Introduction

For a moderately performing athlete a simple lactate sample taken in training may be sufficient to improve training times and subsequent race performance( Vuorimaa et al,2000 ). Optimal performance is widely sought and the continuing trend of improvement demands that individual athletes train at optimal intensities and compete at velocities with a maximum steady state Blood Lactate response (Lass). By sampling Blood Lactate (BL) with incremental loading an athleteís energy contribution can be deduced from aerobic and anaerobic capacity/power (Hill,1999). 

Lactate as a by-product of the anaerobic/glycolytic energy pathway can be measured by sampling (BL). The accumulation of (BL) in response to incremental loading is traditionally thought to reflect the levels of lactate that are produced in muscles(Hilderbrand et Lormes,2000 ). Interpolation of the oxidative aerobic and lactic acid, anaerobic, contribution can thus help determine appropriate training intensities and help predict endurance performance (Foxdal et al,1994).

However spurious authors question the validity and reliability of (BL) testing citing variant methods and sites of sampling procedures, (Foxdal et al,1994) variant exercise protocols,(Hagberg,1984) recovery periods (Weltman,1995), time of) and analysis and calculation of results as causes for concern (Foxdal et al,1994).

Foxdal et al,(1994) considers that different individual physiological levels of tolerance exist (ie inter subject variances in individual anaerobic threshold accumulation of 4mmol.L) and the tested (BL) levels are no more than a mere reflection of muscle lactate levels. The circulating lactate measured does not include stored lactate in non working muscles and liver, thus production and tolerance to higher levels may therefore be underestimated.

Different terminology is frequently used and can confuse readers, thus for further clarity the following definitions have been explained.

The Anaerobic Threshold (AT) is the point of exercise at which the demand for energy (Adenosine Triphosphate,(Atp)) is greater than that which can be supplied aerobically. Hence an Individualised Anaerobic Threshold (IAT) is the highest metabolic rate at which lactate concentration is maintained at Steady State during prolonged exercise (Baldarie et Guidetti 2000). 
The Lactate Threshold (LT) is the level of exercise intensity at the point of lactate accumulation and powerfully predicts aerobic performance (McArdle, Katch & Katch 2000). The (LT) can be expressed as a % of VO2 (maximal oxygen utilised) or commonly at set levels of 4mmol.L. Similarly the Onset of Blood Lactate Accumulation (OBLA) is defined as the running velocity that corresponds to a lactate concentration of 4mmol.L (Mader,1991) and the Maximal lactate Steady State (MLSS) corresponds to the highest workload that can be maintained over time (20 minutes or more) without constant (BL) accumulation. Thus lactate elimination equals production and therefore the speed reached determines the aerobic power.
 

Short term Anearobic Glycolytic (Lactic Acid ) Energy System

Shorter to mid distance events ( 400 to 800 metre races) that take between 40seconds to 120 are thought to primarily rely upon an individualís lactic acid (LA) energy producing capacity. Initially at sub-maximal exercise levels small amounts of (Atp) and pyruvic acid are generated from the breakdown of glucose and the availability of oxygen determines that the pyruvic acid is converted to Carbon Dioxide (CO2), H2O and (Atp) via aerobic glycolysis. Continued strenuous exercise for prolonged periods means less reliance upon the oxidative aerobic capacity and a  subsequent pyruvic to (LA) conversion. The lactate produced within the muscles was traditionally assumed to disperse in the blood (McArdle, Katch & Katch 2000) and if such activity was to continue the accumulation of lactate was believed to impair performance due to fatiguing metabolic activity. Reduced efficiency of muscular contractility in this more acidic environment followed. On resumption of satisfactory oxygen levels the (LA) is reconverted to pryuvic acid and again into CO2, H2O and Atp.

Table 1

Duration (secs)	Classification	Energy Supply
1 to 4	Anaerobic	ATP stores
4 to 20	Anaerobic	ATP and PCr stores
20 to 45	Anaerobic	ATP and PCr and muscle glycogen stores
45 to 120	Anaerobic	lactic muscle glycogen
120 to 240	Aerobic	muscle glycogen and lactic acid
240+	Aerobic	muscle glycogen and fatty acids

ATP, adenosine triphosphate; PCr, phosphocreatine. 
Note that all systems overlap.

Nevertheless contemporary opinion suggests that the lactate produced via anaerobic glycolysis frequently fails to even reach the circulating blood and is shuttled within muscle fibres and slower fibre types as a store of energy for future oxidisation, or to fire other type II fast twitch fibres directly. Coupled with the physiological concept that up to 80% of the lactate is transported via the blood, to the liver for re-conversion to glycogen the question remains is it accurate to test blood lactate levels.

Lactate Formation

During glycolysis two pairs of hydrogen atoms are stripped from the glucose and electrons accepted by NAD+ to form NADH, which is impermeable to mitochondria. The electrons therefore have to be shuttled in to mitochondria to be oxidized. Thus aerobic glycolysis predominates under ample supply of cellular oxygen in non-strenuous exercise.

At rest constant low levels of lactate are formed (2.5mmol.L) due to cellular respiration of the mitochondria-free red blood cells and their associated glycolytic energy drive. When energy demands are raised, by increasing exercise stress, the respiratory chain fails to process all the hydrogen adjoined to NADH due to the lack of availability of sufficient oxygen. Thus in order for the rapid pace of glycolysis to continue NAD+ needs to shed the H+ to return for pick up of more H+ and to oxidise phosphoglyceraldehyde. In anaerobic glycolysis the H+ are catalysed by the enzyme lactate dehydrogenase and combined and temporarily stored with pyruvate to form lactate. Once formed within muscle lactate is assumed to rapidly diffuse in to the blood for buffering and removal to allow continued Atp resynthesis via anaerobic glycolysis. It is thought that fatigue follows from lactate accumulation culminating in lowered pH, acidity and cellular metabolism and reduced contractility. However lactate is not only a waste product but can act as a store of energy during prolonged and strenuous exercise. This source of energy occurs when NAD re-scavenges the lactate holding H+ and oxidises them for Atp. A second energy source is considered when the liver uptakes and recycles lactate and pyruvate to glucose and replenishes liver/muscle glycogen stores and circulating blood glucose via the Cori Cycle. (McArdle, Katch & Katch,2000)

However anaerobic glycolysis is thought to only realise 10% of energy from the glucose molecule. The remainder occurs in the mitochondria via the second stage, the Krebbs Cycle, where the two pyruvate molecules join with two co-enzyme A molecules to produce two AcetylCoa that generates multiple H atoms that are subsequently carried to the electron transport chain for energy creation.

Blood Lactate Accumulation

Lactate produced under light to moderate exercise is removed by liver, heart and non-active skeletal muscle. Aerobic metabolism matches the energy demand and lactate is shuttled to non-active tissue to oxidise the lactate formed. Hence relative stability occurs. Endurance trained individuals who raise their maximal oxygen uptake (VO2max) reap the benefits of aerobic conditioning by increasing size, number and efficiency of mitochondria, increased capillary networks and concentration of enzymes producing faster metabolism (Mader et al1979 cited by Keskinen et l 1989). Thus individuals can aim to delay the point at which lactate accumulates (OBLA 4mmol.L) under more strenuous exercise by becoming less reliant upon anaerobic glycolysis. By mobilising fatty acids, improving cellular adaptation in uptake of lactate by skeletal and heart muscle and liver an improved shuttle effect can occur (Tomlin & Wenger,2001). 

Thus as oxygen demand is exceeded anaerobic glycolysis complements aerobic metabolism and as the H+ release exceeds its oxidisation pyruvate is converted to lactate by accepting the hydrogen. Hence the key question follows how can athletes control which way their pyruvate goes, to lactate via lactate dehydrogenase or for shuttling in to the mitochondria via pyruvate dehydrogenase for oxidisation and high Atp production. By advancing their ability to use oxygen and improving aerobic fitness their ability to tolerate lactate can be increased and (LT) increased accordingly as their body adapts to using and dispersing lactate levels. Thus by training to raise lactate levels incrementally by stacking with (1min:3min / work : rest )rather than continuously accumulating athletes can learn to use their lactate as a source for energy in endurance events (Anderson et al 2001).

Thus as tissues work to resynthesise lactate during exercise it is possible that testing circulating (BL) can underestimate the true lactate levels produced by muscles. The latency of testing after incremental loading means that results may correspond to previous test stages (Myburgh et al, 2000) and also peak levels post exercise testing may be missed and hence the ability to determine how an athlete can effectively disperse lactate may produce inaccurate inferences. The siting of sampling proximal or at distance from the exercising muscle also raises questions concerning accuracy and validity of testing (Thin et al,1999).
 

Indicators of Lactate Threshold

Fixed BL Concentration

As exercise intensity increases BL increases. The VO2 (exercise intensity) associated with fixed BL concentration that exceeds the normal resting variation denotes the LT. 
This often coincides with 2.5mMol.L value, whilst a 4mMol.L according to Mader et al(1978) reflects the OBLA. Bourdon (2000) argues this figure can be underestimated and a more realistic Independent Anaerobic Threshold can vary between 2.5-6.4mM.L.

Ventilatory Threshold (VT)

The (VT) detremines the LT from the relationship between pulmonary ventilation and oxygen uptake during incremental exercise . (McArdle, Katch & Katch,2000)

Blood Lactate / Exercise VO2 response

By plotting BL concentration against VO2, or exercise intensity, LT can be determined. Exercise for 3-4 minutes (pause at end stage) the intersection represents the LT. For cyclists this corresponds to 30-45% VO2 for runners 55-65% VO2, 80% for elite endurance trained. (McArdle, Katch & Katch,2000)
 

Oxygen Debt / Recovery

In light exercise recovery to a resting condition occurs without problem. However strenuous exercise, lactate producing activities of 40 sec duration, takes greater time to return to resting levels. Hillís oxygen debt theory has been superseeded by the EPOC, Excess Post-exercise Oxygen Consumption that identifies the excess oxygen required above the resting level in recovery. Such a period has both fast and slow components. 
Hillís theory assumed that the majority of lactate produced resynthesises to liver glycogen in recovery whilst the rapid phase recovery in strenuous exercise worked to restore intramuscular Atp and Phospho-Creatine stores depleted. Nevertheless a significant percentage of recovery oxygen uptake identifies that during recovery physiological functioning occurs.

Thus in the fast recovery phase BL does not accumulate when steady submaximal aerobic exercise or 5-10 second bouts of all out effort intramuscular high energy phosphates are used. Anaerobic exercise significantly disrupts metabolism and the active recovery with submaximal aerobic (to increase blood perfusion to non exercising muscle, liver and heart) at 35% and 655 VO2 and passive recovery components is deemed optimal  (McArdle, Katch & Katch,2000).   BL testing can thus indicate the strenuousness of the exercise and the adequacy of recovery and can be used as an important indicator for endurance performance and to identify individual anaerobic thresholds.
 

Research / Validity and accuracy of BL testing

The choice of blood sample site and the type analysed have been shown to alter the exercise intensity response to fixed lactate concentrations (Harris & Dudley, 1989). Similarly the exercise design can affect outcomes. Weltman et alís (1995) choice of 3 minute exercise durations produced valid relationships with the LT whilst Hagberg (1984) used 10 minute durations on 3 separate occasions to produce similar results. Tests used between 1-5 minutes indicate a non-steady state concentration of BL (Heck et al 1991, Mader 1991), an important consideration when setting training intensities. Foxdal et al (1994) revealed significant and similar relationships and found no difference in mean prediction error between the predicted and measures maximal endurance running velocities with all tested protocols. They discovered a 5% risk of over/under estimation for prediction of endurance capacity and found the 8 minute run the most accurate performance predictor.

The increase of intensity between exercise periods plus the exercise/rest ratio are also important factors to consider as research supports the view that up to 90% of the BL concentration results from the accumulation phase during the oxygen deficit at the start of the exercise.

Since Mader et al (1978) cited by Foxdal et al 1995, identified the 4mMol.L OBLA, research has focused on intensities designed about this predicted maximal endurance running velocity. However in an effort to realise a more individual level and improve prediction (Baldari et Guidetti 2000) sought to determine the most effective work rate at which prolonged performance can be maintained without adverse lactate accumulation. (Baldari et Guidetti 2000)  found that the individual AT for the antecedent stage was more valid for determining a workload at which constant prolonged exercise was in LASS than using the same stage of its measurement. 

Myburgh et al (2000) further raised the spectre of doubt and validity of BL laboratory  testing for optimal performance at the 4mmol.L mark of OBLA. They found that greater individual response and variation occurred and favoured field tests over laboratory tests as the time trials or distance trial performance test can be more inferred to populations than the constant incremental loading in laboratories.
 

Conclusion

Thus many debateable issues contribute to the debate concerning the se of BL as a valid and reproducible physiological test to predict endurance performance. Timing (Myburgh et al,2000) design (Foxdal et al 1994) and intensity (Palmer et al,1999) coupled with sampling, analysis and calculation issues (Foxdal et al 1994) compound the spurious nature for inference. Albrecht (1998) used rating of perceived exertion and performance results to conclude that BL was a more favourable LT test than Heart Rate, as HR fails to provide an accurate physiological profile in response to exercise intensity testing. 

Nevertheless the results of BL for specific exercising muscle mass is questioned due to the variant designs and the underlying physiological responses of the lactate shuttle within fibres and less active skeletal muscle. Such response may underestimate the circulating levels of BL and therefore inferences on how much lactate is produced peripherhally and locally by muscle. Hence athletes can improve endurance performance by targetting optimal training intensities, with adequate recovery periods, depending on the system to be overloaded.
 

Short Answer Review Questions

Can endurance athletes target performance improvement by longer duration training or multiple short interval training ?

Anderson (2001) advocates that lactate stacking progressively enhances the ability of muscles to clear lactate from the working muscle to alternate sites for store or for future oxidisation as a store of energy. Such shorter duration repetitions allows for continuing ability to run at higher lactate levels for longer periods without adverse effects as opposed to longer duration runs that can not maintain the same velocity over the equivalent distance. Thus such shorter duration also allows for a higher aerobic workout at higher % VO2 max and is thought to correlate to improved performance. However it is still necessary to incorporate efficiency and VO2 improvement throughout training. Thus in conclusion training for AT should work at 80-95%VO2 for 15-30 minutes and 65-75%VO2, 45-120 minutes duration for aerobic.
 
 

References

Anderson O, (2001) Peak Performance.  July 2001. P 151-160

Weltman A (1995)  The Blood Lactate response to Exercise. AM Jnl Sp Med (1995) 120-125

Foxdal,P, Sjodin B, Sjodin A, Ostman,B (1994)  The validity & accuracy of Blood Lactate testing. Am Jnl Sp Med 15 (1994) p89-95.

Hagberg, J (1984) Physiological Implications of the Lactate Threshold .  Int Jnl Sp Med p106-109.

HarrisJ & Dudley, G (1989)  Exercise alters the distrribution of Lactate in the blood. Jnl App Phys. 66: 313-317.

Mader A (1991) Evaluation of the endurance performance of mararthon runners & theoretical analysis of test results. Jnl Sp Med Physical Fitness (31) 1-19

Keskinen,K Komi,P & Rusko H (1989) Lactic Acid evaluation in energy contribution. Br Jnl Sp Med 10, p197-201.

Myburgh, K, Viljoen A Tereblanche S (2001) Plasma lactate concentrations for self selected maximal tests  33. Medicine & SP Sience p152-156.

Palmer,A Potteiger A, Nau K et Tong R (1999)  A 1 day self maximal lactate steady state assessment protocol.   Med & SC in SP & Exc 31, 9 , p1336-1341.

Tomlin D & Wenger H (2001)  The relationship between aerobic fitness and recovery from high intensity exercise  Sports Med 31, (1) 1-11.

Thin et al (1999) Lactate determination in exercise testing using analysers.  Eur Jnl Applied Phys 79(2) 155-159

Olbrecht J (1998)  Details of lactate testing. Reliabillity. http//www.lactate.

Hilderbrand A Lormes W   (2000)   Lactate concentration in plasma & red blood cells during incremental exercise. Int Jnl Sp Med 21(7) Oct

Baldari C et Guidetti l (2000) A simple method for IAT as predictor of max lactate steady state  . Med & SC in Sp & Exc 32(10) 1798-1802.

Vuorima T , Vasankari V et Rusko H (2000) Physiological comparison during 2 intermittent running exercise tests at the velocity associated with VO2 max. Int Jnl Sp Med 21(2) p96-101

Hill,D (1999)  Energy system contribution in middle distance running events , Jnl SP Sc 17(6) p477-83.

McArdle,W Katch F & Katch V (1996)  Exercise Physiology concepts 2nd ED 2000.