Predictive value of strength loss as an indicator of muscle damage across multiple drop jumps

2011 ◽  
Vol 36 (3) ◽  
pp. 353-360 ◽  
Author(s):  
Albertas Skurvydas ◽  
Marius Brazaitis ◽  
Tomas Venckūnas ◽  
Sigitas Kamandulis

The aim of the present study was to compare the time-course of indirect symptoms of exercise-induced muscle damage after 50 and 100 drop jumps. A high-force, low intensity exercise protocol was used to avoid discrepancies regarding metabolic fatigue immediately after exercise. Healthy untrained men performed 50 (“50 group”, n = 13) or 100 (“100 group”, n = 13) intermittent (30-s interval between each jump) drop jumps, respectively, from the height of 0.5 m with a counter-movement to a 90° knee flexion angle and immediate maximal rebound. Voluntary and electrically evoked knee extensor strength was assessed using an isokinetic dynamometer immediately before and at 2 min after exercise, as well as 3, 7, and 14 days after exercise. Creatine kinase (CK) activity and muscle soreness within 7 days after exercise were also determined. The results showed that the decrease in voluntary isometric and isokinetic torque as well as 100 Hz stimulation torque at the end of the 50 and 100 drop jumps was very similar, while substantial differences were found in low-frequency fatigue, shift in optimal knee joint angle, muscle soreness, and CK activity. In addition, there was slower muscle strength recovery after the 100 drop jumps. It is concluded that the predictive value of strength loss immediately after exercise as an indicator of muscle damage decreases as the jump number increases. Still, stimuli must be large enough for muscle torque to reach the reduction plateau. Therefore, magnitude of exercise becomes a major factor in accuracy of muscle damage predictions.

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Giedrius Gorianovas ◽  
Albertas Skurvydas ◽  
Vytautas Streckis ◽  
Marius Brazaitis ◽  
Sigitas Kamandulis ◽  
...  

This study investigated possible differences using the same stretch-shortening exercise (SSE) protocol on generally accepted monitoring markers (dependent variables: changes in creatine kinase, muscle soreness, and voluntary and electrically evoked torque) in males across three lifespan stages (childhood versus adulthood versus old age). The protocol consisted of 100 intermittent (30 s interval between jumps) drop jumps to determine the repeated bout effect (RBE) (first and second bouts performed at a 2-week interval). The results showed that indirect symptoms of exercise-induced muscle damage after SSE were more expressed in adult males than in boys and elderly males, suggesting that the muscles of boys and elderly males are more resistant to exercise-induced damage than those of adult males. RBE was more pronounced in adult males than in boys and elderly males, suggesting that the muscles of boys and elderly males are less adaptive to exercise-induced muscle damage than those of adult males.


2018 ◽  
Vol 1 (108) ◽  
pp. 25-29
Author(s):  
Albertas Skurvydas ◽  
Gediminas Mamkus ◽  
Dalia Mickevičienė ◽  
Diana Karanauskienė ◽  
Dovilė Valančienė ◽  
...  

Background. The aim of this study was to follow symptoms of exercise induced muscle damage in response to 50, 100 and 200 drop jumps with maximal intensity. Methods. Three groups of young healthy men (n = 10 in each group) performed a bout of mechanically demanding stretch shortening cycle exercise consisting of 50, 100 and 200 drop jumps. Voluntary and electrically induced knee extension torque, creatine kinase, muscle soreness were measured before and 24 h after exercise. Results. Indirect symptoms of exercise induced damage were dependent on DJs volume: the higher the numbers of jumps, the more symptoms were observed. Only after 200 DJs compared to 50-100 DJ there was decrease of CAR and H of DJ, and 24 h after 200 DJs CK was greater than after 50-100 DJs. Conclusion. In response to acute severe muscle-damaging exercise (after 200 DJs), indirect symptoms of exercise-induced muscle damage occurred.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yvoni Kyriakidou ◽  
Isabella Cooper ◽  
Igor Kraev ◽  
Sigrun Lange ◽  
Bradley T. Elliott

Background: Exercise-induced muscle damage (EIMD) results in transient muscle inflammation, strength loss, and muscle soreness and may cause subsequent exercise avoidance. Research has recently proven that skeletal muscle can also release extracellular vesicles (EVs) into the circulation following a bout of exercise. However, EV’s potential role, including as a biomarker, in the response to eccentric resistance exercise stimulus remains unclear.Methods: Twelve (younger, n=7, 27.0±1.5years and older, n=5, 63.0±1.0years) healthy, physically active males, undertaking moderate, regular physical activity (3–5 times per week) performed a unilateral high intensity eccentric exercise protocol. Venous plasma was collected for assessment of EVs and creatine kinase (CK) prior to EIMD, immediately after EIMD, and 1–72h post-EIMD, and maximal voluntary isometric contraction (MVIC) and delayed onset muscle soreness (DOMS) were assessed at all time points, except 1 and 2h post-EIMD.Results: A significant effect of both time (p=0.005) and group (p<0.001) was noted for MVIC, with younger participants’ MVIC being higher throughout. Whilst a significant increase was observed in DOMS in the younger group (p=0.014) and in the older group (p=0.034) following EIMD, no significant differences were observed between groups. CK was not different between age groups but was altered following the EIMD (main effect of time p=0.026), with increased CK seen immediately post-, at 1 and 2h post-EIMD. EV count tended to be lower in older participants at rest, relative to younger participants (p=0.056), whilst EV modal size did not differ between younger and older participants pre-EIMD. EIMD did not substantially alter EV modal size or EV count in younger or older participants; however, the alteration in EV concentration (ΔCount) and EV modal size (ΔMode) between post-EIMD and pre-EIMD negatively associated with CK activity. No significant associations were noted between MVIC or DOMS and either ΔCount or ΔMode of EVs at any time point.Conclusion: These findings suggest that profile of EV release, immediately following exercise, may predict later CK release and play a role in the EIMD response. Exercise-induced EV release profiles may therefore serve as an indicator for subsequent muscle damage.


2017 ◽  
Vol 122 (3) ◽  
pp. 631-641 ◽  
Author(s):  
Matthew R. Ely ◽  
Steven A. Romero ◽  
Dylan C. Sieck ◽  
Joshua E. Mangum ◽  
Meredith J. Luttrell ◽  
...  

Histamine contributes to elevations in skeletal muscle blood flow following exercise, which raises the possibility that histamine is an important mediator of the inflammatory response to exercise. We examined the influence of antihistamines on postexercise blood flow, inflammation, muscle damage, and delayed-onset muscle soreness (DOMS) in a model of moderate exercise-induced muscle damage. Subjects consumed either a combination of fexofenadine and ranitidine (blockade, n = 12) or nothing (control, n = 12) before 45 min of downhill running (−10% grade). Blood flow to the leg was measured before and throughout 120 min of exercise recovery. Markers of inflammation, muscle damage, and DOMS were obtained before and at 0, 6, 12, 24, 48, and 72 h postexercise. At 60 min postexercise, blood flow was reduced ~29% with blockade compared with control ( P < 0.05). Markers of inflammation were elevated after exercise (TNF-ɑ, IL-6), but did not differ between control and blockade. Creatine kinase concentrations peaked 12 h after exercise, and the overall response was greater with blockade (18.3 ± 3.2 kU·l−1·h−1) compared with control (11.6 ± 2.0 kU·l−1·h−1; P < 0.05). Reductions in muscle strength in control (−19.3 ± 4.3% at 24 h) were greater than blockade (−7.8 ± 4.8%; P < 0.05) and corresponded with greater perceptions of pain/discomfort in control compared with blockade. In conclusion, histamine-receptor blockade reduced postexercise blood flow, had no effect on the pattern of inflammatory markers, increased serum creatine kinase concentrations, attenuated muscle strength loss, and reduced pain perception following muscle-damaging exercise. NEW & NOTEWORTHY Histamine appears to be intimately involved with skeletal muscle during and following exercise. Blocking histamine’s actions during muscle-damaging exercise, via common over-the-counter antihistamines, resulted in increased serum creatine kinase, an indirect marker of muscle damage. Paradoxically, blocking histamine’s actions attenuated muscle strength loss and reduced perceptions of muscle pain for 72 h following muscle-damaging exercise. These results indicate that exercise-induced histamine release may have a broad impact on protecting muscle from exercise-induced damage.


2018 ◽  
Vol 50 (3) ◽  
pp. 142-143 ◽  
Author(s):  
P. Baumert ◽  
M. J. Lake ◽  
B. Drust ◽  
C. E. Stewart ◽  
R. M. Erskine ◽  
...  

Unaccustomed strenuous exercise can lead to muscle strength loss, inflammation and delayed-onset muscle soreness, which may be influenced by genetic variation. We investigated if a missense single nucleotide polymorphism (A>G, rs2275950 ) within the TRIM63 gene (encoding MuRF-1 and potentially affecting titin mechanical properties) was associated with the variable response to unaccustomed eccentric exercise. Sixty-five untrained, healthy participants (genotyped for rs2275950 : AA, AG, and GG) performed 120 maximal eccentric knee extensions (ECC) to induce muscle damage. Isometric and isokinetic maximal voluntary knee extension contractions (MVCs) and muscle soreness were assessed before, immediately after, and 48 h after ECC. AA homozygotes were consistently stronger [baseline isometric MVC: 3.23 ± 0.92 Nm/kg (AA) vs. 2.09 ± 0.67 Nm/kg (GG); P = 0.006] and demonstrated less muscle soreness over time ( P = 0.022) compared with GG homozygotes. This may be explained by greater titin stiffness in AA homozygotes, leading to intrinsically stronger muscle fibers that are more resistant to eccentric damaging contractions.


Author(s):  
Yvoni Kyriakidou ◽  
Carly Wood ◽  
Chrystalla Ferrier ◽  
Alberto Dolci ◽  
Bradley Elliott

Abstract Background Exercise-induced muscle damage (EIMD) results in transient muscle inflammation, strength loss, muscle soreness and may cause subsequent exercise avoidance. Omega-3 (n-3) supplementation may minimise EIMD via its anti-inflammatory properties, however, its efficacy remains unclear. Methods Healthy males (n = 14, 25.07 ± 4.05 years) were randomised to 3 g/day n-3 supplementation (N-3, n = 7) or placebo (PLA, n = 7). Following 4 weeks supplementation, a downhill running protocol (60 min, 65% V̇O2max, − 10% gradient) was performed. Creatine kinase (CK), interleukin (IL)-6 and tumour necrosis factor (TNF)-α, perceived muscle soreness, maximal voluntary isometric contraction (MVIC) and peak power were quantified pre, post, and 24, 48 and 72 h post-EIMD. Results Muscle soreness was significantly lower in N-3 vs PLA group at 24 h post-EIMD (p = 0.034). IL-6 was increased in PLA (p = 0.009) but not in N-3 (p = 0.434) following EIMD, however, no significant differences were noted between groups. Peak power was significantly suppressed in PLA relative to pre-EIMD but not in N-3 group at 24 h post-EIMD. However, no significant difference in peak power output was observed between groups. MVIC, CK and TNF-α were altered by EIMD but did not differ between groups. Conclusion N-3 supplementation for 4 weeks may successfully attenuate minor aspects of EIMD. Whilst not improving performance, these findings may have relevance to soreness-associated exercise avoidance.


Author(s):  
R Candia Luján ◽  
RA Paredes Carrera ◽  
O Costa Moreira ◽  
KF Candia Sosa ◽  
JA De Paz Fernández

El masaje es una de las terapias más utilizadas para aliviar el dolor muscular tardío (DMT). El objetivo del presente estudio fue determinar la efectividad del masaje en el tratamiento del DMT, para lo cual se llevó a cabo una revisión sistemática en las bases de datos, Pubmed, Scopus, SportDiscus, Web of Science y el buscador Google académico, usando las palabras clave delayed onset muscle soreness y exercise induced muscle damage combinado con massage. Se incluyeron en el estudio 23 artículos en los cuales el 78% mostró disminución del DMT mientras que en el restante 22% no hubo mejoras o bien empeoró. El análisis de los estudios permite concluir que el masaje es una terapia efectiva en el tratamiento del dolor muscular tardío.


2017 ◽  
Vol 122 (3) ◽  
pp. 559-570 ◽  
Author(s):  
Jonathan M. Peake ◽  
Oliver Neubauer ◽  
Paul A. Della Gatta ◽  
Kazunori Nosaka

Unaccustomed exercise consisting of eccentric (i.e., lengthening) muscle contractions often results in muscle damage characterized by ultrastructural alterations in muscle tissue, clinical signs, and symptoms (e.g., reduced muscle strength and range of motion, increased muscle soreness and swelling, efflux of myocellular proteins). The time course of recovery following exercise-induced muscle damage depends on the extent of initial muscle damage, which in turn is influenced by the intensity and duration of exercise, joint angle/muscle length, and muscle groups used during exercise. The effects of these factors on muscle strength, soreness, and swelling are well characterized. By contrast, much less is known about how they affect intramuscular inflammation and molecular aspects of muscle adaptation/remodeling. Although inflammation has historically been viewed as detrimental for recovery from exercise, it is now generally accepted that inflammatory responses, if tightly regulated, are integral to muscle repair and regeneration. Animal studies have revealed that various cell types, including neutrophils, macrophages, mast cells, eosinophils, CD8 and T-regulatory lymphocytes, fibro-adipogenic progenitors, and pericytes help to facilitate muscle tissue regeneration. However, more research is required to determine whether these cells respond to exercise-induced muscle damage. A large body of research has investigated the efficacy of physicotherapeutic, pharmacological, and nutritional interventions for reducing the signs and symptoms of exercise-induced muscle damage, with mixed results. More research is needed to examine if/how these treatments influence inflammation and muscle remodeling during recovery from exercise.


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