Delayed-Onset Muscle Soreness
Delayed-Onset Muscle Soreness, A Physiological Update
Darius Randeria, Pharmacist
Muscle pain after intense exercise will be no stranger to most athletes. There are a number of fairly predictable physiological reasons why repetitive loading would be expected to leave the athlete with a few aches and pains. However, there is a difference between the intensity and duration of this pain compared to the almost debilitating pain that many will have suffered after an intense workout following a hiatus from activity.
Delayed-Onset Muscle Soreness or, DOMS, is not a term that most will recognize. However, it is something that nearly all athletes will have felt. It is characterized by severe muscular pain and is most acute not the day after exercise but anywhere from 24-72 hours afterwards, hence the term, “Delayed-Onset”.
Having played squash my whole life, I have experienced it many times. Squash is one of the most demanding physical games, featuring high frequency eccentric movements and prolonged bouts of activity such as lunging and sprinting. However, DOMS is a common result of any intense, unaccustomed activity. Eccentric activity can be thought of as muscle loading beyond the muscle's ability to resist that load. Remember, there is a difference in “Static”, loading and “Momentum”, loading. In squash, for example, a sprint followed by a sudden stop and lunge causes the front foot to plant and the muscles of the leg to contract as an emergency brake. At that braking point, the muscles must overcome the forward momentum of the body based on weight and speed. That load may be in excess of the normal static load limit of the corresponding muscles. At an extreme, tendons or muscles can tear but, at a point below that and with repetition, the exercise has the characteristic eccentricity that we refer to. As a result of over-loading, microscopic injury can be seen through micro-imaging.
The major muscles used when playing squash include:
The muscles of the shoulder girdle; the pectorals, and the deltoids.
The muscles of the upper legs and hips; the gluteals, the hamstrings, and the quadriceps
The muscles of the forearm and upper arm; the wrist flexors and extensors, the biceps, and the triceps.
The core muscles; the rectus abdominus, obliques, and the spinal erectors.
Sarcomere Structure: Mechanisms of Concentric and Eccentric Actions
a) With a concentric action, the myosin cross-bridges attach and draw the actin proteins towards each other, shortening the sarcomere
b) With an eccentric action, the myosin cross-bridges attach and the actin proteins move away from each other (as the weight is greater than the force of the muscle), lengthening the sarcomere
The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury. However, one of the most effective ways to alleviate the soreness is often to engage in the same activity, albeit at a reduced intensity.
DOMS is defined as a Type 1 Muscle Strain Injury and is characterized by tenderness and stiffness on palpation. It generally begins with pain to the distal myotendinous junction, an area diffuse with pain receptors, and then spreads inwards along the muscle. Let's take a look at the current hypotheses for the pathophysiology of DOMS.
Lactic Acid
Lactic acid is a metabolic by-product that accumulates during exercise. It is known to activate pain receptors in muscle and connective tissue. However, studies have shown that similar amounts of lactic acid build up, produced in repetitive concentric activity and eccentric activity, do not cause the unique symptoms found in DOMS. Additionally, Lactic acid levels seem to return to normal within an hour after activity and are probably responsible for acute pain during and after exercise. Their levels do not explain the relative pain-free period, lasting up to 24-48 hours after exercise.
Muscle Spasm Theory
Electromyography or EMG measures the electrical activity of skeletal muscle. It has been postulated that the soreness in DOMS can be explained by an increased resting muscle tone that continues after eccentric activity. This increased “Resting contraction”, can compress blood vessels and lead to local ischaemia and the further production of pain markers.
Connective Tissue Damage Theory
Muscle fibres come in different varieties, broadly “Slow Twitch”, and “Fast Twitch”. The connective tissue, mostly made of Collagen, that surrounds the fibres, varies in composition. During eccentric exercise, the connective tissue suffers mechanical stress and as these cells break down, they release Hydroxyproline and Hydroxylysine. Hydroxyproline, a product of connective tissue breakdown has been detected in the urine of subjects suffering from DOMS (McArdle, Katch and Katch, 1986), suggesting connective tissue damage. The cytoskeleton of the muscle, when damaged, becomes more permeable, allowing excess leakage of muscle enzymes and an increased uptake of injected radioisotopes (Newham, 1991). Further, changes in the sarcoplasmic reticulum of the muscle cell have been shown to depress calcium muscle metabolism, altering muscle contraction and causing pain (McBride, 1998).
Muscle Damage Theory
This would seems to be a simple explanation for DOMS. Indeed, it is the explanation offered up by almost everyone that is unfamiliar with DOMS. Without going in to complex physiology, muscle cells are arranged in nice straight lines. When they contract, their chemical structure changes and the muscle units (myofibrils) become shorter, hence the tightening of the muscle. When we overload these contractile units, they become damaged. The cells become leaky and they produce an enzyme, Creatine Kinase, or “CK”. In addition, there are pain Receptors in the muscle tissue that are activated. Measurement of CK after intense exercise is well documented. Normal plasma levels are in the range of 100 IU/Litre. After activity, levels as high as 40,000 IU/Litre have been reported.
Unfortunately, CK rises very quickly and peaks early. It is likely that its rise sets in motion an inflammatory cascade involving white blood cell activation.
The Inflammation Theory
This theory showed some promise as experts looked at the inflammatory cascade as a potential culprit in DOMS. Eccentric exercise cause the muscle cells to produce Proteolytic enzymes that attack damaged muscle cells. The breakdown and local inflammation leads to a rise in certain substances such as Bradykinin, Prostaglandin and Histamine. Eventually, osmosis leads to fluid leaving the smaller blood vessels and accumulating in the spaces between the muscle cells. This is called Oedema and leads to a slight increase in the size of the whole muscle and consequently, the whole limb, such as the thigh. Pain corresponds well to increases in limb Girth. Again, however, this does not correlate with the delay in onset until we consider a certain type of white blood cell called Monocytes. These large “Rubbish Digesting cells”, circulate in the plasma until a local injury and the release of certain substances, makes the small blood vessels leaky enough for them to escape. When they do, it takes about 24 hours for them to develop in to Macrophages, their active form. It is known that macrophages produce certain substances that can sensitize type III and IV Muscle fibres.
Enzyme Efflux Theory
This hypothesis states that the soreness might be due to an increase in Calcium outside of the Sarcoplasmic Reticulum. In short, during concentric exercise, Calcium is released, causes tightening of the Actin filaments across the Myosin and is then pumped back in using ATP. During eccentric exercise, Actin filaments that have been pulled close together by contraction, are at the same time pulled apart by the increased load on the muscle. Imagine a person curling his bicep and another person pulling his arm the other way. The muscle is contracting but the muscle is being pulled apart. During this time and possibly due in part to damage of the sarcomere, ATP generation is slowed and Calcium starts to accumulate. Calcium, which has two positive charges, can alter the membrane potential of the cells and also causes the release of inflammatory mediators such as prostaglandins and leukotrienes.
These mechanisms are all linked together to some extent. It is probably
sufficient to characterize DOMS as acute micro-insults to muscle tissue, leading
to delayed inflammatory changes and oedema and ending in a repair process that
temporarily reduces muscle function.
DOMS and related oedema result in failure in the excitation-contraction coupling process and loss of contractile protein, which reduce the force-generating capacity of the affected muscles. Failure in excitation-contraction coupling appears to be the most important, particularly during the first 5 days after injury. Muscle glycogen re-synthesis is also impaired when a muscle is damaged. Re-synthesis is not affected for the first 6 to 12 hours after exercise, but it gradually stops completely as the muscle undergoes repair. This energy redistribution reduces the fuel-storage capacity of the injured muscle and makes it weak, such that muscle retraining may be needed. Maximal force-generating capacity gradually returns over days or weeks
Now that we have an idea of what DOMS is, we might ask what significance it has in athletic performance, injury rates and what can be done to minimize it?
We often use the phrase, “No Pain, No Gain”. That is particularly appropriate here. Whereas there are negative aspects of DOMS, there is a great deal of evidence that controlled, eccentric training regimens do increase performance and strength. It is also becoming popular in rehabilitation, for example in Patellar Tendinitis or after ACL reconstruction. It is believed by some that using the same concentric movements in rehabilitation is inferior to eccentrically forcing the muscle and tendons to adapt to a new challenge. This may cause some re-modelling or alignment of the muscle tissues that would not have otherwise occurred.
There are a number of likely scenarios that might be faced
After a hiatus, an athlete returns to training but a day later is too sore to continue
An athlete suffering from DOMS decides to “Play Away", the soreness and sustains an acute injury
A person taking up a new activity, suffers from DOMS and decides that it is too much for them and quits
An athlete does not time his training well and pushes too hard leading to poor performance at an event or match.
What is the Repeated Bout Effect of Eccentric Training?
One area of research that has much promise in relation to DOMS and eccentric exercise is the repeated bout effect (RBE). One of the only ways, it seems, to prevent or lessen the soreness caused by DOMS (or hasten the recovery of DOMS) from eccentric exercise is to eccentrically stimulate the muscles about one week (or more) prior to the eccentric training bout (Pettitt et al., 2005). The reduced DOMS response to eccentric resistance, after the prior eccentric exposure, is referred to as the RBE. Several studies have shown that performing a bout of exercise leading to DOMS, and then repeating the eccentric bout of exercise several days (and/or up to six months) later results in the following: significantly lower levels of DOMS after the repeated eccentric workout, reduced circulating creatine kinase levels (a marker of muscle damage), increased range of motion recovery and enhanced strength recovery (Nosaka et al., 2001; Pettitt et al., 2005; Balnave & Thompson, 1993). Performing about of 2, 6, or 10 maximal eccentric contractions has been shown to provide a protective effect for a subsequent repeated bout of 24 to 50 maximal muscular contractions weeks later (McHugh, 2003). What causes the RBE is still yet to be decided upon conclusively, however, there are several theories suggesting it is a contribution of adaptations from neural input to the muscle, connective tissue in muscle restructuring, and cellular adaptations (increase in sarcomeres) (McHugh, 2003; McHugh et al., 1999).
Is there a Difference in the Response of Old and Young Persons to Eccentric Training?
Older men are not as susceptible to muscle damage caused by eccentric exercise as is seen with their younger counterparts. Lavender and Nosaka (2006) investigated the responses of 6 sets of 5 eccentric exercise reps (at 40% of their 1-RM) of the elbow flexors with older (ave. age = 70 years) and younger (ave. age = 19 years) males. The younger men experienced greater DOMS and showed greater metabolic markers of DOMS (i.e., increased levels of creatine kinase) after the eccentric training. The authors proposed that slight decreases in range of motion in the older group (due to age-related changes in muscles) might partially explain the lower levels of DOMS as compared to the younger group. In addition, with aging there is a propensity for the loss or atrophy (decrease in size) of fast-twitch muscle fibers, which are particularly challenged (leading to DOMS) in eccentric training (Lavender and Nosaka). In addition, Lavender and Nosaka hypothesize that the older adults may 'instinctively' have developed neural inhibitory mechanisms to avoid exercise-induced muscle damage. With females, Ploutz-Snyder et al. (2001) found that older women (66 yrs of age) showed no difference in DOMS then younger women (23 yrs of age) in either concentric or eccentric strength training in a 12-week study evaluating knee extension strength.
Due to muscle mass and strength decreases associated with aging and inactivity (referred to as sarcopenia), it is valuable to know that eccentric strength training is a principal training technique that can be incorporated with older male and female clients. In fact eccentric exercise has been shown to increase the size of type II (fast-twitch) muscle fibers in men (18-80 years of age) and significantly improve the strength of women (20-74 yrs of age) (Hortobagyi et al., 1995).
Conclusion
DOMS can be a temporarily debilitating result of intense eccentric muscle loading. It is not particularly well studied, likely because its effects are temporary. However, there are important lessons to be learned that can help both amateur athletes as well as professionals. We can look on it as something that can be avoided in most cases. Professional athletes have intense, repetitive training regimens that constantly stretch contracted muscles leading to better muscle performance and faster recovery.
“Weekend warriors”, particularly older athletes are most at risk. Stretching needs to be load-based and involve movement rather than stasis. Cross-training before a particular activity is very important, as is low-impact weight-based training. Heavy weights can also cause DOMS and should be avoided for 72 hours prior to activity.
Once DOMS has occurred, it is easy to shy away from exercise but, as we have learned, modest exercise is helpful, especially if it is a lower impact version of the initial insult.