The lactate shuttle and endurance training

Races from 5000m to marathon are run at a pace that is strongly predicted by pace at lactate threshold because the accumulation of acidity is a major factor limiting muscle performance.  During the combustion of glucose to generate energy, the major source of acid is lactic acid.   Lactic acid is a compound of two ions: negatively charged lactate ions and positively charged hydrogen ions.  Under normal circumstances within the body, lactic acid dissociates into these two constituent parts, lactate and hydrogen ions, and it is the latter that create the acidity.   At least in part, the hydrogen ions are buffered (i.e. mopped-up by  other negative ions within tissue) but once this buffering capacity is saturated, hydrogen ions accumulation creates an acid environment that impairs the efficiency of muscle contraction.

However lactate itself can be used as fuel in various locations in the body, and as it is itself metabolised hydrogen ions are removed.    Thus, understanding the mechanisms by which lactate is transported around the body and the mechanisms by which it is itself metabolised provides the basis for rational planning of training.

The orthodox view

The scientific studies of Louis Pasteur, in the nineteenth and early twentieth century, and subsequently by Hans Krebs, AV Hill and others, early in the twentieth century uncovered the mechanisms of anaerobic and aerobic metabolism of glucose, and established the orthodox view that shaped the theory of training for distance training through the second half of the twentieth century. According to this orthodox view, glucose is initially metabolized by the process of glycolysis, to produce pyruvate,  This anaerobic transformation of glucose to pyuvate releases a modest amount of energy which is transferred into the high energy bonds of the energy-rich molecule, ATP, and ultimately can be used to fuel muscle contraction.  But in the presence of oxygen much more energy can be derived via aerobic metabolism of pyruvate. The pyruvate is transported into mitochondria and converted to acetyl-CoA by an enzyme complex known as the pyruvate dehydrogenase complex.  Acetyl-CoA then undergoes a series of chemical transformations catalysed by the aerobic enzymes within mitochondria.  The acetyl group is oxidized to carbon dioxide, releasing a relatively large amount of energy which is incorporated into ATP, thereby providing a substantial enhancement of the supply of energy for muscle contraction.   In contrast, when the rate of delivery of oxygen to muscle is inadequate, muscle contraction must be fueled via the modest energy yielded by conversion of glucose to pyuvate, and the pyruvate is converted to lactate, thereby generating potentially harmful acidity.

The lactate shuttle

The orthodox view is indeed substantially correct, but is misleading because a substantial proportion of pyruvate is converted to lactate even when oxygen supply is adequate to sustain aerobic metabolism in mitochondria.   The way in which the body deals with this lactate is of crucial importance to coaches and athletes.  It was not until the final years of the twentieth century that an adequate understating of the way in which lactate in handled in the body emerged.    The newly emerging understanding was based largely on the work of George Brooks of the University of California, Berkeley Campus, who developed the concept of the lactate shuttle.  Lactate shuttling refers to a group of processes by which lactate is transported within and between cells to locations where is undergoes metabolism.   There is still debate about the details of these mechanisms but the broad principles are now clear, and these principles have major implications for optimum training for distance running.

The first key point is that a proportion of the pyruvate generated in the first stage of glucose metabolism is converted to lactate in the cytosol (the fluid medium inside cells) of muscle fibres, across a very wide range of work-rates, extending from the low aerobic to anaerobic zones.  In the low and mid-aerobic range, the majority of the lactate is transported across various membranes to various different sites where it is metabolized, so there is very little observable accumulation of lactate in blood until the rate of generation of lactate rises near to the limit of the body’s ability to transport and utilize lactate.  Beyond this point, the concentration of lactate and hydrogen ions in blood rises rapidly (the Onset of Blood Lactate Accumulation, OBLA); respiration becomes very effortful, and the ability to maintain that pace is limited by the limited ability to tolerate acidity.

It is helpful to understand the various processes by which lactate is transported out of the cytosol of muscle cells and subsequently metabolized, in order to design a training program that is likely to enhance these processes.

There are four major pathways by which lactate is transported and metabolized:

  • Transport across the outer mitochondrial membrane to a site where lactate dehydrogenase converts lactate back to pyruvate which then undergoes aerobic metabolism within the same muscle cell. This process results in dissipation of lactate and acidity in the cell where it was created and hence is merely a mechanism that ensures that acid does not accumulate when oxygen supply is adequate to sustain aerobic metabolism.
  • Transport out of the muscle fibre where it was created, into nearby fibres where is can be transported across the outer mitochondrial membrane and metabolized. This mechanism makes it possible for lactate to be generated in type 2 muscle fibres, which are powerful but have relatively low aerobic capacity, and then metabolized in type 1 fibres which have high aerobic capacity.  Training ‘at a good aerobic pace’ as advocated by Lydiard is potentially a good strategy for developing this mechanism.  Although the training pace might be comfortably below OBLA, the ability to dissipate lactate and acidity will be enhanced, leading to a an increase in pace at OBLA and improved performance over distances from 1500m to marathon.
  • Transport out of the muscle fibre where it was created into the blood and thence to other organs, such as heart and brain where it can be metabolized to generate energy
  • Transport out of the muscle fibre where it was created into blood and thence to liver where it can be converted back to glucose by the process of gluconeogenesis. This mechanism is likely to help conserve glucose stores in a manner that is useful in long events such as the marathon.

It is important to note that all of these processes entail transport across a membrane or several membranes prior to metabolism.   Transport is an active process that is performed by specialised proteins known as monocarboxylate transporters (MCTs). There are several different type of MCT located in different types of membrane.   Like many proteins in the body, utilization encourages production of increased amounts of the protein.

Aerobic base-building

Low intensity running is not merely about developing the capillaries to deliver blood to muscle and mitochondrial enzymes that perform aerobic metabolism.  Because appreciable amounts of lactate are produced, transported and metabolized even at work-rates well below OBLA, low intensity training  helps build capacity to handle lactate.

Think of the flow of glucose into the energy metabolic pathway as being like water flowing from an inflow pipe into a sink. The inflow pipe is actually the anaerobic pathway (glycolysis).  A pool of interchangeable pyruvate and lactate tends to accumulate in the sink.  There are two ways out of the sink: transport out of the cell or down the plug hole into mitochondria where aerobic metabolism occurs.  In fibres in which the aerobic system has been well developed , the flow down the plughole can accommodate a large flow of glucose into the system without the sink overflowing.  Shuttling from type 2 fibres which have less well developed aerobic capacity, into nearby type 1 fibres also helps maintain the flow.  There is minimal accumulation of acid in either muscle or blood.  So purely aerobic development, which can be achieved by low intensity training, minimizes accumulation of acid at 10K and 5K pace.   Shuttling explains why runners who only do low intensity running during base building nonetheless usually find that 10K and 5K pace improve despite doing no training near race pace.

The important conclusion for the endurance athlete is that low intensity training is an effective way to develop an aerobic base which helps raise lactate threshold.  It enhances performance at all distances for 1500m to ultramarathon.

Interval training and fartlek

Lactate shuttling also provides an explanation for the effectiveness of interval training and fartlek.  A brief intense effort epoch above threshold generates a surge of lactic acid, and is followed by a recovery epoch during which lactic acid levels fall rapidly, before the sequence of effort and recovery is repeated.  Thus, large gradients in lactate concentration develop, resolve and develop again.  It is noteworthy that the drop in lactate during recovery is likely to be facilitated by low intensity running which maintains transport and utilization of lactate during recovery.  A high lactate gradient across a membrane makes high demand on the transport process and is likely to stimulate production of the relevant transporters, the MCTs.

It is plausible that this will be achieved most effectively by ‘cruise’ intervals of the type employed by Emil Zatopek, or by fartlek sessions in which intensity is high enough during the effort epochs to ensure substantial  production of lactate, while intensity during the recovery epochs is adequate to ensure transport and utilization of the lactate produced during the preceding effort epoch


The various pathways by which lactate is transported out of the muscle cells where it is created to locations where it can be usefully metabolized provide a set of mechanisms by which either low intensity training at a pace comfortably below lactate threshold, or by interval training in which lactate is generated in brief surges, can develop  the ability to cope with lactate production at race pace.    Thus training for sustained periods at or near race pace, which tends to be quite demanding by virtue of the sustained stress, has only a relatively limited role to play in training for endurance events.  This might be an explanation for the observation that many elite endurance athletes adopt a polarized approach to training, in which the majority of training is done at a pace comfortably below threshold, together with an appreciable minority of training at higher intensity during interval sessions and  a modest amount of sustained running near to threshold.


4 Responses to “The lactate shuttle and endurance training”

  1. padraigjapan Says:

    Fascinating as always. Thank you.

  2. Ewen Says:

    Thanks Canute. Good to hear from you again – it’s been a while.

    I may have mentioned that I have a problem in my 5k Parkruns of feeling the effects of lactic acid if I increase my pace ever so slightly during the run. 4:30 per kilometre produces little feeling of lactic acid accumulation whereas 4:24 does. Like you mentioned, historically, most of my running training has been at MAF heart rates (around 5:30 ks) and I have no problem running at 4:30-40s without “going lactic.”

    Do you think there would be a cross-over between cycling and running were I to do anaerobic cycling sessions such as hill repeats and maximum effort sprints during a longer ride? Do you know of any studies of that?

    • canute1 Says:


      It appears that you reach the stage where you are generating lactate in muscle faster than you can transport it away and metabolise it, at a pace between 4:30 and 4:24 per Km. You have probably reached a plateau where additional training at MAF pace will not produce further appreciable improvements. The available studies, eg Esteve-Lanao et al, Stoggl et al, Neal et al (links in my previous post on polarised training) suggest that the best way to make further improvement is via a polarised approach. You raise the issue of whether or not you can get the relevant benefits if you do the relevant high intensity sessions on the bike. The studies by Stoggl et al and Neal et al demonstrates that bike performance is likely to improve, but this does not directly answer your question of whether the benefits of high intensity sessions on the bike transfer to running.

      I would anticipate that high intensity on the bike should specifically develop ability to transport lactate out of type 2 fibres, and utilise it elsewhere (in type 1 fibres, heart, liver etc). Any increase in ability to metabolise lactate in these other tissues should transfer to running. While the changes that favour recruitment of type 2 fibres might have less relatively benefit for running than for cycling, I suspect that type 2 development will help you run a faster 5K. So I anticipate that doing high intensity session on the bike will help your 5K pace, though of course you will need to ensure that you re-establish appropriate neuromuscular coordination for running before the 5K race.

      I will do my next post on the issue of neuromuscular coordination – an issue relevant to the bike-run transition

  3. Ewen Says:

    Thanks Canute. Looking forward to that post.
    I felt the early signs of benefit from bike sprints on yesterday’s XC race – ran a good time and didn’t feel overly stressed with a 4:10 3rd k, even though it was downhill on rough ground.

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