A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms.
Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. If your DOMS is bad, you may need to take a day of complete rest to give your muscles a chance to repair.
That may only worsen and delay your recovery from DOMS. Think about trying some gentle movement throughout the day. To keep your muscles moving, try gentle yoga or some low- to moderate-intensity walking, cycling, or swimming. Time is the only treatment for DOMS, but you can also take steps to ease the pain and stiffness while you wait for your muscles to repair themselves.
Research findings are mixed, and more study is needed. Some findings suggest the following treatments and self-care steps may help lessen the discomfort. Getting a massage 48 hours after workout seemed to work best. Getting a massage after every workout may not be feasible, but you can try self-massage on your:. To massage your muscles, apply some oil or lotion to the area and knead, squeeze, and gently shake your muscles.
Using a foam roller right after a workout may also help head off a bad case of DOMS. Topical analgesics are products meant to help relieve pain. Menthol-based topical analgesics and those with arnica may help ease the pain of DOMS. Always following packaging instructions about how much and how often to apply.
Does an ice bath sound extreme? Try a soak in a warm tub, instead. Moist heat wraps or a warm bath may also ease the pain and stiffness that come with DOMS.
More research is needed, but some findings suggest that eating certain foods or taking certain supplements may help ease DOMS. Learn what kinds of foods to eat after a workout to support optimal muscle recovery. Upper right insets in a , b show the location of the receptive field of the fiber.
The 1st and 3rd traces are raw recordings of the fiber, and the 2nd and 4th traces show readouts of the mechanical force applied to the receptive field. NGF was injected at time 0. From Murase et al. Because our model showed no apparent inflammatory signs, inflammatory cells are unlikely to be responsible for the production of NGF. When inflammation is produced after severe LC or LC induced by surface electrical stimulation [ 8 ], or after LC for 2 weeks [ 5 ], NGF is produced in inflammatory cells and regenerating muscle fibers.
This time course is a good fit for a trigger of NGF upregulation. On the basis of these findings we conclude that GDNF upregulation via COX-2 activation is essential to mechanical hyperalgesia after exercise. The method of presentation is similar to Fig. The black triangles in b represent the GDNF injection group. Involvement of acid-sensing ion channels ASIC in DOMS mechanical hyperalgesia has been demonstrated pharmacologically by use of an antagonist, amiloride [ 37 ].
GDNF-induced muscular mechanical hyperalgesia was reversed by amiloride [ 76 ]. Fujii et al. The receptor subtype for prostaglandin-E2 [ 77 ] that is involved in GDNF production after LC was sought by use of a pharmacological method and EP2 deficient mice, and was demonstrated to be the EP2 subtype [ 78 ].
A schematic diagram of the new mechanism for DOMS proposed on the basis of our observations is shown in Fig. Schematic diagram of the mechanism proposed for DOMS. The upper part of the figure in the shaded area was based on Boix et al. Modified from Mizumura et al. This observation might suggest that NGF produced after LC is not present in amounts large enough to sensitize muscle thin fiber afferents and induce mechanical hyperalgesia. The concentrations of NGF and GDNF used in the experiments that showed sensitization of muscle thin-fiber afferents to mechanical stimulation would have been much higher than those produced after LC.
Further experiments are needed to clarify this point. It is well known that DOMS is reduced when the same exercise is repeated after a specific interval. In addition, adaptation in excitation—contraction coupling or adaptation in the inflammatory response have also been proposed as mechanisms reviewed elsewhere [ 81 , 82 ]; also see Ref. Hoping to shed light on this effect, on the basis of our findings described above, we found that mechanical hyperalgesia and NGF upregulation were reduced after the 2nd bout of exercise in rats [ 83 ].
In addition, these adaptation phenomena were observed even when downstream pathways of the B2 bradykinin receptor were unaffected by its antagonist HOE This observation suggests adaptation occurs in the process of BK release, or at a level upstream of adenosine release. Some reports indicate fascia is important in DOMS. Itoh et al. Gibson et al. This observation may indicate that the fascial afferents are important in DOMS.
However, the response to hypertonic saline of muscle afferent fibers was not sensitized after LC [ 56 ], only mechanical sensitivity was increased [ 52 , 53 ]. A recent report showed that the electrical pain threshold decrease after LC was greater for fascia than for muscle [ 85 ].
To understand the relative contribution of both structures to DOMS, we must differentially measure the mechanical pain threshold of both tissues, or record afferent activity after LC. Innervation of the fascia and its afferent characteristics were only recently reported [ 86 , 87 ]. Whether fascial thin-fiber afferents are more strongly sensitized in DOMS than muscle afferents remains to be analyzed. Because DOMS may interfere with everyday life and the performance of athletes, and because it may make it difficult for those who are not familiar with exercise to continue exercise for fitness, effective methods for preventing from DOMS are needed.
For the moment, the only drugs applicable for humans are COX-2 inhibitors. As described in the introduction, the effectiveness of non-steroidal anti-inflammatory drugs NSAID against DOMS is variable, depending on the time of administration and dosage [ 9 ]. A recent systematic review [ 29 ] of a large number of reports on the effects of NSAID found that many did not follow an appropriate experimental design. Therefore, they performed a randomized, double-blind, placebo-controlled within-subject experiment.
It would be interesting to study how this works in the context of the mechanism we have proposed Fig. Exercise consisting of a small number of maximal isometric contractions [ 88 ] or weak LC [ 89 , 90 ] beforehand up to 2 weeks before is reported to be effective in preventing DOMS. Massage after exercise has been proved to be effective in reducing DOMS in rats [ 91 ]. Several aspects of DOMS must still be studied. This might suggest an interaction between the two pathways. In addition, the very early event that induces adenosine possibly ATP release from the muscle or activates muscle COX-2 during LC, and which might be related to the adaptation mechanism, is also unknown.
The DOMS model has been used for study of myofascial pain syndrome, because it shows taut band-like muscle hardening, and localized decreased nociceptive threshold in it trigger point , which are of diagnostic importance for myofascial pain symptoms.
When LC was repeated every day, instead of adaptation there were longer-lasting mechanical hyperalgesia and muscle signs of degeneration and regeneration [ 5 ]. This observation suggests that this repetitive model is clinically relevant for study of myofascial pain syndrome.
Further study of the DOMS mechanism might reveal the mechanism of myofascial pain syndrome and may suggest possibilities for treatment. Asmussen E Observations on experimental muscular soreness. Acta Rheum Scand — Armstrong RB Mechanisms of exercise-induced delayed onset muscular soreness: a brief review. Med Sci Sports Exerc — Newham DJ The consequences of eccentric contractions and their relationship to delayed onset muscle pain. Eur J Appl Physiol — Graven-Nielsen T, Arendt-Nielsen L Induction and assessment of muscle pain, referred pain, and muscular hyperalgesia.
Curr Pain Headache Rep — Article PubMed Google Scholar. J Pain — Int J Sports Med — Physiol Rep 2 11 :e Sports Med — Smith LL Acute inflammation: the underlying mechanism in delayed-onset muscle soreness. Hough T Ergographic studies in muscular soreness.
Am J Physiol — Google Scholar. Clin Sci — Research shows that DOMS is caused by microscopic damage to muscles and the surrounding connective tissues, which leads to inflammation and shifts of fluid and electrolytes. When your body starts to repair the damage, you begin feeling sore. And unlike what your high school track coach may have told you, lactic acid buildup in your muscles is not what causes DOMS.
It turns out that old-school theory has long been debunked, says Wilder.
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