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.     

Exercise-induced muscle damage: absence of adaptive effect after a single session of eccentric isokinetic heavy resistance exercise

BACKGROUND: Unaccustomed eccentric exercise induces muscle damage. A single session of eccentric exercise can induce an "adaptive effect" protecting exercised muscles during several weeks. Our aim was to verify this phenomenon in isokinetic exercise. Tested hypothesis was: the progressive muscle rise in tension due to isokinetic eccentric actions would be insufficient to induce the adaptive effect. METHODS: Experimental design: prospective study. Setting: general community. Participants: six healthy and moderately active (untrained) males (29.1 yr +/- 1.5 SEM). Interventions: subjects performed two isokinetic eccentric exercises (EE1 and EE2) of the quadriceps femoris of both legs (120 degrees.s-1; 8 sets of 15 repetitions) separated by 4 weeks. Measures: type I serum myosin heavy chains (MHC) and creatine kinase concentrations (CK), and rate of perceived soreness (DOMS) were collected before each exercise and on days 1, 2, 4, 6 and 9. RESULTS: Both exercises induced significant (p < 0.01) increases in MHC and CK concentrations, and DOMS score. There was no significant difference between EE1 and EE2, at any measurement time for any parameter. Mean peak values (SEM) were respectively (EE1; EE2): MHC (microU.l-1): 308 (192); 285 (191). CK (U.l-1): 1217 (760); 1297 (1039). DOMS score: 2.67 (0.52); 2.33 (0.52). CONCLUSIONS: The first session of eccentric isokinetic exercise (EE1) had no adaptive effect against muscle damage when an identical session was performed 4 weeks later (EE2). Muscle adaptation could have resulted in increased work production (+10.2%; p < 0.05; from EE1 to EE2).     

Shift of peak torque angle after eccentric exercise

This study aims to investigate the changes in the mechanical properties of quadriceps muscle following a sub-maximal concentric-eccentric stepping exercise protocol. Twenty-four untrained healthy subjects aged 21.9 +/- 0.55 years were asked to perform a 10-minute stepping exercise where the dominant leg worked eccentrically and the non-dominant leg worked concentrically at a rate of 15 cycles/min. The quadriceps isokinetic peak torque and the corresponding peak torque angle at angular velocity of 60 degrees /sec, and muscle soreness were determined at baseline, immediately after, day 1 and day 2 after the exercise protocol. Repeated measures of ANOVA showed no change in the peak torque after the eccentric exercise and concentric exercise (p > 0.05). There was a significant shift in the peak torque angle to longer muscle lengths in the eccentrically-exercised leg immediately (65.6 +/- 2.21 degrees ) and on the following two days after exercise (day 1: 68.3 +/- 2.71 degrees ; day 2: 67.4 +/- 2.51 degrees ) when compared with baseline (61.4 +/- 1.55 degrees , p < 0.05). These features were not observed in the concentrically-exercised leg. Eccentric exercise produced a higher level of soreness than concentric exercise at day 1 and 2 after the protocol. Submaximal eccentric exercise could bring about changes in the muscle properties resulting in a shift in the angle-torque relationship to longer muscle length without significant force deficit.     

Greater muscle damage induced by fast versus slow velocity eccentric exercise

Debate exists concerning the effect of contraction velocity on muscle damage, and few human studies have yet to address this issue. This study examined whether the velocity of eccentric exercise affected the magnitude of muscle damage. Twelve untrained subjects performed a series of slow velocity isokinetic eccentric elbow flexions (SV: 30 degrees . s (-1)) of one arm and a fast velocity exercise (FV: 210 degrees . s (-1)) of the other arm, separated by 14 days. In order to standardise the time under tension (120 s) for the two conditions, the number of muscle actions for SV was 30 and 210 for FV. Criterion measures consisted of maximal voluntary torque for isometric, concentric (4 velocities) and eccentric contractions (2 velocities), range of motion (ROM) and relaxed elbow joint angle (RANG), upper arm circumference, muscle soreness and plasma creatine kinase (CK) activity. Measures were taken before, immediately after, 0.5 hour and 24 - 168 hours (240 hours for CK) after each eccentric exercise protocol, and changes in the measures over time were compared between FV and SV by two-way repeated measures ANOVA. Both protocols resulted in significant decrements in isometric and dynamic torque (p < 0.01), but FV showed significantly (p < 0.05) greater reductions over time ( approximately 55 %) and a slower recovery compared to SV ( approximately 30 %). Significantly (p < 0.05) larger decreases in, and delayed recovery of, ROM and RANG were evident after FV compared to SV. FV had significantly (p < 0.05) larger increases in upper arm circumference and soreness compared to SV, and peak plasma CK activity was 4.5-fold greater (p < 0.05) following FV than SV. These results suggest that, for the same time under tension, fast velocity eccentric exercise causes greater muscle damage than slow velocity exercise in untrained subjects.     

Effects of downhill treadmill running on uncoupling protein 3 mRNA expression

Eccentric biased exercise has been reported to elicit more muscle injury than concentric or isometric exercise and potentially generate increased oxidative stress one to two days post exercise. Increased oxidative stress has been shown to up-regulate the expression of UCP3 mRNA. The aim of this study was to investigate the effects of downhill running on skeletal muscle UCP3 mRNA expression. Twenty-four male Sprague Dawley rats were randomly assigned to run continuously for 30 minutes (30-C, n = 6), or run six 5-minute bouts separated by rest periods of 2 minutes (2-R, n = 6), 4 minutes (4-R, n = 6), and 6 minutes (6-R, n = 6) on a 16 degree declined treadmill at a speed of 16 m. min (-1). Sham control animals (n = 8) were placed in a treadmill chamber during the 30-minute run session. Semi-quantitative RT-PCR was conducted to evaluate UCP3 mRNA levels in the plantaris, a muscle used eccentrically during downhill running and tibialis anterior, a muscle which undergoes very little eccentric muscle contraction during this exercise. The level of gene expression was normalized to 18 S ribosomal mRNA expression from the same PCR product. Results are reported as mean +/- standard error. UCP3 of the plantaris muscles from 2-R animals (2.36 +/- 0.13) was significantly greater than UCP3 of the plantaris from control animals (1.72 +/- 0.13), p < 0.05. UCP3 of the tibialis anterior from the continuous group (1.51 +/- 0.17) was significantly less than the UCP3 of the tibialis anterior of the control group (2.09 +/- 1.4), p < 0.05. These data suggest that downhill treadmill running is associated with an increase in UCP3 mRNA expression in the plantaris muscle. These results indicate that exercise which is biased toward eccentric exercise may up-regulate UCP3 mRNA during the period post exercise when muscle damage and repair is elevated.     

Phosphatidylserine supplementation and recovery following downhill running

PURPOSE: This study investigated the effects of 750 mg of soybean-derived phosphatidylserine (S-PtdSer), administered daily for 7 d prior to a bout of eccentric exercise and for 2d following exercise, on delayed onset of muscle soreness and markers of muscle damage, inflammation, and oxidative stress that followed prolonged downhill running. METHODS: Following preliminary testing and a familiarization session, eight recreationally active males repeated an individualized downhill run at -16.5% for 51.0 +/- 1.5 min at 8.7 +/- 0.3 km x h(-1) on four occasions (trials 1-4). Trials 1 and 37 were presupplementation control trials. After trials 1 and 3 the subjects received, in a double-blind and crossover fashion, either S-PtdSer or a glucose polymer placebo. Trials 2 and 3 were separated by a 4-wk washout period. Venous blood, perceived soreness ratings, and feeling states were assessed prior to exercise, after exercise, and at 24 and 48 h after exercise during each trial. RESULTS: Downhill running led to elevations in perceived soreness (P < 0.05), creatine kinase activities (P < 0.001), myoglobin concentrations (P < 0.001), interleukin-6 (IL-6) concentrations (P < 0.001), and lipid hydroperoxide concentrations (P < 0.01). However, supplementation did not significantly attenuate these responses. CONCLUSION: These results suggest that supplementation with 750 mg x d(-1) S-PtdSer for 10 d does not afford additional protection against delayed onset of muscle soreness and markers of muscle damage, inflammation, and oxidative stress that follow prolonged downhill running.     

Effects of a 7-day eccentric training period on muscle damage and inflammation

PURPOSE: This study examined the effects of a 7-d repeated maximal isokinetic eccentric training period on the indicators of muscle damage and inflammatory response. METHODS: Twenty-two college-age males were randomly assigned to eccentric training (ET) (N = 12) and control groups (CON) (N = 10). The initial exercise was 30 repetitions of maximal voluntary isokinetic eccentric contraction (ECC1) on nondominant elbow flexors with Cybex 6000 at 60 degrees.s-1 angular velocity. The ET group performed the same exercise for the following 6 consecutive days (referred to as ECC2 to ECC7) after ECC1. Upper arm circumference (CIR), range of motion (ROM), and maximal isometric force (MIF) were measured before, immediately after, and every 24 h for 7 consecutive days after ECC1. Plasma creatine kinase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetate transaminase (GOT), leukocyte counts, and serum interleukin-1beta and -6 (IL-1beta, IL-6) levels were assessed before; at 2 h; and at 1, 3, 4, 6, and 7 d after ECC1. Muscle soreness was measured before and for 7 consecutive days after ECC1. RESULTS: The ECC1 produced significant changes in most of the measures for both groups (P < 0.05), with the exception of leukocyte counts (P > 0.05). No indicators of increased damage (P > 0.05) were found from ECC2 to ECC7 for the ET group. CONCLUSION: Continuous intensive isokinetic eccentric training performed with damaged muscles did not exacerbate muscle damage and inflammation after ECC1. In addition, a muscular "adaptation effect" may occur as early as 24 h after ECC1, as shown by the ET group's performance for 6 consecutive days after ECC1.     

Leg heating and cooling influences running stride parameters but not running economy

To evaluate the effect of temperature on running economy (RE) and stride parameters in 10 trained male runners (VO2peak 60.8 +/- 6.8 ml . kg (-1) . min (-1)), we used water immersion as a passive temperature manipulation to contrast localised pre-heating, pre-cooling, and thermoneutral interventions prior to running. Runners completed three 10-min treadmill runs at 70 % VO2peak following 40 min of randomised leg immersion in water at 21.0 degrees C (cold), 34.6 degrees C (thermoneutral), or 41.8 degrees C (hot). Treadmill runs were separated by 7 days. External respiratory gas exchange was measured for 30 s before and throughout the exercise and stride parameters were determined from video analysis in the sagittal plane. RE was not affected by prior heating or cooling with no difference in oxygen cost or energy expenditure between the temperature interventions (average VO2 3rd-10th min of exercise: C, 41.6 +/- 3.4 ml . kg (-1) . min (-1); TN, 41.6 +/- 3.0; H, 41.8 +/- 3.5; p = 0.94). Exercise heart rate was affected by temperature (H > TN > C; p < 0.001). During minutes 3 - 5 of running the respiratory-exchange and minute ventilation/oxygen consumption ratios were greater in cold compared with thermoneutral (p < 0.05). Averaged over the full 10 min of exercise, stride length was shorter and stride frequency higher for the C trial compared to TN and H (p < 0.01). Leg temperature manipulation did not influence running economy despite changes in stride parameters that might indicate restricted muscle-tendon elasticity after pre-cooling. Larger changes in stride mechanics than those produced by the current temperature intervention are required to influence running economy.     

Muscle damage and soreness after endurance exercise of the elbow flexors

PURPOSE: This study investigated changes in indirect markers of muscle damage after endurance exercise of the elbow flexors and compared the changes with those after maximal eccentric actions (Max-ECC) of the elbow flexors. METHODS: Eighteen male students rhythmically lifted (1 s) and lowered (1 s) a light dumbbell (1.1-1.8 kg: 9% of MIF) in 60-180 degrees of elbow joint angle for 2 h (2-h Ex). Maximal isometric force (MIF), relaxed (RANG) and flexed elbow joint angles (FANG), upper-arm circumference (CIR), muscle soreness (SOR), B-mode ultrasound (US), and plasma creatine kinase (CK) activity were assessed before and immediately after, and up to 96 h after exercise. RESULTS: All measures were altered significantly (P < 0.05) after 2-h Ex in a similar time course to Max-ECC; however, changes in RANG, FANG, CIR, US, and CK (peak: 356 +/- 121 IU.L-1) were significantly (P < 0.05) smaller compared with those after Max-ECC. SOR developed immediately after 2-h Ex and peaked 24-48 h after exercise. MIF dropped to 44.1% of the preexercise level, which was significantly (P < 0.05) lower than that after Max-ECC (58.1%), immediately postexercise. MIF recovered to 79.8% at 24 h, and 97.8% at 96 h postexercise, which was a significantly (P < 0.05) faster recovery compared with that of Max-ECC (73.1% at 96 h). CONCLUSION: These results showed low-intensity continuous muscle contractions (3600 times) resulted in muscle damage; however, the magnitude of the muscle damage was less severe, and the recovery was faster compared with 12 maximal eccentric muscle actions.     

Serum concentrations of collagen degrading enzymes and their inhibitors after downhill running

In the present study the release of proteins degrading extracellular matrix compounds to circulation was measured after damaging exercise in humans. Muscle damage was induced by downhill running; furthermore, the exercise was performed at both cold temperature (5 degrees C) and room temperature (22 degrees C) to study also the possible effect of environmental temperature on serum concentrations of matrix metalloproteinases MMP-2 and MMP-9, tissue inhibitors of metalloproteinases TIMP-1 and TIMP-2, and MMP-2/TIMP-2 complex, and muscle damage monitored by serum creatine kinase measurements. Results were compared with those obtained from patients having rhabdomyolysis, myositis and Becker muscular dystrophy. The present study demonstrates an acute increase in serum concentrations of MMP-9, TIMP-1, and MMP-2/TIMP-2 complex, but no changes in serum MMP-2 concentrations in response to eccentric exercise. Serum creatine kinase activity data suggest greater muscle damage after downhill running in a cold environment than at room temperature. The present observations about at most slight changes in serum MMP and TIMP concentrations and lack of their correlation to increased serum creatine kinase after exercise indicate that serum measurements of MMPs and TIMPs do not sensitively respond to exercise induced skeletal muscle damage and extracellular matrix regeneration. On the other hand, severe skeletal muscle damage, such as rhabdomyolysis, myositis and Becker muscular dystrophy, seemed to have an effect on serum MMP and TIMP concentrations.     

Is eccentric exercise-induced torque decrease contraction type dependent?

PURPOSE: This study was designed to determine whether torque decrease following an acute eccentric exercise is contraction type dependent. METHODS: Ten active males performed an exercise session consisting of five sets of ten maximal eccentric muscle actions of the elbow flexors. Before and immediately after the exercise, maximal voluntary eccentric (-60 degrees.s-1; Ecc60), isometric (0 degrees.s-1; Iso) and concentric (60 degrees.s-1; Con60 and 240 degrees.s-1; Con240) torque were measured. In order to distinguish central from peripheral factors involved in torque decrement, activation level (twitch interpolation technique), myoelectrical activity (RMS) of biceps brachii, as well as electrically evoked M-wave and peak twitch torque (Pt) were recorded. RESULTS: The eccentric exercise induced a significant torque reduction (P < 0.01), whatever the muscular contraction type [mean (SD): -22.3 (8.1)% for Ecc60; -20.8 (11.2)% for Iso; -18.5 (6.1)% for Con60 and -12.5 (8.9)% for Con240]. Relative torque decrement was however significantly less for Con240 compared with Ecc60, Iso, and Con60 (P < 0.05). Torque decreases were associated with a reduction of both M-wave amplitude (P < 0.01) and Pt (P < 0.001), probably related to an impairment of the excitation-contraction coupling. Concurrently, activation level was reduced (P < 0.01), therefore indicating the occurrence of central fatigue, as also confirmed by RMS decreases for all the conditions (P < 0.05), except Con240. DISCUSSION: An acute eccentric exercise induced a significant voluntary maximal torque reduction during eccentric, isometric, and concentric muscle actions ascribed to both peripheral and central failure of force production capacity. It can be concluded that eccentric exercise-induced torque decrease is not contraction type dependent.     

Specific effects of eccentric training on muscular fatigability

This study was designed to test the hypothesis that an eccentric training period induces a reduction of neuromuscular fatigability following an eccentric exercise. Before (Pre-T) and after (Post-T) a 7-wks sub-maximal eccentric training, ten active males performed a fatiguing exercise consisting of five sets of ten maximal eccentric elbow flexions. Before (Pre-T-1 and Post-T-1) and after (Pre-T-2 and Post-T-2) each fatiguing exercise, the voluntary torque and its associated agonistic electromyographic activity (RMS), assessed at four angular velocities (-60 degrees x s (-1); 0 degrees x s (-1); 60 degrees x s (-1); 240 degrees x s (-1)) were measured. The isometric voluntary activation level and twitch contractile properties were measured. The training period induced significant eccentric and isometric torque gains. While isometric and concentric torque decreases were similar Pre-T-2 and Post-T-2, the eccentric torque loss was significantly lower Post-T-2 than Pre-T-2 (-11.7 +/- 10.2 % and -20.5 +/- 6.5 %, respectively; p < 0.05). The reduction of the twitch maximal rate of torque rise was also significantly lower Post-T-2 (-49.4 +/- 11.9 %) than Pre-T-2 (-65.2 +/- 9.8 %) (p < 0.05). The loss of maximal voluntary activation and RMS were similar Pre-T-2 and Post-T-2. The present experiment showed that a 7-wks eccentric training period produced contraction-type specific adaptations that significantly reduced the exercise-induced torque loss during eccentric muscle actions.     

Changes in markers of muscle damage of middle-aged and young men following eccentric exercise of the elbow flexors

It is well documented that unaccustomed eccentric exercise induces muscle damage, but the responses of middle-aged individuals to a bout of eccentric exercise have not been reported. The purpose of this study was to compare changes in indirect markers of muscle damage following eccentric exercise of the elbow flexors between 12 young (age: 19.4+/-0.4 years, height: 173.5+/-2.0cm, body mass: 65.8+/-3.5kg) and 12 middle-aged men (48.0+/-2.1 years, 169.5+/-1.7cm, 67.3+/-1.6kg). It was hypothesized that middle-aged men would be more susceptible to muscle damage than young men. All subjects performed six sets of five eccentric actions of the elbow flexors using a dumbbell of 40% of maximal isometric strength (MVC). Changes in MVC, elbow joint angles and range of motion, upper arm circumference, plasma creatine kinase activity and myoglobin concentration, and muscle soreness before, immediately after, and 1, 2, 3, and 4 days after exercise were compared between the young and middle-aged groups by a two-way repeated measures ANOVA. All criterion measures changed significantly (P<0.05) after exercise, but no significant differences in the changes in the measures except for muscle soreness were evident between groups. Development of muscle soreness after exercise was significantly (P<0.05) lower (approximately a half of the value) for the middle-aged group compared with the young group. These results did not support the hypothesis that middle-aged men would be more susceptible to muscle damage than young men.     

Characteristics of isometric and dynamic strength loss following eccentric exercise-induced muscle damage

Angle-specific isometric strength and angular velocity-specific concentric strength of the knee extensors were studied in eight subjects (5 males and 3 females) following a bout of muscular damaging exercise. One hundred maximal voluntary eccentric contractions of the knee extensors were performed in the prone position through a range of motion from 40 degrees to 140 degrees (0 degrees = full extension) at 1.57 rads(-1). Isometric peak torque was measured whilst seated at 10 degrees and 80 degrees knee flexion, corresponding to short and optimal muscle length, respectively. Isokinetic concentric peak torque was measured at 0.52 and 3.14 rad x s(-1). Plasma creatine kinase (CK) activity was also measured from a fingertip blood sample. These measures were taken before, immediately after and on days 1, 2, 4, and 7 following the eccentric exercise. The eccentric exercise protocol resuited in a greater relative loss of strength (P< 0.05) at short muscle length (76.3 +/- 2.5% of pre-exercise values) compared to optimal length (82.1 +/- 2.7%). There were no differences in the relative strength loss between isometric strength at optimal length and isokinetic concentric strength at 0.52 and 3.14 rad x s(-1). CK activity was significantly elevated above baseline at days 4 (P < 0.01) and 7 (P < 0.01). The greater relative strength loss at short muscle length appeared to persist throughout the seven-day testing period and provides indirect evidence of a shift in the angle-torque relationship towards longer muscle lengths. The results lend partial support to the popping sarcomere hypothesis of muscle damage, but could also be explained by an impairment of activation at short muscle lengths.     

The effects of a prolonged running exercise on strength characteristics

The aim of this study was to examine concentric, isometric, and eccentric strength reductions in the quadriceps muscle following a prolonged running exercise. Before and after a 2 h run (28.4+/-1.4 km) peak torque (PT) of the knee extensors at angular velocities of -120, -90, -60, 0, 60, 120, 180, 240 degrees x s(-1) using an isokinetic dynamometer, electromyographic (EMG) activity of the vastus lateralis (VL) and vastus medialis (VM) muscles and height of a counter movement jump were recorded in twelve well-trained triathletes. Counter movement jump performances decreased by 10% and PT values were all significantly lower (p < 0.01) at each angular velocity following the run. The torque loss was significantly (p < 0.01) greater under eccentric contractions (from 18 to 21%) than under concentric ones (from 11 to 14%). EMG activity (RMS) was lower in both VL and VM muscles after the 2 h run but no difference existed in RMS losses between concentric and eccentric contractions. The present results demonstrate that 1) a prolonged running exercise more greatly affects eccentric force production in the quadriceps muscle, and 2) this specificity seems to be due to an impairment of the muscular contractile mechanism rather than a modification to the neural input.     

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.     

The magnitude of muscle damage induced by downhill backward walking

While various models for exercise-induced muscle damage (EIMD) have been introduced, many of them use maximal voluntary contractions of the elbow flexors and knee extensors performed on isokinetic dynamometers. Few studies have used exercise protocols that attempt to replicate submaximal eccentric muscle actions that commonly occur during daily activities. Downhill backwards walking has been used previously as an EIMD model. However, the common markers of muscle damage have not been systematically examined for this model. The purpose of this study was to determine the magnitude of muscle damage induced by downhill backward walking with regard to changes in commonly-used indirect markers of EIMD. Twenty subjects aged between 19 y and 42 y completed a bout of 60 min of downhill (-15%) backward walking in which a single limb performed submaximal eccentric actions at a stepping rate of 30 - 35 strides per min. A repeated measures ANOVA revealed significant (p < 0.05) increases from baseline for soreness (24 hr- 96 hr), tenderness (24 hr - 96 hr), and plasma creatine kinase activity (0.5 hr - 96 hr), and significant decreases (p < 0.05) in maximal voluntary isometric (approximately 25%) and isokinetic (-15%) strength (0.5 hr - 96 hr) post-walk for the exercised limb. The time course of observed changes in these markers was similar to that reported for EIMD models of the elbow flexors and knee extensors. However, the magnitude of muscle damage appeared more consistent with that demonstrated following submaximal eccentric exercise.     

Short-term immobilization after eccentric exercise. Part II: creatine kinase and myoglobin

PURPOSE: Although creatine kinase (CK) is commonly used as a marker of muscle damage, there is large variability in the response to exercise. We previously found short-term immobilization blunted the rise in plasma CK after eccentric exercise, suggesting subsequent movement of damaged muscle may contribute to variability. We hypothesized that immobilization decreases lymphatic transport of CK from damaged muscle, blunting the CK response. In this study, we compared changes in plasma CK and myoglobin (Mb), as Mb is released from damaged muscle directly into the bloodstream whereas CK is released first into the lymph. METHODS: Twenty-five college-age males were matched according to force loss after 50 maximal eccentric contractions of the elbow flexors and placed into an immobilization (IMM, N = 12) or control (CON, N = 13) group. IMM had their arm immobilized at 90 degrees and secured in a sling for 4 d (treatment). Venipuncture was performed during baseline, treatment, and for 5 d after treatment (recovery) to assess plasma CK activity and Mb. Urine specific gravity (USG) and muscle activity (ACT) were assessed. RESULTS: Immobilization significantly blunted increases in CK activity (IMM: 955 +/- 316 IU.L-1 vs CON: 2884 +/- 1083 IU.L-1; P < 0.05) but not increases in Mb (IMM: 712 +/- 278 ng.mL-1 vs CON: 891 +/- 253 ng.mL-1; P > 0.05). There were no differences in USG between groups over time (P > 0.05) and no group differences in ACT (P > 0.05). CONCLUSIONS: Short-term immobilization after eccentric exercise blunted the CK response but not the Mb response, suggesting lymphatic transport of CK may be responsible. Because hydration status and muscular activity after exercise were not different between groups, the blunted CK response was likely due to inactivation of CK activity before entering circulation.     

Effect of stretching on strength loss and pain after eccentric exercise

PURPOSE: The purposes of the this study were to determine whether stretch-induced strength loss was muscle length dependent (study 1) and whether passive stretching prior to eccentric exercise affected strength loss and pain on subsequent days (study 2). METHODS: For study 1, knee flexion strength was measured isometrically (six angles) and isokinetically (eccentric and concentric) in 10 men (33 +/- 9 yr). The subjects then performed six 90-s static hamstring stretches, after which isometric and isokinetic strength were retested. For study 2, the dominant and nondominant legs of eight men (34 +/- 9 yr) were assigned to a stretch (six 60-s stretches) or control condition prior to eccentric hamstring exercise. Isometric strength and pain were assessed prior to, immediately after, and on the 3 d after exercise. RESULTS: After stretching, strength was decreased by 17% at 80 degrees , 11% at 65 degrees , 5% at 50 degrees , 7% at 35 degrees , and 8% at 20 degrees , and it was increased by 6% at 5 degrees (angle effect P < 0.01). Strength loss following eccentric exercise was less on the stretched versus the unstretched control limb at 37 degrees (P < 0.05), but not at other angles (stretch by time by angle P < 0.01). Pain was not different between the stretched and the unstretched control limb (P = 0.94). CONCLUSION: Stretch-induced strength loss was dependent on muscle length, such that strength was decreased with the muscle group in a shortened position, but not with the muscle group in a lengthened position. Strength loss and pain after eccentric exercise were generally unaffected by prior stretching, with the exception that stretching prevented strength loss when assessed with the muscle in a lengthened position.     

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.