madman
Super Moderator
ABSTRACT
Delayed-onset muscle soreness (DOMS) is a type of ultrastructural muscle injury. The manifestation of DOMS is caused by eccentric or unfamiliar forms of exercise. Clinical signs include reduced force capacities, increased painful restriction of movement, stiffness, swelling, and dysfunction of adjacent joints. Although DOMS is considered a mild type of injury, it is one of the most common reasons for compromised sportive performance. In the past few decades, many hypotheses have been developed to explain the aetiology of DOMS. Although the exact pathophysiological pathway remains unknown, the primary mechanism is currently considered to be the ultrastructural damage of muscle cells due to unfamiliar sporting activities or eccentric exercise, which leads to further protein degradation, apoptosis and local inflammatory response. The development of clinical symptoms is typically delayed (peak soreness at 48 – 72 h post-exercise) as a result of complex sequences of local and systemic physiological responses. The following narrative review was conducted to present an overview of the current findings regarding the damaging mechanisms as well as the pathophysiology of DOMS and its diagnostic evaluation.
▶ Fig.1 Z-disk disintegration and myofilament disarrangement as sign of ultrastructural damage was evaluated by electron microscopy of biopsies of human vastus lateralis 24h after strenuous resistance exercise for 70s time under tension leading to DOMS.
▶ Fig.2 T1-weighted (A,D), T2-weighted fat-suppressed (B, E) and T2-mapping images (C, F) of the lower leg before (A–C) and after eccentric exercise (D–F) in the same participant. The increased signal intensity (E) and T2 time value ( F) reflect a rising fluid content in the gastrocnemius medialis muscle as equivalent of DOMS.
▶ Fig.3 MRI of DOMS in the triceps brachii muscle of a 41 years old recreational crossfit athlete four days after exhausting training. In addition to an intramuscular edema, an edema in the subcutaneous tissue is evident.
▶ Fig.4 Transversal ultrasound scan of a dorsal calf (S 2000, linear probe 9L4, Siemens Healthineers, Erlangen, Germany). Physiological conditions (A), and DOMS conditions within direct signs of ultrastructural muscle damage, 48 hours after exhausting exercises (B) .Triangles: demonstrating a diffuse hyperechoic area, located at the center of pain; GM: gastrocnemius medialis muscle, SM: Soleus muscle.
Conclusions
The present work provides an overview of the damaging mechanisms, pathogenesis and diagnostics of DOMS. Currently, the exact trigger mechanism of the muscle damages and and related cellular mechanisms in DOMS are not fully understood, but many hypotheses exist to explain these phenomena. The primary mechanism of DOMS is currently thought to be a mechanical damage of skeletal muscle tissue due to eccentric exercise and not familiarized and not well coordinated sporting activities, which lead to further protein degradation, autophagy and a local inflammatory response. The predominant significance of preceding eccentric contraction may be explained by passive force generating factors including titin and an altered motor unit activation, which have both to be researched in future studies. To date, magnetic resonance imaging (MRI) has been reported as the preferred modality, providing detailed image analysis and characterization of DOMS and muscle lesions. However, newly emerging ultrasound modalities demonstrate promising results in a noninvasive functional approach
Delayed-onset muscle soreness (DOMS) is a type of ultrastructural muscle injury. The manifestation of DOMS is caused by eccentric or unfamiliar forms of exercise. Clinical signs include reduced force capacities, increased painful restriction of movement, stiffness, swelling, and dysfunction of adjacent joints. Although DOMS is considered a mild type of injury, it is one of the most common reasons for compromised sportive performance. In the past few decades, many hypotheses have been developed to explain the aetiology of DOMS. Although the exact pathophysiological pathway remains unknown, the primary mechanism is currently considered to be the ultrastructural damage of muscle cells due to unfamiliar sporting activities or eccentric exercise, which leads to further protein degradation, apoptosis and local inflammatory response. The development of clinical symptoms is typically delayed (peak soreness at 48 – 72 h post-exercise) as a result of complex sequences of local and systemic physiological responses. The following narrative review was conducted to present an overview of the current findings regarding the damaging mechanisms as well as the pathophysiology of DOMS and its diagnostic evaluation.
▶ Fig.1 Z-disk disintegration and myofilament disarrangement as sign of ultrastructural damage was evaluated by electron microscopy of biopsies of human vastus lateralis 24h after strenuous resistance exercise for 70s time under tension leading to DOMS.
▶ Fig.2 T1-weighted (A,D), T2-weighted fat-suppressed (B, E) and T2-mapping images (C, F) of the lower leg before (A–C) and after eccentric exercise (D–F) in the same participant. The increased signal intensity (E) and T2 time value ( F) reflect a rising fluid content in the gastrocnemius medialis muscle as equivalent of DOMS.
▶ Fig.3 MRI of DOMS in the triceps brachii muscle of a 41 years old recreational crossfit athlete four days after exhausting training. In addition to an intramuscular edema, an edema in the subcutaneous tissue is evident.
▶ Fig.4 Transversal ultrasound scan of a dorsal calf (S 2000, linear probe 9L4, Siemens Healthineers, Erlangen, Germany). Physiological conditions (A), and DOMS conditions within direct signs of ultrastructural muscle damage, 48 hours after exhausting exercises (B) .Triangles: demonstrating a diffuse hyperechoic area, located at the center of pain; GM: gastrocnemius medialis muscle, SM: Soleus muscle.
Conclusions
The present work provides an overview of the damaging mechanisms, pathogenesis and diagnostics of DOMS. Currently, the exact trigger mechanism of the muscle damages and and related cellular mechanisms in DOMS are not fully understood, but many hypotheses exist to explain these phenomena. The primary mechanism of DOMS is currently thought to be a mechanical damage of skeletal muscle tissue due to eccentric exercise and not familiarized and not well coordinated sporting activities, which lead to further protein degradation, autophagy and a local inflammatory response. The predominant significance of preceding eccentric contraction may be explained by passive force generating factors including titin and an altered motor unit activation, which have both to be researched in future studies. To date, magnetic resonance imaging (MRI) has been reported as the preferred modality, providing detailed image analysis and characterization of DOMS and muscle lesions. However, newly emerging ultrasound modalities demonstrate promising results in a noninvasive functional approach
