Bout Of Eccentric Contractions Research Articles

Contraction-Induced Loss of Plasmalemmal Electrophysiological Function Is Dependent on the Dystrophin Glycoprotein Complex.

Weakness and atrophy are key features of Duchenne muscular dystrophy (DMD). Dystrophin is one of the many proteins within the dystrophin glycoprotein complex (DGC) that maintains plasmalemmal integrity and cellular homeostasis. The dystrophin-deficient mdx mouse is also predisposed to weakness, particularly when subjected to eccentric (ECC) contractions due to electrophysiological dysfunction of the plasmalemma. Here, we determined if maintenance of plasmalemmal excitability during and after a bout of ECC contractions is dependent on intact and functional DGCs rather than, solely, dystrophin expression. Wild-type (WT) and dystrophic mice (mdx, mL172H and Sgcb−/− mimicking Duchenne, Becker and Limb-girdle Type 2E muscular dystrophies, respectively) with varying levels of dystrophin and DGC functionality performed 50 maximal ECC contractions with simultaneous torque and electromyographic measurements (M-wave root-mean-square, M-wave RMS). ECC contractions caused all mouse lines to lose torque (p<0.001); however, deficits were greater in dystrophic mouse lines compared to WT mice (p<0.001). Loss of ECC torque did not correspond to a reduction in M-wave RMS in WT mice (p=0.080), while deficits in M-wave RMS exceeded 50% in all dystrophic mouse lines (p≤0.007). Moreover, reductions in ECC torque and M-wave RMS were greater in mdx mice compared to mL172H mice (p≤0.042). No differences were observed between mdx and Sgcb−/− mice (p≥0.337). Regression analysis revealed ≥98% of the variance in ECC torque loss could be explained by the variance in M-wave RMS in dystrophic mouse lines (p<0.001) but not within WT mice (R2=0.211; p=0.155). By comparing mouse lines that had varying amounts and functionality of dystrophin and other DGC proteins, we observed that (1) when all DGCs are intact, plasmalemmal action potential generation and conduction is maintained, (2) deficiency of the DGC protein β-sarcoglycan is as disruptive to plasmalemmal excitability as is dystrophin deficiency and, (3) some functionally intact DGCs are better than none. Our results highlight the significant role of the DGC plays in maintaining plasmalemmal excitability and that a collective synergism (via each DGC protein) is required for this complex to function properly during ECC contractions.

Eccentric exercise causes delayed sensory nerve conduction velocity but no repeated bout effect in the flexor pollicis brevis muscles.

This study was aimed at investigating the effect of eccentric contractions (ECCs) of flexor pollicis brevis muscles (FPBMs) on motor and sensory nerve functions as well as the ipsilateral repeated bout effect (IL-RBE) and contralateral (CL)-RBE of motor and sensory nerve conduction velocities following ECCs. Thirty-two young healthy men (age: 19.6 ± 0.2years, height: 173.2 ± 1.2cm, body mass: 69.7 ± 1.9kg) performed two bouts of ECCs. During the first ECCs bout (ECCs-1), all participants performed 100 ECCs with 1 hand; for the second bout, 3 groups (2weeks [W]: n = 11, 4W: n = 10, 8W: n = 11) performed ECCs with both hands 2, 4, or 8weeks after ECCs-1. The maximal voluntary isometric contraction (MVC), range of motion (ROM), visual analog scale for pain (VAS), motor and sensory nerve conduction velocities were measured before, immediately after, and 1, 2, 3, and 5days after ECCs. ECCs-1 decreased the MVC, limited the ROM, developed VAS, and decreased the motor and sensory nerve conduction velocities compared tonon-exercise hand (p < 0.05). The repeated bout effect was observed in the ROM for IL-RBE in 2W and 4W, VAS for IL-RBE in 2W, and ROM and VAS for CL-RBE in 2W (p < 0.05). However, RBEs of MVC and motor and sensory nerve conduction velocities were not observed, and no differences were confirmed depending on the interval. In the present study, ECCs of the FPBM caused a sensory nerve dysfunction, while IL- or CL-RBE was not observed.

Muscle Strength Does Not Adapt From a Second to Third Bout of Eccentric Contractions: A Systematic Review and Meta-Analysis of the Repeated Bout Effect

Lindsay, A, Abbott, G, Ingalls, CP, and Baumann, CW. Muscle strength does not adapt from a second to third bout of eccentric contractions: A systematic review and meta-analysis of the repeated bout effect. J Strength Cond Res 35(2): 576-584, 2021-The greatest muscle strength adaptations to repeated bouts of eccentric contractions (ECC) occur after the initial injury, with little to no change in subsequent bouts. However, because of the disparity in injury models, it is unknown whether three or more bouts provide further adaptation. Therefore, we performed a systematic review of the literature to evaluate whether a third bout of skeletal muscle ECC impacts immediate strength loss and rate of strength recovery compared with a second bout. A search of the literature in Web of Science, SCOPUS, Medline, and the American College of Sports Medicine database was conducted between May and September 2019 using the keywords eccentric contraction or lengthening contraction and muscle and repeated or multiple, and bout. Eleven studies with 12 experimental groups, using 72 human subjects, 48 mice, and 11 rabbits, met the inclusion criteria. A meta-analysis using a random effects model and effect sizes (ESs; Hedges' g) calculated from the standardized mean differences was completed. Calculated ESs for immediate strength loss provided no evidence that a third bout of ECC results in greater loss of strength compared with a second bout (ES = -0.12, 95% confidence interval [CI] = -0.41 to 0.17). Furthermore, the rate of strength recovery was not different between a second and third bout (ES = -0.15, 95% CI = -1.01 to 0.70). These results indicate a third bout of skeletal muscle ECC does not improve indices of strength loss or rate of strength recovery compared with a second bout. Therefore, coaches and athletes should expect some level of persistent weakness after each of their initial training sessions involving ECC, and the faster recovery of strength deficits in the second bout documented by previous research is not different from a third bout.

Plasmalemma Function Is Rapidly Restored in Mdx Muscle after Eccentric Contractions

Muscle that lacks dystrophin, as in the mdx mouse, has a heightened sensitivity to eccentric (ECC) contraction-induced strength loss but an enhanced rate of recovery. However, the timeline and mechanisms underlying why mdx muscle recovers quicker have yet to be determined. We used an EMG approach to analyze plasmalemma electrophysiological function during and after ECC contraction-induced injury to test the hypothesis that loss of plasmalemmal excitability is a transient event in mdx muscle. Mice were implanted with stimulating electrodes on the common peroneal nerve and EMG electrodes on the tibialis anterior muscle. Anterior crural muscles of anesthetized mice performed one or two bouts of 50 injurious ECC contractions, and recovery of maximal isometric torque and M-wave root mean square (RMS) were assessed after each bout. Maximal isometric torque and M-wave RMS were equally reduced 62% (P < 0.001) in mdx mice immediately after the initial ECC injury. For these mdx mice, M-wave RMS was still reduced at 2 d postinjury (P = 0.034) but was not different from preinjury values by 6 d (P = 0.106), whereas torque took up to 9 d to recover (P = 0.333). M-wave RMS did not change (P = 0.390) in wild-type mice in response to ECC injury, whereas torque decreased 35% (P < 0.001) and recovered by day 2 (P = 0.311). Results from the second bout of ECC contractions were similar to those observed during and after the initial injury. Functional dystrophin is necessary for excitation to occur at the plasmalemma during ECC contractions but is not essential for the complete recovery of plasmalemma electrophysiological function or maximal isometric strength.

PO-064 A potential role of stretch-activated channels in anabolic mechanotransduction in the atrophied rat soleus muscle

Objective Prolonged immobilization or unloading of skeletal muscle causes muscle disuse atrophy, which is characterized by a reduction in muscle cross-sectional area and compromised contractile function. To date, the mechanisms of anabolic mechanotransduction in the atrophied mammalian skeletal muscle remain poorly understood. The aim of the present study was to assess a possible role of stretch-activated ion channels (SAC) in the propagation of a mechanical signal to anabolic signaling and protein synthesis (PS) in an isolated rat soleus muscle following mechanical unloading.&#x0D; Methods The mechanical unloading was performed via hindlimb suspension (HS). Twenty-eight male Wistar rats weighing were randomly assigned to the following 4 groups (n=7/group): 1) vivarium control (C), 2) control + SAC inhibitor (gadolinium) (C+Gd3+), 3) 7-day HS (HS), 4) 7-day HS + SAC inhibitor (HS+Gd3+). Following unloading, an isolated rat soleus was placed in an organ culture medium and subjected to a bout of eccentric contractions (EC). Upon completion of the EC, muscles were collected for Western blot analyses to determine the content of the key anabolic markers. The rate of PS was measured by SUnSET technique.&#x0D; Results EC-induced increase in PS was significantly less in the HS and HS+ Gd3+ groups vs. the C group. There was no statistically significant difference between the HS and HS+ Gd3+ groups in terms of EC-induced increase in muscle PS. A decrease in EC-induced phosphorylation of p70S6K, 4E-BP1, RPS6 and GSK-3beta in the 7-day unloaded soleus treated with SAC inhibitor did not differ from that of the 7-day unloaded soleus without SAC blockade. Thus, the inhibition of SAC with gadolinium did not lead to further decline in EC-induced phosphorylation of the key anabolic markers and muscle PS.&#x0D; Conclusions The results of the study suggest that attenuation of mTORC1-signaling and PS in response to EC in unloaded soleus muscle may be associated with inactivation of SAC. The study was supported by the RFBR grant # 16-34-60055.

Effects of a combined protein and antioxidant supplement on recovery of muscle function and soreness following eccentric exercise

BackgroundAn acute bout of eccentric contractions (ECC) cause muscle fiber damage, inflammation, impaired muscle function (MF) and muscle soreness (MS). Individually, protein (PRO) and antioxidant (AO) supplementation may improve some aspects of recovery from ECC, though have yet to be combined. We sought to determine if combined PRO and AO supplementation (PRO + AO) improves MS and MF following damaging ECC over PRO alone.MethodsSixty sedentary college-aged males participated in a randomized, single–blind, parallel design study of peak isometric torque (PIMT), peak isokinetic torque (PIKT), thigh circumference (TC), and muscle soreness (MS) of knee extensor muscles measured at baseline, immediately after and 1, 2, 6, and 24 h after completion of 100 maximal ECC. Immediately, 6 h, and 22 h post-ECC, participants consumed either: carbohydrate control (CHO; n = 14), PRO (n = 16), or PRO + AO (n = 17).ResultsAt baseline MS, TC, MF, macro- and micro-nutrient intakes, and total work during the ECC were not different between groups (p > 0.05). PIMT and PIKT (both −25%∆), TC (~1%∆) and MS (~35%∆) all changed with time (p < 0.05). We observed a group by time effect for PIKT (PRO + AO and PRO > CHO, p < 0.05). At 24 h post ECC, there was a trend towards improved relative PIMT (~11%) and PIKT (~17%) for PRO + AO (~17%) and PRO (~11%) compared to CHO. An interaction indicated PRO + AO had lowest MS over time (PRO + AO > PRO & CHO, p < 0.05).ConclusionsOur results suggest PRO facilitates recovery of muscle function within 24 h following ECC, and addition of AO ameliorates MS more than PRO or CHO alone.

The realization of a mechanical signal during gravitational unloading: The response of mTORC1 targets to eccentric contractions

The aim of this study was to assess the response of key mTORC1 substrates to a bout of contractile stimuli under different times of functional unloading. Functional unloading of hind-limb muscles was carried out by the method of antiorthostatic suspension. Twenty-eight Wistar rats were divided into four groups: control, and hindlimb suspension for 1, 3, and 7 days. After hindlimb suspension, isolated soleus muscles of rats were subjected to a bout of ex vivo eccentric contractions. The contents of phosphorylated forms of p70s6k and 4E-BP1 were then determined using western blotting. It was found that an eccentric load resulted in a significant increase in p70s6k phosphorylation and reduced 4E-BP1 phosphorylation both in control and suspended rats, but in the case of suspension the response was dramatically reduced. Thus, it can be concluded that a bout of eccentric contractions of isolated rat soleus muscle during functional unloading causes a weaker activation of the Akt-mTORC1-p70s6k signaling pathway compared with the control. This may indicate that it is important to maintain muscle tone for a more efficient muscle perception of an external mechanical signal and subsequent activation of anabolic signaling pathways.

Regional adaptation of collagen in skeletal muscle to repeated bouts of strenuous eccentric exercise.

This study investigated the injured region-specific alterations of factors related to the "repeated bout effect" (RBE), i.e., when the first bout of eccentric exercise generates resistance to injuries from the second bout of the same exercise. Wistar rats were divided into single injury (SI) and repeated injury (RI) groups. The right gastrocnemius muscle was subjected to a bout of eccentric contractions (ECs) at the age of 14weeks in the SI group and 10 and 14weeks in the RI group. The number of injured fibers after the last bout of ECs was lower in RI than in SI. In the SI group, injured fibers after ECs were mainly located in the superficial region of muscle and expressed myosin heavy chain (MHC) IIx and IIb. Prior to the second bout of ECs, the fiber-type composition in the RI group showed decreased MHC IIx and IIb fibers and increased MHC IIa fibers compared with those in the SI group. However, most regenerating fibers showed either MHC IIx or IIb expression. Heat shock protein 72 and total collagen contents in whole muscle were higher in the RI group than in the SI group; however, only the collagen expression in the RI group was more intense than that in the SI group in the superficial region of muscle. These findings suggest that increased collagen may play a more important role in the injured region of muscle than the other factors in RBE.

Utility of 17-(allylamino)-17-demethoxygeldanamycin treatment for skeletal muscle injury.

Repeated eccentric contractions can injure skeletal muscle and result in functional deficits that take several weeks to fully recover. The 70-kDa heat shock protein (Hsp70) is a stress-inducible molecular chaperone that maintains protein quality and plays an integral role in the muscle's repair processes following injury. Here, we attempted to hasten this recovery by pharmacologically inducing Hsp70 expression in mouse skeletal muscle with 17-(allylamino)-17-demethoxygeldanamycin (17-AAG) (40mg/kg) both prior to and throughout the first 7days after an injurious bout of 150 maximal eccentric contractions. Hsp70 content in the injured skeletal muscle was strongly induced following the eccentric contractions and remained elevated over the next 7days as the muscle underwent repair. Treatment with 17-AAG increased Hsp70 content ∼fivefold; however, this was significantly less than that induced by the injury. Moreover, 17-AAG treatment did not recover the decrements to in vivo isometric torque production following the bout of eccentric contractions. Together, these findings demonstrate that although Hsp70 content was induced in the uninjured skeletal muscle, treatment of 17-AAG (40mg/kg) was not a preventive measure to either reduce the severity of skeletal muscle damage or enhance functional recovery following a bout of maximal eccentric contractions.

The Contribution of the Neuromuscular System in the Repeated Bout Effect

Maximal eccentric contractions induce an immediate strength loss that results from skeletal muscle damage, the symptoms of which can persist for several days after the exercise insult. The repeated bout effect (RBE) refers to the acute adaptive response precipitated from a single bout of eccentric contractions that result in an attenuated damage response on subsequent, potentially damaging, bouts of exercise. The mechanisms for this adaptive response are thought to be, at least in part, from neural adaptations.

Intramuscular Inflammatory Response Following Repeated Bouts of Eccentric Exercise

INTRODUCTION: Skeletal muscle rapidly adapts to exercise induced damage, showing reduced evidence of damage after a second bout of damaging exercise. This phenomenon is called the repeated bout effect (RBE). The mechanisms of the RBE are not well understood. Modulation of the inflammation response may play a role in adaptations that precipitate the RBE. PURPOSE: This study broadly characterized the inflammatory response to repeated bouts of eccentric exercise in human skeletal muscle by measuring a large contingent of inflammatory markers. METHODS: Fourteen inactive men (n=7; 23.3 ± 2.1yrs; 178.5 ± 8.3cm and 84.8 ± 23.4kg) and women (n=7; 25.6 ± 2.5yrs; 166.0 ± 8.3cm and 76.6 ± 32.7kg) were in the study. Subjects did 2 bouts of eccentric contractions (EC) separated by 28 days. Muscle biopsies were taken before the first bout of EC (pre-b1) and at 2 days after the first bout (post-b1). The same procedure was followed for the second bout of EC and muscle tissue was collected before the second bout (pre-b2) and two days after (post-b2). Pre-b1 biopsy was taken from the non-exercised leg. All others were from the exercised leg. Macrophages per muscle fiber were quantified by immunohistochemistry and fluorescence microscopy from 10 of the 14 subjects. An array of 29 cytokines was quantified using a Luminex multiplex assay. Serum creatine kinase (CK) was measured before and 2 days after each bout. RESULTS: CK significantly increased from pre-b1 to post-b1 (86 U/l vs. 1292 U/l, p0.05). Macrophage/fiber between pre-b1 and post-b2 increased (0.079 cells/fiber vs. 0.14 cells/fiber, p<0.05). Among the 29 cytokines measured interleukin 4 (IL4), monocyte chemoattractant protein (MCP1) and interferon gamma-induced protein 10 (IP10) showed significant changes. IL4 decreased between pre-b1 and post-b2 (26 pg/ml to 13 pg/ml, p<0.05). MCP1 increased between pre-b1 and post-b2 (7 pg/ml to 52 pg/ml, p<0.05). IP10 increased between pre-b1 and post-b2 (11 pg/ml to 36 pg/ml, p<0.05). CONCLUSIONS: EC results in an altered intramuscular inflammatory response that is manifest primarily following the second, rather than the first bout of EC.

Extracellular Matrix Remodeling Following Repeated Bouts of Eccentric Contractions in Human Skeletal Muscle

Extracellular Matrix Remodeling Following Repeated Bouts of Eccentric Contractions in Human Skeletal Muscle

STAT3 Regulation In Cachectic Skeletal Muscle After Repeated Eccentric Contractions

Introduction The cachectic muscle's response to multiple bouts of eccentric contractions (ECC) has not been examined. We examined if 2 weeks of repeated ECC training could alter STAT3 regulation in cachectic muscle. Methods Male C57BL/6 (B6; N=9) and ApcMin/+ mice were subjected to 7 bouts of high-frequency electrical stimulation (100 Hz, 6-12V, 10 sets of 6 repetitions) over 2 weeks. The left tibialis anterior (TA) muscle performed ECC while the right TA served as an intra-animal control. ApcMin/+ mice were stratified into mild (7%; N=5) and severe (16% loss; N=4) cachexia based on the percentage of body weight loss at the end of the study. Results ApcMin/+ mice had smaller control TA muscle mass (-26%; P<.01) and type IIA and IIB myofiber cross-sectional area (CSA) compared to B6 mice. Cachexia increased control TA muscle STAT3 phosphorylation (9-fold; P<.05), p42/44 MAPK phosphorylation (8-fold; P<.05), and Atrogin-1 protein expression (9-fold; P<.05). Independent of cachexia ECC increased TA muscle mass and type IIA and IIB myofiber CSA. ECC had no effect on TA muscle STAT3 phosphorylation in mildly cachectic mice, but there was a 30% reduction (P<.01) in severely cachectic mice. ECC had no effect on muscle p42/p44 MAPK phosphorylation in ApcMin/+ mice. The induction of Atrogin-1 protein expression was attenuated 31% (P<.01) by ECC in severely cachectic mice. Conclusion These results suggest that repeated bouts of ECC can alter cachexia-induced muscle signaling. The contraction-induced regulation of STAT3 signaling during cachexia progression warrants further investigation. Supported by NIH/NCI R01CA121249 to JAC.

D-16 Thematic Poster - Exercise Training in Cardiac Patients

While branched-chain amino acids (BCAA) leucine is known to stimulate the activation of mTOR and protein synthesis, the contribution of leucine supplementation to the adaptive process and performance improvement to eccentric resistance training is unclear. PURPOSE: This study investigated the effect of BCAA on eccentric training efficiency in rats. METHODS: Male Wistar rats of 12 weeks of age were allocated into BCAA-supplemented (n=7), casein -supplemented (CS) (n=8) or non-supplemented (CONT) (n=8) groups. The BCAA group was fed a BCAA solution (1.35 g/kg, valine: leucine: isoleucine = 1:2:1) by oral gavage twice per day, and had free access to water containing BCAA (3% BCAA solution). The CS group was fed isonitrogen casein and CONT group received 1% hydroxypropyl methylcellulose solution (without nitrogen source) administered in the same manner as the BCAA group. Rats achieved one bout of eccentric contractions, elicited by forty intermittent electric stimulations in the tibialis anterior (TA) muscles every other day for 6 weeks. The isometric strength was monitored throughout the training period and assessed 24 hours after the last session in blinded manner. RESULTS: During the first 4 to 9 days of the training, the isometric strength of all groups declined by 57-62% of the initial value but increased consecutively thereafter. In the last two weeks of the training period, the isometric strength in the BCAA group exceeded that of CONT group by 8-10% (p<0.05) but the increase was not significantly different in the CS group compared to the CONT group (by 5-7%). The increase in the post training isometric force was statistically significant in the BCAA (34.0±2.8 mNm, p<0.05) as compared to the CONT group (25.3±1.9 mNm) but was not statistically significant in the CS group (29.1±1.4 mNm). The average cross-sectional area of the fibers with central nuclei was significantly larger in the BCAA (4291±117 μm2) and CS (4116±100 μm2) as compared to the CONT (3763±93 μm2) group. The muscle weight, myogenic regulatory factors, cytoskeletal protein and satellite cells increased significantly over time but there were no significant differences between the groups. CONCLUSION: These results suggest that BCAA supplementation may be an effective tool in facilitating adaptation to training and improve muscle strength.

Satellite Cell Response to a Repeated Bout of Eccentric Contractions in Human Skeletal Muscle

Satellite Cell Response to a Repeated Bout of Eccentric Contractions in Human Skeletal Muscle

A role for Raptor phosphorylation in the mechanical activation of mTOR signaling

The activation of mTOR signaling is necessary for mechanically-induced changes in skeletal muscle mass, but the mechanisms that regulate the mechanical activation of mTOR signaling remain poorly defined. In this study, we set out to determine if changes in the phosphorylation of Raptor contribute to the mechanical activation of mTOR. To accomplish this goal, mouse skeletal muscles were subjected to mechanical stimulation via a bout of eccentric contractions (EC). Using mass spectrometry and Western blot analysis, we found that ECs induced an increase in Raptor S696, T706, and S863 phosphorylation, and this effect was not inhibited by rapamycin. This observation suggested that changes in Raptor phosphorylation might be an upstream event in the pathway through which mechanical stimuli activate mTOR. To test this, we employed a phospho-defective mutant of Raptor (S696A/T706A/S863A) and found that the EC-induced activation of mTOR signaling was significantly blunted in muscles expressing this mutant. Furthermore, mutation of the three phosphorylation sites altered the interactions of Raptor with PRAS40 and p70S6k, and it also prevented the EC-induced dissociation of Raptor from p70S6k. Combined, these results suggest that changes in the phosphorylation of Raptor play an important role in the pathway through which mechanical stimuli activate mTOR signaling.

Role of nitric oxide in muscle regeneration following eccentric muscle contractions in rat skeletal muscle

We examined the role of nitric oxide (NO) in muscle repair and regeneration following repetitive eccentric contractions (ECC). A standardized exercise protocol was used to create eccentric contraction-induced injury to the left tibialis anterior muscle of 48 male Wistar rats (body wt 250-350g), using a customized isokinetic test device and a bout of 40 ECCs under electrical stimulation. A nitric oxide synthase inhibitor, N(G)-nitro-L-arginine-methyl ester (L-NAME; 35mgkg(-1)day(-1)), was included in the diet for half the animals (n=24) beginning 3days prior to the ECC and continuing throughout the experiment, whereas the other half (n=24) received a control diet. ECC/+L-NAME and ECC/-L-NAME were killed after the ECC protocol at 0, 1, 3 and 7days (n=6 on each day). An unexercised contralateral limb with and without L-NAME infusion served as a respective control muscle at each time point. Muscle NO content, skeletal muscle damage, leukocyte infiltration, calpain activity, and MyoD and myogenin expression were assessed. NO has both pro-inflammatory and anti-inflammatory properties, and several possible roles for NO in skeletal muscle damage have been postulated. NO content was greater in the ECC/-L-NAME group at all time points (p<0.05) compared to ECC/+L-NAME. Additionally, significant differences in NO content were observed on day0 (p<0.05), and day3 (p<0.05), ECC/+L-NAME versus ECC/-L-NAME. One day following the bout of ECC, and NO levels were increased in the ECC/-L-NAME group. Three days following ECC, there was greater myofiber damage (measured by β-glucuronidase activity) and leukocyte invasion in the ECC/-L-NAME group as compared to the ECC/+L-NAME group. One day after ECC, calpain activity was significantly increased in ECC/-L-NAME compared with control muscles (p<0.05). On days3 and 7, Myo-D and myogenin gene expression was increased in both groups; however, the degree of regeneration was less in the ECC/+L-NAME-treated animals. These data suggest that NO dynamics have important implications in the regulation of various factors during skeletal muscle regeneration following damaging eccentric muscle contractions.

Mechanomyography and electromyography during and after fatiguing shoulder eccentric contractions in males and females

The aim of this study was to investigate changes in mechanomyographic (MMG) and the surface electromyographic (EMG) signals during and after fatiguing shoulder eccentric contractions in a group consisting of 12 males and 12 females. Exerted force, MMG, EMG, pain and rate of perceived exertion were assessed before, during and after repeated high-intensity eccentric exercises. Bouts of eccentric contractions caused a decrease in the exerted force for males (P<0.05) and an increase in the rate of perceived exertion and pain for both genders (P<0.05). During eccentric exercise, the root mean square (RMS) values of the MMG signal increased (P<0.05). The mean power frequency (MPF) values of the EMG signal decreased at the end of each eccentric bout for both genders (P<0.05); the decrease was higher for females compared with males (P<0.05). Immediately after eccentric exercise in static abduction of the upper limbs, the MMG RMS and MPF values increased (P<0.05). The present study showed that (1) neuromuscular changes associated with pain and changes in muscle stiffness and (2) changes in motor units strategy during fatigue development in shoulder muscle are reflected in the MMG and EMG signals.

Effects of Muscle Damage on Stretch-Shortening Cycle Function and Muscle Stiffness Control

This experiment examined the effect of eccentric contraction-induced muscle damage on the stretch-shortening cycle and vertical leg spring stiffness during jumping activities. Ten moderately active male and female adult volunteers participated in this study (aged 23 +/- 2.3 years). Temporary muscle damage to the knee extensors was administered by a bout of eccentric contractions on an isokinetic dynamometer. Measurements were obtained of maximum voluntary force and of take-off velocities for single-leg countermovement jumps (CMJs), squat jumps (SJs), and drop jumps (DJs), performed on a specially constructed sledge and force plate apparatus. These measurements were obtained before and after the damage intervention, and the undamaged leg was used as a control. The results indicated that eccentric muscle damage significantly affected stretch-shortening cycle performance by causing relatively greater reductions in SJ performance than CMJ or DJ. The muscle damage intervention also significantly increased leg-spring stiffness, which indicates that the changes in leg stiffness may be an important adaptation resulting from eccentric exercise.

Decreased EMG median frequency during a second bout of eccentric contractions.

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. 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. 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. 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.