Ibuprofen and acetaminophen: effect on muscle inflammation after eccentric exercise

PURPOSE: We examined the influence of ibuprofen and acetaminophen on muscle neutrophil and macrophage concentrations after novel eccentric contractions. METHODS: Twenty-four males (25 +/- 3 yr) were divided into three groups that received the maximal over-the-counter dose of either ibuprofen (1200 mg x d-1), acetaminophen (4000 mg x d-1), or a placebo after eccentric contractions of the knee extensors. Biopsies from the vastus lateralis were taken before and 24 h after exercise. Inflammatory cells were quantified in muscle cross-sections using immunohistochemistry. RESULTS: Macrophage concentrations were elevated by 1.5- to 2.5-fold (P < 0.05) at 24 h postexercise relative to preexercise concentrations, whereas neutrophil concentrations were not significantly elevated. Muscle inflammatory cell concentrations were unaffected by treatment with ibuprofen or acetaminophen when compared with placebo. CONCLUSIONS: Maximal over-the-counter doses of ibuprofen or acetaminophen, when administered therapeutically, do not affect muscle concentrations of neutrophils or macrophages 24 h after a novel bout of eccentric contractions.     

Acute adaptation to low volume eccentric exercise.

PURPOSE: Many symptoms of eccentric muscle damage can be substantially reduced if a similar eccentric bout is repeated within several weeks of the initial bout. The purpose of this study was to determine whether a nondamaging, low repetition, low volume eccentric exercise bout could also provide a protective/adaptive effect. METHODS: Subjects were assigned to a control (CON), eccentric exercise (ECC), or low volume familiarized eccentric exercise group (LV+ECC). Before the study, the LV+ECC group performed six maximal eccentric contractions during two familiarization sessions. The main eccentric bout targeted the elbow flexor muscle group and consisted of 36 maximal eccentric contractions. Muscle soreness, upper arm girth, elbow angle, creatine kinase activity, isometric torque, and concentric and eccentric torque at 0.52 and 3.14 rad.s-1 were assessed 0, 1, 2, 3, 4, 7, and 10 d postexercise. RESULTS: No evidence of muscle damage was observed as a result of the low volume eccentric bouts. Nevertheless, with the exception of muscle soreness and concentric torque, all variables recovered more rapidly in the LV+ECC group (P < 0.05). CONCLUSION: Adaptation to eccentric exercise can occur in the absence of significant muscle damage. Exposure to a small number of nondamaging eccentric contractions can significantly improve recovery after a subsequent damaging eccentric bout. Furthermore, this adaptation appears to be mode-specific and not applicable to concentric contractions.     

Decreased EMG median frequency during a second bout of eccentric contractions

PURPOSE: Others have reported preferential recruitment of fast motor units in muscles during performance of eccentric contractions and there is evidence that fast muscle fibers are more susceptible to eccentric contraction-induced injury. We tested the hypothesis that during a second bout of maximal eccentric contractions 1 wk after the first, there would be a reduction in the electromyographic (EMG) median frequency (MF) with minimal change in the EMG root-mean-square (RMS), indicating greater reliance on slower motor units. This could provide an explanation for the enhanced resistance to eccentric contraction-induced injury after a single bout of eccentric exercise. METHODS: Human subjects performed 50 maximal voluntary eccentric (N = 10) or concentric (N = 10) contractions of the anterior crural muscles on two occasions separated by 1 wk. To determine whether MF changes during the second bout could be a consequence of injury to fibers in fast motor units, the anterior crural muscles of mice were electrically stimulated to perform 50 maximal eccentric (N = 10) or concentric (N = 9) contractions on two occasions separated by 1 wk. In both the humans and mice, torque production and tibialis anterior muscle RMS and MF were measured during the two exercise bouts. RESULTS: In human tibialis anterior muscle, MF was 30% lower (P < 0.01) during the second eccentric bout although RMS was the same. In the mice, RMS and MF were unchanged at any time after the first eccentric bout despite torque deficits similar to those observed in the humans. CONCLUSIONS: The data indicate that with repetition of maximal voluntary eccentric contractions, there is an increased activation of slow motor units and a concomitant decrease in activation of fast units.     

Short-term immobilization after eccentric exercise. Part I: contractile properties

PURPOSE: The purpose of this study was to examine the compound muscle action potential (M-wave) and evoked contractile properties of immobilized muscle after high-force eccentric exercise. We believed that changes in these variables would contribute to the enhanced recovery of maximal voluntary force observed after short-term immobilization of damaged muscle. We hypothesized that immobilization after eccentric exercise would result in an enhanced M-wave and a change in contractile properties toward characteristics of faster muscle fibers. 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 during a 4-d treatment. Maximal isometric torque (MVC) was assessed at baseline and for 8 d after treatment. M-wave and evoked contractile properties of the muscle (twitch torque [TT], maximal rate of torque development [MRTD], time to peak torque [TPT], and one-half relaxation time [HRT]) were assessed at baseline and for the first 5 d after treatment. RESULTS: Immediately postexercise, MVC was reduced 43% and 42% in IMM and CON, respectively. Recovery of MVC was significantly greater in IMM during recovery (P < 0.05), 95% of baseline MVC compared with 83% in CON. M-wave was reduced 32%, and all contractile properties were altered immediately postexercise. M-wave, MRTD, TPT, and HRT were not significantly different between groups during recovery (P > 0.05). TT demonstrated enhanced recovery in IMM (P < 0.05). CONCLUSIONS: Short-term immobilization after eccentric exercise resulted in enhanced recovery of maximal voluntary force. However, enhanced force recovery cannot be explained by muscle activation and evoked contractile properties of the muscle.     

The effects of a repeated bout of eccentric exercise on indices of muscle damage and delayed onset muscle soreness

This study examined markers of muscle damage following a repeated bout of maximal isokinetic eccentric exercise performed prior to full recovery from a previous bout. Twenty non-resistance trained volunteers were randomly assigned to a control (CON, n=10) or experimental (EXP, n=10) group. Both groups performed 36 maximal isokinetic eccentric contractions of the elbow flexors of the non-dominant arm (ECC1). The EXP group repeated the same eccentric exercise bout two days later (ECC2). Total work and peak eccentric torque were recorded during each set of ECC1 and ECC2. Isometric torque, delayed onset muscle soreness (DOMS), flexed elbow angle and plasma creatine kinase (CK) activity were measured prior to and immediately following ECC1 and ECC2. at 24h intervals for 7 days following ECC1 and finally on day 11. In both groups, all dependent variables changed significantly during the 2 days following ECC1. A further acute post-exercise impairment in isometric torque (30 +/- 5%) and flexed elbow angle (20 +/- 4%) was observed following ECC2 (p<0.05), despite EXP subjects producing uniformly lower work and peak eccentric torque values during ECC2 (p<0.05). No other significant differences between the CON and EXP groups were observed throughout the study (p>0.05). These findings suggest that when maximal isokinetic eccentric exercise is repeated two days after experiencing of contraction-induced muscle damage, the recovery time course is not significantly altered.     

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.     

Structural and mechanical basis of exercise-induced muscle injury.

It is well documented in both animal and human studies that unaccustomed, particularly eccentric, muscle exercise may cause damage of muscle fiber contractile and cytoskeletal components. These injuries typically include: Z-band streaming and dissolution, A-band disruption, disintegration of the intermediate filament system, and misalignment of the myofibrils. The mechanical basis for this damage is suggested to be due to the fiber strain magnitude rather than the absolute stress imposed on the fiber. We hypothesize that eccentric contraction-induced damage occurs early in the treatment period, i.e., within the first few minutes. The structural abnormalities predominate in the fast-twitch glycolytic fibers. In the final section of this paper, we hypothesize a damage scheme, based on the muscle fiber oxidative capacity as a determining factor.     

Vitamin E supplementation and endurance exercise: are there benefits?

It has been widely noted that vitamin E shows numerous beneficial effects through and beyond its antioxidative properties; consequently, vitamin E is expected to prevent degenerative diseases. In the field of sports medicine, many studies dealing with vitamin E have been conducted originally from the point of view of its effects on physical performance. Although some earlier studies indicated that vitamin E supplementation could improve physical performance, defects in the study design or statistical analysis were pointed out at a later time. The majority of subsequent well controlled studies have reported no significant effect on physical performance from vitamin E supplementation. Recent studies suggest that endurance exercise may promote free radical generation in the body, and vitamin E may play an important role in preventing the free radical damage associated with endurance exercise. Although there is evidence of free radical involvement in exercise-induced muscle injury, vitamin E supplementation might not be expected to prevent muscle damage caused by exercise in humans without a vitamin E deficiency. Since it is still unclear whether exercise induces lipid peroxidation in the human body, the beneficial effect of vitamin E supplementation on exercise-induced lipid peroxidation has not yet been established. However, it is proposed that as a result of exercise vitamin E may be mobilised from store tissues and redistributed in the body to prevent oxidative damage. Therefore, we are convinced that vitamin E contributes to preventing exercise-induced lipid peroxidation. It has also been indicated that strenuous endurance exercise may enhance the production of oxidised low density lipoprotein (LDL), which plays a key role in the initiation and progression of atherosclerosis. It is also suggested that this enhanced production of oxidised LDL could be reduced if a higher vitamin E status is maintained. Supplementation with 100 to 200mg of vitamin E daily can be recommended for all endurance athletes to prevent exercise-induced oxidative damage and to reap the full health benefits of exercise.     

Mechanisms of variability in strength loss after muscle-lengthening actions

PURPOSE: Profound strength loss is a marker of exercise-induced muscle damage; however, there is a large intersubject variability in the response, even when subjects are exposed to standardized exercise protocols. We sought to identify factors including neural drive and peripheral function underlying variability in early development of muscle strength loss after lengthening actions. We objectively characterized subjects on the basis of postexercise strength loss and analyzed voluntary and stimulated muscle function before and after exercise to test the hypothesis that greater strength loss would be associated with greater losses in peripheral, but not central, function. METHODS: Forty-six subjects were tested. Central measures were integrated electromyographic activity (iEMG), compound muscle action potential (CMAP), and central activation ratio (CAR). Peripheral measures were maximal isometric and eccentric voluntary action torques and stimulated tetanic and twitch torques. Subjects performed 50 maximal lengthening (eccentric) actions of the elbow flexors. Isometric strength was assessed pre- and postexercise and for 4 d after exercise. Central and peripheral functions were assessed before and 5 min after exercise. RESULTS: Cluster analysis of isometric strength loss at 0 and 24 h after exercise generated three groups: higher responders (HR) (N = 21; 49% average loss), lower responders (LR) (N = 22; 23% average loss), and nonresponders (N = 3; no loss). Maximal eccentric torque losses were greater in the HR group than in the LR group. Greater dysfunction was found for all peripheral measures (torque after tetanic stimuli; torque after twitch stimuli) in the HR group, whereas central measures (iEMG, CMAP, and CAR) were not different between groups (P > 0.05). CONCLUSION: Greater voluntary strength loss after lengthening exercise was associated with greater impairment of peripheral function, but similar central function, suggesting that the mechanism(s) driving variations in strength loss after lengthening actions are localized within the periphery.     

The efficacy of ice massage in the treatment of exercise-induced muscle damage

The purpose of this investigation was to, firstly, examine the effects of repeated applications of ice massage on the indirect markers associated with muscle damage using a within-subjects cross-over design and secondly, to examine how ice massage affects muscle function in both static and dynamic contractions following unaccustomed eccentric exercise. Twelve males performed damaging exercise on two separate occasions. The protocol consisted of three sets of 10 maximal eccentric repetitions of the elbow flexors using isokinetic dynamometry. Subjects were randomly assigned to an ice massage group or placebo group and received treatments immediately post-exercise, 24 and 48 h post-exercise. Muscle function (maximal isometric, slow and fast isokinetic contractions), creatine kinase, myoglobin, muscle soreness, limb girth and range of motion were measured pre, immediately post, 24, 48, 72 and 96 h post-exercise. Significant time effects were observed for all dependent variables (P<0.05). There were no significant differences between treatments. Ice massage is ineffective in reducing the indirect markers associated with exercise-induced muscle damage and enhancing recovery of muscle function in male exercisers unaccustomed to eccentric biased exercise.     

Vitamin E supplementation attenuates leakage of enzymes following 6 successive days of running training

The purpose of this study was to examine whether vitamin E supplementation in humans would attenuate an increase of serum enzymes as an indirect marker of muscle damage following a sudden large increase in the running distance in a 6-day running training or not. A randomized and placebo-controlled study was carried out on fourteen male runners who were supplied vitamin E (alpha-tocopherol 1200 IU x day(-1); E) or placebo (P) 4 weeks prior to (T1) and during 6 successive days of running training (48.3 +/- 5.7 km x day(-1), means +/- SD). Resting venous blood samples were obtained before maximal treadmill running, at T1, the day immediately before (T2), the next day (T3), and three weeks (T4) after the running training. Serum levels of alpha-tocopherol, lipid peroxidation products (thiobarbituric acid; TBA), creatine kinase (CK), lactate dehydrogenase (LDH), and LDH isozyme 1-5 were quantitatively analyzed. No significant difference was found in maximal oxygen uptake (VO2max) and maximal heart rates following the exhaustive exercise between the P and E group during the experiments. Vitamin E supplementation significantly increased serum alpha-tocopherol (p<0.001) and decreased TBA levels (p < 0.001) compared with pre-supplementation levels. Although serum CK and LDH activities increased significantly at T3 in either group, significantly lower CK (p < 0.05) and LDH (p < 0.001) levels were observed in the E group compared with the P group. The ratio of LDH1 to LDH2 (LDH1/LDH2) decreased significantly at T3 in either group compared with the T1 levels, since there was no significant difference in the LDH1/LDH2 between the P and E group throughout the experiments. These results indicate that vitamin E supplementation can reduce the leakage of CK and LDH following 6 successive days of endurance running. The protective effect of vitamin E against free radicals probably inhibits free-radical-induced muscle damage caused by a sudden large increase in the running distance.     

补充复方1,6-二磷酸果糖及谷氨酰胺对训练大鼠游泳运动能力和运动后骨骼肌损伤的影响

目的:探讨补充复方1,6-二磷酸果糖(FDP)和谷氨酰胺对训练大鼠运动能力与运动后骨骼肌损伤的影响。方法:76只雄性Wistar大鼠被随机分为安静对照组、运动对照组、训练组、训练加补充谷氨酰胺组和训练加补充活性糖组。游泳训练6周后,除安静对照组外,其余大鼠进行1次力竭游泳运动,记录力竭时间;检测各组大鼠血浆CK及其同工酶活性变化;取比目鱼肌制备电镜切片,观察骨骼肌细胞Z线变化。结果:训练加补充活性糖组大鼠力竭游泳时间显著长于训练组和训练加补充谷氨酰胺组(P<0.05),训练加补充谷氨酰胺组大鼠运动后即刻比目鱼肌Z线异常率分别显著低于对照组和训练加补充活性糖组(P<0.05),训练组大鼠力竭运动后即刻比目鱼肌Z线异常率亦分别显著低于对照组和训练加补充活性糖组(P<0.05)。结果提示,补充活性糖有助于提高训练大鼠的运动能力;补充谷氨酰胺对于降低运动导致的骨骼肌细胞损伤是否有积极作用尚待进一步探讨。     

Combined antioxidant treatment effects on blood oxidative stress after eccentric exercise

PURPOSE: This study was designed to ascertain the effects of a combination antioxidant therapy on plasma protein carbonyls (PC), malondialdehyde (MDA), and whole blood total (TGSH), oxidized (GSSG), and reduced (GSH) glutathione in non-resistance trained females after eccentric resistance exercise. METHODS: Eighteen women (aged 19-31 yr) were randomized in a double-blind manner to either an antioxidant supplement (N = 9; 400 IU vitamin E, 1 g vitamin C, and 90 mug selenium per day) or a lactose placebo (N = 9) for 14 d before and for 2 d after eccentric elbow flexor exercise. Blood samples taken before and immediately, 2, 6, 24, and 48 h postexercise were analyzed for PC, MDA, TGSH, and GSSG. RESULTS: No treatment by time interaction was noted for any variable, with all blood markers experiencing a change after the exercise in both conditions. Time main effects were observed for PC, MDA, and GSSG, with values elevated above preexercise after the eccentric exercise, whereas GSH concentration decreased after the eccentric exercise. Antioxidant supplementation resulted in a condition main effect for PC and MDA, with lower values compared with placebo. The antioxidant treatment attenuated the rise in both PC (75%) and MDA (100%). CONCLUSION: These data suggest that eccentric resistance exercise can increase blood biomarkers of oxidative stress in non-resistance trained females, and this vitamin E, C, and selenium supplementation can attenuate the rise in PC and MDA.     

Effect of single bout versus repeated bouts of stretching on muscle recovery following eccentric exercise

ObjectivesTo analyze the effects of a single bout and repeated bouts of stretching on indirect markers of exercise-induced muscle damage.DesignA randomized controlled clinical trial at a university human research laboratory was conducted.MethodsFifty-six untrained males were randomly divided into four groups. (I) a single stretching group underwent a single bout of stretching on the quadriceps muscle; (II) an eccentric exercised group underwent eccentric quadriceps muscle contractions until exhaustion; (III) an eccentric exercise group followed by a single bout of stretching; (IV) an eccentric exercised group submitted to repeated bouts of stretching performed immediately and 24, 48, and 72 h post-exercise. Muscle stiffness, muscle soreness, maximal concentric peak torque, and plasma creatine kinase activity were assessed before exercise and 1, 24, 48, 72, and 96 h post-exercise.ResultsAll exercised groups showed significant reduction in maximal concentric peak torque and significant increases in muscle soreness, muscle stiffness, and plasma creatine kinase. There were no differences between these groups in all assessed variables, with the exception of markers of muscle stiffness, which were significantly lower in the eccentric exercise group followed by single or repeated bouts. The single stretching group showed no change in any assessed variables during the measurement period.ConclusionsMuscle stretching performed after exercise, either as single bout or as repeated bouts, does not influence the levels of the main markers of exercise-induced muscle damage; however, repeated bouts of stretching performed during the days following exercise may have favorable effects on muscle stiffness.     

Effects of dietary protein on enzyme activity following exercise-induced muscle injury

PURPOSE: The objective of this investigation was to determine the effects of varying levels of dietary protein on the postexercise increase in serum and muscle enzyme activity normally observed following exercise-induced muscle injury. METHODS: Serum creatine kinase (CK), serum aspartate aminotransferase (AST), and muscle glucose-6-phosphate dehydrogenase (G-6-PD) activities were measured in rats fed for 10 d on high (50%), normal (12%), or low (4%) protein diets following a single bout of eccentric exercise (treadmill running at 16 m.min(-1), -16 degrees incline, 90 min). RESULTS: The exercise intervention resulted in significant increases in serum CK and AST activities in all diet groups. Serum CK demonstrated peak activity immediately postexercise with increases reaching 910+/-94, 594+/-53, and 283+/-52 IU.L(-1) for animals on high, normal, and low protein diets, respectively. Similarly, peak postexercise AST activity for high, normal, and low protein diets reached 193+/-10, 147+/-3, and 162+/-9 IU.L(-1), respectively. The exercise intervention resulted in increases in muscle G-6-PD activity for all diet groups; however, LP rats demonstrated significantly lower values than NP or HP rats. CONCLUSIONS: These data show that dietary protein intake can significantly effect both serum and muscle enzyme activity following acute exercise-induced muscle injury.     

The effects of massage on delayed onset muscle soreness

OBJECTIVES: The purpose of this study was to investigate the physiological and psychological effects of massage on delayed onset muscle soreness (DOMS). METHODS: Eighteen volunteers were randomly assigned to either a massage or control group. DOMS was induced with six sets of eight maximal eccentric contractions of the right hamstring, which were followed 2 h later by 20 min of massage or sham massage (control). Peak torque and mood were assessed at 2, 6, 24, and 48 h postexercise. Range of motion (ROM) and intensity and unpleasantness of soreness were assessed at 6, 24, and 48 h postexercise. Neutrophil count was assessed at 6 and 24 h postexercise. RESULTS: A two factor ANOVA (treatment v time) with repeated measures on the second factor showed no significant treatment differences for peak torque, ROM, neutrophils, unpleasantness of soreness, and mood (p > 0.05). The intensity of soreness, however, was significantly lower in the massage group relative to the control group at 48 h postexercise (p < 0.05). CONCLUSIONS: Massage administered 2 h after exercise induced muscle injury did not improve hamstring function but did reduce the intensity of soreness 48 h after muscle insult.     

Effects of eccentric exercise on trunk extensor torque and lumbar paraspinal EMG

PURPOSE: Little is known about the effects of eccentric contractions on the function of the lumbar paraspinal muscles. The purpose of this study was to determine the effects of a single bout of eccentric contractions using the trunk extensor muscles on torque and lumbar paraspinal electromyographic (EMG) parameters. METHODS: Twenty healthy men between the ages of 18 and 49 yr participated in the study. Subjects performed a single bout of 50 maximal voluntary concentric (N = 10) or eccentric (N = 10) trunk extension movements while surface EMG signals were recorded from the multifidus and iliocostalis lumborum muscles. A series of isometric contractions were performed both before the exercise protocol and at five additional time points over the following 7 d. RESULTS: During the exercise protocol, peak torque decreased 30% and 24% in the eccentric and concentric groups, respectively, whereas no change occurred in EMG root-mean-square (RMS). There were no group differences in peak torque generation at any of the postexercise protocol time points. Compared with the preexercise protocol values, multifidus EMG was elevated 27% immediately post and 15 min post in the eccentric group. Similarly, compared with the concentric group, multifidus EMG in the eccentric group was increased 34%, 40%, and 25% immediately post, 15 min post, and 1 d after the exercise protocol, respectively. CONCLUSION: Eccentric contractions using the trunk extensor muscles result in higher levels of multifidus EMG activity to produce a given level of torque. This reduction in neuromuscular efficiency persisted for one day with recovery to baseline levels by the third day. Contrary to studies using other muscle groups, no sustained alteration in muscle function was observed.     

Antioxidants did not prevent muscle damage in response to an ultramarathon run

PURPOSE: This study was conducted to determine if 6 wk of supplementation with vitamins E and C could alleviate exercise-induced muscle damage. We studied 22 runners during a 50-km ultramarathon. METHODS: Subjects were randomly assigned to one of two groups: (a) placebos (PL) or (b) antioxidants (AO) (1000 mg vitamin C and 300 mg RRR-alpha-tocopheryl acetate). Blood samples were obtained before supplementation (baseline), 24 h pre-, 12 h pre-, and 1 h prerace; midrace, postrace, 2 h postrace, and for 6 d postrace. Plasma alpha-tocopherol (alpha-TOH), ascorbic acid (AA), and muscle damage markers (creatine kinase (CK) and lactate dehydrogenase (LDH)), as well as maximal voluntary contraction (MVC) of the hamstring and quadriceps were assessed. RESULTS: With supplementation, plasma alpha-TOH and AA increased in the AO but not the PL group. LDH and CK increased in response to the race; LDH peaked at postrace and CK reached maximal values 2 h and 1 d postrace; neither was affected by treatment. Adjusting for between-subject differences in baseline CK values revealed that men had higher levels of CK than did women throughout the study. Correcting CK values for lean body mass (kg) eliminated sex differences, but not changes over time. CK was significantly correlated (R = 0.52, P < 0.0001) with C-reactive protein, an acute phase response marker. MVC decreased 14-26% in all groups in response to the run. Eccentric hamstring (EH) torque and concentric quadriceps (CQ) power exhibited the largest deficits, 26 and 24%, respectively, with no effect of treatment. CQ recovered at a faster rate in women than in men. CONCLUSION: Antioxidants appeared to have no effect on exercise-induced increases in muscle damage or recovery, but important sex differences were observed.     

Serum creatine kinase levels and renal function measures in exertional muscle damage

PURPOSE: Serum creatine kinase (CK) levels are commonly used to judge the severity of muscle damage and to determine when to hospitalize patients who present with symptoms of exertional rhabdomyolysis in order to prevent renal failure. However, no CK standard exists because of the limited information available regarding exercise-induced CK elevation and renal function. This study determined the magnitude of CK elevation and the effect on renal function produced by exercise in a large subject group. METHODS: Blood samples were obtained from 203 volunteers who performed 50 maximal eccentric contractions of the elbow flexor muscles. The samples, taken before and 4, 7, and 10 d after exercise, were analyzed for markers of muscle damage (CK, myoglobin (Mb), lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase and for measures of renal function (creatinine, blood urea nitrogen, phosphorus, potassium, osmolality, and uric acid). RESULTS: All indicators of muscle damage increased significantly after exercise (P < 0.01). CK levels were 6420, 2100, and 311% above baseline on days 4, 7, and 10 after the exercise, respectively (P < 0.01), and Mb was 1137, 170, and 28% above baseline on days 4, 7, and 10 after exercise, respectively (P < 0.01). Of the 203 participants, 111 had CK values at 4 d postexercise > 2,000 U x L(-1) and 51 had values > 10,000 U x L(-1), levels used to diagnose myopathy (e.g., statin myositis) and rhabdomyolysis, respectively. There were no significant increases in any measure of renal function. Despite marked CK and Mb elevations in some subjects, none experienced visible myoglobinuria or required treatment for impaired renal function. CONCLUSIONS: Exertional muscle damage produced by eccentric exercise in healthy individuals can cause profound CK and Mb elevations without renal impairment.     

Effect of Vitamin C and E supplementation on biochemical and ultrastructural indices of muscle damage after a 21 km run.

This study investigated whether 4 weeks of daily supplementation with 500 or 1000 mg of Vitamin C and 500 or 1000 IU of Vitamin E could modify biochemical and ultrastructural indices of muscle damage following a 21 km run. Fifteen experienced male distance runners were divided into two groups (vitamin or placebo) and received supplementation for four weeks before completing the first 21 km run in as fast a time as possible. A four-week "washout" period followed before the subjects crossed over and received the alternate supplement for the next four weeks. They then completed a second 21 km run. Before, immediately after and 24 h after each run venous blood samples were taken and analysed for serum creatine kinase, myoglobin, malondialdehyde and vitamin C and E (before-samples only) concentrations. A subgroup of six subjects also had muscle biopsy (gastrocnemius) samples taken 24 h before and 24 h after each 21 km run, which were later analysed by electron microscopy. The two dosages of supplementation produced similar results, so a single vitamin group was formed for further analysis of results. Significant increases (p < 0.05) in creatine kinase and myoglobin, but not in malondialdehyde, were found post-run in both groups. However, no significant differences were found between the vitamin and placebo groups for creatine kinase, myoglobin and malondialdehyde concentrations recorded after the 21 km runs. A qualitative ultrastructural examination of pre-run muscle samples revealed changes consistent with endurance training, but little further change was seen after the 21 km run in either the vitamin or placebo groups. It was concluded that vitamin C and E supplementation (500 or 1000 mg or IU per day) for four weeks does not reduce either biochemical or ultrastructural indices of muscle damage in experienced runners after a half marathon.