Cellular adaptation to repeated eccentric exercise-induced muscle damage.

Eccentrically biased exercise results in skeletal muscle damage and stimulates adaptations in muscle, whereby indexes of damage are attenuated when the exercise is repeated. We hypothesized that changes in ultrastructural damage, inflammatory cell infiltration, and markers of proteolysis in skeletal muscle would come about as a result of repeated eccentric exercise and that gender may affect this adaptive response. Untrained male (n = 8) and female (n = 8) subjects performed two bouts (bout 1 and bout 2), separated by 5.5 wk, of 36 repetitions of unilateral, eccentric leg press and 100 repetitions of unilateral, eccentric knee extension exercises (at 120% of their concentric single repetition maximum), the subjects' contralateral nonexercised leg served as a control (rest). Biopsies were taken from the vastus lateralis from each leg 24 h postexercise. After bout 2, the postexercise force deficit and the rise in serum creatine kinase (CK) activity were attenuated. Women had lower serum CK activity compared with men at all times (P < 0.05), but there were no gender differences in the relative magnitude of the force deficit. Muscle Z-disk streaming, quantified by using light microscopy, was elevated vs. rest only after bout 1 (P < 0.05), with no gender difference. Muscle neutrophil counts were significantly greater in women 24 h after bout 2 vs. rest and bout 1 (P < 0.05) but were unchanged in men. Muscle macrophages were elevated in men and women after bout 1 and bout 2 (P < 0.05). Muscle protein content of the regulatory calpain subunit remained unchanged whereas ubiquitin-conjugated protein content was increased after both bouts (P < 0.05), with a greater increase after bout 2. We conclude that adaptations to eccentric exercise are associated with attenuated serum CK activity and, potentially, an increase in the activity of the ubiquitin proteosome proteolytic pathway.     

Indices of skeletal muscle damage and connective tissue breakdown following eccentric muscle contractions

 Indirect indices of exercise-induced human skeletal muscle damage and connective tissue breakdown were studied following a single bout of voluntary eccentric muscle contractions. Subjects (six female, two male), mean (SD) age 22 (2) years performed a bout of 50 maximum voluntary eccentric contractions of the knee extensors of a single leg. The eccentric exercise protocol induced muscle soreness (P < 0.05 Wilcoxon test), chronic force loss, and a decline in the 20:100 Hz percutaneous electrical myostimulation force ratio [P < 0.01, repeated measures analysis of variance (ANOVA)]. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities were elevated (P < 0.01, repeated measures ANOVA) following the bout. The mean (SD) CK and LDH levels recorded 3 days post-exercise were 2815 (4144) IU · l^–1 and 375 (198) IU · l^–1, respectively. Serum alkaline phosphatase activity showed no changes throughout the study, and a non-significant increase (P = 0.058, repeated measures ANOVA) in pyridinoline was recorded following the bout. Urinary hydroxyproline (HP) and hydroxylysine (HL) excretion, expressed in terms of creatinine (Cr) concentration, increased after exercise (P < 0.05 and P < 0.01, respectively, repeated measures ANOVA). An increased HP:Cr was recorded 2 days post-exercise and HL:Cr was increased above baseline on days 2, 5, and 9 post-exercise. This indirect evidence of exercise-induced muscle damage suggests that myofibre disruption was caused by the eccentric muscle contractions. Elevated urine concentrations of indirect indices of collagen breakdown following eccentric muscle contractions suggests an increased breakdown of connective tissue, possibly due to a localised inflammatory response. Accepted: 9 October 1996     

MR measurements of muscle damage and adaptation after eccentric exercise.

The purposes of this study were, first, to clarify the long-term pattern of T2 relaxation times and muscle volume changes in human skeletal muscle after intense eccentric exercise and, second, to determine whether the T2 response exhibits an adaptation to repeated bouts. Six young adult men performed two bouts of eccentric biceps curls (5 sets of 10 at 110% of the 1-repetition concentric maximum) separated by 8 wk. Blood samples, soreness ratings, and T2-weighted axial fast spin-echo magnetic resonance images of the upper arm were obtained immediately before and after each bout; at 1, 2, 4, 7, 14, 21, and 56 days after bout 1; and at 2, 4, 7 and 14 days after bout 2. Resting muscle T2 [27.6 +/- 0.2 (SE) ms] increased immediately postexercise by 8 +/- 1 ms after both bouts. T2 peaked 7 days after bout 1 at 47 +/- 4 ms and remained elevated by 2.5 ms at 56 days. T2 peaked lower (37 +/- 4 ms) and earlier (2-4 days) after bout 2, suggesting an adaptation of the T2 response. Peak serum creatine kinase values, pain ratings, and flexor muscle swelling were also significantly lower after the second bout (P < 0.05). Total volume of the imaged arm region increased transiently after bout 1 but returned to preexercise values within 2 wk. The exercised flexor compartment swelled by over 40%, but after 2 wk it reverted to a volume 10% smaller than that before exercise and maintained this volume loss through 8 wk, consistent with partial or total destruction of a small subpopulation of muscle fibers.     

Repeated bout effect is not correlated with intraindividual variability during muscle-damaging exercise

The aim of this study was to test the hypothesis that the repeated bout effect depends on intraindividual variability during a second bout of eccentric exercise. Eleven healthy men performed 2 resistance training bouts consisting of maximal eccentric exercise (EE1 and EE2) using the knee extensor muscles. The interval between the exercise bouts was 2 weeks and consisted of 10 sets of 12 repetitions at 160° · s(-1). Maximal isokinetic concentric torque at 30° · s(-1) was measured before the bouts and 2 minutes and 24 hours thereafter. Muscle soreness score and creatine kinase activity were determined before and after exercise. Intraindividual variability in torque during each eccentric repetition was measured during exercise. Repeated bout effect manifested after EE2: Muscle soreness was less, the shift in optimal knee joint angle to a longer muscle length was less, and the decrease in isokinetic concentric torque 2 minutes after exercise was less for EE2 compared with that for EE1. During concentric (isokinetic) contraction, length-dependent changes in isokinetic torque (IT) occurred after both EE1 and EE2: The shorter the muscle length, the greater the change in IT. There was a significant relationship between the decrease in maximal isokinetic knee extension torque 24 hours after EE1 and intraindividual variability of EE1 (R2 = 0.71, p < 0.05), but this relationship was not significant for EE2 (R2 = 0.18). It seems that intraindividual variability during eccentric exercise protects against muscle fatigue and damage during the first exercise bout but not during a repeat bout. These findings may be useful to coaches who wish to improve muscle function in resistance training with less depression in muscle function and discomfort of their athletes, specifically, when muscle is most sensitive to muscle-damaging exercise.     

Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40 min of bench stepping (knee high step; 15 steps · min⁻¹). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150 W, with increments of 50 W every 2 min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P < 0.05). Endurance time and peak V˙O₂ during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P < 0.05) during cycling after eccentric exercise compared with the control condition. Peak blood lactate concentration, observed at 2 min post-exercise was also higher [12.6 (SD 1.4) vs 10.9 SD (1.3) mM; P < 0.01]. The higher blood lactate concentration during cycling exercise after prior eccentric exercise may be attributable to an increased rate of glycogenolysis possibly arising from an increased recruitment of Type II muscle fibres. It follows that determination of lactate thresholds for the purpose of fitness assessment in subjects experiencing DOMS is not appropriate. Accepted: 27 September 1997     

Intramuscular adaptations to eccentric exercise and antioxidant supplementation

Prophylactic supplementation of N-acetyl-cysteine (NAC) and epigallocatechin gallate (EGCG) was studied for physiological and cellular changes in skeletal muscle after eccentric muscle contractions. Thirty healthy, active males (20.0 ± 1.8 years, 160 ± 7.1 cm, 76.1 ± 17.0 kg) ingested for 14 days either 1,800 mg of NAC, 1,800 mg of EGCG, or 1,000 mg of fiber (glucomannan) placebo (PLC) in a double blind, prophylactic fashion. Subjects completed one eccentric exercise bout (100 repetitions at 30°/s) using the dominant knee extensors. Strength and soreness were assessed, and blood and muscle samples obtained before and 6, 24, 48, and 72 h with no muscle sample being collected at 72 h. Separate mixed factorial repeated measures ANOVA (P < 0.05) were used for all statistical analysis. All groups experienced significantly reduced peak torque production after 6 and 24 h, increased soreness at all time points from baseline [with even greater soreness levels 24 h after exercise in PLC when compared to EGCG and NAC (P < 0.05)], increased lactate dehydrogenase at 6 h, and increased creatine kinase 6, 24 and 48 h after exercise. No significant group × time interaction effects were found for serum cortisol, neutrophil counts, and the neutrophil:lymphocyte ratio; although, all values experienced significant changes 6 h after exercise (P < 0.05), but at no other time points. At 48 h after the exercise bout the Neu:Lym ratio in EGCG was significantly less than NAC (P < 0.05), whereas there was a trend (P = 0.08) for the EGCG values to be less when compared to PLC at this time point. Markers of intramuscular mitochondrial and cytosolic apoptosis were assessed (e.g., bax, bcl-2, cytochrome C, caspase-3 content/enzyme activity, and total DNA content). Significant increases (P < 0.05) in muscle levels of bax and bcl-2 were observed in all groups with no significant differences between groups, whereas no changes (P > 0.05) were reported for cytochrome C, caspase-3 content, caspase-3 enzyme activity, and total DNA. Caspase-3 enzyme activity was significantly greater in all groups 48 h after exercise when compared to baseline (P < 0.05) and 6 h (P < 0.05) after exercise. An eccentric bout of muscle contractions appears to significantly increase muscle damage, markers of mitochondrial apoptosis, apoptotic enzyme activity, and whole-blood cell markers of inflammation with no changes in oxidative stress. While soreness ratings were blunted in the two supplementation groups 24 h after exercise when compared to PLC values, more research is needed to determine the potential impact of EGCG and NAC supplementation on changes related to oxidative stress, apoptosis, and eccentric exercise.     

The effect of severe eccentric exercise-induced muscle damage on plasma elastase, glutamine and zinc concentrations

The aim of this study was to determine if severe exercise-induced muscle damage alters the plasma concentrations of glutamine and zinc. Changes in plasma concentrations of glutamine, zinc and polymorphonuclear elastase (an index of phagocytic cell activation) were examined for up to 10 days following eccentric exercise of the knee extensors of one leg in eight untrained subjects. The exercise bout consisted of 20 repetitions of electrically stimulated eccentric muscle actions on an isokinetic dynamometer. Subjects experienced severe muscle soreness and large increases in plasma creatine kinase activity indicative of muscle fibre damage. Peak soreness occurred at 2 days post-exercise and peak creatine kinase activity [21714 (6416) U · l⁻¹, mean (SEM)] occurred at 3 days post-exercise (P < 0.01 compared with pre-exercise). Plasma elastase concentration was increased at 3 days post-exercise compared with pre-exercise (P < 0.05), and is presumably indicative of ongoing phagocytic leucocyte infiltration and activation in the damaged muscles. There were no significant changes in plasma zinc and glutamine concentrations in the days following eccentric exercise. We conclude that exercise-induced muscle damage does not produce changes in plasma glutamine or zinc concentrations despite evidence of phagocytic neutrophil activation. Accepted: 3 November 1997     

Neuromuscular dysfunction with the experimental arm acting as its own reference following eccentric and isometric exercise

Eccentric exercise has been extensively used as a model to study muscle damage-induced neuromuscular impairment, adopting mainly a bilateral matching task between the reference (unexercised) arm and the indicator (exercised) arm. However, little attention has been given to the muscle proprioceptive function when the exercised arm acts as its own reference. This study investigated muscle proprioception and motor control, with the arm acting both as reference and indicator, following eccentric exercise and compared them with those observed after isometric exercise. Fourteen young male volunteers were equally divided into two groups and performed an eccentric or isometric exercise protocol with the elbow flexors of the non-dominant arm on an isokinetic dynamometer. Both exercise protocols induced significant changes in indicators of muscle damage, that is, muscle soreness, range of motion and maximal isometric force post-exercise (p < 0.05–0.001), and neuromuscular function was similarly affected following both protocols. Perception of force was impaired over the 4-day post-exercise period (p < 0.001), with the applied force being systematically overestimated. Perception of joint position was significantly disturbed (i.e., target angle was underestimated) only at one elbow angle on day 4 post-exercise (p < 0.05). The misjudgements and disturbed motor output observed when the exercised arm acted as its own reference concur with the view that they could be a result of a mismatch between the central motor command and an impaired motor control after muscle damage.     

Repeated eccentric exercise bouts do not exacerbate muscle damage and repair

This study examined whether performing repeated bouts of eccentric exercise 2 and 4 days after an initial damaging bout would exacerbate muscle damage. One arm performed 3 sets of 10 eccentric actions of the elbow flexors (ECC1) using a dumbbell set at 50% of the maximal isometric force at 90 degrees (SINGLE). Two weeks later the same exercise was performed by the opposite arm with the exception that subsequent bouts were performed 2 (ECC2) and 4 (ECC3) days after ECC1 (REPEATED). In the REPEATED condition, maximal isometric force (MIF) decreased to the same level immediately after ECC1-3, and the decreases in range of motion (ROM) and increases in upper arm circumference immediately postexercise were similar among the bouts. However, no significant differences in changes in MIF, ROM, muscle soreness, and plasma creatine kinase activity were evident between the SINGLE and REPEATED conditions when excluding the changes immediately after ECC2 and ECC3. These results suggest that ECC2 and ECC3 did not exacerbate muscle damage or affect the recovery process.     

Magnetic resonance imaging and electromyography as indexes of muscle function.

Electromyography (EMG) is commonly used to determine the electrical activity of skeletal muscle during contraction. To date, independent verification of the relationship between muscle use and EMG has not been provided. It has recently been shown that relaxation- (e.g., T2) weighted magnetic resonance images (MRI) of skeletal muscle demonstrate exercise-induced contrast enhancement that is graded with exercise intensity. This study was conducted to test the hypothesis that exercise-induced magnetic resonance (MR) contrast shifts would relate to EMG amplitude if both measures reflect muscle use during exercise. Both MRI and EMG data were collected for separate eccentric (ECC) and concentric (CON) exercise of increasing intensity to take advantage of the fact that the rate of increase and amplitude of EMG activity are markedly greater for CON muscle actions. Seven subjects 30 +/- 2 (SE) yr old performed five sets of 10 CON or ECC arm curls with each of four resistances representing 40, 60, 80, and 100% of their 10 repetition maximum for CON curls. There was 1.5 min between sets and 30 min between bouts (5 sets of 10 actions at each relative resistance). Multiple echo, transaxial T2-weighted MR images (1.5 T, TR/TE 2,000/30) were collected from a 7-cm region in the middle of the arm before exercise and immediately after each bout. Surface EMG signals were collected from both heads of the biceps brachii and the long head of the triceps brachii muscles. CON and ECC actions resulted in increased integrated EMG (IEMG) and T2 values that were strongly related (r = 0.99, P < 0.05) with relative resistance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of one bout of endurance exercise on the expression of myogenin in human quadriceps muscle

The objective of this study was to investigate the cellular localisation of MyoD and myogenin in human skeletal muscle fibres as well as the possible alterations in the expression of MyoD and myogenin in response to a single bout of endurance exercise at 40% and 75% of maximum oxygen uptake (VO₂ max). Twenty-five biopsies (5 per subject) from the vastus lateralis muscle were obtained before exercise, from the exercising leg at 40% and 75% of VO₂ max and from the resting leg following these exercise bouts. The tyramide signal amplification-direct and the Vectastain ABC methods using specific monoclonal antibodies were used to determine the exact location of myogenin and MyoD, to identify muscle satellite cells and to determine myosin heavy chain (MyHC) composition. At rest, myonuclei did not express MyoD or myogenin. Following a single bout of exercise at 40% and 75% of VO₂ max, an accumulation of myogenin in myonuclei and not in satellite cells was observed in biopsies from the exercised leg but not in biopsies before exercise and from the resting leg. The number of myogenin-positive myonuclei varied among individuals indicating differences in the response to a single exercise bout. In conclusion, this immunohistochemical study showed that a rapid rearrangement of myogenin expression occurs in exercised human skeletal muscles in response to a single bout of exercise.     

Repeated bout effect is absent in resistance trained men: An electromyographic analysis

A prior bout of exercise is well known to confer protection from subsequent eccentric bouts (i.e. repeated bout effect; RBE), which may be fostered through neural adaptations, specifically a shift in the frequency content of the surface electromyogram (EMG). It is currently not clear whether chronically resistance trained men are capable of a RBE driven by neural adaptations. Eleven resistance trained men (23.5 ± 3.4 yrs) performed 100 eccentric actions of the barbell bench press exercise, followed by an equivalent bout 14 days later. Indirect markers of muscle damage (i.e. force production, soreness) along with surface EMG were measured before and through 48 h of recovery. Median frequency and maximal isometric force demonstrated time main effects (p > 0.05), but no RBE. A prior bout of eccentric exercise does not confer a RBE for indirect markers of muscle injury or elicit changes in the frequency content of the EMG signal in resistance trained men.     

The effects of antagonist moment on the resultant knee joint moment during isokinetic testing of the knee extensors

The purpose of this study was to examine the effects of moment of antagonistic muscle on the resultant joint moment during isokinetic eccentric and concentric efforts of the knee extensors. Ten males performed maximum eccentric and concentric knee extension and flexion efforts on a Biodex dynamometer at 0.52 rad · s⁻¹ (30° · s⁻¹). Electromyographic (EMG) activity of vastus medialis and biceps femoris (hamstrings) was also recorded. The antagonistic moment of the hamstrings was determined by recording the integrated EMG (iEMG)/moment relationship at different levels of muscle effort. The iEMG/moment curves were fitted using second-degree polynomials. The polynomials were then used to predict the antagonistic moment exerted by the hamstrings from the antagonist iEMG. The antagonistic moment had a maximum of 42.92 Nm and 28.97 Nm under concentric and eccentric conditions respectively; paired t-tests indicated that this was a significant difference (P < 0.05). These results indicate that the resultant joint moment of knee extensors is the result of both agonist and antagonist muscle activation. The greater antagonist muscle activity under concentric activation conditions may be partly responsible for the lower resultant joint concentric moment of knee extensors compared with the corresponding eccentric activation. The antagonist moment significantly affects comparisons between the isokinetic moments and agonist EMG and in vitro force measurements under different testing (muscle action and angular velocity) conditions. Accepted: 25 February 1997     

Muscle metabolites and performance during high-intensity, intermittent exercise

Six men werestudied during four 30-s "all-out" exercise bouts on anair-braked cycle ergometer. The first three exercise bouts wereseparated by 4 min of passive recovery; after the third bout, subjectsrested for 4 min, exercised for 30 min at 30-35% peakO₂ consumption, and rested for afurther 60 min before completing the fourth exercise bout. Peak powerand total work were reduced (P < 0.05) during bout 3 [765 ± 60 (SE) W; 15.8 ± 1.0 kJ] compared withbout 1 (1,168 ± 55 W, 23.8 ± 1.2 kJ), but no difference in exercise performance was observed betweenbouts 1 and4 (1,094 ± 64 W, 23.2 ± 1.4 kJ). Before bout 3, muscle ATP,creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR)Ca²⁺ uptake were reduced, whilemuscle lactate and inosine 5'-monophosphate wereincreased. Muscle ATP and glycogen before bout4 remained lower than values beforebout 1 (P < 0.05), but there were no differences in muscle inosine 5'-monophosphate, lactate, pH, and SR Ca²⁺ uptake. Muscle CP levelsbefore bout 4 had increased aboveresting levels. Consistent with the decline in muscle ATP wereincreases in hypoxanthine and inosine before bouts3 and 4. The decline in exercise performance does not appear to be related to a reduction inmuscle glycogen. Instead, it may be caused by reduced CP availability, increased H⁺ concentration,impairment in SR function, or some other fatigue-inducing agent.

     

FKBP12 deficiency reduces strength deficits after eccentric contraction-induced muscle injury.

Strength deficits associated with eccentric contraction-induced muscle injury stem, in part, from excitation-contraction uncoupling. FKBP12 is a 12-kDa binding protein known to bind to the skeletal muscle sarcoplasmic reticulum Ca2+ release channel [ryanodine receptor (RyR1)] and plays an important role in excitation-contraction coupling. To assess the effects of FKBP12 deficiency on muscle injury and recovery, we measured anterior crural muscle (tibialis anterior and extensor digitorum longus muscles) strength in skeletal muscle-specific FKBP12-deficient and wild-type (WT) mice before and after a single bout of 150 eccentric contractions, as well as before and after the performance of six injury bouts. Histological damage of the tibialis anterior muscle was assessed after injury. Body weight and peak isometric and eccentric torques were lower in FKBP12-deficient mice compared with WT mice. There were no differences between FKBP12-deficient and WT mice in preinjury peak isometric and eccentric torques when normalized to body weight, and no differences in the relative decreases in eccentric torque with a single or multiple injury bouts. After a single injury bout, FKBP12-deficient mice had less initial strength deficits and recovered faster (especially females) than WT mice, despite no differences in the degree of histological damage. After multiple injury bouts, FKBP12-deficient mice recovered muscle strength faster than WT mice and exhibited significantly less histological muscle damage than WT mice. In summary, FKBP12 deficiency results in less initial strength deficits and enhanced recovery from single (especially females) and repeated bouts of injury than WT mice.     

Changes in magnetic resonance images in human skeletal muscle after eccentric exercise

To investigate the time-course of changes in transverse relaxation time (T₂) and cross-sectional area (CSA) of the quadriceps muscle after a single session of eccentric exercise, magnetic resonance imaging was performed on six healthy male volunteers before and at 0, 7, 15, 20, 30 and 60 min and 12, 24, 36, 48, 72 and 168 h after exercise. Although there was almost no muscle soreness immediately after exercise, it started to increase 1 day after, peaking 1–2 days after the exercise (P<0.01). Immediately after exercise, T₂ increased significantly in the rectus femoris, vastus lateralis and intermedius muscles (P<0.05) and decreased quickly continuing until 60 min after exercise. At and after the 12th h, a significant increase was perceived again in the T₂ values of the vastus lateralis and intermedius muscles (P<0.01) [maximum 9.3 (SEM 2.8)% and 10.9 (SEM 2.2)%, respectively]. The maximal values were exhibited at 24–36 h after exercise. In contrast, the rectus femoris muscle showed no delayed-stage increase. Also, in CSA, an increase after 12 h was observed in addition to the one immediately after exercise in the vastus lateralis, intermedius and medialis and quadriceps muscles as a whole (P < 0.01), reaching the maximal values at 12–24 h after exercise. The plasma creative kinase activity remained unchanged up to 24 h after and then increased significantly 48 h after exercise (P < 0.05). Beginning 12 h after exercise, the subjects whose T₂ and CSA increased less than the others displayed a faster decrease in muscle soreness. These results suggested that T₂ and CSA displayed bimodal responses after eccentric exercise and the time-courses of changes in them were similar to those in muscle soreness.     

Effect of antioxidant vitamin supplementation on muscle function after eccentric exercise

This study investigated the effects of antioxidant vitamin supplementation upon muscle contractile function following eccentric exercise and was performed double blind. Twenty-four physically active young subjects ingested either placebo (400 mg; n = 8), vitamin E (400 mg; n=8) or vitamin C (400 mg; n = 8) for 21 days prior to and for 7 days after performing 60 min of box-stepping exercise. Contractile function of the triceps surae was assessed by the measurement of maximal voluntary contraction (MVC) and the ratio of the force generated at 20 Hz and 50 Hz tetanic stimulation before and after eccentric exercise and for 7 days during recovery. Following eccentric exercise, MVC decreased to 75 (4) % [mean (SE); n = 24; P < 0.05] of the preexercise values and the 20/50 Hz ratio of tetanic tension from 0.76 (0.01) to 0.49 (0.03) [mean (SE); n = 24; P<0.05). Compared to the placebo group no significant changes in MVC were observed immediately post-exercise, though recovery of MVC in the first 24 h post-exercise was greater in the group supplemented with vitamin C. The decrease in 20/50 Hz ratio of tetanic tension was significantly less (P < 0.05) post-exercise and in the initial phase of recovery in subjects supplemented with vitamin C but not with vitamin E. These data suggest that prior vitamin C supplementation may exert a protective effect against eccentric exercise-induced muscle damage.     

Changes in ventilation related to changes in electromyograph activity during repetitive bouts of isometric exercise in simulated sailing

This study examined the control of ventilation during repetitive bouts of isometric exercise in simulated sailing. Eight male sailors completed four successive 3-min bouts of similar isometric effort on a dinghy simulator, bouts were separated by 15-s rest intervals. Quadriceps muscle integrated electromyograph activity (iEMG) was recorded during each bout and expressed as a percentage of activity during maximal voluntary contraction (%iEMG_max). From the first to the fourth bout, the 3-min mean averages for ventilation and for %iEMG_max increased from 19.8 (SEM 1.1) to 37.5 (SEM 3.0) l · min^–1 and from 31 (SEM 4) to 39 (SEM 4)% respectively; also, ventilation and %iEMG_max over each minute throughout the four bouts were significantly correlated (r = 0.85;P < 0.05). Progressive hyperventilation reduced the mean end-tidal partial pressure of carbon dioxide from 5.0 (SEM 0.3) kPa during bout 1 to 4.3 (SEM 0.4) kPa during bout 4 [37.7 (SEM 2.0) to 32.4 (SEM (3.0) mmHg]. From the first to the fourth bout the end-of-bout blood lactate concentration did not increase significantly although the concentration from the third bout onwards was significantly greater than at rest. The results suggested that the development of muscle fatigue, which was enhanced by the insufficiency of recovery during the 15-s intervals and mirrored in the progressive increase in iEMG, was linked with stimuli causing progressive hyperventilation. Though these changes in ventilation and iEMG could not be associated with changes in blood lactate concentration, they could both have been related to accumulating metabolites within the muscles themselves.     

Effect of concentric and eccentric muscle actions on muscle sympathetic nerve activity

The purpose ofthis study was to determine the effects of concentric (Con) andeccentric (Ecc) muscle actions on leg muscle sympathetic nerve activity(MSNA). Two protocols were utilized. In protocol1, eight subjects performed Con and Ecc arm curls for 2 min, with a resistance representing 50% of one-repetition maximum forCon curls. Heart rate (HR) and mean arterial pressure (MAP) weregreater (P < 0.05) during Con thanduring Ecc curls. Similarly, the MSNA was greater(P < 0.05) during Con than during Ecc curls. In protocol 2, eightdifferent subjects performed Con and Ecc arm curls to fatigue, followedby postexercise muscle ischemia, by using the same resistanceas in protocol 1. Endurance time wassignificantly greater for Ecc than for Con curls. The increase in HR,MAP, and MSNA was greater (P < 0.05)during Con than during Ecc curls. However, when the data werenormalized as a function of endurance time, the differences in HR, MAP,and MSNA between Con and Ecc curls were no longer present. HR, MAP, andMSNA responses during postexercise muscle ischemia were similar for Con and Ecc curls. Con curls elicited greater increase(P < 0.05) in blood lactateconcentration than did Ecc curls. In summary, Con actions contributesignificantly more to the increase in cardiovascular and MSNA responsesduring brief, submaximal exercise than do Ecc actions. However, whenperformed to a similar level of effort (i.e., fatigue), Con and Eccmuscle actions elicit similar cardiovascular and MSNA responses. Theseresults indicate that the increase in MSNA during a typical bout ofsubmaximal dynamic exercise is primarily mediated by the musclemetaboreflex, which is stimulated by metabolites produced predominantlyduring Con muscle action.