I received this message from one of my athletes a few years ago, “I can’t even sit on the toilet!” my reply was “why are you sitting down to take a piss!”. All jokes aside DOMS can leave you in some serious pain that can affect your sleep and training schedule, but as an athlete they don’t need to be a badge of honor that you train hard. Here is what you need to know to reduce the effects of DOMS!

What is DOMS?

DOMS stands for Delayed Onset of Muscle Soreness and it is a symptom of Exercise Induced Muscle Damage (EIMD) (1). EIMD is temporary, repairable and the term used for microscopic damage to muscle induced by exercise (2). EIMD can be stimulated by unaccustomed, excessive or most commonly eccentric exercise (3). Eccentric muscle contractions can generate more force at a lower metabolic cost, lower motor unit activation (predominately fast twitch muscle fibers) and create more damage at longer muscle lengths when compared to isometric and concentric contractions (4).

Why do DOMS occur?

Proposed mechanisms of EIMD are catergorised into primary and secondary damage, with primary damage occurring during the bout of exercise (4).
Primary Damage
It is theorised that when a muscle is subject to mechanical damage induced by eccentric lengthening it is first exposed to “sarcomere popping” (5). Sarcomere popping is a result of non-uniform lengthening of sarcomeres beyond their optimal length operating on the descending limb (a region of inherent instability) of the length-tension curve (5).
DON’T GET LOST YET!
This basically means that as the muscle stretches during eccentric contractions the sarcomeres are also stretched and they may be stretched beyond their optimal length (which means the perfect amount of overlap between actin and myosin to produce maximal force). At this length  (beyond optimal), tension cannot be produced (this is known as the descending limb of the length-tension curve) and this will cause “popping” or disruption of the sarcomere (5).
Further damage also includes inhibited components (t-tubles, and sarcoplasmic reticulm membrane) of the excitation-contraction coupling complex, which is a process of converting an electrical impulse (action potential) into a muscle contraction (4). This may affect the release of calcium (Ca2+) per action potential for muscle contractions, which can lead to an immediate reduction in force production (6).
Secondary Damage
Following mechanical damage caused in the primary process an activation of ionic channels (stretch-activated calcium channels) elevates concentrations of Ca2+ disrupting intracellular Ca2+ homeostasis (7). This increase in Ca2+ has been associated with Ca2+ activated cysteine proteases know as calpains which digest individual myofibrillar proteins causing protein degradation leading to further muscle damage (8). The secondary phase has also been associated with an acute inflammatory response, initiated due to the resultant protein degradation within muscle fibers (9).

When will I feel DOMS?

As mentioned earlier DOMS is the most common symptom in athletes and the symptoms of DOMS include muscle soreness, swelling, stiffness and strength loss (1). Research investigating the time course and magnitude of symptoms associated with DOMS post eccentric exercise showed muscle soreness, swelling and stiffness peak in magnitude between 24-96 hours post intervention. However, strength levels decrease immediately post exercise and peak in magnitude within 24 hours. By 48 hours post eccentric exercise strength levels have commenced a linear recovery pattern which suggests strength levels follow a different temporal pattern to muscle soreness, swelling and stiffness (1).
Practical Applications:
1. DOMS  should not be a subjective measurement of muscle soreness, swelling and stiffness only, as reductions in muscle function may already be at a deficit (0-24 hours) or in a state of recovery (24-48 hours).
2. Although an athlete may be free of muscle soreness, swelling and stiffness. Planning high intensity training sessions 0-24 hours post eccentric exercise may put an athlete at risk of injury due to a possible reduction in strength levels
 3. At 36 hours post eccentric exercise despite a possible peak in muscle soreness, swelling and stiffness, it is possible to still train with a high intensity as muscle function has recovered and the 3 other symptoms may subside with a sufficient warm up.

What will happen?

DOMS can have a significant affect on important athletic qualities that constitute to success in many sports. Sprinting times have been shown to be significantly slower over 5m and 10m at 48 hours post eccentric exercise (10). Vertical jumping performance decrements have been shown to last for 3 days before a linear return to recovery 7 days later (11). Endurance performance assessed with the distance covered in a 30-minute time trial was reduced by 4%, 48 hours post eccentric exercise (12).

How do I reduce the affect of DOMS?

Several preventative strategies are proposed to attenuate the effects of DOMS (13). One modality is the repeat bout effect (RBE), a phenomenon that provides an adaption resulting in a protective mechanism to subsequent bouts of eccentric exercise (14). This protective adaption is activated by the initial bout of eccentric exercise and can last for weeks or months (15). The sarcomere strain theory is theorised to be the mechanism for the RBE (5). It is suggested the initial bout of eccentric exercise results in an increase of sarcomeres in series (addition of sarcomeres longitudinally) increasing the sarcomeres length-tension relationship which decreases the amount of strain placed on the sarcomeres in the subsequent eccentric bout. This shift in the length-tension relationship increases the optimal length at which the sarcomeres can produce force and therefore not operate on the descending limb of the length-tension curve, as mentioned earlier this is where sarcomere popping may occur.
The RBE has been shown to increase in its protective magnitude in relation to the intensity adopted in the initial eccentric exercise bout. Thus, the greater the intensity bout (100% maximal voluntary contraction) the greater the protective effect on markers of muscle damage, although a protective effect has also been found at a lower intensity (40% maximal voluntary contraction) to a lesser degree and for a shorter duration (16). The RBE highlights the ability of muscle to adapt to eccentric exercise with a muscle that is less susceptible to damage upon future bouts.

Practical Applications:

1. New stimulus involving eccentric contractions should follow a progressive build up in intensity/volume across training sessions to reduce the possibility of extensive damage allowing the protective adaption of the RBE to build.
2. As the RBE duration of protection can be limited depending on the intensity of exercise, training sessions should not be scheduled too far apart as this may allow the symptoms of DOMS to be exposed. Therefore, weekly sessions should be implemented across consecutive weeks that follow similar if not identical training days.

References

1. Cleak, M.J., & Eston, R.G. (1992). Muscle soreness, swelling, stiffness and strength loss after intense eccentric exercise. British Journal of Sports Medicine, 26, 267-272
2. Ebbling, C.B., & Clarkson, P.M. (1989). Exercise-induced muscle damage and adaption. Sports Medicine, 7, 207-234.
3.Byrne, C., Twist, C., & Eston, R. (2004). Neuromuscular function after exercise-induced muscle damage. Sports Medicine, 34, 49-69.
4. Thiebaud, R.S. (2012). Exercise-induced muscle damage: is it detrimental or beneficial? Journal of Trainology, 1, 36-44.
5. Morgan, D.L. (1990). New insights into the behaviour of muscle during active lengthening. Biophysical Journal, 57, 209-221.
6. Morgan, D.L., & Allen, D.G. (1999). Early events in stretch-induced muscle damage. Journal of Applied Physiology, 87, 2007-2015.
7. Allen, D.G., Whitehead, N.P., & Yeung, E.W. (2005). Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changes. Journal of Physiology, 567, 723-735.
8. Huang, J., & Forsberg, N.E. (1998). Role of calpain in skeletal-muscle protein degradation. Proceedings of the National Academy of Sciences, 95, 12100-12105.
9. MacIntyre, D. L., Reid, W.D., & McKenzie, D.C. (1995). Delayed muscle soreness: the inflammatory response to muscle injury and its clinical implications. Sports Medicine, 20, 24-40.
10. Highton, J.M., Twist, C., & Eston, R.G. (2009). The effects of exercise-induced muscle damage on agility and sprint running performance. Journal of Exercise Science & Fitness, 7, 24-30.
11. Byrne, C., & Eston, R. (2002). The effect of exercise induced muscle damage on isometric and dynamic knee extensor strength and vertical jump performance. Journal of Sports Science, 20, 417-425.
12. Marcora, S.M., & Bosio, A. (2007). Effect of exercise induced muscle damage on endurance running performance in humans. Scandinavian Journal of Medicine and Science in Sports, 17, 662-671.
13. Howatson, G., & van Someran, K.A. (2008). The prevention and treatment of exercise-induced muscle damage. Sports Medicine, 38, 483-503.
14. Nosaka, K., & Clarkson, P.M. (1995). Muscle damage following repeated bouts of high force eccentric exercise. Medicine and Science in Sports and Exercise, 27, 1263-1269.
15. Nosaka, K., Sakamoto, K., Newton, M., & Sacco.P. (2001). How long does the protective effect on eccentric exercise-induced muscle damage last? Medicine and Science in Sports and Exercise, 33, 1490-1495.
16. Chen, T.C., Nosaka, K., & Sacco, P. (2007). Intensity of eccentric exercise, shift of optimum angle, and the magnitude of repeated-bout effect. Journal of Applied Physiology, 102, 992-999.
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