Sports massage after eccentric exercise

BACKGROUND: The use of sports massage is very common in the athletic community. However, only a few studies have shown any therapeutic effect of massage. HYPOTHESIS: Sports massage can improve the recovery after eccentric exercise. STUDY DESIGN: Prospective randomized clinical trial. METHODS: Sixteen subjects performed 300 maximal eccentric contractions of the quadriceps muscle bilaterally. Massage was given to 1 leg, whereas the other leg served as a control. Subjects were treated once daily for 3 days. Maximal strength was tested on a Kin-Com dynamometer, and functional tests were based on 1-leg long jumps. Pain was evaluated using a visual analog scale. RESULTS: There was a marked loss of strength and function of the quadriceps directly after exercise and on the third day after exercise. The massage treatment did not affect the level or duration of pain or the loss of strength or function following exercise. CONCLUSION: Sports massage could not improve the recovery after eccentric exercise.     

Muscle damage and resting metabolic rate after acute resistance exercise with an eccentric overload

PURPOSE: The purpose of this investigation was to determine whether muscle damage caused from acute resistance exercise with an eccentric overload would influence resting metabolic rate (RMR) up to 72 h postexercise in resistance-trained (RT) and untrained (UT) subjects. METHODS: Nine RT and 9 UT male subjects (mean +/- SD; age = 20.7 +/- 2.1 yr; body mass = 79.0 +/- 1.4 kg; height = 178.4 +/- 3.1 cm; and body fat = 10.2 +/- 1.6%) were measured for RMR, creatine kinase concentration ([CK]), and rating of perceived muscle soreness (RPMS) on five consecutive mornings. To induce muscle damage, after the measurements on day 2, each subject performed leg presses that emphasized the eccentric movement for 8 sets at his six-repetition maximum (6-RM). RESULTS: Compared with baseline, the RMR (kJ x d(-1) and kJ x kg FFM(-1) x h(-1) was significantly elevated for RT and UT at 24 h and 48 h postexercise. From 24 h to 48 h to 72 h postexercise, RMR significantly decreased within both groups. The UT group had a significantly higher RMR at 24 h (9,705.4 +/- 204.5 kJ x d(-1)) and 48 h postexercise (8,930.9 +/- 104.4 kJ x d(-1)) when compared with the RT group (9,209.3 +/- 535.3 and 8,601.7 + 353.7 kJ x d(-1)). Both [CK] and RPMS showed a similar time course. CONCLUSION: There was a significantly higher [CK] for the UT group at 24 h postexercise (320.4 +/- 20.1 U x L(-1)) and for both [CK] and RPMS at 48 h (1,140.3 +/- 37.1 U x L(-1) and 4.4 +/- 0.5, respectively) and 72 h postexercise (675.9 +/- 41.7 U x L(-1) and 1.67 +/- 0.5, respectively) when compared with the RT group (24 h, 201.9 +/- 13.4 U x L(-1); 48 h, 845.4 +/- 30.7 U x L(-1) and 3.7 +/- 0.5: and 72 h postexercise, 420.2 +/- 70.2 U x L(-1) and 0.89 +/- 0.3). These data indicate that eccentrically induced muscle damage causes perturbations in RMR up to 48 h postexercise.     

Muscle soreness, swelling, stiffness and strength loss after intense eccentric exercise.

High-intensity eccentric contractions induce performance decrements and delayed onset muscle soreness. The purpose of this investigation was to study the magnitude and time course of such decrements and their interrelationships in 26 young women of mean(s.d.) age 21.4(3.3) years. Subjects performed 70 maximal eccentric contractions of the elbow flexors on a pulley system, specially designed for the study. The non-exercised arm acted as the control. Measures of soreness, tenderness, swelling (SW), relaxed elbow joint angle (RANG) and isometric strength (STR) were taken before exercise, immediately after exercise (AE), analysis of variance and at 24-h intervals for 11 days. There were significant (P < 0.01, analysis of variance) changes in all factors. Peak effects were observed between 24 and 96 h AE. With the exception of STR, which remained lower (P < 0.01), all variables returned to baseline levels by day 11. A non-significant correlation between pain and STR indicated that pain was not a major factor in strength loss. Also, although no pain was evident, RANG was decreased immediately AE. There was no relationship between SW, RANG and pain. The prolonged nature of these symptoms indicates that repair to damaged soft tissue is a slow process. Strength loss is considered particularly important as it continues when protective pain and tenderness have disappeared. This has implications for the therapeutic management of patients with myopathologies and those receiving eccentric exercise for rehabilitation.     

Effect of ketoprofen on muscle function and sEMG activity after eccentric exercise

PURPOSE: This study examined whether ketoprofen, a nonsteroidal anti-inflammatory drug, attenuated muscle soreness (SOR), improved maximal isometric force (MIF) recovery, and/or altered myoelectric activity after high-force eccentric exercise. METHODS: 48 subjects were randomly assigned to one of four groups: CON: no exercise/no drug (N = 12); PLA: exercise + placebo (N = 12); TRT-100: exercise + 100 mg oral ketoprofen (N = 12); and TRT-25: exercise + 25 mg oral ketoprofen (N = 12). PLA, TRT-100, and TRT-25 were administered in a double-blind fashion. Baseline measurements of SOR, MIF, and surface electromyographic (EMG) amplitude were taken, and PLA, TRT-100, and TRT-25 performed 50 maximal eccentric contractions of the elbow flexors; 36 h later, subjects reporting moderate soreness were given ketoprofen or placebo and SOR measures were taken hourly for 8 h. EMG amplitude was assessed during MIF before dosing and again 8 h later and during submaximal contractions of 5%, 10%, and 20% of MIF before dosing and hourly for 8 h. RESULTS: Eccentric exercise increased myoelectric activity during submaximal force measurements in PLA, TRT-100, and TRT-25 in all conditions. Ketoprofen had no effect on reducing this increase in EMG activity. Ketoprofen attenuated perceived SOR (P < 0.05) and enhanced MIF recovery (P < 0.05) compared with placebo. TRT-100 and TRT-25 demonstrated 10% and 19% reductions in SOR, respectively, and 16% and 9% increases in MIF, respectively, whereas PLA demonstrated a 1% increase in SOR and 9% decrease in MIF over 8 h. CONCLUSION: Ketoprofen treatment after muscle damaging exercise reduces muscle soreness and improves force recovery.     

Activity and immobilization after eccentric exercise: I. Recovery of muscle function

PURPOSE: The purpose of the present study was to determine whether activity would affect the recovery of muscle function after high-force eccentric exercise of the elbow flexors. METHODS: Twenty-six male volunteers were randomly assigned to one of three groups for a 4-d treatment period: immobilization (N = 9), control (N = 8), and light exercise (N = 9). Relaxed arm angle (RANG), flexed arm angle (FANG), maximal isometric force (MIF), and perceived muscle soreness (SOR) were obtained for 3 consecutive days pre-exercise (baseline), immediately post-exercise, and for 8 consecutive days after the 4-d treatment period (recovery). During the treatment period, the immobilization group had their arm placed in a cast and supported in a sling at 90 degrees. The control group had no restriction of their arm activity. The light exercise group performed a daily exercise regimen of 50 biceps curls with a 5-lb dumbbell. RESULTS: All subjects showed a prolonged decrease in RANG, increase in FANG, loss in MIF, and increase in SOR in the days after eccentric exercise. During recovery, there was no significant interaction observed among groups over time in RANG (P > 0.05) or FANG (P > 0.05), but there was a significant interaction observed among groups over time in both MIF (P < 0.01) and SOR (P < 0.01). Recovery of MIF was facilitated by light exercise and immobilization, whereas recovery from SOR was facilitated by light exercise and delayed by immobilization. CONCLUSIONS: The recovery of MIF in both the light exercise and immobilization groups suggests that more than one mechanism may be involved in the recovery of isometric force after eccentric exercise.     

Repeated bout effect after maximal eccentric exercise

We hypothesized that a bout of high or low volume eccentric exercise would protect against muscle damage following a subsequent high volume bout and that adaptation would be attributable to neural changes, independent of the initial exercise volume. Sixteen males performed either 45 (ECC45) or 10 (ECC10) maximal eccentric contractions using the elbow flexors, followed by an ECC45 bout 2 weeks later. Damage markers were measured for the following 96 h; EMG and work done during the first 10 eccentric contractions were also recorded. CK, soreness, and decrements in MVC and range of motion (ROM) were greater in bout 1 than bout 2 (p < 0.01). Soreness, MVC and ROM were greater after the initial ECC45 bout compared to the initial ECC10 bout and the repeated bouts of ECC45 exercise in both groups (p < 0.01). Median frequency decreased from bout 1 to bout 2 (p < 0.001), no differences between groups were observed. An ECC45 bout of maximal eccentric exercise causes more initial damage than an ECC10 bout of maximal eccentric exercise, although both confer protection from subsequent ECC45 bouts of maximal eccentric contractions, which are attributable, at least in part, to a shift in the frequency content of EMG.     

Myofibers express IL-6 after eccentric exercise

BACKGROUND: Interleukin (IL)-6 is locally produced in skeletal muscles and shows a remarkable increase in plasma after eccentric exercises. OBJECTIVE: To elucidate the cell types in the muscles responsible for IL-6 production after eccentric exercises. STUDY DESIGN: Controlled laboratory study. METHODS: An eccentric contraction model was made using electrical stimulation. The authors investigated the muscle damage and regeneration processes after eccentric exercises histologically, and the cell types expressing IL-6 and its subcellular compartimentalization with time immunohistochemically after eccentric exercises. RESULTS: Swollen myofibers were detected from 8 hours to 3 days after exercises. Disrupted myofibers were detected from 24 hours to 7 days, with a peak of 3 days. IL-6 was detected only in the cytoplasm of myofibers until 12 hours; thereafter, it was found in the inflammatory cells and proliferating satellite cells as well. The swollen myofibers were negatively stained for IL-6. The positive ratios of IL-6 in myofibers immediately increased after exercises, peaked in 12 hours, and then decreased. CONCLUSIONS: After eccentric exercises, IL-6 expression increased in myofibers preceding the disruption of myofibers. IL-6 might be closely related to muscle damage caused by strenuous exercises.     

Cyclic compressive loading facilitates recovery after eccentric exercise

PURPOSE: To assess the biologic basis of massage therapies, we developed an experimental approach to mimic Swedish massage and evaluate this approach on recovery from eccentric exercise-induced muscle damage using a well-controlled animal model. METHODS: Tibialis anterior muscles of six New Zealand White rabbits were subjected to one bout of damaging, eccentric contractions. One muscle was immediately subjected to cyclic compressive loads, and the contralateral served as the exercised control. RESULTS: We found that commencing 30 min of cyclic compressive loading to the muscle, immediately after a bout of eccentric exercise, facilitated recovery of function and attenuated leukocyte infiltration. In addition, fiber necrosis and wet weight of the tissue were also reduced by compressive loading. CONCLUSION: We conclude that subjecting muscle to compressive loads immediately after exercise leads to an enhanced recovery of muscle function and attenuation of the damaging effects of inflammation in the rabbit model. Although these observations suggest that skeletal muscle responds to cyclic compressive forces similar to those generated by clinical approaches, such as therapeutic massage, further research is needed to assess the translational efficacy of these findings.     

Improvements in multi-joint leg function following chronic eccentric exercise

Previous authors have reported that chronic eccentric cycling facilitates greater changes in multi-joint leg function (hopping frequency, maximum jumping height) compared with concentric cycling. Our purpose was to evaluate changes in leg spring stiffness and maximum power following eccentric and concentric cycling training. Twelve individuals performed either eccentric (n=6) or concentric (n=6) cycling for 7 weeks (3 sessions/week) while training duration progressively increased. Participants performed trials of submaximal hopping, maximal counter movement jumps, and maximal concentric cycling to evaluate leg spring stiffness, maximum jumping power, and maximum concentric cycling power respectively, before and 1 week following training. Total work during training did not differ between eccentric and concentric cycling (126 ± 15-728 ± 91 kJ vs 125 ± 10-787 ± 76 kJ). Following training, eccentric cycling exhibited greater changes in k(leg) and jumping P(max) compared with CON(cyc) (10 ± 3% vs -2 ± 4% and 7 ± 2% vs -2 ± 3%, respectively, P=0.05). Alterations in CON(cyc) P(max) did not differ between ECC(cyc) (1035 ± 142 vs 1030 ± 133 W) and CON(cyc) (1072 ± 98 vs 1081 ± 85 W). These data demonstrate that eccentric cycling is an effective method for improving leg spring stiffness and maximum power during multi-joint tasks that include stretch-shortening cycles. Improvements in leg spring stiffness and maximum power would be beneficial for both aging and athletic populations.     

Shift of peak torque angle after eccentric exercise

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

Muscle degeneration after exercise in rats

To search for morphological changes in muscle, related to overuse syndromes of muscle due to exercise, groups of untrained rats ran on a treadmill for 1 h at submaximal intensity. Each group was sacrificed at a different interval after the end of the exercise. To evaluate the physiologic load, the colonic temperature and blood lactate level were determined. The right hindlimb was fixated with buffered glutaraldehyde, injected into the femoral artery, and different muscles were dissected and prepared for electron and light microscopy. The muscles of the left limb were frozen in liquid Freon and used for histochemistry. Signs of degeneration were noted in the soleus, rectus femoris, and vastus lateralis muscles, but were absent in the gastrocnemius, tibialis anterior, extensor digitorum, and biceps femoris muscles. Immediately after exercise, only minor signs of degeneration were observed at the ultrastructural level, while after 2-3 h degeneration became clearly visible at the light microscopic level. The most pronounced changes were observed 24-48 h after exercise, whereafter regeneration occurred. Only 2%-5% of all fibers in the soleus muscle showed signs of degeneration, while in the vastus lateralis and rectus femoralis muscle less than 0.5% of the fibers were affected. The affected fibers showed degeneration only in segments with a length between 150-1250 micrometers. The affected fibers in the soleus and vastus lateralis muscles belong to the type I population, while in the rectus femoris type I as well as type II fibers were affected.     

Interleukin-6 expression after repeated bouts of eccentric exercise

Plasma interleukin-6 (IL-6) is known to increase in response to eccentric exercise due to an acute-phase immune response. However, the severity of muscle injury is reduced with repeated bouts of eccentric exercise, possibly as a result of decreases in plasma IL-6. This study determined the response of IL-6 mRNA and IL-6, troponin-I (sTnI), muscle strength, and soreness as a result of repeated bouts of eccentric exercise. Eight males underwent two eccentric exercise bouts (3 wk apart) involving 7 sets of 10 repetitions at 150 % of the isotonic 1-RM of the dominant knee extensors. Blood samples were taken before, after and 2, 4, 6, 24, 48 and 96 h post-exercise. Strength and soreness ratings were assessed before and at 24, 48 and 96 h-post. Data were analyzed with 2 x 4 and 2 x 8 ANOVAs and the non-parametric Friedman test (p < 0.05). Both IL-6 mRNA and IL-6 underwent peak increases (p < 0.05) at 4 h-post and 6 h-post, respectively, but were not different between bouts. However, there were significant changes (p < 0.05) in sTnI, strength, and soreness that were greater after the first bout than the second, characteristic of the repeated bout effect. These results indicate that changes in sTnI, strength and soreness were less with the second eccentric exercise bout whereas the changes in both IL-6 mRNA and protein were not effected between bouts.     

Glucocorticoid receptor and ubiquitin expression after repeated eccentric exercise

INTRODUCTION/PURPOSE: Eccentric exercise causes muscle proteolysis that may be attenuated with repeated exercise. Therefore, this study determined the effect of repeated bouts of eccentric exercise on ubiquitin (UBI), ubiquitin conjugating enzyme (E2), and 20S proteasome (20S) and glucocorticoid receptor (GR) mRNA and protein expression, myofibrillar protein content, DNA content, caspase-3 activity, serum skeletal muscle troponin-I (sTnI) and cortisol (CORT), and muscle strength. METHODS: Nine males underwent two identical eccentric exercise bouts (BT1 and BT2) 3 wk apart involving seven sets of 10 repetitions at 150% one-repetition maximum of the dominant knee extensors. Blood and muscle biopsy samples were obtained before and at 6 and 24 h postexercise whereas muscle strength was assessed before and at 24, 48, and 72 h postexercise. Data were analyzed with separate 2 x 3 and 2 x 4 factorial ANOVA (P < 0.05). RESULTS: Decrements in strength and increased soreness occurred at 24 and 48 h postexercise for both bouts (P < 0.05); however, the changes for BT1 were greater than BT2. Serum CORT and sTnI were greater immediately after and at 6, 24, and 48 h postexercise for both bouts; however, the differences in BT1 were greater than BT2 (P < 0.05). Caspase-3 activity and the mRNA and protein levels of UBI, E2, 20S, and GR were increased at 6 and 24 h postexercise, and these differences were greater for BT1 than BT2 (P < 0.05). For BT1, DNA and myofibrillar protein content decreases were apparent at 24 h postexercise (P < 0.05) but not in BT2. CONCLUSION: These results indicate that muscle injury occurring from an initial bout of eccentric exercise seems to decrease muscle strength and myofibrillar protein, possibly due to apoptosis and up-regulation of glucocorticoid receptor mediated increases in UBI-proteolytic pathway activity, all of which appear to be tempered with a repeated eccentric exercise bout.     

Plasma creatine kinase activity and glutathione after eccentric exercise

PURPOSE: This study examined whether plasma total glutathione levels could explain the intersubject variability in the creatine kinase (CK) response to eccentric exercise. We hypothesized that the increase in plasma CK activity after eccentric exercise would be lower for individuals with low plasma total glutathione (<2.5 micromol x L-1) compared with individuals with high total glutathione (>3.8 micromol x L-1), but other indicators of muscle damage would be the same between groups. METHODS: Resting blood samples were obtained over 2 d from 60 subjects and analyzed for plasma total glutathione. Eight subjects who had total glutathione values below 2.5 micromol x L-1 (LG), and nine who had values above 3.8 micromol x L-1 (HG) performed 50 maximal eccentric actions of the elbow flexors. Maximal voluntary isometric contraction (MVC), relaxed arm angle (RANG), and blood samples for CK, myoglobin (Mb), and total glutathione were obtained pre, post (except blood samples), 24, 48, 72, 96, and 120 h after exercise. RESULTS: There was a significant group-by-time interaction in analysis of MVC, RANG, total glutathione, CK, and Mb response to exercise. Although LG showed a smaller CK response to eccentric exercise compared with HG, LG also showed a smaller increase in plasma Mb, a faster recovery of MVC and RANG, and an increase in plasma total glutathione. CONCLUSION: Subjects with low plasma total glutathione levels had a smaller plasma CK and Mb response and a faster recovery from eccentric exercise compared with subjects having high plasma total glutathione levels. We suggest that a blunted inflammatory response in subjects with low plasma glutathione may be one explanation for these findings.     

Selective serotonin reuptake inhibitors and rhabdomyolysis after eccentric exercise

PURPOSE: The purpose of this report was to review three cases of clinically significant rhabdomyolysis that developed in research subjects after completing an eccentric exercise protocol. All three cases occurred in subjects who reported use of selective serotonin reuptake inhibitors (SSRI). METHODS: Sixty-three subjects enrolled in the study. Subjects performed 15 sets of 15 repetitions of maximal eccentric contractions of the elbow flexors. Subjects were then monitored on a daily basis for development of delayed onset muscle soreness (DOMS). Subjects received either microcurrent electrical neuromuscular stimulation (MENS) or sham treatment. RESULTS: Three subjects developed clinically significant rhabdomyolysis after performing this exercise protocol. Affected subjects were the only subjects who reported use of SSRI during the study period. CONCLUSION: This report raises suspicion of SSRI use as a predisposing factor to muscle injury after eccentric exercise.     

Blood leukocyte and glutamine fluctuations after eccentric exercise.

Skeletal muscle, as a producer of glutamine, is important for lymphocytes, monocytes and macrophages. Exercise-induced muscle damage could burden the immune system by concurrently eliciting a local inflammatory response and decreasing glutamine availability. The aim of this study was to determine whether blood leukocyte and glutamine concentrations were affected in individuals with high serum creatine kinase (CK) activity (indirect indication of muscle damage) compared to those with no change in CK. Twelve females performed maximal eccentric resistance exercise using one arm and one leg. Blood leukocyte subsets and glutamine were measured at 24 and 0 h pre-exercise, and post-exercise at intervals up to 9 d post-exercise. Eleven subjects were placed in High (n = 6) and Low CK (n = 5) groups. Lymphocytes, (total, natural killer, and T), monocytes, and granulocytes did not change significantly in either group, at any time. Whole blood glutamine concentration decreased (p < 0.05) from 437 microM pre-exercise to 332 microM 3 d post-exercise in both groups. The decrease in glutamine suggests that the metabolism of the muscle may be affected by this exercise, however, the occurrence of this decrease in both groups suggests that this change was not a response to muscle damage.     

Muscle glycogen synthesis before and after exercise

The importance of carbohydrates as a fuel source during endurance exercise has been known for 60 years. With the advent of the muscle biopsy needle in the 1960s, it was determined that the major source of carbohydrate during exercise was the muscle glycogen stores. It was demonstrated that the capacity to exercise at intensities between 65 to 75% VO2max was related to the pre-exercise level of muscle glycogen, i.e. the greater the muscle glycogen stores, the longer the exercise time to exhaustion. Because of the paramount importance of muscle glycogen during prolonged, intense exercise, a considerable amount of research has been conducted in an attempt to design the best regimen to elevate the muscle's glycogen stores prior to competition and to determine the most effective means of rapidly replenishing the muscle glycogen stores after exercise. The rate-limiting step in glycogen synthesis is the transfer of glucose from uridine diphosphate-glucose to an amylose chain. This reaction is catalysed by the enzyme glycogen synthase which can exist in a glucose-6-phosphate-dependent, inactive form (D-form) and a glucose-6-phosphate-independent, active form (I-form). The conversion of glycogen synthase from one form to the other is controlled by phosphorylation-dephosphorylation reactions. The muscle glycogen concentration can vary greatly depending on training status, exercise routines and diet. The pattern of muscle glycogen resynthesis following exercise-induced depletion is biphasic. Following the cessation of exercise and with adequate carbohydrate consumption, muscle glycogen is rapidly resynthesised to near pre-exercise levels within 24 hours. Muscle glycogen then increases very gradually to above-normal levels over the next few days. Contributing to the rapid phase of glycogen resynthesis is an increase in the percentage of glycogen synthase I, an increase in the muscle cell membrane permeability to glucose, and an increase in the muscle's sensitivity to insulin. The slow phase of glycogen synthesis appears to be under the control of an intermediate form of glycogen synthase that is highly sensitive to glucose-6-phosphate activation. Conversion of the enzyme to this intermediate form may be due to the muscle tissue being constantly exposed to an elevated plasma insulin concentration subsequent to several days of high carbohydrate consumption. For optimal training performance, muscle glycogen stores must be replenished on a daily basis. For the average endurance athlete, a daily carbohydrate consumption of 500 to 600g is required. This results in a maximum glycogen storage of 80 to 100 mumol/g wet weight.(ABSTRACT TRUNCATED AT 400 WORDS)     

Muscle enzyme and fiber type‐specific sarcomere protein increases in serum after inertial concentric‐eccentric exercise

Muscle damage induced by inertial exercise performed on a flywheel device was assessed through the serum evolution of muscle enzymes, interleukin 6, and fiber type‐specific sarcomere proteins such as fast myosin (FM) and slow myosin (SM). We hypothesized that a model of muscle damage could be constructed by measuring the evolution of serum concentration of muscle proteins following inertial exercise, according to their molecular weight and the fiber compartment in which they are located. Moreover, by measuring FM and SM, the type of fibers that are affected could be assessed. Serum profiles were registered before and 24, 48, and 144 h after exercise in 10 healthy and recreationally active young men. Creatine kinase (CK) and CK‐myocardial band isoenzyme increased in serum early (24 h) and returned to baseline values after 48 h. FM increased in serum late (48 h) and remained elevated 144 h post‐exercise. The increase in serum muscle enzymes suggests increased membrane permeability of both fast and slow fibers, and the increase in FM reveals sarcomere disruption as well as increased membrane permeability of fast fibers. Consequently, FM could be adopted as a fiber type‐specific biomarker of muscle damage.     

Changes in motor unit characteristics after eccentric elbow flexor exercise

Morphological evidence suggests that fast-twitch fibers are prone to disruption of their membrane structures by eccentric exercise. However, it is unclear how this is reflected in the discharge rate and action potential propagation of individual motor units, especially at high contraction levels. High-density surface electromyograms were recorded from biceps brachii muscle and decomposed to individual motor unit action potentials at isometric contraction levels between 10% and 75% of maximal voluntary contraction (MVC) before intermittent maximal elbow flexor eccentric exercise, and two hours (2H), two days (2D) and four days (4D) post-exercise. Maximal voluntary force decreased by 21.3±5.6% 2H and by 12.6±11.1% 2D post-exercise. Motor unit discharge rate increased and mean muscle fiber conduction velocity decreased, at the highest isometric contraction levels only (50% and 75% of MVC) at 2H post-exercise. These results indicate that eccentric exercise can disturb the function of motor units active at high contraction levels in the early stages after exercise, which seems to be compensated by the central nervous system with an increase in neural drive during submaximal isometric contractions.     

Muscular performance after concentric and eccentric exercise in trained men

PURPOSE: We studied previously resistance-trained men and compared the effects of concentric and eccentric training on performance and structural muscle parameters. METHODS: Seventeen trained individuals (age 26.9 +/- 3.4 yr) participated in 12 wk of either maximum concentric (N = 8) or eccentric (N = 9) resistance training of the elbow flexors. The functional performance was measured as the maximum concentric and eccentric strength and angular velocity at standard loads. Muscle cross-sectional area and cross-sectional area of single cells were used as measures of muscular hypertrophy. Fiber-type proportions were assessed by staining cells for myofibrillar ATPase. RESULTS: Both eccentric and concentric training increased concentric strength to a similar extent (14 vs 18%), whereas eccentric training led to greater increases in eccentric strength than concentric training did (26 vs 9%). The maximum angular velocity at all loads was enhanced equally in both training groups. The cross-sectional area of both the elbow flexors (+11%) and of the type I and type IIA fibers increased only after the eccentric training. In addition, the relative cross-sectional area occupied by the type II fibers increased from 64 to 73% after the eccentric training. There were only minor changes in the fiber-type proportions. CONCLUSION: The present data suggest that for resistance-trained men, increases in concentric strength and velocity performance after eccentric training are largely mediated by changes in fiber and muscle cross-sectional area. However, hypertrophy alone could not explain the increase in eccentric strength. Because the increases in strength and velocity performance after concentric training could not be ascribed to muscular adaptations alone, we suggest that they may be attributable to additional neural factors.