Protective effect by maximal isometric contractions against maximal eccentric exercise-induced muscle damage of the knee extensors

This study investigated whether maximal voluntary isometric contractions (MVIC) performed before maximal eccentric contractions (MaxEC) would attenuate muscle damage of the knee extensors. Untrained men were placed to an experimental group that performed 6 sets of 10 MVIC at 90° knee flexion 2 weeks before 6 sets of 10 MaxEC or a control group that performed MaxEC only (n = 13/group). Changes in muscle damage markers were assessed before to 5 days after each exercise. Small but significant changes in maximal voluntary concentric contraction torque, range of motion (ROM) and plasma creatine kinase (CK) activity were evident at immediately to 2 days post-MVIC (p < 0.05), but other variables (e.g. thigh girth, myoglobin concentration, B-mode echo intensity) did not change significantly. Changes in all variables after MaxEC were smaller (p < 0.05) by 45% (soreness)–67% (CK) for the experimental than the control group. These results suggest that MVIC conferred potent protective effect against MaxEC-induced muscle damage.     

Concentric or eccentric training effect on eccentric exercise-induced muscle damage.

PURPOSE: The purpose of this study was to compare changes in muscle damage indicators following 24 maximal eccentric actions of the elbow flexors (Max-ECC) between the arms that had been previously trained either eccentrically or concentrically for 8 wk. METHODS: Fifteen subjects performed three sets of 10 repetitions of eccentric training (ECC-T) with one arm and concentric training (CON-T) with the other arm once a week for 8 wk using a dumbbell representing 50% of maximal isometric force of the elbow flexors (MIF) determined at the elbow joint of 90 degrees (1.57 rad). The dumbbell was lowered from a flexed (50 degrees, 0.87 rad) to an extended elbow position (180 degrees, 3.14 rad) in 3 s for ECC-T, and lifted from the extended to the flexed position in 3 s for CON-T. Max-ECC was performed 4 wk after CON-T and 6 wk after ECC-T. Changes in MIF, range of motion (ROM), upper arm circumference (CIR), muscle soreness (SOR), and plasma creatine kinase (CK) activity were compared between the ECC-T and CON-T arms. RESULTS: The first ECC-T session produced larger decreases in MIF and ROM, and larger increases in CIR and SOR compared with CON-T. CK increased significantly (P < 0.01) and peaked 4 d after the first training session, but did not increase in the following sessions. All measures changed significantly (P < 0.01) following Max-ECC; however, the changes were not significantly different between ECC-T and CON-T arms. CONCLUSION: These results showed that ECC-T did not mitigate the magnitude of muscle damage more than CON-T, and CON-T did not exacerbate muscle damage.     

Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage

This study investigated the relationship between delayed-onset muscle soreness and other indicators of muscle damage following eccentric exercise. Male students (n = 110) performed 12 (12ECC), 24 (24ECC), or 60 maximal eccentric actions of the elbow flexors (60ECC). Maximal isometric force, relaxed and flexed elbow joint angles, upper arm circumference, and plasma creatine kinase activity were assessed immediately before and after, and for 4 days after exercise. Muscle soreness (SOR) was evaluated by a visual analog scale (a 50-mm line, 0: no pain, 50: extremely painful) when the elbow flexors were palpated (SOR-Pal), flexed (SOR-Flx) and stretched (SOR-Ext). Although 24ECC and 60ECC resulted in significantly (P <; 0.05) larger changes in all indicators and slower recovery compared to 12ECC, no significant differences were evident for SOR-Pal and SOR-Flx between 12ECC and 24ECC, or 12ECC and 60ECC. In contrast, SOR-Ext was significantly (P <; 0.05) lower for 12ECC compared to 24ECC and 60ECC. A Pearson product-moment correlation showed SOR-Pal did not correlate significantly with any indicators, however, SOR-Ext and SOR-Flx showed weak (r <; 0.32) but significant (P <; 0.05) correlations with other indicators. Because of generally poor correlations between DOMS and other indicators, we conclude that use of DOMS is a poor reflector of eccentric exercise-induced muscle damage and inflammation, and changes in indirect markers of muscle damage and inflammation are not necessarily accompanied with DOMS.     

Identical twins are discordant for markers of eccentric exercise-induced muscle damage

This study investigated whether the variability observed in the markers of exercise-induced muscle damage (EIMD) has a genetic etiology. Sixteen pairs of identical twins performed 24 maximal eccentric contractions (24MAX) using the elbow flexors. EIMD indicators were measured pre-24MAX and three days post-24MAX and included: post-exercise force deficit, maximal isometric force (ISO), plasma creatine kinase (CK), myoglobin (Mb), and joint range of motion. Force-time curves were recorded throughout the 24MAX. Twin siblings were alike for pre-exercise ISO (intraclass R = 0.89) and CK (R = 0.76) (p < 0.001), but were discordant for post-exercise force deficit (R = 0.29), CK (R = 0.15), and Mb (R = 0.17) (p > 0.05). In comparison with individuals minimally affected by the 24MAX, those who experienced the greatest force deficit 3 days post-exercise (> 50 %) were characterised by the greater application of eccentric force at longer muscle lengths (23.1 % vs 17.3 %) (p < 0.05). This study demonstrates that twins do not experience the same level of EIMD following identical exercise bouts. This suggests that the individual variability following high-force eccentric exercise cannot be attributed to genetic differences, refuting the idea that an inherited subclinical predisposition is responsible. From these results, a potential mechanism for the repeated bout effect is discussed.     

Low-intensity elbow flexion eccentric contractions attenuate maximal eccentric exercise-induced muscle damage of the contralateral arm

Objectives

The magnitude of muscle damage induced by maximal eccentric contractions (MaxEC) of the elbow flexors (EF) is reduced when it is preceded by low-intensity (10% of maximal voluntary isometric contraction strength) eccentric contractions (10%EC) of the same muscle, or by MaxEC of the opposite EF. This study investigated whether 10%EC would reduce the magnitude of muscle damage after MaxEC performed by the opposite arm.

Moderate intensity cycling is better than running on recovery of eccentric exercise-induced muscle damage

ObjectiveTo compare the effects of moderate intensity running and cycling on markers of exercise-induced muscle damage in men.Study designRandomized controlled trial.SettingLaboratory.ParticipantsThirty volunteers were randomized in three groups [running (RG; n = 10), cycling (CG; n = 10) and control (CON; n = 10)] and were evaluated at baseline, post 24, 48 and 72 h of knee extensors’ muscle damage protocol. CON performed passive recovery, while RG and CG performed active recovery immediately after the protocol, as well as 24 h and 48 h afterwards.Main outcomes(i) maximal voluntary isometric contraction (MVIC); (ii) delayed-onset muscle soreness (DOMS); (iii) plasma creatine kinase (CK) and lactate dehydrogenase (LDH) levels.ResultsNo group-by-time interaction was found in any outcome evaluated (p > 0.05). All groups presented decreases in MVIC and increases in DOMS (p < 0.001), without differences in CK and LDH. Compared with CON, exercise groups presented likely beneficial effects for LDH, while only CG had a likely beneficial effect for DOMS. Lastly, CG presented likely/very likely beneficial effects for MVIC and DOMS compared to RG.ConclusionAlthough the null hypothesis analysis did not find differences, the magnitude-based inference analysis suggested that moderate intensity cycling have likely beneficial effects on knee extensor muscle recovery after eccentric exercise protocol.     

Effects of local cryotherapy for recovery of delayed onset muscle soreness and strength following exercise-induced muscle damage: systematic review and meta-analysis

Sport Sciences for Health - The aim of the current study was to evaluate the effects of local cryotherapy on the main symptoms of exercise-induced muscle damage (EIMD) through a systematic...     

The effects of muscle damage following eccentric exercise on gait biomechanics

To examine the effects of knee extensors muscle damage on walking and running biomechanics in healthy males. Muscle damage was caused by 60 (6x10) maximal eccentric knee flexions of both legs, selected in a random order, at an angular velocity of 1.05rad/s in 10 volunteers (mean age 20+/-1.0 years). Muscle damage indicators (creatine kinase (CK), lactate dehydrogenase (LDH), delayed onset muscle soreness (DOMS), eccentric and isometric (110 degrees knee flexion) peak torque), pelvic three dimensional (3D) orientation, as well as hip, knee and ankle-joint flexion/extension angles during gait (walking at 1.2m/s and running at 2.8m/s) were assessed pre- and 48h post-eccentric exercise. All muscle damage indicators revealed significant changes post- compared to pre-exercise data (P<0.05) confirming that muscle damage did occur. Kinematic analysis revealed that muscle damage significantly decreased the knee-joint angle range of movement at the stance and swing phases during walking (P<0.05) and running (P<0.05), respectively. These changes were accompanied by corresponding increases of pelvic rotation (P<0.05) and decrease of pelvic tilt (P<0.05). The present data demonstrate that damage of knee extensors result in changes of treadmill walking and running kinematics at both knee joint and pelvis. The fact that these alterations occur at different gait phases could be attributed to the speed of movement and to a self-protection mechanism to prevent further damage.     

Metabolic consequences of exercise-induced muscle damage

Exercise-induced muscle damage (EIMD) is commonly experienced following either a bout of unaccustomed physical activity or following physical activity of greater than normal duration or intensity. The mechanistic factor responsible for the initiation of EIMD is not known; however, it is hypothesised to be either mechanical or metabolic in nature. The mechanical stress hypothesis states that EIMD is the result of physical stress upon the muscle fibre. In contrast, the metabolic stress model predicts that EIMD is the result of metabolic deficiencies, possibly through the decreased action of Ca(2+)-adenosine triphosphatase. Irrespective of the cause of the damage, EIMD has a number of profound metabolic effects. The most notable metabolic effects of EIMD are decreased insulin sensitivity, prolonged glycogen depletion and an increase in metabolic rate both at rest and during exercise. Based on current knowledge regarding the effects that various types of damaging exercise have on muscle metabolism, a new model for the initiation of EIMD is proposed. This model states that damage initiation may be either metabolic or mechanical, or a combination of both, depending on the mode, intensity and duration of exercise and the training status of the individual.     

A review on strength exercise-induced muscle damage: applications, adaptation mechanisms and limitations

This study aims to review the main aspects that induce muscle damage, and to discuss the adaptations of this phenomenon, applications and limitations of this study area. Damage induced by strength training has been utilized for two purposes: 1) verification of the recovery period required between training sessions, which has a direct influence on designing exercise programs; and 2) as indication for higher training intensity, mainly in studies on the "repeated bout effect". There is some speculation about the role of muscle damage in inducing hypertrophy. However, studies demonstrate that exercise-induced muscle damage may not be a consistent indicator of higher chronic hypertrophic response, because hypertrophy also occurs in training strategies with very low mechanical overloads. In addition, aerobic exercise, also induces muscle damage, exhibits no hypertrophic response after training. The remodeling process induced bay muscle damage promotes alterations to strength x length relationship for stretched positions, indicating an increased number of sarcomeres in series, due to strength exercises. Therefore, the study on strength exercise-induced damage seems to be adequate for implementing adequate rest periods to recovery from different sessions of strength training, and not to suggest chronic hypertrophy.     

The effect of acute and repeated ischemic preconditioning on recovery following exercise-induced muscle damage

ObjectivesThe aim of this investigation was to determine if acute or repeated applications of ischemic preconditioning (IPC) could enhance the recovery process, following exercise induced muscle damage (EIMD).DesignRandomized control trial.MethodsTwenty-three healthy males were familiarised with the muscle damaging protocol (five sets of 20 drop jumps from a 0.6 m box) and randomly allocated to one of three groups: SHAM (3 × 5 min at 20 mmHg), Acute IPC (3 × 5 min at 220 mmHg) and Repeated IPC (3 days x 3 × 5 min at 220 mmHg). The indices of muscle damage measured included creatine kinase concentration ([CK]), thigh swelling, delayed onset muscle soreness, counter movement jumps (CMJ) and maximal voluntary isometric contraction (MVIC).ResultsBoth acute and repeated IPC improved recovery in MVIC versus SHAM. Repeated IPC led to a faster MVIC recovery at 48 h (101.5%) relative to acute IPC (92.6%) and SHAM (84.4%) (P < 0.05). Less swelling was found for both acute and repeated IPC vs. SHAM (P < 0.05) but no group effects were found for CMJ, soreness or [CK] responses (P > 0.05).ConclusionTaken together, repeated IPC can enhance recovery time of MVIC more than an acute application, and both reduce swelling following EIMD, relative to a SHAM condition.     

The prevention and treatment of exercise-induced muscle damage

Exercise-induced muscle damage (EIMD) can be caused by novel or unaccustomed exercise and results in a temporary decrease in muscle force production, a rise in passive tension, increased muscle soreness and swelling, and an increase in intramuscular proteins in blood. Consequently, EIMD can have a profound effect on the ability to perform subsequent bouts of exercise and therefore adhere to an exercise training programme. A variety of interventions have been used prophylactically and/or therapeutically in an attempt to reduce the negative effects associated with EIMD. This article focuses on some of the most commonly used strategies, including nutritional and pharmacological strategies, electrical and manual therapies and exercise. Long-term supplementation with antioxidants or beta-hydroxy-beta-methylbutyrate appears to provide a prophylactic effect in reducing EIMD, as does the ingestion of protein before and following exercise. Although the administration of high-dose NSAIDs may reduce EIMD and muscle soreness, it also attenuates the adaptive processes and should therefore not be prescribed for long-term treatment of EIMD. Whilst there is some evidence that stretching and massage may reduce muscle soreness, there is little evidence indicating any performance benefits. Electrical therapies and cryotherapy offer limited effect in the treatment of EIMD; however, inconsistencies in the dose and frequency of these and other interventions may account for the lack of consensus regarding their efficacy. Both as a cause and a consequence of this, there are very few evidence-based guidelines for the application of many of these interventions. Conversely, there is unequivocal evidence that prior bouts of eccentric exercise provide a protective effect against subsequent bouts of potentially damaging exercise. Further research is warranted to elucidate the most appropriate dose and frequency of interventions to attenuate EIMD and if these interventions attenuate the adaptation process. This will both clarify the efficacy of such strategies and provide guidelines for evidence-based practice.     

Mechanomyographic responses of the vastus medialis to isometric and eccentric muscle actions

PURPOSE: The mechanomyographic (MMG) signal may be used to examine the motor control strategies used to modulate torque during various types of muscle actions. Therefore, the purpose of this study was to examine the MMG amplitude and mean power frequency (MPF) versus torque relationships during isometric and eccentric isokinetic muscle actions. METHODS: Eleven adults (mean age +/- SD = 20.8 +/- 1.4 yr) volunteered to perform isometric and eccentric isokinetic leg extension muscle actions at 10, 20, 30, 40, 50, 60, 70, 80, 90, and 100% of peak torque on a Cybex 6000 dynamometer. A piezoelectric crystal contact sensor was placed on the vastus medialis to detect the MMG signal. RESULTS: Polynomial regression analyses indicated that for the isometric muscle actions, the relationships for MMG amplitude (r2 = 0.984) and MPF (r2 = 0.989) versus torque were linear. For the eccentric isokinetic muscle actions, the relationships for MMG amplitude (r2 = 0.580) and MPF (r2 = 0.961) versus torque were also linear. CONCLUSION: The patterns for MMG amplitude and MPF may reflect the motor control strategies that modulate torque production for isometric and eccentric isokinetic muscle actions. Based on the results of this and previous studies, it appears that for the vastus medialis, torque is modulated in a similar manner for isometric, concentric, and eccentric isokinetic muscle actions. Specifically, these findings suggest that gradation of torque involves increases in recruitment and firing rate to 100% voluntary torque production.     

Differential expression of muscle damage in humans following acute fast and slow velocity eccentric exercise

We sought to determine if the velocity of an acute bout of eccentric contractions influenced the duration and severity of several common indirect markers of muscle damage. Subjects performed 36 maximal fast (FST, n = 8: 3.14 rad x s(-1)) or slow (SLW, n = 7: 0.52 rad x s(-1)) velocity isokinetic eccentric contractions with the elbow flexors of the non-dominant arm. Muscle soreness, limb girth, plasma creatine kinase (CK) activity, isometric torque and concentric and eccentric torque at 0.52 and 3.14 rad x s(-1) were assessed prior to and for several days following the eccentric bout. Peak plasma CK activity was similar in SLW (4030 +/- 1029 U x 1(-1)) and FST (5864 +/- 2664 U x 1(-1)) groups, (p > 0.05). Both groups experienced similar decrement in all strength variables during the 48 hr following the eccentric bout. However, recovery occurred more rapidly in the FST group during eccentric (0.52 and 3.14 rad x s(-1)) and concentric (3.14 rad x s(-1)) post-testing. The severity of muscle soreness was similar in both groups. However, the FST group experienced peak muscle soreness 48 hr later than the SLW group (24 hr vs. 72 hr). The SLW group experienced a greater increase in upper arm girth than the FST group 20 min, 24 hr and 96 hr following the eccentric exercise bout. The contraction velocity of an acute bout of eccentric exercise differentially influences the magnitude and time course of several indirect markers of muscle damage.     

肌红蛋白基因多态性与运动性肌肉损伤的相关性

 目的 探讨肌红蛋白（myoglobin, Mb）基因第2外显子单核苷酸多态（A79G）与运动性肌肉损伤的关系。方法 85名武警战士进行一次大强度负重运动,检测血清肌酸激酶（creatine kinase,CK）活性的时程变化;聚合酶链反应-限制性片段长度多态（PCR-RFLP）法测定Mb基因多态性;分析基因多态性与安静CK（CK_pre）、峰值CK（CK_peak）及CK最大变化值（△CK）的关系。结果 CK_pre为（145±33）U/L,大强度运动后24 h开始逐渐升高,72 h达峰值［CK_peak：（2972±1648）］U/L,随后缓慢下降,120 h仍高于安静水平。3种基因型的分布频率分别为AA（54.1%）、AG（40.0%）、GG（5.9%）,等位基因分布频率为A（74.1%）、G（25.9%）,符合Hardy-Weinberg遗传平衡定律。组间比较,（AG+GG）组CK_pre、CK_peak和△CK均高于AA组（均P＜0.01）。结论 运动性肌肉损伤易感性与Mb基因第2外显子单核苷酸多态（A79G）有关,G等位基因具有肌肉损伤易感性,而AA基因型则具有运动性肌肉损伤保护作用。     

Ice massage. Effects on exercise-induced muscle damage

AIM: The purpose of this study was to examine the effects of ice massage on the signs and symptoms associated with exercise-induced muscle damage. METHODS: Nine recreationally resistance trained males performed an exercise protocol designed to induce muscle damage on 2 separate occasions; this was performed on the dominant or non-dominant arm in a random cross over design. The protocol consisted of 3 sets of 10 repetitions of single arm biceps curls, at 70% of a pre-determined one repetition maximum (1RM), with the eccentric phase of the contraction extended to 7 seconds. Subjects were also randomly assigned to an ice massage group or control group in the cross over design and received treatments immediately post-exercise, 24 hours and 48 hours post-exercise. 1RM, plasma creatine kinase (CK), muscle soreness (DOMS), limb girth and range of motion (ROM) were measured pre, immediately post, 24 hours, 48 hours and 72 hours post-exercise. RESULTS: Significant time effects were observed for all dependent variables (p<0.05), though no significant group effects were observed. A group by time interaction was found for CK (p<0.05), which at 72 hours post-exercise was significantly lower in the ice massage group (p<0.05). CONCLUSION: These results indicate that although ice massage reduces the appearance of CK it has no other effect on signs and symptoms associated with exercise-induced muscle damage.     

Nifedipine diminishes exercise-induced muscle damage in mouse.

The purpose of this study was to evaluate the effects of a calcium channel blocker (nifedipine) on the severity of muscle damage induced by intensive exercise. Male Charles River mice were assigned to four groups (8 mice/group): normal control (C), nifedipine (N), nifedipine and exercise (N + E) and exercise (E). The animals of the C group were not submitted to any exercise nor to drug administration. The animals of the N group received 1 mg.kg-1 per day of nifedipine (Adalat 10 mg, Bayer AG), per os, during 3 days. The mice of the N + E group were submitted to a treadmill run (0 degree slope) at 1000 m.h-1 (80% of their maximal speed) for 1 hour. In this group, the administration of the drug was under the same conditions as for the N group. The administration started 24 h before the run. The E group was submitted to the same exercise protocol as the animals of N + E group. The soleus muscle was excised for light and electron microscopic evaluation using routine histological techniques. In the C and N groups no morphological alterations were detected. In the E group the number of alterations of striated pattern was twice that in the N + E group. The number of fibres with central nuclei was 35% in the E group but only 8% in the N + E group. The total number of damaged fibres was significantly higher in the E group. The results suggest that nifedipine may give protection to exercise-induced skeletal muscle damage in mouse, probably because the blocking of channels impaired Ca2+ influx; and the results of this study therefore confirm earlier contentions about the possible role of calcium ions in producing muscle damage after work.