You’re running and suddenly you can run no more. You slow to a walk until your muscles feel “ready” to run again and you do. Or, you are squatting a barbell for reps and on the last one, you pause at the bottom of the movement as your muscles temporarily fail. (Hopefully, you are in the cage or have someone to lift said barbell off your back with minimal damage.) What exactly is going on here?

Over the years, we’ve been lead to believe that this is a simply linear process of depletion of fuel and build-up of waste products that cause our muscle to reach a point of temporary failure to contract. Makes sense, right? This is because a long time ago, skeletal muscle cells in culture were made to contract with electrical impulses and when they failed to contract despite stimulation, it was shown that they were depleted of nutrients and/or had accumulated a high level of metabolic waste.

However, what happens in the petri dish does not always happen in real live organisms. When muscle from exercising individuals was taken during a fatigued state after exercise, there actually wasn’t a catastrophic depletion of ATP or extremely high levels of metabolic waste. Why the difference?

Well, people are complex. Those muscle cells from the petri dish are actually part of a complex organ system that interacts with other complex organ systems and is controlled by a central nervous system. Our bodies are pretty complex and perhaps sophisticated beyond simple termination of activity due to a catastrophic metabolic or physiologic condition that could possibly lead to a whole host of other problems such as organ failure.

So, I’m going to get very technical here and describe the current thoughts on what exactly causes muscle fatigue.

Although the process of muscle contraction is driven by the presence of ATP, depletion of ATP is not necessarily responsible for muscle fatigue as levels of ATP measured in fatigued muscle have not been found to be severely reduced. Instead, it is thought that other factors, possible involving temporary inability of the muscle cell to respond to nerve impulses, may be to blame. (Rhoades and Pflanzer 1989, 508)

There are many mechanisms thought to be involved in skeletal muscle fatigue including metabolism, heat, hypoxia (lack of oxygen), and depletion of glycogen stores. Somehow, a combination of increased body temperature, decreased oxygen saturation, an increase in metabolic waste products such as lactic acid, a decrease in ATP, and depletion in muscle and liver glycogen is thought to bring about fatigue at which point a period of recovery must take place before further activity can continue. However, this “linear” characterization of fatigue as a catastrophic endpoint is not supported by the current research. (St Clair Gibson and Noakes 2004)

In the previous model, it was hypothesized that the perception of fatigue was the result of the impairment of skeletal muscle by metabolic and other changes. These results were based on experiments performed in cell culture. However, in in vivo experiments, where the experiments were carried out in live subjects, feelings of fatigue did not correlate with significant metabolic changes or other peripheral endpoint changes. Therefore, the link between the perception of fatigue and physiologic variables has not been demonstrated. (St Clair Gibson and Noakes 2004)

The role of the brain as a “central governor” in fatigue has been hypothesized in recent years to account for the lack of evidence pointing to fatigue being the result of a metabolic or peripheral catastrophic endpoint. In this hypothesis, the brain acts on information gathered from the body such as heart rate, oxygen saturation, and changes in metabolites to manage muscle fiber recruitment in such a way as to maintain homeostasis while completing tasks. In this manner, fatigue may be another way in which the body self-regulates homeostasis. (St Clair Gibson and Noakes 2004) (Lambert, St Clair Gibson and Noakes 2005)

So, how can we use this information to our advantage?

Rate of Perceived Exertion

When performing a task such as running or lifting weights, it may seem easy or quite difficult. Gunnar Borg created a scale by which to gauge difficulty of a task and demonstrated that it correlated to measurable physiologic parameters such as heart rate. This scale is known at the rate of perceived exertion (RPE) and using a target RPE has been shown to be as effective as using a device to measure exercise intensity level such as a heart rate monitor. (Alberton, et al. 2010) (Borg 1998) (Celine, et al. 2010) (Tiggemann, et al. 2010)

There is currently some disagreement among exercise physiologists regarding the RPE and what exactly it measures, ie, is it a sensation generated by the brain or is it a direct product of peripheral nervous system feedback? A review of the current literature indicates that the sensation of effort may be generated centrally from the brain whereas sensations such as pain or temperature may be generated directly from the peripheral nervous system. (Smirmaul 2010)

So, I can summarize this in two sentences to make this very clear: It is hypothesized (this is the important part) that our brain acts on subtle cues such as metabolite levels, body temperature, respiratory and circulatory rate, etc. to induce fatigue in order to maintain homeostasis. Using a rate of perceived exertion, the sensation of effort related to peripheral signals and neurological input perceived by the brain, we can accurately pace our workouts. The key is knowing when to listen. And just so you know, this is NOT at the beginning of the workout or before you even get to the gym when you are quite certain your brain is telling you to go get a latte or stay in bed.

Bibliography

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Amann, Markus, Lee Romer, Andrew Subudhi, David Pegelow, and Jerome Dempsey. “Severity of arterial hypoxaemia affects the relative contributions of peripheral muscle fatigue to exercise performance in healthy humans.” Journal of Physiology, 2007: 389-403.

Amann, Markus, Marlowe, Lovering, Andrew Eldridge, Michael Stickland, David Pegelow, and Jerome Dempsey. “Arterial oxygenation influences central motor output and exercise performance via effects on peripheral locomotor muscle fatigue in humans.” Journal of Physiology, 2006: 937-952.

Borg, Gunnar. Perceived Exertion and Pain Scale. Champaigne, IL: Human Kinetics, 1998.

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