What Causes Muscle Soreness and How Can I Minimize This?
By Kris Walker MD

“No pain, no gain.” All athletes experience muscle soreness at one time or another during training or competition. But what causes muscle soreness? How can it be minimized? Could it or should it be prevented? We’ll discuss two types of muscle pain here: the acute burning type that occurs during strenuous activity and delayed onset muscle soreness, or DOMS, which occurs one to three days after the inciting activity. These are caused by different mechanisms and warrant different coping strategies.

Acute muscle pain is the burning you get when you are pushing yourself. Your muscles seem to scream, “Stop! You’re hurting me!” If you continue at the same pace, your muscles will slow down or stop working. The pain occurs when muscles are forced to work anaerobically, or without oxygen. Muscles require fuel to perform work, in the form of blood glucose or muscle glycogen. If oxygen is available, the fuel is burned “clean” and no by-products accumulate in the muscle. When there is not enough oxygen available, lactic acid is produced as a by-product in the muscle cell. It is thought that the hydrogen ions from the lactic acid decrease the pH in the cell and stimulate pain receptors, causing the burning sensation.

Some ways to lessen this pain have been proposed. One method is to buffer the acidity by taking sodium bicarbonate and some athletes try this. However, 1 teaspoon of sodium bicarbonate provides more than twice the RDA of sodium, and to get effective buffering, you would have to use many times this amount. Other supplements have been marketed to buffer the acidity, containing potassium hydroxide, magnesium hydroxide, and calcium carbonate. Phosphate loading is also claimed to reduce lactic acid production and increase ATP (energy) production. Phosphate loading, though, is likely to cause stomach cramping, and the body will adapt to it, requiring cycling on and off supplementation for effectiveness.

Recent research has suggested that, far from being a poison that stops muscles from contracting effectively, lactic acid is actually an important fuel. George A Brooks, a biology professor and exercise physiologist at UC Berkeley, has studied lactic acid for years and has developed the “lactate shuttle theory.” This theory shows that the lactate is transferred from the cytoplasm of the cell into the mitochondria, where it is used as fuel. Heart muscle, slow twitch muscle fibers, and breathing musculature actually prefer lactate as fuel over glucose or glycogen. In order to minimize the lactic acid burn, it may be more beneficial to increase mitochondrial capacity to burn the lactate, rather than minimize the production of the lactic acid.

Interval training, generates big lactate loads and the body adapts by building more mitochondria. Endurance training also increases mitochondrial mass. To build mitochondria without destroying muscle, intervals should gradually increase in intensity. A combination of endurance training and intervals may be optimal to increase mitochondrial numbers and the ability to use lactate as fuel. This also will increase cardiovascular capacity and increase oxygen delivery to the muscle, decreasing lactic acid production.

In delayed onset muscle soreness, the pain starts a day or two after the new or excessive activity: You’re a fit cyclist, so you jump into a 5k running race. The next day every step is painful, and going down stairs is excruciating. The pain can last from three to seven days after the inciting event. Muscle soreness is most frequently caused by resistance to gravity, momentum, or a stronger force. The soreness is thought to be caused by actual damage to the muscle fiber. Eccentric contractions, in which the muscle is forced to contract while lengthening, cause the most damage. Microscopic study of muscle fibers has shown ruptured cell membranes and other damage. This damage causes inflammation, histamine release, and an influx of white blood cells. The white blood cells then release prostaglandins. Prostaglandins are chemicals which sensitize nerve fibers and increase pain sensation. The inflammatory response also causes swelling and increased pressure in the muscle which may increase pain.

How can this pain be minimized? Some proposed forms of pain relief include stretching, balms and creams, ice, hot baths, massage, and sauna exposure. These methods provide temporary relief, at best.

Non-steroidal anti-inflammatories, or NSAIDs, such as ibuprofen, block prostaglandin synthesis. In fact, the NSAIDs ketoprofen and diclofenacmay be more effective in reducing pain, as they block two pathways of prostaglandin synthesis. However, over twenty-five studies have looked at DOMS and these medications with inconsistent results. This may be, in part, because of individual response differences: some people do not experience DOMS. Other caveats of NSAID use are the risk of stomach and gastrointestinal ulcers and liver or kidney problems from overuse. Plus, interfering with the inflammatory process may be detrimental to long term muscle health and may actually delay recovery. (for more on NSAID’s see First Endurance research article Ibuprofen-NSAIDS and endurance).

Promising methods of proposed relief include muscle compression, yoga, light activity, use of TENS units, ultrasound, and hyperbaric oxygen therapy. These all need more study before strong recommendations can be made.

It may be that once the muscle damage is caused, nothing will halt the process. The process, may, in fact be an important step in muscle hypertrophy: overload > slight tearing > soreness > repair > rebuild/remodel > stronger. Some literature suggests a “repeated bout effect.” Once you have experienced soreness from a particular activity, you may be protected from soreness from the same intensity of that activity for up to six weeks. Perhaps prevention is the best strategy, using pre-conditioning and gradual habituation.