treningsfrik75 said:
DOMS are definately a sign og muscle growth... trying to get rid of it as fast as possible through good nutrition and supplements is different. We want to be sore.. thats for sure.
Tear down muscle fiber through training and build up better and bigger muscles thereafter through good nutrition.
Initial events in exercise-induced muscular injury.
* Armstrong RB.
Department of Physical Education, University of Georgia, Athens 30602.
Immediately following unaccustomed exercise, particularly that with eccentric contractions, there is evidence of injury to skeletal muscle fibers: a) disruption of the normal myofilament structures in some sarcomeres, observable with both light and electron microscope and b) loss of intramuscular proteins (e.g., creatine kinase enzymes) into the plasma, indicating damage to sarcolemma. T
his pathology is probably responsible for the temporary reductions in muscle force and delayed-onset soreness that can occur following eccentric exercise. The mechanisms underlying this injury are not known, although loss of intracellular Ca2+ homeostasis could play a primary role. In other experimental muscle injury models, elevated [Ca2+]i appears to cause release of muscle enzymes through activation of phospholipase A2, which in turn could induce injury to sarcolemma through production of leukotrienes and prostaglandins, through free O2 radical formation (in the subsequent lipoxygenase and cyclooxygenase reactions), and/or through release of detergent lysophospholipids. On the other hand, the mechanism responsible for the rapid damage to myofibrils caused by increased [Ca2+]i is unknown. Regardless of the cause(s), the initial and early events in the injury process are autogenetic; i.e., they are indigenous to the muscle cells and occur before phagocytic cells enter the injury site.
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Mechanisms of exercise-induced delayed onset muscular soreness: a brief review.
* Armstrong RB.
Delayed-onset muscular soreness (DOMS), the sensation of pain and stiffness in the muscles that occurs from 1 to 5 d following unaccustomed exercise, can adversely affect muscular performance, both from voluntary reduction of effort and from inherent loss of capacity of the muscles to produce force. This reduction in performance is temporary; permanent impairment does not occur. A number of clinical correlates are associated with DOMS, including elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure; exertional rhabdomyolysis appears to be the extreme form of DOMS. Presently, the best treatment for DOMS appears to be muscular activity, although the sensation again returns following the exercise. Training for the specific contractile activity that causes DOMS reduces the soreness response.
The etiology and cellular mechanisms of DOMS are not known, but a number of hypotheses exist to explain the phenomenon. The following model may be proposed: 1) high tensions (particularly those associated with eccentric exercise) in the contractile/elastic system of the muscle result in structural damage; 2) cell membrane damage leads to disruption of Ca++ homeostasis in the injured fibers, resulting in necrosis that peaks about 2 d post-exercise; and 3) products of macrophage activity and intracellular contents accumulate in the interstitium, which in turn stimulate free nerve endings of group-IV sensory neurons in the muscles leading to the sensation of DOMS.
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I cant find any research correlating DOMS with recovery/repair but rather evidence showing that DOMS is related somehow with the inflammatory effect of intense eccentric exercise but lagged.
