I’ve been thinking about lactate and low carb lately, and haunted by guilt for not writing anything here in some while, I thought I’d share my thoughts.
If you’re even just remotely interested in exercise, chances are that you still know buildup of lactate should be avoided. Those with more exercise experience will have heard of the benefits of exercising at the lactate threshold, the exercise level where lactate production will exceed the rate of removal, and lactate accumulates. Those with expert knowledge will perhaps pray for more lactate while exercising. It’s a funny thing really.
Lactate is produced when glucose is broken down. Glucose is first broken down to pyruvate, and lactate is then made from pyruvate via the enzyme lactate dehydrogenase (LDH). Lactate can be burned as energy and can also be turned back into glucose in the process called gluconeogenesis. The thing with lactate production is that we produce more at higher intensities of exercise. It is with dread that i remember the 800 meter competitions I competed in when I was younger. The last 100 m of those races was an exercise in willing my legs to move even though they felt like they would burst from pressure of lactate build up. Lactate has a poor reputation, but as it seems, it is quite undeserved.
Because lactate is produced from glucose, an athlete primarily fueling his body on carbohydrates will produce more lactate than one primarily fueled on fat.
In fact, lactate levels are notoriously lower after low carb, high fat diets and this is in one of the hallmarks of fat adaptation. Even 4 days of high fat dieting followed by a carb loading day will make you produce less lactate during exercise (and also burn proportionately more fat) (1).
In «The art and science of low carbohydrate performance», Volek and Phinney has this to say on the matter:
«An increased reliance on fat and a corresponding decrease in glycolysis during exercise is associated with less accumulation of lactate (a surrogate for hydrogen ion accumulation). As cellular lactate and hydrogen ion levels increase at higher intensities of exercise, there are several events that cause force production and work capacity to decrease. A key contributor in this process is the acidity (i.e., decreasing pH) associated with hydrogen ion buildup. Along with maximal oxygen consumption, lactate threshold (the exercise intensity where blood lactate begins to accumulate) is a major determinant of endurance performance. With the enhanced ability to oxidize lipid associated with keto-adaptation, there is less lactate production at any one workload, and thus an elevation in the threshold exercise intensity associated with increased acidity.»
As you see, reduced lactate production is used as an argument in favor of low carbohydrate dieting. But, this reasoning might be based on a shaky foundation. It rest on the assumption that more lactate is bad and that less is good. Also, acidity doesn’t seem to be the problem (2).
When we exercise, potassium ions (K+) leak out of the muscle cells and into the extracellular compartment causing the muscles be depolarized and losing their excitability. Muscles are sort of like batteries. There has to be a difference in electrical charge between the inside and the outside of the cell to make them contract. Loss of contractile force has often been blamed on lactic acid build up and the reduced pH that follows.
So it seems that lactate is in fact what keeps muscles from fatiguing when extracellular potassium is high and removing lactic acid would only cause us to fatigue earlier. We can no longer blame lactate.
But if this is true, as it seems to be, what then of the claims that low carb is beneficial because less lactate is produced?
Studies of low carbohydrate diets and endurance exercise performance indicate that lower carb may reduce the ability for high intensity sprints during endurance races (5). I wonder if this may in fact partly be explained by the reduced lactate output (of course it could simply be because fatty acids takes too darn long to oxidize). I asked Kristian Overgaard, one of the Danish researchers, and he answered:
«I would say that if a dietary intervention influences the glycolytic flux and production of lactic acid, this may affect muscle function through a number of different mechanisms – one of them being a reduction in excitability-protective effect of acidification, which our group has demonstrated in skeletal muscle. Whether this particular mechanism is important in explaining the reduced performance is speculative. But it is a possibility.»
Now, it was first believed that the effect of lactic acid on depolarization was due to the fact that it was an acid. For example, the Danish researchers exposed rat muscles, that were incubated in a high potassium ion solution, to CO2 and this caused an increased excitability. Because of this, my thinking was that increased levels of the ketone bodies beta-hydroxybutyrate and acetoacetate, might fulfill the same function as lactic acid, because they also are acids. But results from the Danish group suggested that the effect of lactic acid was on chloride channels and not a result of reduced pH. This does not however mean that ketone bodies may not exert some other positive influence, minimizing the proposed negative consequence of the reduced lactate output.
(1) Burke LM, Hawley JA, Angus DJ, Cox GR, Clark SA, Cummings NK et al. Adaptations to short-term high-fat diet persist during exercise despite high carbohydrate availability. Med Sci Sports Exerc 2002; 34(1):83-91.
(2) de Paoli FV, Ortenblad N, Pedersen TH, Jorgensen R, Nielsen OB. Lactate per se improves the excitability of depolarized rat skeletal muscle by reducing the Cl- conductance. J Physiol 2010; 588(Pt 23):4785-4794.
(3) Overgaard K, Hojfeldt GW, Nielsen OB. Effects of acidification and increased extracellular potassium on dynamic muscle contractions in isolated rat muscles. J Physiol 2010; 588(Pt 24):5065-5076.
(4) de Paoli FV, Overgaard K, Pedersen TH, Nielsen OB. Additive protective effects of the addition of lactic acid and adrenaline on excitability and force in isolated rat skeletal muscle depressed by elevated extracellular K+. J Physiol 2007; 581(Pt 2):829-839.
(5) Havemann L, West SJ, Goedecke JH, Macdonald IA, St Clair GA, Noakes TD et al. Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance. J Appl Physiol 2006; 100(1):194-202.