Pathogenesis of Musculotendinous and Fascial Injuries After Physical Exercise - Short Review

Abstract

Purpose

The identification of sports and physical exercises with injury risk is necessary to preserve the capacity of athletes and people who perform physical education and also to prevent the installation of functional deficiencies.

Methods

We have selected the articles related to the pathogenic mechanisms involved in musculotendinous and fascial injuries produced as a result of physical exercise.

Results and Discussions

The lesional pathogenesis is complex and incompletely clarified. Recent theories put in a new light the mechanisms of muscle pain and tendinopathy production. The accumulation of lactate anion, known to be a residue that induces fatigue and muscle pain, has been reconsidered by some authors. It appears that lactate anion is an excellent fuel for the myocardial fiber. Moreover, the accumulation of lactic acid after intense physical exercise could prevent the inexcitability of the sarcolemma induced by the increased concentration of interstitial K⁺. Most of the time, overuse injuries are not limited to muscles. They can cause myofascial, myotendinous or purely muscular injuries. The muscular fascia is more susceptible to injuries produced under the action of large external forces. Also, fascia is more sensitive to pain compared to muscle when external forces act eccentrically. Overloading the tendon and putting it under tension repeatedly is followed by ruptures of the tendon fibers. The regeneration of the degenerated tendon is defective in the context of the inflammation produced by the injury. Tendon fibers undergo a process of fibrosis, scarring, adhesion and heterogeneous calcification. Oxidative stress is responsible for inflammation, degeneration and apoptosis of tenocytes.

Conclusion

The benefits brought by physical education and sports are indisputable, but their practice requires a coordinated program to prevent possible traumatic and overuse injuries.

Keywords:

• sport muscle injury
• musculofascial injury
• pathogenesis
• stress tendinopathy
• delayed onset muscle soreness

Abbreviations

α-SMA, alpha-smooth muscle actin; DOMS, delayed onset muscle soreness; ATP, adenosine triphosphate; MCP-1, monocyte chemoattractant protein-1; CCL2, C-C motif chemokine ligand 2; CCR2, C-C chemokine receptor type 2; IL, interleukin; TNFα, tumor necrosis factor-alpha; TGFβ, transforming growth factor beta; NOX, nicotinamide adenine dinucleotide phosphate oxidase; mTOR, mammalian target of rapamycin; MMPs, matrix metalloproteinases; TIMPs, tissue inhibitors of matrix metalloproteinases; NO, nitric oxide; NOS, nitric oxide synthases family; iNOS, inducible nitric oxide synthase; eNOS, endothelial nitric oxide synthase; bNOS, neuronal nitric oxide synthase; VEGF, vascular endothelial growth factor.

Acknowledgments

The authors wish to acknowledge that the present study was academically supported by the “Dunărea de Jos” University of Galați, Romania.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors report no conflicts of interest in this work.

Additional information

Funding

The article publishing charge was paid by the “Dunărea de Jos” University of Galaţi, Romania.