Skeletal muscle adapts to exercise-induced damage by orchestrating several but still poorly understood mechanisms that endow protection from subsequent damage. Known widely as the repeated bout effect, we propose that neural adaptations, alterations to muscle mechanical properties, structural remodeling of the extracellular matrix, and biochemical signaling work in concert to coordinate the protective adaptation.

This study tested the hypothesis that changes in indirect markers of muscle damage following maximal eccentric exercise would be smaller for the knee extensors (KE) and flexors (KF) compared with the elbow flexors (EF) and extensors (EE). A total of 17 sedentary men performed five sets of six maximal isokinetic (90° s(-1)) eccentric contractions of EF (range of motion, ROM: 90°-0°, 0 = full extension), EE (55°-145°), KF (90°-0°), and KE (30°-120°) using a different limb with a 4-5-week interval in a counterbalanced order. Changes in maximal isometric and concentric isokinetic strength, optimum angle, limb circumference, ROM, plasma creatine kinase activity and myoglobin concentration, muscle soreness, and echo-intensity of B-mode ultrasound images before and for 5 days following exercise were compared amongst the four exercises using two-way repeated-measures ANOVA. All variables changed significantly following EF, EE, and KF exercises, but KE exercise did not change the optimum angle, limb circumference, and echo-intensity. Compared with KF and KE, EF and EE showed significantly greater changes in all variables, without significant differences between EF and EE. Changes in all variables were significantly greater for KF than KE. For the same subjects, the magnitude of change in the dependent variables following exercise varied among the exercises. These results suggest that the two arm muscles are equally more susceptible to muscle damage than leg muscles, but KF is more susceptible to muscle damage than KE. The difference in the susceptibility to muscle damage seems to be associated with the use of muscles in daily activities.

In this study, we examined the time course of changes in running economy following a 30-min downhill (-15%) run at 70% peak aerobic power (VO2peak). Ten young men performed level running at 65, 75, and 85% VO2peak (5 min for each intensity) before, immediately after, and 1 - 5 days after the downhill run, at which times oxygen consumption (VO2), minute ventilation, the respiratory exchange ratio (RER), heart rate, ratings of perceived exertion (RPE), and blood lactate concentration were measured. Stride length, stride frequency, and range of motion of the ankle, knee, and hip joints during the level runs were analysed using high-speed (120-Hz) video images. Downhill running induced reductions (7 - 21%, P < 0.05) in maximal isometric strength of the knee extensors, three- to six-fold increases in plasma creatine kinase activity and myoglobin concentration, and muscle soreness for 4 days after the downhill run. Oxygen consumption increased (4 - 7%, P < 0.05) immediately to 3 days after downhill running. There were also increases (P < 0.05) in heart rate, minute ventilation, RER, RPE, blood lactate concentration, and stride frequency, as well as reductions in stride length and range of motion of the ankle and knee. The results suggest that changes in running form and compromised muscle function due to muscle damage contribute to the reduction in running economy for 3 days after downhill running.

This study compared the effect of four different intensities of initial eccentric exercise (ECC1) on optimum angle shift and extent of muscle damage induced by subsequent maximal eccentric exercise. Fifty-two male students were placed into 100%, 80%, 60%, or 40% groups (n = 13 per group), performing 30 eccentric actions of the elbow flexors of 100%, 80%, 60%, or 40% of maximal isometric strength [maximal voluntary contraction (MVC)] for ECC1, followed 2-3 wk later by a similar exercise (ECC2) that used 100% MVC load. MVC at six elbow joint angles, range of motion, upper arm circumference, serum creatine kinase activity, myoglobin concentration, and muscle soreness were measured before and for 5 days following ECC1 and ECC2. A rightward shift of optimum angle following ECC1 was significantly (P < 0.05) greater for the 100% and 80% than for the 60% and 40% groups, and it decreased significantly (P < 0.05) from immediately to 5 days postexercise. By the time ECC2 was performed, only the 100% group kept a significant shift (4 degrees). Changes in most of the criterion measures following ECC1 were significantly greater for the 100% and 80% groups compared with the 60% and 40% groups. Changes in the criterion measures following ECC2 were significantly (P < 0.05) greater for the 40% group compared with other groups. Although the magnitude of repeated bout effect following ECC2 was significantly (P < 0.05) smaller for the 40% and 60% groups, all groups showed significantly (P < 0.05) reduced changes in criterion measures following ECC2 compared with the ECC1 100% bout. We conclude that the repeated-bout effect was not dependent on the shift of optimum angle.

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This study examined whether a second bout of maximal eccentric exercise performed 3 days after the first exercise bout would produce further changes in muscle damage and electromyographic activity (EMG). Male students (n=26) were randomly assigned to experimental 70 (EX70; n=9), experimental 30 (EX30; n=8), and control (CON; n=9) groups. The initial exercise was 30 maximal voluntary isokinetic eccentric contractions (MAX1) on non-dominant elbow flexors at 60 degrees s(-1) (1.05 rad s(-1)). The EX70 and EX30 groups performed a second bout of 70 and 30 eccentric contractions (MAX2), respectively, 3 days after MAX1. Upper arm circumference, range of motion, strength, integrated EMG (IEMG), and mean power frequency (MPF) were measured before, immediately after, and once a day for 9 days after MAX1. Plasma creatine kinase (CK) activity and muscle soreness were assessed before and for 9 days after MAX1. Total work, work per contraction, IEMG, and MPF were also recorded during MAX1 and MAX2. All indicators of muscle damage changed following MAX1 for each group (P<0.05), but no indicators of additional damage (P>0.05) were apparent after MAX2 for either the EX70 or EX30 groups. IEMG (P=0.03) and MPF (P=0.04) were lower for MAX2 compared with MAX1 for both the EX30 and EX70 groups. It is concluded that performing a second bout of eccentric exercise with damaged muscles 3 days after the initial bout does not produce further damage or retard recovery, even when the second bout of exercise is more strenuous. EMG findings were consistent with reduced activation of fast-twitch motor units during the second eccentric bout. These results may be interpreted as evidence of a neural protective mechanism.

This study proposed that attenuated expression of inflammatory factors is an underlying mechanism driving the repeated-bout effect (rapid adaptation to eccentric exercise). We investigated changes in mRNA levels and protein localization of inflammatory genes after two bouts of muscle-lengthening exercise. Seven male subjects performed two bouts of lower body exercise (separated by 4 wk) in which one leg performed 300 eccentric-concentric actions, and the contralateral leg performed 300 concentric actions only. Vastus lateralis biopsies were collected at 6 h, and strength was assessed at baseline and at 0, 3, and 5 days after exercise. mRNA levels were measured via semiquantitative RT-PCR for the following genes: CYR61, HSP40, HSP70, IL1R1, TCF8, ZFP36, CEBPD, and MCP1. Muscle functional adaptation was demonstrated via attenuated strength loss (16% less, P = 0.04) at 5 days after bout 2 compared with bout 1 in the eccentrically exercised leg. mRNA expression of three of the eight genes tested was significantly elevated in the eccentrically exercised leg from bout 1 to bout 2 (+3.9-fold for ZFP36, +2.3-fold for CEBPD, and +2.6-fold for MCP1), while all eight mRNA levels were unaffected by bout in the concentrically exercised leg. Immunohistochemistry further localized the protein of one of the elevated factors [monocyte chemoattractant protein-1 (MCP1)] within the tissue. MCP1 colocalized with resident macrophage and satellite cell populations, suggesting that alterations in cytokine signaling between these cell populations may play a role in muscle adaptation to exercise. Contrary to our hypothesis, several inflammatory genes were transcriptionally upregulated (rather than attenuated) after a repeated exercise bout, potentially indicating a role for these genes in the adaptation process.

Purpose: Unilateral resistance training increases muscle strength of the contralateral homologous muscle by the cross-education effect. Muscle damage induced by second eccentric exercise bout is attenuated, even when it is performed by the contralateral limb. The present study compared the effects of unilateral eccentric training (ET) and concentric training (CT) of the elbow flexors (EF) on maximal voluntary isometric contraction (MVC) strength and muscle damage of the contralateral untrained EF. Methods: Young men were placed into ET, CT, ipsilateral repeated bout (IL-RB), and contralateral repeated bout (CL-RB) groups (n = 12 per group). The ET and CT groups performed unilateral EF training consisting of five sets of six eccentric and concentric contractions, respectively, once a week for 5 wk by increasing the intensity from 10% to 100% of MVC, followed by 30 maximal eccentric contractions (30MaxEC) of the opposite EF 1 wk later. The IL-RB group performed two bouts of 30MaxEC separated by 2 wk using the nondominant arm, and CL-RB group performed two bouts of 30MaxEC with a different arm for each bout in 1-wk apart. Results: The MVC increased (P < 0.05) greater for the trained (19% ± 8%) and untrained (11% ± 5%) arms in ET when compared with those in CT (10% ± 6%, 5% ± 2%). The magnitude of changes in muscle damage markers was reduced by 71% ± 19% after the second than the first bout for IL-RB group, and by 48% ± 21% for CL-RB group. Eccentric training and CT attenuated the magnitude by 58% ± 25% and 13% ± 13%, respectively, and the protective effect of ET was greater (P < 0.05) than CL-RB, but smaller (P < 0.05) than IL-RB. Conclusions: These results showed that cross-education effect was stronger for ET than CT, and progressive ET produced greater contralateral muscle damage protective effect than a single eccentric exercise bout.