Exercise-Associated Muscle Cramps: Knowns and Unknowns

Number of Scientific Sources: 4

Comprehension Level: Intermediate

Table of Contents:

• What Are Exercise-Associated Muscle Cramps?
• Poking Holes In The Electrolyte/Hydration Hypotheses
• What’s Missing: Neuromuscular Fatigue
• Treatments

What Are Exercise-Associated Muscle Cramps?

If you have never had an exercise-associated muscle cramp (EAMC) during physical activity, consider yourself lucky. They are intense, involuntary muscular contractions. Depending on where they occur and the magnitude of the severity, they can be debilitating. A calf cramp will likely floor you because your leg is under a spell of excruciating plantarflexion. Abdominal cramps feel like your stomach is imploding and you can’t stop yourself from curling forward. Despite EAMCs being nothing new, we still don’t exactly know why they occur.

Poking Holes In The Electrolyte/Hydration Hypotheses

It has been echoed since the land before time that if you want to prevent or get rid of cramps, you should eat your bananas and drink more water.

Where does this thought process stem from?

This is based on the premise that EAMCs are caused by a fluid and electrolyte imbalance. In other words, if you are dehydrated or when sodium levels are relatively mismatched with water and other electrolytes (i.e. potassium (found in bananas), calcium, magnesium, and chloride) in and around your cells, this can cause your muscles to cramp. Thus, sweating from exercise, especially in hot environments, is thought to cause cramping, especially if you are not properly replenishing yourself with electrolyte-enriched fluids.

There has been some evidence that suggests this to be true. For example, some athletes that have higher sweat rates, sodium losses, and/or chloride losses may be more likely to have cramps (Miller et al, 2022).

However, the support for this hypothesis can be contrasted for the following reasons, according to Miller et al (2022):

1. EAMCs are not only correlated with high body temperature or hot environments. Some research suggests application of cooling modalities do not relieve cramps. Further, cramping can occur in any temperature/environment.
2. Plasma characteristics (i.e. electrolyte concentrations in the blood and plasma volume) in athletes with and without EAMCs were often within normal limits and comparable after exercise (although this likely does not represent intracellular concentrations).
3. Some research has shown that dehydration of up to 6% loss of body mass has not shown to affect resting membrane potential (aka the balance of electrical charges across a cell’s membrane are undisturbed, which has a fundamental role in muscle contraction). If you weighed 200 lbs, that would be losing 12 lbs from fluid loss. The evidence in favor of electrolyte administration is weak and limited, at best.
4. Water and electrolyte losses are often systemic, but muscle cramps are usually localized to a specific muscle.
5. Stretching can alleviate a muscle cramp without affecting fluid status or electrolyte concentrations, suggesting the mechanism(s) behind cramping are not as relevant to hydration or nutrition as previously believed.

So if heat, hydration, and nutritional status may not be the primary culprits, what explains the onset of a muscular cramp during or after exercise?

What’s Missing: Altered Neuromuscular Control

One common denominator that early research failed to account or control for is neuromuscular fatigue. There are various types of fatigue (i.e. mental/psychological, peripheral, central, etc) and most are intertwined to some extent. In this case, neuromuscular fatigue might fill in the gap and offer an explanation as to why EAMCs occur.

What is neuromuscular fatigue, though?

Basically, it is fatigue stemming from the nervous system that impairs or alters muscular homeostasis and contraction. The brain and spinal cord are losing their connection with the muscles.

Some basic neurophysiology will be important to highlight, when it comes to understanding the connection between neural fatigue and muscle cramps.

Motor neurons (or motor nerves) are components of our intricate nervous systems that permit voluntary and involuntary movement via activation of muscles and glands (Zayia & Tadi, 2023). Motor neurons can be split up into upper and lower motor neurons. Lower motor neurons can be divided into somatic motor neurons, special visceral efferent (branchial) motor neurons, and general visceral motor neurons. Somatic motor neurons can be further divided into alpha, beta, and gamma neurons.

For the sake of this article, we will mostly care about the alpha motor neurons (which are largely responsible for muscle contraction) and gamma motor neurons (which primarily respond to stretch of muscle spindles (muscle spindles = receptors in our muscles that detect the rate of change in length/stretch)). When excessive lengthening is detected, the stretch reflex occurs, which tells (excites) our muscles to shorten/contract.

Golgi tendon organs (GTO) will also need an honorable mention, which are receptors in our tendons that detect the rate of change in tension. When excessive tension is detected, the inverse stretch reflex occurs, which inhibits muscle contraction (aka promotes relaxation). This is also referred to as the Golgi tendon reflex or autogenic inhibition.

Altogether, these have a role in muscle contraction and the regulation of muscle tone (muscle tone = the involuntary, continuous partial contraction of our muscles that is always happening (our muscles are never truly relaxed)). Our muscles are under constant surveillance from our central nervous system that respond to various feedback mechanisms, which manifests as a dynamic balance between inhibitory and excitatory inputs. An abnormal deviation from this balance (less inhibition + more excitation) caused by neuromuscular fatigue and altered neural control is what is thought to be the foundation of EAMCs (Miller et al, 2022). In other words, your brain and spinal cord are losing control of your muscles from fatigue-related factors.

This hypothesis is fortified by the following reasons, according to Miller et al (2022):

1. Previous research identified risk factors that were better associated with fatigue-induced alterations in nervous system excitability (i.e. poor conditioning and high exercise intensities) than dehydration or electrolyte losses.
2. EAMCs usually happen near the end of competitions or events, when fatigue is likely the greatest.
3. Most EAMCs occur in contracting, multi-joint muscles (i.e. gastrocnemius (the calf muscle)). Multi-joint muscles often contract in already shortened positions, which means the amount of muscle inhibition coming from Golgi tendon organs is reduced.
4. People that experience little-to-no cramps produce more inhibitory inputs than people who experience cramping.

That said, neuromuscular fatigue might not fully explain the onset of EAMCs. In reality, they (EAMCs) are likely multifactorial (see image below from Miller et al (2022)).

According to this proposed model of EAMCs, there must be a factor threshold that allows a cramp to manifest. This can explain why cramps might happen in some people, while others are spared. Nevertheless, science is still trying to find ways to explain exactly why EAMCs happen.

Treatments

Just because we do not fully understand why EAMCs happen, it does not mean that we do not know how treat them after they occur.

As of now, stretching is the most recommended treatment strategy for alleviating cramps. Physically, stretching while pry apart the contractile proteins in your muscles that are shortened during a cramp. However, the effect from doing this also has a neural component, which is likely the primary reason as to why stretching works. Stretching will activate the Golgi tendon organ to produce inhibitory signals, potentially restoring balance to muscular tone. Interestingly, stretching prior to exercise does not have much evidence to support its use as a preventive method (Evers-Smith & Miller, 2023; Miller et al (2022)).

Pickle juice is gaining popularity for cramping and probably not because of the sodium content from a nutritional standpoint. Parts of our digestive system (i.e. mouth, oropharynx, esophagus, and stomach) contain receptors that detect temperatures and sensations that can be stimulated by strong tastes, such as the sensation when they interact with acetic acid (a main component of vinegar). The stimulation of these receptors can trigger the oropharyngeal reflex, which might stop cramping via inhibiting the alpha motor neuron (Hooper et al, 2020; Miller et al, 2022).

Further, acetic acid might aid in the role of acetylcholine plays in muscular contraction/relaxation (Hooper et al, 2020). Acetylcholine is a neurotransmitter that is released from our nerves and binds to our muscles to facilitate contraction. Acetylcholine is broken down by an enzyme (acetylcholinesterase), which yields choline and acetic acid, and promotes muscular relaxation. More acidic acid after consumption = possibly more muscle relaxation.

Despite the interesting bits of information we now know (or confidently believe, based on the current evidence), the current body of research is still quite limited. EAMCs are hard to study due to the spontaneity of them. In addition, what can be provoked in a lab setting might not be safe to assume and generalize in real world settings. At the very least, we can confidently assume 1) that cramps can occur for a variety of reasons, 2) the central mechanism likely involves the nervous system, and 3) they can be treated with stretching and/or acetic acid consumption (but more research is needed on the latter).

References

Evers-Smith & Miller. (2023). Does Prophylactic Stretching Reduce the Occurrence of Exercise-Associated Muscle Cramping? A Critically Appraised Topic.

Hooper et al. (2020). Quantitative Analysis of the Acetic Acid Content in Substances Used by Athletes for the Possible Prevention and Alleviation of Exercise-Associated Muscle Cramps.

Miller et al. (2022). An Evidence-Based Review of the Pathophysiology, Treatment, and Prevention of Exercise-Associated Muscle Cramps.

Zayia & Tadi. (2023). Neuroanatomy, Motor Neuron.

About the Author

Alex Tran is a personal trainer, nutrition coach, and virtual coach that is based in Chicago, IL. He has a Master’s degree in Applied Exercise Science with a Sports Nutrition emphasis. Additionally, he is a Certified Strength & Conditioning Specialist through the National Strength & Conditioning Association and a Certified Pre/Postnatal Coach. To see more of his content, follow him here: instagram.com/atperformance_. To contact him, follow this link.