Despite research dating back over 30 years, several misconceptions surrounding lactic acid (lactate) still exist amongst fitness practitioners and the general public (1). Common misconceptions include that it was considered a primary cause of fatigue during exercise as well as the cause of delayed onset muscle soreness (DOMS) sometimes experienced 12-to-72 hours following exercise. Furthermore, it was also incorrectly regarded as a waste product of metabolism that would impair athletic performance if it was allowed to accumulate within the muscle cell.
On the contrary, we have come to learn that lactic acid (lactate) is more friend-than-foe and actually serves as a viable energy reserve for both our aerobic and anaerobic pathways (2, 3). It is true that the accumulation of this product during intense exercise can alter muscle pH and impede muscle contraction while simultaneously activating pain receptors (aka acute muscle pain), but this issue normally resolves itself within 30 to 60 minutes following the cessation of an exercise bout (3). The DOMS experienced over subsequent hours to days has nothing to do with this metabolic by-product, but is believed to be more aligned with microtrauma occurring within the muscle fibers due to excessive loads or volumes of eccentric muscle action.
As we can see, there is much to be shared and learned about this compound, but before we dive into this topic in more detail, let’s first resolve another source of confusion – that being the difference between the terms ‘lactic acid’ and ‘lactate.’ Although lactic acid is produced as a by-product of glucose or glycogen metabolism (glycolysis) when the demands for energy exceed the availability of oxygen, it is a weak acid implying that it easily dissociates in water, the primary component of the muscle sarcoplasm where glycolysis takes place. The products of this dissociation are the formation of a lactate ion (negatively charged) and a hydrogen ion (positively charged). So technically, although lactic acid is generally considered everyday vernacular, we are actually referring to the presence of lactate (L-) and hydrogen (H+) in the human body. And it is actually these H+ ions and not the lactate that lower the pH of tissue which interferes with muscle action. The lowering of pH in any tissue (e.g., cells, blood) is called acidosis.
As illustrated in Figure 1-1, the body contains two basic energy systems; the aerobic pathway which functions in the presence of oxygen, and the anaerobic pathways which function in the absence of oxygen. The anaerobic pathway is further sub-divided into two systems; the more immediate phosphagen system and the glycolytic system, (also known as the fast-glycolytic or lactate system) which is the topic of interest in this article.
Figure 1-1: Overview of the bioenergetics pathways
It is important to recognize that these systems do not function independently of each other, but function in a more complementary manner as illustrated in Figure 1-2. Think to the function of a dimmer on a light switch. As exercise intensity progresses, we come to rely more upon our anaerobic systems for many reasons including (3):
- the capacity to generate ATP more rapidly.
- rapid utilization of ATP molecules increases H+ ion concentration in the cell which in turn lowers the cell’s pH – this inhibits the action of carnitine palmitoyltransferase I (CPT1) or carnitine acyltransferase which is needed to transport fats into the mitochondria for aerobic respiration.
- an increased use of carbohydrates as exercise intensity increases also elevates levels of a compound called Malonyl-CoA which also inhibits CPT1 action.
Figure 1-2: Relative Contributions of the Aerobic and Anaerobic Pathways
Glycolysis, Fast Glycolytic or Lactate System
By definition, glycolysis represents the metabolic pathway that breaks down glucose or muscle glycogen into two pyruvates (3). Although pyruvate is technically considered the end product of glycolysis, it actually suffers two general fates:
- it is either converted to lactate in the absence of sufficient oxygen.
- it is shuttled into the mitochondria (aerobic fuel factories) for aerobic respiration.
However, what is important to remember, is that the fate of pyruvate does not follow an all-or-nothing principle (i.e., both occur simultaneously depending on the availability of oxygen). The quantity of pyruvate that enters the mitochondria for aerobic respiration is contingent upon the capacity of the aerobic pathway (i.e., availability of oxygen, size and number of mitochondria). Any excess pyruvate that cannot pass to the mitochondria are converted to lactic acid which then dissociate into L- and H+. The use of an analogy may help illustrate this point:
- Think of a four-lane highway upon which an accident happens in the northbound lanes. With less cars now moving through this section of the highway, we essentially create a backlog slowing down all traffic. In a similar manner, if pyruvate accumulates and is not cleared, it too will create a backlog and slow all glycolysis.
As a high-level summary illustrated in Figure 1-3, glycolysis is a sequence of 10 reactions involving intermediate compounds that ultimately manufacture the two pyruvate structures and in the process produce ATP. During glycolysis, H+ ions are removed from some of the intermediate products produced during the 10 steps and are also produced during the utilization of ATP. Under steady-state (aerobic) exercise, these H+ ions are passed to the mitochondria to generate ATP, but under non-steady-state (anaerobic) exercise, these H+ ions begin to accumulate as they all cannot be cleared to the mitochondria (due to limited oxygen availability). This results in acidosis (lowered tissue pH) which also slows glycolysis.
Figure 1-3: A General Overview of Glycolysis
So how does the body resolve this issue of accumulating pyruvate and H+ ions? Because these compounds cannot be removed directly from the cell, the body combines the excess pyruvate with these H+ ions to form lactic acid (L- and H+), which can both be removed from the cells and placed into the blood. In other words, the formation of these compounds enables the muscle to continue working longer than it ordinarily is capable of doing. Although the muscle has been temporarily alleviated of this problem, it is the blood that has now has inherited the problem. Now you can understand why the production of lactate is actually more friend-than-foe – allowing the muscle to work longer. But like muscle, the accumulation of H+ ions in any medium produces acidosis which will become a problem at some point (3).
Another important fact to consider – glycolysis is a set of reversible reactions as illustrated in Figure 1-3 implying that although glucose or glycogen can be broken down to produce pyruvate and ATP (e.g., during exercise), pyruvate molecules can move backwards through the pathway to produce glucose (e.g., recovery), but this requires ATP in the process which is provided during recovery by metabolizing other fuels like fats. Likewise, lactate can also be converted back to pyruvate. In essence, lactate can be converted back to pyruvate which in turn can be reconverted back to glucose, helping establish the fact that lactate is a viable fuel rather than a waste product. This reversible process plays a significant role in energy production, carbohydrate preservation and replenishment.
Lactate Production and Clearance
The human body is constantly producing L- and H+ considering how certain cells (e.g., red blood cells) lack mitochondria and therefore only generate energy via the anaerobic pathways (i.e., glycolysis). Furthermore, our lives are represented by a series of continual stops-and-starts (e.g., walking up three flights of stairs, suddenly having to run after your child at the park) where we constantly call upon our anaerobic energy systems to provide immediate energy that cannot be completely supplied aerobically. This results in a continual presence of L- and H+ in the blood, which if left unattended would become disastrous because blood acidosis can potentially impair or damage protein structures like red and white blood cells, enzymes and hormones. Fortunately, our blood has the capacity to tolerate the accumulation of these compounds because it contains an assortment of buffers to maintain a relatively stable and near neutral blood pH at all times.
Although various buffers exist in the blood, each with a unique function, sodium bicarbonate (NaHCO3), more commonly known as baking soda, acts as our principal hydrogen buffer. As illustrated in Figure 1-4, sodium or potassium present in our blood binds with lactate to form a sodium lactate or potassium lactate which has several options:
- Removal from the blood into different cells for conversion back to pyruvate to produce energy or glucose (pathway called the Lactate Shuttle) (2)
- Removal into the liver where any glucose produced can be re-released back into circulation (pathways called the Cori Cycle) – only the liver cells are capable of releasing glucose back into the blood, a function that is not possible in muscle cells (3).
However, it is important to also note that some lactate may actually never even leave the cell and enter the blood in the first place, especially when muscle glycogen levels within that cell become depleted. This lactate can actually be shuttled directly into the cell’s mitochondria where it is used as a fuel (pathways called the Intracellular Shuttle) (2).
Figure 1-4: Buffering Lactate and Hydrogen with Sodium Bicarbonate
The remaining bicarbonate binds with H+ ions to form carbonic acid (H2CO3), a weak acid that then dissociates into water and carbon dioxide. Although we have no real need to remove this metabolic water from the body, any excess carbon dioxide not needed by the body can be expelled via the lungs.
At rest, or during lower or more steady-state exercise intensities, we maintain a balance between lactate production and clearance into the blood, and the amount of available buffer, but at higher intensities this can become a problem. Let’s use an analogy of baking soda that we place in our refrigerator to help explain this point. Many use this compound to buffer smells. Now imagine placing a bowl of baking soda on a shelf and each time your refrigerator develops a smell you remove a tablespoon of the powder. Eventually, you might run out and need to replenish the compound. Similarly, we need to constantly replenish this buffer as we use it (combining sodium, water and carbon dioxide – all present within the blood) and as long as we can replenish at the same rate or faster than our rate of utilization, we can sustain L- and H+ clearance from muscles and the intensity of work. At any time however, if we exceed our capacity to replenish this buffer, the blood will prevent any more L- and H+ from spilling over from our cells, forcing their accumulation within the cell which will impair glycolysis. The accumulation of H+ ions in the cell will alter muscle pH and impede muscle contraction, while simultaneously activating pain receptors. The symptoms experienced include a mild burning or tingling sensation within the muscle coupled with a gradual inability to maintain muscle action. This is often referred to as the lactate threshold (LT) by practitioners and the public which we will discuss shortly. At this point what you need is simply time to recover your buffer so you can continue to spill L- and H+ out of the cell, or to reduce your exercise intensity. Regardless of how much mental fortitude you believe you might have, here is where physiology trumps psychology. In essence then, this pathway is not necessarily limited by your muscles, but perhaps more by what your blood is capable or incapable of handling.
Now think to your circuits – do you believe that by continually rotating muscle groups, without proper recovery, you are allowing yourself to maintain exercise intensity? In fact you are not, because all the L- and H+ produced within the different muscles ends up spilling over into the blood (systemic) and once we’ve reached capacity, you will need to recover or slow down. This is where we see a transition from exercise intensity to exercise effort – two completely different training parameters.
- Exercise intensity emphasizes overload to get bigger, stronger, faster; represents more calories expended per unit of time; ensures better form given its inclusion of appropriate recoveries and can be measured objectively (e.g., wattage, 40-sec sprint time, 1 RM).
- Exercise effort emphasizes volume of work with reduced emphasis on appropriate recoveries; does not necessarily burn significantly more calories per unit of time despite the increased amount of work performed (i.e., at lower intensities); is usually associated with greater likelihood of bad technique, higher injury-risk and poorer experiences; and is usually only measured subjectively (e.g., ratings of perceived exertion).
Lactate Threshold (LT) and Onset of Blood Lactate Accumulation (OBLA)
Let’s explain these two terms because confusion exists between the scientific definitions of each and how they are commonly used within fitness and performance. We will always have a minimal amount of blood lactate given what was discussed previously - red blood cells lack mitochondria and therefore only produce energy anaerobically. During exercise however, a slight, but manageable increase in H+ ions levels in the blood reflects a small imbalance between H+ spill over from cells and our buffering removal from blood, and this illustrates the first accumulation of blood lactate above resting concentrations (refer to Figure 1-5). This is scientifically defined as the lactate threshold (LT), but is often misunderstood by practitioners and the general public. Technically, this point represents an intensity where carbohydrates now become the body’s primary fuel or where the body begins to lose its aerobic efficiency (i.e., the ability to keep burning fats as a primary fuel) and starts relying more upon the anaerobic systems to assist in producing energy (5).
Further increases in exercise intensity continue to raise L- levels (and H+ ions), suggesting greater disruptions between lactate spill over and removal from the blood. This ultimately leads to a disproportionate increase in blood lactate and subsequent acidosis due to elevated levels of H+. This point is known as the onset of blood lactate accumulation (OBLA), which is the point at which the ability to perform high-intensity exercise cannot be sustained for much longer (6).
Physiologically, this marker indicates an inability by the body to dispose or manage the rate at which L- and H+ ions are entering the blood and the body’s ability to dispose of H+ ions becomes overwhelmed. In practical terms, this is the marker of intensity that is of interest to athletes and coaches because intensities immediately below this level represent the highest sustainable intensity of exercise. Practitioners and athletes however, often refer to this point as LT which is technically incorrect. To avoid confusion, the terms ventilatory threshold 1 (VT1) and ventilatory threshold 2 (VT2) are more commonly used to represent LT and OBLA respectively.
Figure 1-5: Lactate Accumulation Markers - LT and OBLA
From a performance standpoint, implementing strategies to boost both VT1 and VT2 will improve fuel utilization efficiency and overall athletic performance. Although aerobic training provides the basis for VT1 training, anaerobic training (intervals) should be emphasized to boost VT2 which adapts by:
- Spilling L- and H+ more rapidly into the blood from muscle cells.
- Removing these compounds from the blood more efficiently.
- Regenerating the lactate buffer more rapidly.
- Increasing the total amount of buffer within the blood marginally.
However, expanding your blood volume, achieved primarily via aerobic training is also an effective method to increase the total amount of lactate buffer held in your blood. Aerobic training can expand blood volume by 12-to-20% in order to accommodate more red blood cells, but this same expansion also allows for a greater, and sustained quantity of buffer to be stored within the blood without raising blood pH. Sodium bicarbonate (NaHCO3) is a base which raises blood pH which generally cannot exceed 7.45 (refer Figure 1-4).
An individual can also increase their levels of buffer in the blood temporarily (last a few hours) via a nutritional intervention (7, 8):
- Consuming an alkalizing agent like sodium bicarbonate (baking soda) at a recommended dose of 0.2 - 0.4 g per Kg of body weight (0.1 - 0.18 g per pound lb.) with one liter (33.8 oz.) of fluid 60-120 minutes before exercising can improve performance by reducing metabolic acidosis which limits high-intensity exercise performance. As this has a bitter and unpleasant taste, one might need to add flavors to make the beverage more palatable.
- However, there are side-effects associated with ingesting sodium bicarbonate that include gastrointestinal distress (e.g., nausea, diarrhea, stomach acidity) that should be considered.
Over recent years, research has examined bioenergetics (energy) pathway differences between men and women (3). Considering how women generally have a slightly lower concentration of type II fibers than men (fibers more responsible for anaerobic respiration) and smaller blood volumes (and therefore less lactate buffer), it is assumed that they have a lower capacity for anaerobic exercise in comparison to men. These assumptions are further supported by research into the role of estrogen and the anaerobic pathways where estrogen is believed to:
- reduce the rates of glycolysis, which reduces rates of ATP availability.
- reduce the activity levels of the glycolytic enzymes, thus slowing glycolysis.
- reduce activity levels of lactate dehydrogenase (LDH), the enzyme that facilitates the conversion of pyruvate to lactate, thereby slowing lactate clearance from the muscle.
- reduces glycogen loading capacity, which translates into less available glycogen being stored within the muscles
Collectively, these factors diminish the overall efficacy and efficiency of the anaerobic pathways in women, which merits consideration when programming. Although no clear guidelines exist, the overall takeaways are that work intervals probably need to be shorter in duration for women given their potential inability to produce and clear lactate as quickly, coupled with smaller amounts of available buffer versus men, but can utilize shorter recovery intervals (e.g., 1-to-2 work-to-recovery ratios or shorter) as they don’t need to regenerate as much buffer. Additionally, work intervals for women should be somewhat less challenging than for men if attempting to match work-interval time frames with men.
As practitioners it is our professional responsibility to comprehend the physiological systems that drive muscle action so that we not only program safely and effectively, but also to provide credible and accurate information to our clients and to the public in our ongoing effort to move our industry forward. As a credible resource you also enhance the equity of your brand so, now that your expanded your toolbox with the lowdown in lactic acid (lactate), help us collectively debunk many misconceptions and myths surrounding this compound.
- Brooks GA, (1985). Anaerobic threshold: review of the concept and directions for future research. Medicine and Science in Sport and Exercise, 17(1):22-34
- Brooks GA, (2009). Cell-cell and intracellular lactate shuttles. The Journal of Physiology, 587(23):5591-5600.
- Pocari J, Bryant CX, and Comana F, (2015). Exercise Physiology, F.A. Davis Company, Philadelphia, PA.
- Pilegaard H, Domino K, Noland T, Juel C, Hellsten Y, Halestrap AP, and Bangsbo J, (1999). Effect of high intensity exercise training on lactate/H+ transport capacity in human skeletal muscle. American Journal of Physiology, 276: E255-E261.
- Brooks GA, Fahey TD, and Baldwin KM, (2005). Exercise Physiology: Human Bioenergetics and its Applications (4th). New York, NY: McGraw-Hill Companies.
- Kenney WL, Wilmore JH, and Costill DL, (2012). Physiology of Sport and Exercise (5th), Champaign, IL: Human Kinetics.
- Bishop D, Girard O, and Mendez-Villanueva A, (2011). Repeated-sprint ability part II: recommendations for training. Sports Medicine, 41:741-756.
- Peart DJ, Siegler JC, and Vince RV, (2012). Practical recommendations for coaches and athletes: a meta-analysis of sodium bicarbonate use for athletic performance. Journal of Strength and Conditioning Research, 26:1975-1983.