Protective effect of nitric oxide on cytoskeletal proteins in rat soleus under eccentric exercise

An in vivo study was performed to see whether deterioration of the muscle cytoskeleton caused by eccentric exercise could be counteracted by raising the tissue content of nitric oxide. In Wistar rats that ran downhill on a treadmill inclined at 16° for 40 min at 20 m/min, the desmin content in m. soleus measured 24 h later declined by 15%, and the percentage of ruptures in the dystrophin layer was three times higher than in the control. Destruction of cytoskeletal proteins was also pronounced in rats pretreated with a blocker of NO synthase before exercise. By contrast, animals that received a nitric oxide donor (L-arginine) prior to running had control levels of desmin and dystrophin. It was concluded that nitric oxide can protect muscle cytoskeletal proteins in a single eccentric exercise.     

Rapid muscle-specific gene expression changes after a single bout of eccentric contractions in the mouse

Eccentric contractions (ECs), in which a muscle is forced to lengthen while activated, result in muscle injury and, eventually, muscle strengthening and prevention of further injury. Although the mechanical basis of EC-induced injury has been studied in detail, the biological response of muscle is less well characterized. This study presents the development of a minimally invasive model of EC injury in the mouse, follows the time course of torque recovery after an injurious bout of ECs, and uses Affymetrix microarrays to compare the gene expression profile 48 h after ECs to both isometrically stimulated muscles and contralateral muscles. Torque dropped by 55% immediately after the exercise bout and recovered to initial levels 7 days later. Thirty-six known genes were upregulated after ECs compared with contralateral and isometrically stimulated muscles, including five muscle-specific genes: muscle LIM protein (MLP), muscle ankyrin repeat proteins (MARP1 and -2; also known as cardiac ankyrin repeat protein and Arpp/Ankrd2, respectively), Xin, and myosin binding protein H. The time courses of MLP and MARP expression after the injury bout (determined by quantitative real-time polymerase chain reaction) indicate that these genes are rapidly induced, reaching a peak expression level of 6–11 times contralateral values 12–24 h after the EC bout and returning to baseline within 72 h. Very little gene induction was seen after either isometric activation or passive stretch, indicating that the MLP and MARP genes may play an important and specific role in the biological response of muscle to EC-induced injury. muscle LIM protein; cardiac ankyrin repeat protein; muscle ankyrin repeat protein; microarray     

Role of the calcium-calpain pathway in cytoskeletal damage after eccentric contractions.

The mechanism(s) underlying eccentric damage to skeletal muscle cytoskeleton remain unclear. We examined the role of Ca(2+) influx and subsequent calpain activation in eccentric damage to cytoskeletal proteins. Eccentric muscle damage was induced by stretching isolated mouse muscles by 20% of the optimal length in a series of 10 tetani. Muscle force and immunostaining of the cytoskeletal proteins desmin, dystrophin, and titin were measured at 5, 15, 30, and 60 min after eccentric contractions and compared with the control group that was subjected to 10 isometric contractions. A Ca(2+)-free solution and leupeptin (100 microM), a calpain inhibitor, were applied to explore the role of Ca(2+) and calpain, respectively, in eccentric muscle damage. After eccentric contractions, decreases in desmin and dystrophin immunostaining were apparent after 5 min that accelerated over the next 60 min. Increased titin immunostaining, thought to indicate damage to titin, was evident 10 min after stretch, and fibronectin entry, indicating membrane disruption, was evident 20 min after stretch. These markers of damage also increased in a time-dependent manner. Muscle force was reduced immediately after stretch and continued to fall, reaching 56 +/- 2% after 60 min. Reducing extracellular calcium to zero or applying leupeptin minimized the changes in immunostaining of cytoskeletal proteins, reduced membrane disruption, and improved the tetanic force. These results suggest that the cytoskeletal damage and membrane disruption were mediated primarily by increased Ca(2+) influx into muscle cells and subsequent activation of calpain.     

Immunological changes after a single bout of moderate-intensity exercise in a hot environment

This study was aimed to evaluate the possible changes caused by a single bout of moderate-intensity exercise in a hot environmental temperature on the immune function and on inflammatory markers. A total of 22 young male adults (VO_2max, 55.4±3.6 ml·kg^?1·min^?1) volunteered to participate in an exercise session of 60 minutes on a treadmill ergometer at moderate speed (60% of the maximum aerobic speed) in hot environmental conditions (35°C and humidity 60%). Total leukocyte numbers, lymphocyte subsets (CD8+, CD4+, CD3+, NK and CD19+), cytokine production capacity by peripheral blood mononuclear cells (PBMCs) (IL-2, IL-4, IL-5, IL-10, IFN-γ and TNF-α) as well as the concentration of several inflammation related proteins (ceruloplasmin, C-reactive protein (CRP), complement factors C3 and C4) were evaluated before and after exercise. The results show that leukocyte and neutrophil absolute values increased (P<0.001) after the exercise period. In contrast, eosinophil values decreased (P<0.05) after the exercise. In addition, ceruloplasmin, C3 and C4 values (P<0.05) increased after exercise. No changes in T lymphocyte subsets, cytokine production, or CRP were observed. These data confirm previous studies suggesting that a 60 min exercise in a hot environment is enough to cause a physiologic adaptation to these special conditions leading to an increase of non-specific immune cells and promoting inflammatory processes. On the other hand, PCR values, lymphocyte subsets and the capacity of cytokine production by PBMC were not changed in a relatively short bout of exercise under these conditions in contrast with previous studies.     

Gender differences in insulin action after a single bout of exercise.

Effects of a single exercise bout on insulin action were compared in men (n = 10) and women (n = 10). On an exercise day, subjects cycled for 90 min at 85% lactate threshold, whereas on a rest (control) day, they remained semirecumbent. The period of exercise, or rest, was followed by a 3-h hyperinsulinemic-euglycemic clamp (30 mU.m(-2).min(-1)) and indirect calorimetry. Glucose kinetics were measured isotopically by using an infusion of [6,6-2H2]glucose. Glucose infusion rate (GIR) during the clamp on the rest day was not different between the genders. However, GIR on the exercise day was significantly lower in men compared with women (P = 0.01). This was mainly due to a significantly lower glucose rate of disappearance in men compared with women (P = 0.05), whereas no differences were observed in the endogenous glucose rate of appearance. Nonprotein respiratory quotient (NPRQ) increased significantly during the clamp from preclamp measurements in men and women on the rest day (P < 0.01). Exercise abolished the increase in NPRQ seen during the clamp on the rest day and tended to decrease NPRQ in men. Our results indicate the following: 1) exercise abolishes the usual increase in NPRQ observed during a hyperinsulinemic-euglycemic clamp in both genders, 2) men exhibit relatively lower whole body insulin action in the 3-4 h after exercise compared with women, and 3) gender differences in insulin action may be explained by a lower glucose rate of disappearance in the men after acute exercise. Together, these data imply gender differences in insulin action postexercise exist in peripheral tissues and not in liver.     

Enhanced procollagen processing in skeletal muscle after a single bout of eccentric loading in humans.

Increases in procollagen processing within skeletal muscle have previously been reported in small animal models only. While indirect measurements in humans have suggested an increase procollagen processing, no intra-skeletal muscle measurements have confirmed these findings. In this study, eight young healthy male subjects performed a single bout of unaccustomed high intensity eccentric exercise on one leg, with the contralateral leg being the control. A significant increase in the muscle interstitial concentration of the N-terminal propeptide of procollagen type I (PINP) was observed (day 0: 1.96 +/- 0.44 ng ml(-1), day 2: 1.94 +/- 0.32 ng ml(-1), day 4: 3.90 +/- 1.03 ng ml(-1), day 8: 7.23 +/- 2.34 ng ml(-1)*, *P < 0.05 vs. basal and control) with no change being noted in the control leg. By day 2 post-exercise, an increase in the histological immunoreactivity of PINP and the N-terminal propeptide of procollagen type III (PIIINP) was also shown in the exercising leg only. Further, from day 2 post-exercise, immunoreactivity for tenascin C and reactive macrophages (CD68+ cells) was seen within the perimysial and endomysial connective tissue of the exercising leg only, indicating a high mechanical load and inflammation. This study shows that following a single bout of high intensity eccentric exercise there is an increase in procollagen processing within skeletal muscle in humans.     

Single bout of exercise eliminates the immobilization-induced oxidative stress in rat brain

We were interested in the effects of immobilization (IM), a single bout of exercise (E) and immobilization followed by exercise (EIM) on memory and oxidative damage of macromolecules in hippocampus of rat brain. Eight hours of IM resulted in impairment of passive avoidance test (memory retrieval deficit) and increased latency to start locomotion in an open-field test. Two hours of swimming did not significantly alter the memory retrieval deficit and latency, while the EIM group had longer latency and similar memory than control and E groups. The oxidative damage of lipids, proteins and nuclear DNA increased significantly in IM group and no increase was observed in E and EIM animals. The activity of proteasome was not altered in any groups. The activity of glutamine synthetase (GS) was decreased in IM group (P < 0.05), this down regulation was not observed in E and EIM groups. These data suggest that oxidative damage of macromolecules is associated with impaired cognitive function. Single bout of exercise after immobilization eliminates the oxidative damage of macromolecules and normalizes memory function, probably by its ability to restore the activity level of GS and eliminate the consequences of immobilization-induced prolonged efflux of glutamate.     

Protein metabolism in rat tibialis anterior muscle after stimulated chronic eccentric exercise.

In another study (J. Appl. Physiol. 69: 1709-1717, 1990) we reported that gastrocnemius (GAST) muscle enlargement failed to occur after 10 wk of 192 contractions performed every 3rd or 4th day. This result was surprising because increased protein synthesis rates were determined after an initial acute exercise bout with the same paradigms. In the same set of animals, tibialis anterior (TA) muscles were enlarged 16-30% compared with sedentary control muscles after the same chronic training regimen. This indicated that the regulation of protein expression may be different between the GAST and TA muscles. The present experiment attempted to define and explain these differences by comparing changes in various indexes of protein metabolism in TA with the same parameters determined in the accompanying study for the GAST. As in the GAST, results showed that TA protein synthesis rates are increased by acute exercise and principally regulated by translational and possibly posttranslational mechanisms. The differential response in muscle mass between the GAST and TA muscles after training may be due, in part, to greater relative resistances imposed on the TA than on the GAST that result in a more-prolonged effect on protein synthesis rates, with lower numbers of stimulated contractions required to stimulate increases in protein synthesis. Data also revealed that although as little as 1 min of total contractile duration (24 repetitions) increased TA protein synthesis rate by 30%, 8 min of total contractile duration (192 repetitions) further increased TA protein synthesis rates to only 45% above control.     

Reduced vascular responsiveness after a single bout of dynamic exercise in the conscious rabbit.

We measured agonist-induced changes in the iliac artery blood flow velocity (IFV) independent of baroreflex-mediated compensatory mechanisms in chronically instrumented New Zealand White rabbits (n = 8). Animals were instrumented with a Doppler flow probe around the right common iliac artery. A Teflon catheter was inserted into the right iliolumbar artery for local infusion of the vasoactive agonists. Another Teflon catheter was inserted in the left femoral artery for the measurement of pulsatile and mean arterial (MAP) blood pressures and heart rate (HR). The alpha-adrenergic receptor agonist phenylephrine (PE, 1.32-10.0 micrograms), the beta 1- and beta 2-adrenergic receptor agonist isoproterenol (IP, 0.022-0.11 micrograms), and the purinergic receptor agonist adenosine (AD, 10.0-100.0 micrograms) were injected into the functionally isolated hindlimb, and dose-response curves were generated. Changes in IFV were obtained without changes in MAP or HR. Exercise increased HR, MAP, and IFV (65.3 +/- 7.1 beats/min, 11.1 +/- 2.2 mmHg, and 2.2 +/- 0.3 kHz, respectively). The maximum responses to PE, AD, and IP were reduced 29.0 +/- 6.7, 50.7 +/- 8.5, and 61.0 +/- 8.1%, respectively, after exercise. In conclusion, exercise attenuated adrenergic and purinergic receptor-mediated vascular responses in the intact conscious rabbit.     

Impaired muscle glycogen resynthesis after eccentric exercise

Eight men performed 10 sets of 10 eccentric contractions of the knee extensor muscles with one leg [eccentrically exercised leg (EL)]. The weight used for this exercise was 120% of the maximal extension strength. After 30 min of rest the subjects performed two-legged cycling [concentrically exercised leg (CL)] at 74% of maximal O2 uptake for 1 h. In the 3 days after this exercise four subjects consumed diets containing 4.25 g CHO/kg body wt, and the remainder were fed 8.5 g CHO/kg. All subjects experienced severe muscle soreness and edema in the quadriceps muscles of the eccentrically exercised leg. Mean (+/- SE) resting serum creatine kinase increased from a preexercise level of 57 +/- 3 to 6,988 +/- 1,913 U/l on the 3rd day of recovery. The glycogen content (mmol/kg dry wt) in the vastus lateralis of CL muscles averaged 90, 395, and 592 mmol/kg dry wt at 0, 24, and 72 h of recovery. The EL muscle, on the other hand, averaged 168, 329, and 435 mmol/kg dry wt at these same intervals. Subjects receiving 8.5 g CHO/kg stored significantly more glycogen than those who were fed 4.3 g CHO/kg. In both groups, however, significantly less glycogen was stored in the EL than in the CL.     

Evidence for altered alpha-adrenoreceptor responsiveness after a single bout of maximal exercise.

We studied hemodynamic responses to alpha- and beta-receptor agonists in eight men to test the hypothesis that adrenoreceptor responsiveness is altered within 24 h of the performance of maximal exercise. Adrenoreceptor responsiveness was tested under two experimental conditions (with and without maximal exercise). Adrenoreceptor tests were performed 24 h after each subject performed graded upright cycle ergometry to volitional exhaustion. The 2 test days (experimental conditions) were separated by at least 1 wk, and the order of exercise and no-exercise conditions was counterbalanced. Steady-state graded infusions of phenylephrine (PE) and isoproterenol (Iso) were used to assess alpha- and beta-adrenoreceptor responsiveness, respectively. Slopes calculated from linear regressions between Iso and PE doses and changes in heart rate, blood pressure, and leg vascular resistance for each subject were used as an index of alpha- and beta-adrenoreceptor responsiveness. The slope of the relationship between heart rate and Iso with maximal exercise was 1773 +/- 164 beats x microm-1x kg-1x min-1 compared with 1987 +/- 142 beats x microg-1x kg-1x min-1 without exercise (P = 0.158), whereas the slopes of the relationship between vascular resistance to Iso were -438 +/- 123 peripheral resistance units (PRU) x microg-1x kg-1x min-1 with maximal exercise and -429 +/- 105 x microg-1x kg-1 x min-1 without exercise (P = 0.904). Maximal exercise was associated with greater (P < 0.05) vascular resistance (15.1 +/- 2.8 PRU x microg-1 kg-1x min-1) and mean arterial blood pressure (15.8 +/- 2.1 mmHg. microg-1x kg-1x min-1) responses to PE infusion compared with no exercise (9.0 +/- 2.0 PRU x microg-1 kg-1 x min-1 and 10.9 +/- 2.0 mmHg. microg-1x kg-1x min-1, respectively). These results provide evidence that a single bout of maximal exercise increases alpha1-adrenoreceptor responsiveness within 24 h without affecting beta-cardiac and vascular adrenoreceptor responses.     

Calpain-3 is autolyzed and hence activated in human skeletal muscle 24 h following a single bout of eccentric exercise.

The function and normal regulation of calpain-3, a muscle-specific Ca(2+)-dependent protease, is uncertain, although its absence leads to limb-girdle muscular dystrophy type 2A. This study examined the effect of eccentric exercise on calpain-3 autolytic activation, because such exercise is known to damage sarcomeric structures and to trigger adaptive changes that help prevent such damage on subsequent exercise. Six healthy human subjects performed a 30-min bout of one-legged, eccentric, knee extensor exercise. Torque measurements, vastus lateralis muscle biopsies, and venous blood samples were taken before and up to 7 days following the exercise. Peak isometric muscle torque was depressed immediately and at 3 h postexercise and recovered by 24 h, and serum creatine kinase concentration peaked at 24 h postexercise. The amount of autolyzed calpain-3 was unchanged immediately and 3 h after exercise, but increased markedly (from approximately 16% to approximately 35% of total) 24 h after the exercise, and returned to preexercise levels within 7 days. In contrast, the eccentric exercise produced little autolytic activation of the ubiquitous Ca(2+)-activated protease, mu-calpain. Eccentric exercise is the first physiological circumstance shown to result in calpain-3 activation in vivo.     

Potential biomarkers of muscle injury after eccentric exercise

Proteomics was utilized to identify novel potential plasma biomarkers of exercise-induced muscle injury. Muscle injury was induced in nine human volunteers by eccentric upper extremity exercise. Liquid chromatography–mass spectrometry identified 30 peptides derived from nine proteins which showed significant change in abundance post-exercise. Four of these proteins, haemoglobin α chain, haemoglobin β chain, α1-antichymotrypsin (ACT) and plasma C-1 protease inhibitor (C1 Inh), met the criterion for inclusion based on changes in at least two distinct peptides. ACT and C1 Inh peptides peaked earlier post-exercise than creatine kinase, and thus appear to provide new information on muscle response to injury.     

Gender differences in muscle inflammation after eccentric exercise.

Unaccustomed exercise is followed by delayed-onset muscle soreness and morphological changes in skeletal muscle. Animal studies have demonstrated that women have an attenuated response to muscle damage. We studied the effect of eccentric exercise in untrained male (n = 8) and female (n = 8) subjects using a unilateral exercise design [exercise (Ex) and control (Con) legs]. Plasma granulocyte counts [before (Pre) and 48 h after exercise (+48h)] and creatine kinase activity [Pre, 24 h after exercise (+24h), +48h, and 6 days after exercise (+6d)] were determined before (Pre) and after (+24h, +48h, +6d) exercise, with biopsies taken from the vastus lateralis of each leg at +48h for determination of muscle damage and/or inflammation. Plasma granulocyte counts increased for men and decreased for women at +48h (P < 0.05), and creatine kinase activity increased for both genders at +48h and +6d (P < 0.01). There were significantly greater areas of both focal (P < 0.001) and extensive (P < 0.01) damage in the Ex vs. Con leg for both genders, which was assessed by using toluidine blue staining. The number of leukocyte common antigen-positive cells/mm(2) tissue increased with exercise (P < 0.05), and men tended to show more in their Ex vs. Con leg compared with women (P = 0.052). Men had a greater total (Ex and Con legs) number of bcl-2-positive cells/mm(2) tissue vs. women (P < 0.05). Atrophic fibers with homogeneous bcl-2-positive staining were seen only in men (n = 3). We conclude that muscle damage is similar between genders, yet the inflammatory response is attenuated in women vs. men. Finally, exercise may stimulate the expression of proteins involved in apoptosis in skeletal muscle.     

Time course of glycogen accumulation after eccentric exercise.

This study examined the time course of glycogen accumulation in skeletal muscle depleted by concentric work and subsequently subjected to eccentric exercise. Eight men exercised to exhaustion on a cycle ergometer [70% of maximal O2 consumption (VO2max)] and were placed on a carbohydrate-restricted diet. Approximately 12 h later they exercised one leg to subjective failure by repeated eccentric action of the knee extensors against a resistance equal to 120% of their one-repetition maximum concentric knee extension force (ECC leg). The contralateral leg was not exercised and served as a control (CON leg). During the 72-h recovery period, subjects consumed 7 g carbohydrate.kg body wt-1.day-1. Moderate soreness was experienced in the ECC leg 24-72 h after eccentric exercise. Muscle biopsies from the vastus lateralis of the ECC and CON legs revealed similar glycogen levels immediately after eccentric exercise (40.2 +/- 5.2 and 47.6 +/- 6.4 mmol/kg wet wt, respectively; P greater than 0.05). There was no difference in the glycogen content of ECC and CON legs after 6 h of recovery (77.7 +/- 7.9 and 85.1 +/- 4.9 mmol/kg wet wt, respectively; P greater than 0.05), but 18 h later, the ECC leg contained 15% less glycogen than the CON leg (90.2 +/- 8.2 vs. 105.8 +/- 8.9 mmol/kg wet wt; P less than 0.05). After 72 h of recovery, this difference had increased to 24% (115.8 +/- 8.0 vs. 153.0 +/- 12.2 mmol/kg wet wt; P less than 0.05). These data confirm that glycogen accumulation is impaired in eccentrically exercised muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Post-exercise increase of lipid oxidation after a moderate exercise bout in untrained healthy obese men.

The aim of the study was to examine whether a moderate exercise increases the utilization of fatty acids during the recovery period in obese men. Six healthy obese participated in a randomized crossover investigation, one with exercise and one without exercise. At 8 a. m., the subjects had a standardized breakfast and they rested in a sitting position for 3 hours. The subjects were maintained in the sitting position for 4 additional hours in one session. In a second session, they exercised for 60 min at 50 % of their VO(2) max and then returned to the sitting position for 3 hours. Respiratory exchange ratio (RER) values were calculated by indirect calorimetry. During the resting session, plasma non-esterified fatty acids (NEFA) and glycerol concentrations rose progressively, whereas RER progressively decreased. During the exercise, plasma catecholamines, NEFA, glycerol, growth hormone and cortisol levels and RER increased while insulin decreased. During the recovery, plasma NEFA increased and glycerol decreased. During the first hour of recovery, RER values were lower and fatty acid utilization higher than during the same period of the resting session. The study shows that exercise induces modifications in hormonal factors promoting lipid mobilization and suggests that exercise provide substantial amounts of NEFA for muscle oxidation during recovery from an exercise bout in obese subjects.     

Sex differences in oxidative stress after eccentric and concentric exercise

Objectives: Comparison of redox balance changes in the blood of women and men as a result of submaximal eccentric (ECC) and concentric (CONC) efforts.

Methods: 10 women and 10 men performed three 45-minute submaximal treadmill runs at constant velocities (downhill run – ECC, uphill run – CONC and level run). Prior to the 45-minute exercises, after their completion and following 24 hours of recovery, the concentration of lactate, oxidized low-density lipoprotein (ox-LDL), 3-nitrotyrosine, uric acid (UA) and the white blood cell count (WBC), neutrophil (NEUT), lymphocyte (LYMPH) and monocyte content in the blood were determined.

Results: In women, the ox-LDL increased significantly 10 minutes and 24 hours following ECC (P?P?P?P?Discussion: ECC cause impaired redox balance only in women. Due to the increase in antioxidant capacity of the blood without accompanying oxidative damage to macromolecules, for both sexes, it is recommended to perform concentric running efforts at the highest possible subliminal intensity.     

Single bout of running exercise changes LC3-II expression in rat cardiac muscle

Macroautophagy (autophagy) is an intracellular catalytic process. We examined the effect of running exercise, which stimulates cardiac work physiologically, on the expression of microtubule-associated protein 1 light chain 3 (LC3)-II, an indicator of autophagy, as well as some autophagy-related proteins in rat cardiac muscle. The left ventricles were taken from rats immediately (0 h), and at 0.5 h, 1 h or 3 h after a single bout of running exercise on a treadmill for 30 min and also from rats in a rest condition. In these samples, we evaluated the level of LC3-II and p62, and the phosphorylation level of mammalian target of rapamycin (mTOR), Akt and AMP-activated protein kinase alpha (AMPKα) by Western blotting. The exercise produced a biphasic change in LC3-II, with an initial decrease observed immediately after the exercise and a subsequent increase 1 h thereafter. LC3-II then returned to the rest level at 3 h after the exercise. A negative correlation was found between the LC3-II expression and mTOR phosphorylation, which plays a role in inhibiting autophagy. The exercise increased phosphorylation of AMPKα, which stimulates autophagy via suppression of mTOR phosphorylation, immediately after exercise. The level of p62 and phosphorylated Akt was not altered significantly by the exercise. These results suggest for the first time that a single bout of running exercise induces a biphasic change in autophagy in the cardiac muscle. The exercise-induced change in autophagy might be partially mediated by mTOR in the cardiac muscle.     

Normal forces and myofibrillar disruption after repeated eccentric exercise

Hortobágyi, Tibor, Joseph Houmard, David Fraser,Ronald Dudek, Jean Lambert, and James Tracy. Normalforces and myofibrillar disruption after repeated eccentric exercise.J. Appl. Physiol. 84(2): 492-498, 1998.To investigate the "rapid-adaptation" phenomenon, weexamined force, neural, and morphological adaptations in 12 subjectswho performed 100 eccentric contractions with the quadriceps muscle(bout 1) and repeated the sameexercise after a 2-wk hiatus (bout2). Two days after bout1, quadriceps muscle strength and surfaceelectromyographic (EMG) activity declined ~37 and 28%, respectively,in the control group (n = 6). Atday 2 after bout 1, significant increases occurred in patellar tendonreflex amplitude (~25%), muscle soreness (fivefold), and serumcreatine kinase (220%), and 65 ± 12% of the total number of pixelsin the EMG indicated myofibrillar disruption. At day7 after bout 1, all variables returned to normal. At day 2 after bout 2, no significant changesoccurred in force, EMG, creatine kinase, or soreness, but reflexamplitude increased, and 23 ± 4% of the total number of pixels inthe EMG still indicated myofibrillar disruption. The results suggestthat the rapid force recovery following eccentric exercise is mediatedat least in part by neural factors and that this recovery may occurindependently of cell disruption.