Is Fatigue All in Your Head?

By Steven Shocki, Alki X Gym trainer

Inspired by a recent review done by Timothy Noakes, an exercise physiologist out of South Africa, I will be discussing what is to me at least, a relatively new model of fatigue.

In school I was taught that exercise induced fatigue was purely a failure of the muscular system to maintain a given intensity of work. This idea was based on of a number of studies performed in the early 1900’s that seemed to show that cessation (termination) of exercise was the result of an oxygen deficit in the working muscles, specifically in the heart. So what this model proposes is that at a certain intensity of exercise oxygen can no longer be delivered to the heart at the rate it is being consumed. In order to protect the heart from essentially having a heart attack, there would then be a slowing of the heart rate in order to reduce its oxygen consumption, which would result in less blood to the muscles, which would ultimately result in the termination of the exercise. This is what I was taught, and it makes sense at first glance.

Noakes however, raises the question that something must be controlling the heart rate and causing it to slow down in order to protect itself from what he calls a “catastrophic failure”, or in other words, to protect homeostasis (the status quo of the body). By bringing the idea of homeostasis into the picture, things have gotten a lot more interesting, because one of the things that we are finding more and more is that when it comes to matters of homeostasis, the brain is almost always the one regulating it. And if the brain is indeed limiting exercise, this has powerful implications for the current model of fatigue because it would then no longer be purely a muscular issue, but rather one that also includes the brain. Noakes refers to this as the “governor hypothesis”, because there is something (in this case the brain) that is governing the intensity of the exercise and limiting it accordingly.

                Noakes goes into a lot more detail, but I will highlight what pertains to us in the gym. First, and this is what is really important, is that your mental state greatly affects your physical performance. He lists a number of factors that he believes play a role in how soon fatigue sets in, including: emotional state, mental fatigue, sleep deprivation, state of recovery from previous exercise session, as well as a bunch of other factors.  

In fact, in 2009 a study was published in the Journal of Applied Physiology displaying this. They had subjects perform a test meant to mentally fatigue them, and they then tested their performance on an exercise bike. With no differences in physiological parameters the subjects all performed worse after having gone through the mental fatigue exercise (Marcora, 2009). I think this really coincides with my experience working out and training in the X Gym; I can usually tell when someone has a lot going in their life outside the gym because it affects their performance in the workout.

When you think about it, there is nothing that is making them physically weaker, yet they often fatigue out faster or simply don’t have the will to keep going. More important than this though, is that while all these factors will certainly make your workout seem harder, in the end what really determines how you perform is whether or not you choose to do well. Noakes gives the example of distance runners sprinting to finish a race. Logically you would think that at the end of a long race you wouldn’t have much energy left and you should theoretically be at your slowest. But this is never the case is it? We always see the runners go even harder at the very end. What changed was their motivation.

If you can find ways to motivate yourself to push through the pain, you will. No matter how bad your day was, if you can find something positive about your workouts to focus on, not only will you fatigue slower, according to these studies there will actually be less pain as well. And that to me is the big take home message: approach your workouts with a positive attitude to get the most out of them.

 I’m not saying you have to get super excited and love everything about them, but just try to have a good attitude towards the whole thing. If all you focus on is the pain, then guess what: it is probably going to hurt. Everyone has it in them to be tough and to be disciplined. Like everything, it just takes practice. So, keep practicing! 

Forget Everything You Thought You Knew About Lactic Acid...

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

For many years, the scientific, medical, athletic communities and the general population have accepted the fact that lactate is a just a by-product created by exercising muscle fibers.

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!

Further, research done in vitro (meaning in a lab using human or animal tissue) and in live rats have suggested that lactate might indeed contribute to increased force production. In an experiment by Nielsen et al. (2001), the reduction in contraction force in isolated muscle fibers caused by elevated potassium (K+) was almost completely reversed following the injection of lactate. Adding to these findings are the findings of Pedersen and colleagues (2004), which suggest that lactate “delays the onset of muscle fatigue by maintaining the excitability of muscle tissue.” However, both studies were done in vitro therefore it is hard to establish what is actually happening during live exercise.

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.

Forget Everything You Thought You Knew About Lactic Acid...

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

For many years, the scientific, medical, athletic communities and the general population have accepted the fact that lactate is a just a by-product created by exercising muscle fibers.

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!

Further, research done in vitro (meaning in a lab using human or animal tissue) and in live rats have suggested that lactate might indeed contribute to increased force production. In an experiment by Nielsen et al. (2001), the reduction in contraction force in isolated muscle fibers caused by elevated potassium (K+) was almost completely reversed following the injection of lactate. Adding to these findings are the findings of Pedersen and colleagues (2004), which suggest that lactate “delays the onset of muscle fatigue by maintaining the excitability of muscle tissue.” However, both studies were done in vitro therefore it is hard to establish what is actually happening during live exercise.

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.