If you work out, you’re already familiar with feelings of fatigue – burning muscles and the sensation that you simply can’t do another rep. It’s fatigue that often limits workout performance. Plus, the level of fatigue you experience on a given day can change. Have you noticed that there are days when exercise feels easier, when you go longer, and push harder than other days? These variations may have to do with how well you slept the night before, what you ate before your workout, stress level, and if you’re well hydrated.
But what about fatigue that happens during a strength-training workout, the kind of fatigue that keeps you from doing another rep and forces you to stop and rest? Believe it or not, we still don’t have a thorough understanding of exercise fatigue, but there seems to be three main types of disturbances that affect the muscle and cause it to fatigue. Let’s look at each.
Local Muscle Fatigue
Local muscle fatigue – you’ve probably experienced it many times. You struggle to do another rep of squats or biceps curls but your muscles feel so heavy that you can barely eke it out. Simply put, your muscles are spent. Why does this happen? One factor is local muscle fatigue. This simply means that something at the level of the muscle limits the muscle’s ability to generate force.
Muscles are instructed to contract by input from the brain and nervous system. The command leads to the generation of an action potential by a motor neuron and the release of acetylcholine. Acetylcholine release, in turn, stimulates the sarcoplasmic reticulum of the muscle cell to release calcium. Once calcium is released, it binds to troponin, which, in turn, allows actin and myosin cross-bridges to form so that muscle contraction can take place.
One theory as to why local muscle fatigue happens has to do with the muscle’s interaction with calcium released from the sarcoplasmic reticulum. As the muscle fatigues, it can’t bind calcium as readily and the necessary cross-bridges between actin and myosin can’t form and the muscle can’t contract. One study even found that with prolonged muscle contraction, muscle cells begin to leak calcium.
Another theory is that repeated muscle contractions lead to a build-up of free radicals. These free radicals damage proteins involved in muscle contraction and reduce the number of actin and myosin cross-bridges that form. In fact, researchers at the University of Kentucky found that giving the antioxidant drug n-acetyl-cysteine to exercisers delayed muscle fatigue, further suggesting that oxidative damage and free radicals may play a role in muscle fatigue.
Metabolic Fatigue
There’s also a metabolic component of fatigue. To contract, your muscles need a constant supply of ATP. When the ATP supply outstrips the demand, muscle cells accumulate metabolic products, such as hydrogen ions and inorganic phosphate. These metabolites interfere with the ability of actin and myosin cross-bridges to form. Fortunately, with five minutes of rest, your muscles clear these metabolites and the muscle recovers. So, metabolic fatigue is short-term fatigue caused by a lack of adequate fuel and is characterized by the build-up of metabolic waste products. Even though lactic acid also accumulates during intense exercise, it does not play a role in fatigue.
Metabolic fatigue happens when you deplete energy reserves like glycogen or build up lactic acid during high-intensity exercise. It’s not lactic acid that causes fatigue but the rise in hydrogen ions that takes place when lactic acid releases a hydrogen ion to form lactate. As hydrogen ions increase, so do potassium ions. As potassium builds up in muscle cells, it interferes with the ability of muscle cells to generate the electrical charge they need to contract. You usually experience this type of fatigue as a burning feeling in your muscles. A 30-second sprint can very quickly bring on the sensation of metabolic fatigue.
Neural Fatigue
Your brain can also be the limiting factor in how quickly you fatigue. As mentioned, the command for a muscle to contract comes from the brain. The brain sends a signal to motor units through the spine and an action potential follows. Then, the previously discussed sequence of events takes place that finally leads to cross-bridge formation in the muscle and muscle contraction. If the signal from the brain is weak, the muscle will have problems contracting even if the muscles still have enough ATP to contract.
Neural fatigue can be brought on by deviations in neurotransmitters, brain chemicals, like dopamine, serotonin, and norepinephrine. What causes these changes? A number of factors, including stress, lack of motivation, overtraining, medications, dehydration, or poor nutrition contribute to neural fatigue. You have receptors in your brain that monitor hydration and nutritional status, heart rate, and body temperature. When your brain detects inadequate hydration, elevated body temperature, or low nutritional status, the signals it sends to the muscles are weaker.
Neural fatigue can also be brought on by a long or grueling workout. Drinking a few cups of caffeinated coffee before a workout may help delay the onset of neural fatigue by altering neurotransmitters like norepinephrine and blocking adenosine receptors. Adenosine is a chemical that causes you to relax, so blocking it boosts motivation, attention, and reduces central fatigue.
Neural fatigue early in a workout can also be a sign that you’re pushing yourself too hard or not giving yourself enough recovery time. Make sure you’re giving your body enough time to recover between workouts.
The Bottom Line
Fatigue is part of the training equation but it’s important to know how to manage it. Don’t push yourself hard and not give yourself enough recovery time between sessions. Make sure you’re going into a workout with adequate energy stores (a pre-workout snack) if you’re doing high-intensity exercise. Stay hydrated as well. Finally, make sure you’re getting sufficient sleep and managing stress to reduce neural fatigue.
References:
J Physiol. 2008 Jan 1; 586(Pt 1): 11–23.
Muscle Nerve. 2005 Nov;32(5):633-8.
Baillieres Clin Endocrinol Metab. 1990 Sep;4(3):441-59.
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