Here is chain of events which contributes to muscle soreness and fatigue after eccentric exercise. Again, we will use publication of Cheung, et al., (2003) as guide because it summarizes everything beautifully:

  • High tensile forces produced during eccentric muscle activity cause disruption of structural proteins in muscle fibres, particularly at the weakened z-lines. This is accompanied by excessive strain of the connective tissue at the myotendinous junction and surrounding muscle fibres (connective tissue damage theory and muscle damage theory).
  • Damage to the sarcolemma results in the accumulation of calcium that inhibits cellular respiration. ATP production is hindered and calcium homeostasis is disturbed. High calcium concentrations activate calcium-dependent proteolyticenzymes that degrade the z-line of sarcomers, troponin and tropomyosin (enzyme efflux theory).
  • Within a few hours there is a significant elevation in circulating neutrophils (inflammation theory).
  • Intracellular components and markers of connective tissue damage and muscle damage (e.g. HP and CK) diffuse into the plasma and interstitium. These substances serve to attract monocytes between 6–12 hours that in turn convert to macrophages. Mast cells and histamine production are activated (inflammation theory). Within hours there is a significant elevation in circulating neutrophils at the injury site (inflammation theory).
  • Monocytes/macrophages peak in number at 48 hours. Upon exposure to the inflammatory environment, macrophages produce prostaglandin (PGE2) that sensitises type III and IV nerve endings to mechanical, chemical or thermal stimulation (inflammation theory).
  • The accumulation of histamine, potassium and kinins from active phagocytosis and cellular necrosis in addition to elevated pressure from tissue oedema and increased local temperature could then activate nociceptors within the muscle fibres and the muscle tendon junction (inflammation theory).
  • These events lead to the sensation of DOMS. Soreness may be increased with movement as the increased intramuscular pressure creates a mechanical stimulus for pain receptors already sensitised by PGE2.

As you can see there is no even mentioning of the lactic acid be the cause of muscle fatigue and soreness.

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