Muscle Soreness and Damage and the Repeated-Bout Effect

Author(s):  
Ken Nosaka
2017 ◽  
Vol 42 (9) ◽  
pp. 978-985 ◽  
Author(s):  
Kenji Doma ◽  
Moritz Schumann ◽  
Anthony Scott Leicht ◽  
Brian Edward Heilbronn ◽  
Felipe Damas ◽  
...  

This study investigated the repeated bout effect of 3 typical lower body resistance-training sessions on maximal and submaximal effort running performance. Twelve resistance-untrained men (age, 24 ± 4 years; height, 1.81 ± 0.10 m; body mass, 79.3 ± 10.9 kg; peak oxygen uptake, 48.2 ± 6.5 mL·kg−1·min−1; 6-repetition maximum squat, 71.7 ± 12.2 kg) undertook 3 bouts of resistance-training sessions at 6-repetitions maximum. Countermovement jump (CMJ), lower-body range of motion (ROM), muscle soreness, and creatine kinase (CK) were examined prior to and immediately, 24 h (T24), and 48 h (T48) after each resistance-training bout. Submaximal (i.e., below anaerobic threshold (AT)) and maximal (i.e., above AT) running performances were also conducted at T24 and T48. Most indirect muscle damage markers (i.e., CMJ, ROM, and muscle soreness) and submaximal running performance were significantly improved (P < 0.05; 1.9%) following the third resistance-training bout compared with the second bout. Whilst maximal running performance was also improved following the third bout (P < 0.05; 9.8%) compared with other bouts, the measures were still reduced by 12%–20% versus baseline. However, the increase in CK was attenuated following the second bout (P < 0.05) with no further protection following the third bout (P > 0.05). In conclusion, the initial bout induced the greatest change in CK; however, at least 2 bouts were required to produce protective effects on other indirect muscle damage markers and submaximal running performance measures. This suggests that submaximal running sessions should be avoided for at least 48 h after resistance training until the third bout, although a greater recovery period may be required for maximal running sessions.


2014 ◽  
Vol 116 (11) ◽  
pp. 1473-1480 ◽  
Author(s):  
Ling Xin ◽  
Robert D. Hyldahl ◽  
Stuart R. Chipkin ◽  
Priscilla M. Clarkson

We investigated the existence of contralateral repeated bout effect and tested if the attenuation of nuclear factor-kappa B (NF-κB; an important regulator of muscle inflammation) induction following eccentric exercise is a potential mechanism. Thirty-one healthy men performed two bouts of knee extension eccentric exercise, initially with one leg and then with the opposite leg 4 wk later. Vastus lateralis muscle biopsies of both exercised and control legs were taken 3 h postexercise. Knee extension isometric and isokinetic strength (60°/sec and 180°/sec) were measured at baseline, pre-exercise, immediately postexercise, and 1/day for 5 days postexercise. Serum creatine kinase (CK) activity and muscle soreness were assessed at baseline and 1/day for 5 days postexercise. NF-κB (p65) DNA-binding activity was measured in the muscle biopsies. Isometric strength loss was lower in bout 2 than in bout 1 at 24, 72, and 96 h postexercise ( P < 0.05). Isokinetic strength (60°/s and 180°/s) was reduced less in bout 2 than in bout 1 at 72 h postexercise ( P < 0.01). There were no significant differences between bouts for postexercise CK activity or muscle soreness. p65 DNA-binding activity was increased following eccentric exercise (compared with the control leg) in bout 1 (122.9% ± 2.6%; P < 0.001) and bout 2 (109.1% ± 3.0%; P < 0.05). Compared with bout 1, the increase in NF-κB DNA-binding activity postexercise was attenuated after bout 2 ( P = 0.0008). Repeated eccentric exercise results in a contralateral repeated bout effect, which could be due to the attenuated increase in NF-κB activity postexercise.


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.


2013 ◽  
Vol 23 (4) ◽  
pp. 378-387 ◽  
Author(s):  
Kelle F. T. Veggi ◽  
Marco Machado ◽  
Alexander J. Koch ◽  
Sandro C. Santana ◽  
Sedison S. Oliveira ◽  
...  

Purpose:We examined the effects of creatine supplementation on the response to repeated bouts of resistance exercise.Methods:Young men (24.1 ± 5.2 yr) were divided into Creatine (CM, n = 9) and Placebo (PL, n = 9) groups. On day (D) 1 and D15, subjects performed four sets of bicep curls at 75% 1-RM to concentric failure. On D8-D13, subjects consumed either 20g/d creatine monohydrate or placebo. Muscle soreness and elbow joint range of motion (ROM) were assessed on D1-D5 and D15-D19. Serum creatine kinase activity (CK) was assessed on D1, D3, D5, D15, D17, and D19.Results:The first exercise bout produced increases in muscle soreness and CK, and decreases in ROM in both groups (p < .001). The second bout produced lesser rises in serum CK, muscle soreness, and a lesser decrease in ROM (bout effect, p < .01 for all), with greater attenuation of these damage markers in CM than PL. CK levels on D17 were lower (+110% over D15 for CM vs. +343% for PL), muscle soreness from D15–19 was lower (–75% for CM vs. –56% for PL compared with first bout), and elbow ROM was decreased in PL, but not CM on D16 (p < .05 for all).Conclusions:Creatine supplementation provides an additive effect on blunting the rise of muscle damage markers following a repeated bout of resistance exercise. The mechanism by which creatine augments the repeated bout effect is unknown but is likely due to a combination of creatine’s multifaceted functions.


Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1867
Author(s):  
Balázs Sonkodi ◽  
Zsolt Kopa ◽  
Péter Nyirády

Post orgasmic illness syndrome is a rare, mysterious condition with an unknown pathomechanism and uncertain treatment. The symptoms of post orgasmic illness syndrome last about 2–7 days after an ejaculation. The current hypothesis proposes that the primary injury in post orgasmic illness syndrome is an acute compression proprioceptive axonopathy in the muscle spindle, as is suspected in delayed onset muscle soreness. The terminal arbor degeneration-like lesion of delayed onset muscle soreness is theorized to be an acute stress response energy-depleted dysfunctional mitochondria-induced impairment of Piezo2 channels and glutamate vesicular release. The recurring symptoms of post orgasmic illness syndrome after each ejaculation are suggested to be analogous to the repeated bout effect of delayed onset muscle soreness. However, there are differences in the pathomechanism, mostly attributed to the extent of secondary tissue damage and to the extent of spermidine depletion. The spermidine depletion-induced differences are as follows: modulation of the acute stress response, flu-like symptoms, opioid-like withdrawal and enhanced deregulation of the autonomic nervous system. The longitudinal dimension of delayed onset muscle soreness, in the form of post orgasmic illness syndrome and the repeated bout effect, have cognitive and memory consequences, since the primary injury is learning and memory-related.


2014 ◽  
Vol 6 (3) ◽  
Author(s):  
Michael Behringer ◽  
Johannes Montag ◽  
Yvonne Kilian ◽  
Molly McCourt ◽  
Anna-Maria Liphardt ◽  
...  

The primary aim of the present study was to investigate if there is a repeated bout effect for cartilage tissue, evident in the marker serum cartilage oligomeric matrix protein (sCOMP). Ten healthy male subjects (26.4±3.14 years) performed two high impact interventions (100 drop jumps with a 30 second interval) carried out at a 3 week interval. After each intervention, sCOMP and muscle soreness were assessed on 8 and 6 occasions respectively. Muscle soreness was determined via a visual analog scale with a maximum pain score of 10. sComp levels did not show a blunted response after the second bout (Bout 1: 12.2±3.3 U/L−1; Bout 2: 13.1±4.0 U/L−1; P&gt;0.05). Remarkably, sCOMP increased from baseline levels by 16% after bout 1 and 15% after bout 2. Muscle soreness was blunted following the second intervention (Bout 1: 5.0±1.8; Bout 2: 1.6±0.8). Unlike the known repeated bout effect for muscle damage markers, sCOMP levels do not show a blunted response after two similar loading interventions. This information on biomarker behavior is essential to clinicians attempting to use this marker as an indicator of cartilage damage associated with the development or progression of osteoarthritis.


2021 ◽  
Vol 11 (1) ◽  
pp. 108
Author(s):  
Balázs Sonkodi

Delayed onset muscle soreness (DOMS) is hypothesized to be caused by glutamate excitotoxicity-induced acute compression axonopathy of the sensory afferents in the muscle spindle. Degeneration of the same sensory afferents is implicated in the disease onset and progression of amyotrophic lateral sclerosis (ALS). A series of “silent” acute compression proprioceptive axonopathies with underlying genetic/environmental factors, damaging eccentric contractions and the non-resolving neuroinflammatory process of aging could lead to ALS disease progression. Since the sensory terminals in the muscle spindle could not regenerate from the micro-damage in ALS, unlike in DOMS, the induced protective microcircuits and their long-term functional plasticity (the equivalent of the repeated bout effect in DOMS) will be dysfunctional. The acute stress invoking osteocalcin, bradykinin, COX1, COX2, GDNF, PGE2, NGF, glutamate and N-methyl-D-aspartate (NMDA) receptors are suggested to be the critical signalers of this theory. The repeated bout effect of DOMS and the dysfunctional microcircuits in ALS are suggested to involve several dimensions of memory and learning, like pain memory, inflammation, working and episodic memory. The spatial encoding of these memory dimensions is compromised in ALS due to blunt position sense from the degenerating proprioceptive axon terminals of the affected muscle spindles. Dysfunctional microcircuits progressively and irreversibly interfere with postural control, with motor command and locomotor circuits, deplete the neuroenergetic system, and ultimately interfere with life-sustaining central pattern generators in ALS. The activated NMDA receptor is suggested to serve the “gate control” function in DOMS and ALS in line with the gate control theory of pain. Circumvention of muscle spindle-loading could be a choice of exercise therapy in muscle spindle-affected neurodegenerative diseases.


Author(s):  
Patricio A. Pincheira ◽  
Eduardo Martinez‐Valdes ◽  
Rodrigo Guzman‐Venegas ◽  
Deborah Falla ◽  
Marta I. Garrido ◽  
...  

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 83
Author(s):  
Christina D. Bruce ◽  
Luca Ruggiero ◽  
Gabriel U. Dix ◽  
Paul D. Cotton ◽  
Chris J. McNeil

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