Research review by Alki X Gym trainer Aaron Wagar
“Lactate—a signal coordinating cell and systemic function”
Andrew Philip, Adam L. Macdonald, & Peter W. Watt
It was first theorized to be the reason for delayed onset muscle soreness (DOMS), the feeling of pain and stiffness the day after a hard workout (or sometimes for up to 4 days after). This theory was proven wrong by a well-controlled study where participants were randomly assigned to 2 different groups. One group, which I will call the Lactate Group (LG), ran “up” an incline treadmill and the other group, the Sore Group (SG) ran “down a decline treadmill. Interestingly, the LG group accumulated the most lactate in the muscles, yet the SG was the group to feel significantly more soreness. Apparently, we got that one wrong.
Next, researchers came up with the “lactate-induced-fatigue theory.” Research dating to way back in the day (early 1900’s) has been correlating increased muscle and blood lactate with fatigue, or exhaustion. As more researchers looked into it, the clearer it became, apparently. Lactate is at its highest peak at or just following exhaustion, therefore lactate is the cause of fatigue, right? Wrong. This evidence is only correlational. Lactate does indeed accumulate as exercise intensity increases, and lactate levels are at their highest right around exhaustion, but this does not mean that the lactate is necessarily causing the fatigue. Much research around the subject has been done, and many theories have been tested as to how a muscle reaches fatigue and what exactly the role of lactate is in this process.
A major hypothesis in muscle exhaustion during the 1920’s and 1930’s was the Oxygen Debt hypothesis. This hypothesis was accepted after Hill, with his colleagues and Meyerhof et al.’s research in 1924 showed that lactate increased dramatically once exercise intensity became so great that enough oxygen was not be delivered to the exercising muscle. This led to the Anaerobic Threshold concept in the 1980’s. However, research has confirmed that lactate production is not associated with hypoxia (decreased O2 levels), or to put it in layman’s terms - running out of oxygen, which is one of the main endurance fuel components for muscles.
Although many scientific breakthroughs occurred during the 1980’s and early 1990’s, most researchers still assumed that lactate was at least in part responsible for muscle fatigue. Researchers came up with a new hypothesis—“intracellular lactate acidification” was most likely responsible for the reduction in force production (fatigue) observed in earlier studies. Basically the researchers hypothesized that the environment within the muscle cells was becoming too acidic (due to lactate production) that muscle contraction force was compromised.
In the mid 90’s to early 2000’s studies were published that seemed to show that lactate ions were not responsible for a decreased muscle contraction force. In fact, the effect of acidosis in muscle fatigue is questioned by many, and recent biochemical evidence suggests that lactate might retard intracellular acidosis, which if anything would delay the onset of fatigue and therefore help to improve endurance!
Other evidence seems to suggest that lactate might play a role in the switch from fat to glucose utilization during periods of high-intensity exercise. Scientists found that lactate can also be reconverted to fuel. (It is actually the preferred fuel source for cardiac muscle). Moreover, following the observations of an in vivo (living human beings) study, researchers concluded that lactate seems to have a glucose-sparring effect. This could allow for glucose stores to be maintained (or at least utilization be slowed) during periods of increased exercise intensity, also contributing to delayed fatigue.
The notion that lactate accumulation causes pain during exercise (the feared quad burn), has been preached for a long time. I heard it, believed it, and even propagated it because I didn’t know any better until now. We all assumed that since it feels like acid burning the muscle, it must be from lactic acid, since we knew that was building up at the time. What I have found however, it that there is no direct scientific evidence supporting this assumption.
In fact, studies in which lactate was directly infused during exercise trials concluded that increased lactate has no effect on perceived effort or in the initiation of pain in muscle or joints. However, new research shows that lactate may influence and even modulate nociceptive sensation via acid-sensitive ion channels (ASIC). In other words, lactate may make certain nerve cells more sensitive to what is happening in the exercising muscle. These cells, in turn, send signals to the brain to cease exercise if the intensity becomes too great and they feel that injury is a risk. However, this has only been observed in vitro and the effects in live exercise have yet to be confirmed. What we do know is that lactate itself is not the direct cause of the “burn” pain during exercise.
To end on an exciting note, lactate may actually act as a pseudo-hormone. Studies have observed that lactate induces a pseudo-hypoxic state, which means that the cells’ environment appears hypoxic (low oxygen) but there is plenty of oxygen available. This pseudo-hypoxic state seems to stimulate tissue growth and repair (especially collagen deposition and increased blood vessels). Moreover, it seems to act as a signal for catecholamine release which regulates (usually adding to) the vasodilation effects and resulting circulation increases of active muscle tissue). Further, some in vitro studies have observed anti-oxidant effects of lactate as it bound free radicals.
In conclusion, the role of lactate during high intensity exercise is far from being fully understood. It most likely acts to delay fatigue (instead of cause it like we previously thought) It also increases or at least maintains force production in the active muscle (instead of decreasing force production as we previously thought). Additionally, it increases nerve and blood flow to and from the active tissue. The hormone-like effects of lactate are not clear and more research (especially in vivo) is warranted, however, lactate seems to be quite an impressive by-product, helping us to perform better, stronger and longer instead of the opposite as previously believed.
On a more anecdotal note, this could help explain why some runners perform at their best 1 or 2 days after a stair-climbing race. Stair-climbing is extremely intense and, just like in the “uphill” lactate group, it induces an incredible amount of lactate production. This increased blood-lactate circulation might be the key to their improved performance the next day.
For those of us merely trying to endure and improve our weight-training sessions at the X Gym, I am still undecided as to which strategy of lactate employment is best. Doing high intensity cardio (i.e www.tabataprotocol.com) the day before weight training could possibly increase force production during weight training. Performing high intensity cardio after weight training could produce recovery benefits. Over-loading the muscle with too much training however, could be detrimental to both force and recovery, and increases the risk of overuse symptoms. For now, I would recommend one high intensity cardio session per week after weight training. This will prevent the sprint training from negatively interfering with your physical and mental state during weight training, but could still likely aid in recovery.