128 Centre-Ville, Montréal, QC, Canada H3C 3J7
Phone: 1 514 743 6737
Fax: 1 514 343 2181