Exercise Associated Muscle Cramp
What is it?
Exercise Associated Muscle Cramping (EAMC) is a phenomenon that many competitive athletes are familiar with. You’re running (or swimming) along when suddenly, as if possessed, you feel a piece of your body seize up. It can put you on the ground quicker than an Italian soccer player looking to draw the referee’s whistle.
Technically, EAMC is a sudden spasm in a working muscle that results from explosive hyperactivity of the ‘neuromuscular junction’ (NM Junction) – the point where the nerve attaches to the muscle. This results in significant pain that may force the athlete to slow significantly or stop their activity altogether.
Symptoms
Signs of hyperexcitability may appear first as mild fasciculation (or twitching) within the muscle that may be visible and/or perceivable by the athlete but do not yet interfere with activity. This may gradually increase in severity leading to a ‘tightening’ that requires a modification or slowing of activity. Conversely, a mild sensation of tightening or twitching may ‘jump’ right to a full seizing up with little additional warning.
Areas most commonly affected include the calf muscles, hamstrings and quadriceps. Swimmers are familiar with EAMC affecting the muscles in the arch of their feet.
EAMC is most pervasive in endurance events such as distance running and tennis.
Differentiating Cramps
EAMC can be tricky to differentiate from another phenomenon – Exertional Heat Cramps (EHC), as both are related to exercise. However, they should be considered separate, as the underlying cause is distinct.
1) EAMC, associated with local muscle fatigue and 2) ‘Exertional heat cramps’ (EHC) is associated with dehydration and a ‘whole body exchangeable sodium deficit.’ 1
At the medical tent of endurance races, we see “crampers” who respond nicely to the neuroinhibition and stretching techniques – these are athletes with local EAMC in overworked muscles. Less frequently we see a person who cramps without relief until given a liter of intravenous saline. This athlete is clearly experiencing a cramp associated with dehydration (EHC).
EHC is a result of profuse sweating often associated with exercise in hot temperatures. Excessive sweat loss results in an electrolyte concentration change that takes place within the muscle (and the surrounding ‘interstitial fluid’).
* For a more detail description see the article: Muscle Cramps during Exercise – Is It Fatigue or Electrolyte Deficit.
Controversy
In the past, muscle cramps have been attributed almost exclusively to dehydration and electrolyte depletion; most experts now agree that these factors often aren’t the primary cause of cramping in athletes. The outdated explanation goes like this: ‘when you exercise, your body sweats, releasing water and electrolytes like sodium, potassium and magnesium. The athlete continues to expel water and electrolytes, eventually becoming depleted. Electrolytes help conduct nerve impulses throughout your body, allowing you to activate muscles to contract. When your body loses enough water and/or electrolytes, the nerve impulses from your brain to your muscles become disrupted. This disruption causes your muscles to cramp.’
This is why you’re told to consume sports drinks, electrolyte tablets, and lots of water during and after your workouts to help prevent or treat all types of muscle cramps. Unfortunately, there’s almost no evidence that this works for the majority of cramping athletes. 2 3 4
* That is not to say that proper hydration, electrolyte and (perhaps more importantly) glycogen replacement strategies aren’t important. But, the importance of these strategies for treating and preventing cramps are equivocal at best.
Experts now agree that the majority of athletic cramps are not caused by these factors. 5 6 7
Consider:
‘Cramping risk’ is not correlated with blood electrolyte depletion during endurance events – One study of ultramarathon runners demonstrated that those who ‘cramped’ had identical electrolyte levels and dehydration levels when compared to those who did not. 8 9
- Dehydration is a systemic phenomenon and therefore does not explain a focused event at one muscle. Real electrolyte deficiencies can result in full body muscle spasms. Even minor imbalances, if symptomatic, should be a more ‘global’ event.
- Stretching and brief rest are frequently effective strategies for cramping – This would obviously have no effect on a true electrolyte imbalance.
What’s Really Happening?
Muscles have sensory structures that help regulate tension. When fatigued, these receptors fail to work properly.
These structures are the Golgi Tendon Organs (GTO) and Muscle Spindles (MS). They send signals to your nervous system in response to either an increase or decrease the tension or ‘excitability’ of the muscle. It appears that the activity of the GTOs (which act to decrease the excitability) are depressed with muscle fatigue. At the same time, the spindles (which act to increase the excitability of the muscle) are enhanced. 10 11
This shift in the ‘balance’ of opposing mechanisms leads to an increase in excitability and therefor an increased propensity to cramp.
Observations that support the ‘fatigue’ hypothesis include:
1) Increased likeliness to cramp during a race compared to training (when the athlete is pushing harder). Additionally, marathoners that ‘go out hard’ in the first half of the event have been shown to cramp more frequently. 12
2) Evidence that ‘pre-race’ muscle damage is associated with an increased cramp risk. The speculation here is that certain muscles may be overused, pre-fatigued and thus have an increased propensity to cramp.13
3) Athletes with less of a ‘taper’ before a race are more likely to cramp. 14
3) Athletes experience cramps almost exclusively in muscle that are ‘working’. 15 16
4) In the laboratory, muscles can be made to cramp by electrically stimulating motorneurons (the nerves that travel from your spinal cord directly to a muscle). Studies have demonstrated that ‘cramp-prone subjects’ require less electrical stimulation to produce a cramp – this finding is completely unrelated to hydration levels. For more detail on the neurophysiology underlying muscle cramps including evidence suggesting spinal mechanisms, see this recent article from the American College of Sports Medicine – (Minetto MA, A Botter. Elicitability of muscle cramps in different leg and foot muscles. (2012) Muscle Nerve 40:535-544.)
Prevention
With a better understanding for the physiology underlying muscle cramps comes new advice for treating and preventing muscle cramps.
If the key modifiable factor is fatigue, then anything that leads to severe muscle fatigue will increase your susceptibility to cramping. This would include inadequate training, poor form/inefficient mechanics, and, yes, to a lesser degree improper hydration strategies.
1) Train properly for event
Training should provide a gradual progression of intensity to ensure proper muscles conditioning and provide graded ‘exposures’ to the strain associated with a particular activity. The idea here is to build tissue tolerance for applied loads. For a great review of the theory of graded exposures see here.
Remember tissues adapt to slow incremental changes, but they react to large sudden changes!
2) Consult with a coach
Consider consulting with a race coach if signing up for a new event to determine an proper training and recovery schedule. This should include an appropriate pre-race taper. You should attempt to establish an optimal pace to make sure you don’t go out too hard early.
3) Consult with a Sports Nutritionist
Determine proper training and race day hydration strategies.
4) Get a foam roll
Trigger points in muscles can indicate a heightened state of excitability at rest. An elevated ‘baseline’ of excitability leads to lower ‘threshold’ for triggering a cramped state.
5) Trigger Point Dry Needling
A more aggressive, but highly effective method for reducing local muscle tension.
Here a trained Physical Therapist utilizes a thin filament (the same as an acupuncture needle) to ‘deactivate’ hyperexcitable bands of muscle tissue (Trigger Points)
4) Have your form assessed
For runner this would mean a video gait analysis to ensure proper form. Poor form leads to overuse of particular muscles (or even particular portions of a particular muscles). With repetitive training this can lead to a ‘baseline’ state of hyperactivity in certain muscles that may contribute to a lowered threshold for cramping
Treatment
1) Tune into early warning signs
If you feel the initial ‘warning signs’ of an impending cramp – small fasciculations or a ‘tightening’ of cramp prone muscles – stop. If you’re close to the end of the event, you might consider stopping for a short break, stretching the effected muscle and then returning at a slower pace. If you ‘push through’ and progress to a full blown cramp, this will not only cause you unnecessary pain, but it will force you to stop and may interrupt your activity/training for days to come.
2) Stretch
Especially with a full-blown cramp, stop the activity (you may have no choice) and place the muscle on stretch.
3) Trick the nervous system
‘Reciprocal Inhibition’ techniques can also be helpful. This is a firing the muscle that opposes the cramping muscle to encourage it to relax. For example – with a cramping hamstring, place yourself in a position that stretches the hamstring lightly and then activate the quadriceps muscle by tightening up the front of the thigh and fully straightening the knee.
4) Massage the muscle
This most likely has a similar effect to stretching – decreasing the hyperexcitability and promoting inhibition.
5) Ice
In severe case, the athlete should do a series of ice treatments. Place the muscle on a very gentle stretch and ice directly over the cramp for 10 minutes. Repeat 3-5 times over the initial ~ 2 hours with some slow paced walking in between rounds.
6) Hydrate
Especially if you have reason to suspect a true ‘exertional heat cramp’ – hydrate immediately with a sports drink with supplemental sodium. Experts recommend a 0.5L carbohydrate-electrolyte drink with 3.0 grams of added salt mixed in thoroughly consumed all at once (or within 5-10 minutes). 17 If the muscle cramps are true EHC you will experience an improvement in your condition in as quickly as a few minutes. In many cases, the athlete with EHC may be able to safely return to activity/competition almost immediately. Intravenous (IV) rehydration with saline solution is rarely needed (and will, of course, be of no use for EAMC!).
Put down the pickle juice! While it is true that pickle juice was shown to decrease cramping better than water (or sports drinks) acutely, this is not a result of ‘rehydration’ or electrolyte replenishment. Researchers believe the strong taste sensation plays a neurophysiological ‘trick’ on the brain and triggers a relaxation response. A similar effect was found with spicy tinctures that are completely devoid of electrolytes. If you’re interested in reading more on this – see here: (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080605/)
So, why ‘put down the pickle juice’ if it works? Because it is not working on hydration or electrolytes imbalances. So, if all you are looking to do is reduce the hyperexcitability of a fatigued and cramping muscle, use the simple options listed above and save yourself the unnecessary burden of drinking something supremely gross!
* Seek Medical attention if:
1) The athlete does not urinate in the ~ 12-24 hours after a race despite drinking fluids.18
2) In the 12-24 hours post race, urine is a very dark color. 19
3) If the cramping is unresponsive to the basic strategies listed above.
4) If the athlete suffers from exertional cramps frequently. 20
The follow series of questions to suggest the need for medical workup comes from. 21
|
- Bergeron. Muscle cramps during exercise – Is it fatigue or electrolyte deficit? Current Sports Medicine Reports.
Abstract: Skeletal muscle cramps during exercise are a common affliction, even in highly fit athletes. And as empirical evidence grows, it is becoming increasingly clear that there are two distinct and dissimilar general categories of exercise-associated muscle cramps. Skeletal muscle overload and fatigue can prompt muscle cramping locally in the overworked muscle fibers, and these cramps can be treated effectively with passive stretching and massage or by modifying the exercise intensity and load. In contrast, extensive sweating and a consequent significant whole-body exchangeable sodium deficit caused by insufficient dietary sodium intake to offset sweat sodium losses can lead to a contracted interstitial fluid compartment and more widespread skeletal muscle cramping, even when there is minimal or no muscle overload and fatigue. Signs of hyperexcitable neuromuscular junctions may appear first as fasciculations during breaks in activity, which eventually progress to more severe and debilitating muscle spasms. Notably, affected athletes often present with normal or somewhat elevated serum electrolyte levels, even if they are “salty sweaters,” because of hypotonic sweat loss and a fall in intravascular volume. However, recovery and maintenance of water and sodium balance with oral or intravenous salt solutions is the proven effective strategy for resolving and averting exercise-associated muscle cramps that are prompted by extensive sweating and a sodium deficit. - Minetto, et all. Origin and development of muscle cramps. Exerc Sport Sci Rev.
Abstract: Cramps are sudden, involuntary, painful muscle contractions. Their pathophysiology remains poorly understood. One hypothesis is that cramps result from changes in motor neuron excitability (central origin). Another hypothesis is that they result from spontaneous discharges of the motor nerves (peripheral origin). The central origin hypothesis has been supported by recent experimental findings, whose implications for understanding cramp contractions are discussed. - Braulick, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med.
Abstract:
Objective: Many clinicians believe that exercise-associated muscle cramps (EAMC) occur because of dehydration. Experimental research supporting this theory is lacking. Mild hypohydration (3% body mass loss) does not alter threshold frequency (TF), a measure of cramp susceptibility, when fatigue and exercise intensity are controlled. No experimental research has examined TF following significant (3-5% body mass loss) or serious hypohydration (>5% body mass loss). Determine if significant or serious hypohydration, with moderate electrolyte losses, decreases TF.Design: A prepost experimental design was used. Dominant limb flexor hallucis brevis cramp TF, cramp electromyography (EMG) amplitude and cramp intensity were measured in 10 euhydrated, unacclimated men (age=24±4 years, height=184.2±4.8 cm, mass=84.8±11.4 kg). Subjects alternated exercising with their non-dominant limb or upper body on a cycle ergometer every 15 min at a moderate intensity until 5% body mass loss or volitional exhaustion (3.8±0.8 h; 39.1±1.5°C; humidity 18.4±3%). Cramp variables were reassessed posthypohydration.
Results: Subjects were well hydrated at the study’s onset (urine specific gravity=1.005±0.002). They lost 4.7±0.5% of their body mass (3.9±0.5 litres of fluid), 4.0±1.5 g of Na(+) and 0.6±0.1 g K(+) via exercise-induced sweating. Significant (n=5) or serious hypohydration (n=5) did not alter cramp TF (euhydrated=15±5 Hz, hypohydrated=13±6 Hz; F1,9=3.0, p=0.12), cramp intensity (euhydrated= 94.2±41%, hypohydrated=115.9±73%; F1,9=1.9, p=0.2) or cramp EMG amplitude (euhydrated=0.18±0.06 µV, hypohydrated= 0.18±0.09 µV; F1,9=0.1, p=0.79).
Conclusions: Significant and serious hypohydration with moderate electrolyte losses does not alter cramp susceptibility when fatigue and exercise intensity are controlled. Neuromuscular control may be more important in the onset of muscle cramps than dehydration or electrolyte losses.
- Miller, K. Stone, M. et al. Exercise-Associated Muscle Cramps. Sports Health.
Abstract:
Context: Exercise-associated muscle cramps (EAMC) are a common condition experienced by recreational and competitive athletes. Despite their commonality and prevalence, their cause remains unknown. Theories for the cause of EAMC are primarily based on anecdotal and observational studies rather than sound experimental evidence. Without a clear cause, treatments and prevention strategies for EAMC are often unsuccessful.Evidence Acquisition: A search of Medline (EBSCO), SPORTDiscus, and Silverplatter (CINHAL) was undertaken for journal articles written in English between the years 1955 and 2008. Additional references were collected by a careful analysis of the citations of others’ research and textbooks.
Results: Dehydration/electrolyte and neuromuscular causes are the most widely discussed theories for the cause of EAMC; however, strong experimental evidence for either theory is lacking.
Conclusions: EAMC are likely due to several factors coalescing to cause EAMC. The variety of treatments and prevention strategies for EAMC are evidence of the uncertainty in their cause. Acute EAMC treatment should focus on moderate static stretching of the affected muscle followed by a proper medical history to determine any predisposing conditions that may have triggered the onset of EAMC. Based on physical findings, prevention programs should be implemented to include fluid and electrolyte balance strategies and/or neuromuscular training.
- Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Minetto, et al. Origin and development of muscle cramps. Exerc Sport Sci Rev.
Abstract: Cramps are sudden, involuntary, painful muscle contractions. Their pathophysiology remains poorly understood. One hypothesis is that cramps result from changes in motor neuron excitability (central origin). Another hypothesis is that they result from spontaneous discharges of the motor nerves (peripheral origin). The central origin hypothesis has been supported by recent experimental findings, whose implications for understanding cramp contractions are discussed. - Braulick, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med.
Abstract:
Objective: Many clinicians believe that exercise-associated muscle cramps (EAMC) occur because of dehydration. Experimental research supporting this theory is lacking. Mild hypohydration (3% body mass loss) does not alter threshold frequency (TF), a measure of cramp susceptibility, when fatigue and exercise intensity are controlled. No experimental research has examined TF following significant (3-5% body mass loss) or serious hypohydration (>5% body mass loss). Determine if significant or serious hypohydration, with moderate electrolyte losses, decreases TF.Design: A prepost experimental design was used. Dominant limb flexor hallucis brevis cramp TF, cramp electromyography (EMG) amplitude and cramp intensity were measured in 10 euhydrated, unacclimated men (age=24±4 years, height=184.2±4.8 cm, mass=84.8±11.4 kg). Subjects alternated exercising with their non-dominant limb or upper body on a cycle ergometer every 15 min at a moderate intensity until 5% body mass loss or volitional exhaustion (3.8±0.8 h; 39.1±1.5°C; humidity 18.4±3%). Cramp variables were reassessed posthypohydration.
Results: Subjects were well hydrated at the study’s onset (urine specific gravity=1.005±0.002). They lost 4.7±0.5% of their body mass (3.9±0.5 litres of fluid), 4.0±1.5 g of Na(+) and 0.6±0.1 g K(+) via exercise-induced sweating. Significant (n=5) or serious hypohydration (n=5) did not alter cramp TF (euhydrated=15±5 Hz, hypohydrated=13±6 Hz; F1,9=3.0, p=0.12), cramp intensity (euhydrated= 94.2±41%, hypohydrated=115.9±73%; F1,9=1.9, p=0.2) or cramp EMG amplitude (euhydrated=0.18±0.06 µV, hypohydrated= 0.18±0.09 µV; F1,9=0.1, p=0.79).
Conclusions: Significant and serious hypohydration with moderate electrolyte losses does not alter cramp susceptibility when fatigue and exercise intensity are controlled. Neuromuscular control may be more important in the onset of muscle cramps than dehydration or electrolyte losses.
- Braulick, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med.
Abstract:
Objective: Many clinicians believe that exercise-associated muscle cramps (EAMC) occur because of dehydration. Experimental research supporting this theory is lacking. Mild hypohydration (3% body mass loss) does not alter threshold frequency (TF), a measure of cramp susceptibility, when fatigue and exercise intensity are controlled. No experimental research has examined TF following significant (3-5% body mass loss) or serious hypohydration (>5% body mass loss). Determine if significant or serious hypohydration, with moderate electrolyte losses, decreases TF.Design: A prepost experimental design was used. Dominant limb flexor hallucis brevis cramp TF, cramp electromyography (EMG) amplitude and cramp intensity were measured in 10 euhydrated, unacclimated men (age=24±4 years, height=184.2±4.8 cm, mass=84.8±11.4 kg). Subjects alternated exercising with their non-dominant limb or upper body on a cycle ergometer every 15 min at a moderate intensity until 5% body mass loss or volitional exhaustion (3.8±0.8 h; 39.1±1.5°C; humidity 18.4±3%). Cramp variables were reassessed posthypohydration.
Results: Subjects were well hydrated at the study’s onset (urine specific gravity=1.005±0.002). They lost 4.7±0.5% of their body mass (3.9±0.5 litres of fluid), 4.0±1.5 g of Na(+) and 0.6±0.1 g K(+) via exercise-induced sweating. Significant (n=5) or serious hypohydration (n=5) did not alter cramp TF (euhydrated=15±5 Hz, hypohydrated=13±6 Hz; F1,9=3.0, p=0.12), cramp intensity (euhydrated= 94.2±41%, hypohydrated=115.9±73%; F1,9=1.9, p=0.2) or cramp EMG amplitude (euhydrated=0.18±0.06 µV, hypohydrated= 0.18±0.09 µV; F1,9=0.1, p=0.79).
Conclusions: Significant and serious hypohydration with moderate electrolyte losses does not alter cramp susceptibility when fatigue and exercise intensity are controlled. Neuromuscular control may be more important in the onset of muscle cramps than dehydration or electrolyte losses.
- Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Bergeron. Muscle cramps during exercise – Is it fatigue or electrolyte deficit? Current Sports Medicine Reports.
Abstract: Skeletal muscle cramps during exercise are a common affliction, even in highly fit athletes. And as empirical evidence grows, it is becoming increasingly clear that there are two distinct and dissimilar general categories of exercise-associated muscle cramps. Skeletal muscle overload and fatigue can prompt muscle cramping locally in the overworked muscle fibers, and these cramps can be treated effectively with passive stretching and massage or by modifying the exercise intensity and load. In contrast, extensive sweating and a consequent significant whole-body exchangeable sodium deficit caused by insufficient dietary sodium intake to offset sweat sodium losses can lead to a contracted interstitial fluid compartment and more widespread skeletal muscle cramping, even when there is minimal or no muscle overload and fatigue. Signs of hyperexcitable neuromuscular junctions may appear first as fasciculations during breaks in activity, which eventually progress to more severe and debilitating muscle spasms. Notably, affected athletes often present with normal or somewhat elevated serum electrolyte levels, even if they are “salty sweaters,” because of hypotonic sweat loss and a fall in intravascular volume. However, recovery and maintenance of water and sodium balance with oral or intravenous salt solutions is the proven effective strategy for resolving and averting exercise-associated muscle cramps that are prompted by extensive sweating and a sodium deficit. - Braulick, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med.
Abstract:
Objective: Many clinicians believe that exercise-associated muscle cramps (EAMC) occur because of dehydration. Experimental research supporting this theory is lacking. Mild hypohydration (3% body mass loss) does not alter threshold frequency (TF), a measure of cramp susceptibility, when fatigue and exercise intensity are controlled. No experimental research has examined TF following significant (3-5% body mass loss) or serious hypohydration (>5% body mass loss). Determine if significant or serious hypohydration, with moderate electrolyte losses, decreases TF.Design: A prepost experimental design was used. Dominant limb flexor hallucis brevis cramp TF, cramp electromyography (EMG) amplitude and cramp intensity were measured in 10 euhydrated, unacclimated men (age=24±4 years, height=184.2±4.8 cm, mass=84.8±11.4 kg). Subjects alternated exercising with their non-dominant limb or upper body on a cycle ergometer every 15 min at a moderate intensity until 5% body mass loss or volitional exhaustion (3.8±0.8 h; 39.1±1.5°C; humidity 18.4±3%). Cramp variables were reassessed posthypohydration.
Results: Subjects were well hydrated at the study’s onset (urine specific gravity=1.005±0.002). They lost 4.7±0.5% of their body mass (3.9±0.5 litres of fluid), 4.0±1.5 g of Na(+) and 0.6±0.1 g K(+) via exercise-induced sweating. Significant (n=5) or serious hypohydration (n=5) did not alter cramp TF (euhydrated=15±5 Hz, hypohydrated=13±6 Hz; F1,9=3.0, p=0.12), cramp intensity (euhydrated= 94.2±41%, hypohydrated=115.9±73%; F1,9=1.9, p=0.2) or cramp EMG amplitude (euhydrated=0.18±0.06 µV, hypohydrated= 0.18±0.09 µV; F1,9=0.1, p=0.79).
Conclusions: Significant and serious hypohydration with moderate electrolyte losses does not alter cramp susceptibility when fatigue and exercise intensity are controlled. Neuromuscular control may be more important in the onset of muscle cramps than dehydration or electrolyte losses.
- Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Minetto, et al. Origin and development of muscle cramps. Exerc Sport Sci Rev.
Abstract: Cramps are sudden, involuntary, painful muscle contractions. Their pathophysiology remains poorly understood. One hypothesis is that cramps result from changes in motor neuron excitability (central origin). Another hypothesis is that they result from spontaneous discharges of the motor nerves (peripheral origin). The central origin hypothesis has been supported by recent experimental findings, whose implications for understanding cramp contractions are discussed. - Bergeron. Muscle cramps during exercise – Is it fatigue or electrolyte deficit? Current Sports Medicine Reports.
Abstract: Skeletal muscle cramps during exercise are a common affliction, even in highly fit athletes. And as empirical evidence grows, it is becoming increasingly clear that there are two distinct and dissimilar general categories of exercise-associated muscle cramps. Skeletal muscle overload and fatigue can prompt muscle cramping locally in the overworked muscle fibers, and these cramps can be treated effectively with passive stretching and massage or by modifying the exercise intensity and load. In contrast, extensive sweating and a consequent significant whole-body exchangeable sodium deficit caused by insufficient dietary sodium intake to offset sweat sodium losses can lead to a contracted interstitial fluid compartment and more widespread skeletal muscle cramping, even when there is minimal or no muscle overload and fatigue. Signs of hyperexcitable neuromuscular junctions may appear first as fasciculations during breaks in activity, which eventually progress to more severe and debilitating muscle spasms. Notably, affected athletes often present with normal or somewhat elevated serum electrolyte levels, even if they are “salty sweaters,” because of hypotonic sweat loss and a fall in intravascular volume. However, recovery and maintenance of water and sodium balance with oral or intravenous salt solutions is the proven effective strategy for resolving and averting exercise-associated muscle cramps that are prompted by extensive sweating and a sodium deficit. - Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC. - Schwellnus. Cause of exercise associated muscle cramps (EAMC)–altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med.
Abstract: Exercise Associated Muscle Cramps (EAMC) is one of the most common conditions that require medical attention during or immediately after sports events. Despite the high prevalence of this condition the aetiology of EAMC in athletes is still not well understood. The purpose of this review is to examine current scientific evidence in support of (1) the “electrolyte depletion” and “dehydration” hypotheses and (2) the “altered neuromuscular control” hypothesis in the aetiology of EAMC. In this review, scientific evidence will, as far as possible, be presented using evidence-based medicine criteria. This is particularly relevant in this field, as the quality of experimental methodology varies considerably among studies that are commonly cited in support of hypotheses to explain the aetiology of EAMC. Scientific evidence in support of the “electrolyte depletion” and “dehydration” hypotheses for the aetiology of EAMC comes mainly from anecdotal clinical observations, case series totalling 18 cases, and one small (n = 10) case-control study. Results from four prospective cohort studies do not support these hypotheses. In addition, the “electrolyte depletion” and “dehydration” hypotheses do not offer plausible pathophysiological mechanisms with supporting scientific evidence that could adequately explain the clinical presentation and management of EAMC. Scientific evidence for the “altered neuromuscular control” hypothesis is based on evidence from research studies in human models of muscle cramping, epidemiological studies in cramping athletes, and animal experimental data. Whilst it is clear that further evidence to support the “altered neuromuscular control” hypothesis is also required, research data are accumulating that support this as the principal pathophysiological mechanism for the aetiology of EAMC.
Leave a Reply
Want to join the discussion?Feel free to contribute!