Exercise associated muscle cramps (EAMC) are voluntary painful contractions that occur during or immediately after exercise. EAMC are localised muscle cramps that affect different muscles, mainly the calf, hamstring, quadriceps and foot muscles. Cramping in triathletes has been reported the most at 67%, cyclists at 60%, rugby players at 52% and marathon runners at 30-50%.
During sports competitions, training or other intense physical activity, repeated loading on certain muscles can result in localised muscle fatigue. Fatigue seems to be an important contributing factor as EAMC mostly occurs at the end or after exercise. The cause of muscle cramps is still unknown but more research is pointing towards a neurological origin, in other words, the communication between your muscles and your nerves. There are 2 sensors that send input to your brain about muscle contraction. The muscles spindles are the first sensors in your muscle and they detect muscle lengths. When you stretch your muscle the muscle spindles send a message to your brain (via sensory neurons) to immediately contract the muscle so that the muscle doesn’t tear. This contraction signal is sent from the brain back to the muscle (via motor neurons). The second sensors are Golgi tendon organs which are found in the tendons. Golgi tendon organs pick up muscle tension, so when your muscle is contracted, these sensors are activated and your brain sends a message to the muscle to relax (via motor neurons). In summary, the muscle spindles tell your brain to contract muscles and Golgi tendon organs tell your brain to relax muscles.
EAMC occurs more often when the muscle is contracting (in a shortened position). This may explain why cramping in the calf muscles of swimmers is common. In swimming races a swimmer must swim with pointed toes that require the calf muscle to contract in a shortened position. In a shortened position there is increased tension on the muscle for the Golgi tendon organs to detect, therefore, there are no “relaxing” signals being sent to your brain. Studies have found that fatigue causes the muscle spindles to be more excitable and the Golgi tendon organs to be inhibited. Your brain receives more “contract” signals and not enough “relax” signals, resulting in your muscle cramping uncontrollably.
EAMC are more likely in less well-trained athletes and events of long durations. A positive family history of cramping, older age, poor conditioning and stretching habits are also risk factors. Cramps are more common in men than in women, and those more susceptible to heat illness.
Different athletes may have different mechanisms leading to EAMC, so a treatment that works for one athlete my not work for another athlete. Passive stretching seems to be the most popular and effective treatment technique. Passive stretching increases the “relax” signal to the motor neuron, which supports the altered neuromuscular control theory. Management aimed at changing fatigability and neuromuscular control may help prevent cramps. Generalised conditioning and endurance, maintaining carbohydrate reserves, plyometric and eccentric exercises improve neuromuscular control. Massage and myofascial trigger point therapy may also improve the effectiveness of the muscle and decrease fatigability.
Many factors cause muscle cramps, each factor being unique to each athlete and caused by changes in the nervous system. We will be more successful preventing EAMC if we identify each athlete’s risk factors and target those risks with interventions.
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- Google images. Viewed 4/6/18, http://www.bowenworkmaui.com/how-does-it-work.html