The soreness is perceived as a dull, aching pain in the affected muscle, often combined with tenderness and stiffness.
DOMS was first described in 1902 by Theodore Hough,[4] who concluded that this kind of soreness is "fundamentally the result of ruptures within the muscle".
[5] The soreness has been attributed to the increased tension force and muscle lengthening from eccentric exercise.
Cellular respiration is inhibited and ATP needed to actively transport calcium back into the sarcoplasmic reticulum is produced at a lower rate.
This accumulation of calcium may activate proteases and phospholipases which in turn break down and degenerate muscle protein.
[7][9] An earlier theory posited that DOMS is connected to the build-up of lactic acid in the blood, which was thought to continue being produced following exercise.
This build-up of lactic acid was thought to be a toxic metabolic waste product that caused the perception of pain at a delayed stage.
This theory has been largely rejected, as concentric contractions which also produce lactic acid have been unable to cause DOMS.
[5] Additionally, lactic acid is known from multiple studies to return to normal levels within one hour of exercise, and therefore cannot cause the pain that occurs much later.
[2]: 69 The magnitude of the effect is subject to many variations, depending for instance on the time between bouts, the number and length of eccentric contractions, and the exercise mode.
[2]: 74 Delayed onset muscle soreness can be reduced or prevented by gradually increasing the intensity of a new exercise program,[11]: 112 thereby taking advantage of the repeated-bout effect.
Physical activity before eccentric exercise helps to prevent delayed-onset muscle soreness.
If treatment is desired, any measure that increases blood flow to the muscle, such as low-intensity activity, massage, nerve mobilization,[15] hot baths,[16][17] or a sauna visit may help somewhat.