PURPOSE The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. METHODS Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. RESULTS In the exercised leg, peak torque was reduced by 47 +/- 5% during exercise and was still 22 +/- 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 +/- 6% of all fibers in exercised muscle and in 2 +/- 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. CONCLUSIONS Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process.

PURPOSE:To investigate the time course of leukocyte accumulation in eccentric exercised human muscles and its relation to recovery of muscle function and soreness. METHODS:Eleven young males performed 300 unilateral, maximal voluntary, eccentric actions with the musculus quadriceps femoris (30 degrees x s(-1)). Before and at regular intervals for 7 d after exercise, force-generating capacity was measured with maximal concentric knee extensions (60 degrees x s(-1)). Accumulation of radiolabeled (autologous) leukocytes was measured with scintigraphy. Biopsies from musculus vastus lateralis were obtained 0.5, 4, 8, 24, 96, and 168 h after exercise from both the exercised leg and the control leg. Muscle cross-sections were stained with antibodies against leukocytes (CD16 and CD68). Muscle soreness was rated on a visual analog scale. RESULTS:Immediately after exercise, the subjects' ability to generate force was reduced by 47 +/- 5%. Muscle function recovered slowly and was not fully restored after 1 wk. Radiolabeled leukocytes accumulated in the muscles during the first hour (3-24 h) after exercise, and leukocytes were at the same time observed histologically, primarily in the endomysium and perimysium. A part of the accumulated radiolabeled leukocytes appeared to be located within local blood vessels. The highest numbers of CD16(+) and CD68(+) cells were found 4 and 7 d after exercise. There was a positive correlation between accumulation of radiolabeled leukocytes and muscle weakness measured 1-3 d after exercise (r = 0.8, P < 0.05) and, surprisingly, a negative correlation between radiolabeled leukocyte accumulation and muscle soreness (r = -0.96, P < 0.01). CONCLUSION:Exercise-induced muscle damage initiated a rapid local inflammatory response that gradually increased over the next days. Halted recovery of muscle function was associated with local accumulation of leukocytes, whereas muscle soreness could not be explained by the presence of leukocytes.

Knowledge about the effects of exercise on myofibrillar protein breakdown in human subjects is limited. Our purpose was to measure the changes in the degradation of myofibrillar proteins in response to different ways of eliciting muscle contractions using the local interstitial 3‐methyl‐histidine (3‐MH) concentration as a marker for myofibrillar protein breakdown. Untrained males (n=8, 22–27 years, range) performed 210 maximal isokinetic eccentric contractions with each leg on an isokinetic dynamometer. One leg performed voluntary (VOL) and the other leg performed electrically induced contractions (ES). Microdialysis probes were placed in m. vastus lateralis in both the legs immediately after, and 1 and 3 days post‐exercise. Interstitial 3‐MH was higher in ES vs VOL immediately after exercise (P<0.05). One and 3 days post‐exercise no difference between the two exercise types was observed. Only after ES did the histochemical stainings show significant disruption of cytoskeletal proteins. Furthermore, intracellular disruption and destroyed Z‐lines were markedly more pronounced in ES vs VOL. In conclusion, the local level of interstitial 3‐MH in the skeletal muscle was significantly enhanced after ES compared with VOL immediately after exercise, while the level of 3‐MH did not change in the post‐exercise period after VOL. These results indicate that the local myofibrillar breakdown is accelerated after ES associated with severe myofiber damage.

The effect of concurrent strength (S) and endurance (E) training on adaptive changes in aerobic capacity, endurance performance, maximal muscle strength and muscle morphology is equivocal. Some data suggest an attenuated cardiovascular and musculoskeletal response to combined E and S training, while other data show unimpaired or even superior adaptation compared to either training regime alone. However, the effect of concurrent S and E training has never been examined in elite level (national team) endurance athletes. PURPOSE: To evaluate the effect of concurrent SE training on maximal muscle strength (MVC), rate of force development (RFD), muscle fiber morphology and composition, capillarization, aerobic capacity (VO2max), economy (VO2 at 75% VO2max), and short/long term endurance capacity in elite level endurance athletes. METHODS: Muscle biopsies (VL) were analyzed for fiber area, fiber type composition, and capillarization (cap/mm2, cap/fiber) pre and post 16 wks of combined SE training (SE, n=7) or E training alone (E, n=7) in young Danish national team cyclists (19.7±0.8 yrs). Maximal quadriceps MVC and RFD was obtained using a dynamometer (KinCom). VO2max, economy and endurance capacity (total cycle work during 5-min and 45-min all out) were evaluated using standardized ergometer cycle tests (own bike). Subjects were thoroughly familiarized to all tests. RESULTS: Post training MVC and RFD increased (+12-20%) in SE (p<0.01) but not E. VO2max and economy remained unchanged. Lean body mass increased (+3%) in SE, without any change in total body mass (69.2 ± 5.8 vs 70.0 ±6.1 kg). Short-term endurance performance increased (+3-4%) both in SE and E (p<0.05), while long-term endurance only increased in SE (+8%) (p<0.05). Muscle fiber area and capillarization remained unchanged with training both in SE and E. Type IIA fiber proportions (%area) increased from 26% to 34% in SE (p<0.05). CONCLUSIONS: Both SE and E training improved short-term endurance capacity, but only combined strength and endurance training (SE) improved the long-term endurance capacity in elite level endurance athletes, which was accompanied by an increased proportion of type IIA fibers and an enhanced capacity for rapid muscle force generation (elevated RFD).

Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n = 8, range 22-27 years) performed 2 10 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.

Acute muscle protein metabolism is modulated not only by resistance exercise but also by amino acids. However, less is known about the long-term hypertrophic effect of protein supplementation in combination with resistance training. The present study was designed to compare the effect of 14 weeks of resistance training combined with timed ingestion of isoenergetic protein vs carbohydrate supplementation on muscle fiber hypertrophy and mechanical muscle performance. Supplementation was administered before and immediately after each training bout and, in addition, in the morning on nontraining days. Muscle biopsy specimens were obtained from the vastus lateralis muscle and analyzed for muscle fiber cross-sectional area. Squat jump and countermovement jump were performed on a force platform to determine vertical jump height. Peak torque during slow (30 degrees s-1) and fast (240 degrees s-1) concentric and eccentric contractions of the knee extensor muscle was measured in an isokinetic dynamometer. After 14 weeks of resistance training, the protein group showed hypertrophy of type I (18% +/- 5%; P < .01) and type II (26% +/- 5%; P < .01) muscle fibers, whereas no change above baseline occurred in the carbohydrate group. Squat jump height increased only in the protein group, whereas countermovement jump height and peak torque during slow isokinetic muscle contraction increased similarly in both groups. In conclusion, a minor advantage of protein supplementation over carbohydrate supplementation during resistance training on mechanical muscle function was found. However, the present results may have relevance for individuals who are particularly interested in gaining muscle size.

We hypothesized that an acute bout of strenuous, non-damaging exercise would increase rates of protein synthesis of collagen in tendon and skeletal muscle but these would be less than those of muscle myofibrillar and sarcoplasmic proteins. Two groups (n = 8 and 6) of healthy young men were studied over 72 h after 1 h of one-legged kicking exercise at 67% of maximum workload (W(max)). To label tissue proteins in muscle and tendon primed, constant infusions of [1-(13)C]leucine or [1-(13)C]valine and flooding doses of [(15)N] or [(13)C]proline were given intravenously, with estimation of labelling in target proteins by gas chromatography-mass spectrometry. Patellar tendon and quadriceps biopsies were taken in exercised and rested legs at 6, 24, 42 or 48 and 72 h after exercise. The fractional synthetic rates of all proteins were elevated at 6 h and rose rapidly to peak at 24 h post exercise (tendon collagen (0.077% h(-1)), muscle collagen (0.054% h(-1)), myofibrillar protein (0.121% h(-1)), and sarcoplasmic protein (0.134% h(-1))). The rates decreased toward basal values by 72 h although rates of tendon collagen and myofibrillar protein synthesis remained elevated. There was no tissue damage of muscle visible on histological evaluation. Neither tissue microdialysate nor serum concentrations of IGF-I and IGF binding proteins (IGFBP-3 and IGFBP-4) or procollagen type I N-terminal propeptide changed from resting values. Thus, there is a rapid increase in collagen synthesis after strenuous exercise in human tendon and muscle. The similar time course of changes of protein synthetic rates in different cell types supports the idea of coordinated musculotendinous adaptation.

No studies to date have reported activation of satellite cells in vivo in human muscle after a single bout of high intensity exercise. In this investigation, eight individuals performed a single bout of high intensity exercise with one leg, the contralateral leg being the control. A significant increase in mononuclear cells staining for the neural cell adhesion molecule (N-CAM) and fetal antigen 1 (FA1) were observed within the exercised human vastus lateralis muscle on days 4 and 8 post exercise. In addition, a significant increase in the concentration of the FA1 protein was determined in intramuscular dialysate samples taken from the vastus lateralis muscle of the exercising leg (day 0: 1.89 +/- 0.82 ng ml(-1); day 2: 1.68 +/- 0.37 ng ml(-1); day 4: 3.26 +/- 1.29 ng ml(-1), P < 0.05 versus basal; day 8: 4.68 +/- 2.06 ng ml(-1), P < 0.05 versus basal and control). No change was noted in the control leg. Despite this increase in N-CAM- and FA1-positive mononuclear cells, an increased expression of myogenin and the neonatal isoform of the myosin heavy chain (MHCn) was not observed. Interestingly, myofibre lesions resulting from extensive damage to the proteins within the myofibre, particularly desmin or dystrophin, were not observed, and hence did not appear to induce the expression of either N-CAM or FA1. We therefore propose that satellite cells can be induced to re-enter the cell growth cycle after a single bout of unaccustomed high intensity exercise. However, a single bout of exercise is not sufficient for the satellite cell to undergo terminal differentiation.

Electrical stimulation training is known to alter skeletal muscle characteristics after a spinal cord injury, but the effect of load on optimizing the training protocol has not been fully investigated. This study investigated two electrical-stimulation training regimes with different loads on intramuscular parameters of the paralyzed lower limbs. Six paraplegic individuals with a spinal cord injury underwent electrical stimulation training (45 min daily for 3 days per week for 10 weeks). One leg was trained statically with load, and the contralateral leg was trained dynamically with minimal load. Isometric force assessed with 35-Hz stimuli increased significantly in both legs from baseline, with the static-trained leg also being significantly higher than the dynamic-trained leg. The vastus lateralis muscle of the statically trained leg showed a significant increase in type I fibers, fiber cross-sectional area, capillary-to-fiber ratio, and citrate synthase activity when compared to both baseline and the dynamically trained leg. Relative oxygenation of the vastus lateralis muscle as determined by near infrared spectroscopy was also significantly greater after static training. This study indicates that the load that is applied to paralyzed muscle during an electrical stimulation training program is an important factor in determining the amount of muscle adaptation that can be achieved.

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

Neuromuscular electrical stimulation has grown in popularity as a therapeutic device for training and an ambulation aid to human paralyzed muscle. Despite its current clinical use, few studies have attempted to concurrently investigate the functional and intramuscular adaptations which occur after electrical stimulation training. Six individuals with a spinal cord injury performed 10 weeks of electrical stimulation leg cycle training (30 min d(-1), 3 d week(-1)). The paralyzed vastus lateralis muscle showed significant alterations in skeletal muscle characteristics after the training, indicated by an improvement in total work output (52-112 kJ; P < 0.05), an increase in fiber cross-sectional area (18 to 41 x 10(2) microm(2); P < 0.05), a reduction in the percentage of type IIX fibers (75% to 12%; P < 0.05), a decrease in myosin heavy chain IIx (68% to 44%; P < 0.05), an increase in capillary density (2-3.5 capillaries around fiber; P < 0.05) and increases in activity levels of citrate synthase (7-16 mU mg(-1) protein) and hexokinase (1.2-2.4 mU mg(-1) protein). This study showed that 10 weeks of electrical stimulation training of human paralyzed muscle induces concurrent improvements in functional capacity and oxidative metabolism.

The vascular endothelium is an important mediator of tissue vasodilatation, yet the role of the specific substances, nitric oxide (NO) and prostaglandins (PG), in mediating the large increases in muscle perfusion during exercise in humans is unclear. Quadriceps microvascular blood flow was quantified by near infrared spectroscopy and indocyanine green in six healthy humans during dynamic knee extension exercise with and without combined pharmacological inhibition of NO synthase (NOS) and PG by l‐NAME and indomethacin, respectively. Microdialysis was applied to determine interstitial release of PG. Compared to control, combined blockade resulted in a 5‐ to 10‐fold lower muscle interstitial PG level. During control incremental knee extension exercise, mean blood flow in the quadriceps muscles rose from 10 ± 0.8 ml (100 ml tissue)−1 min−1 at rest to 124 ± 19, 245 ± 24, 329 ± 24 and 312 ± 25 ml (100 ml tissue)−1 min−1 at 15, 30, 45 and 60 W, respectively. During inhibition of NOS and PG, blood flow was reduced to 8 ± 0.5 ml (100 ml tissue)−1 min−1 at rest, and 100 ± 13, 163 ± 21, 217 ± 23 and 256 ± 28 ml (100 ml tissue)−1 min−1 at 15, 30, 45 and 60 W, respectively (P < 0.05 vs. control). In conclusion, combined inhibition of NOS and PG reduced muscle blood flow during dynamic exercise in humans. These findings demonstrate an important synergistic role of NO and PG for skeletal muscle vasodilatation and hyperaemia during muscular contraction.

Four individuals with a spinal cord injury underwent 16 weeks of isometric electrical stimulation training to both legs for 60 min, five times per week during the first 5 months after injury, while two SCI individuals remained untrained. A baseline biopsy sample of the vastus lateralis muscle was obtained within 1 month of injury, and another biopsy sample was taken after a further 16 weeks. The untrained, paralyzed skeletal muscle displayed a reduction in (1) type I fibers (from 50% to 9%), (2) myosin heavy chain (MHC) I (from 27% to 6%), and (3) fiber cross-sectional area of type I, type IIA and type IIX fibers (-62%, -68%, and -55%, respectively) when compared to the baseline sample of muscle taken within 1 month of injury. In contrast, the trained group showed smaller alterations in type I fibers (from 49% to 40%) and MHC I composition (from 39% to 25%), while fiber cross-sectional area was similar to baseline levels for type I, type IIA and type IIX fibers (-3%, -8%, and -4%, respectively). In conclusion, electrical stimulation training can largely prevent the adverse effects of a spinal cord injury upon paralyzed human skeletal muscle if applied soon after the injury.

The effects of sprint training on muscle metabolism and ion regulation during intense exercise remain controversial. We employed a rigorous methodological approach, contrasting these responses during exercise to exhaustion and during identical work before and after training. Seven untrained men undertook 7 wk of sprint training. Subjects cycled to exhaustion at 130% pretraining peak oxygen uptake before (PreExh) and after training (PostExh), as well as performing another posttraining test identical to PreExh (PostMatch). Biopsies were taken at rest and immediately postexercise. After training in PostMatch, muscle and plasma lactate (Lac(-)) and H(+) concentrations, anaerobic ATP production rate, glycogen and ATP degradation, IMP accumulation, and peak plasma K(+) and norepinephrine concentrations were reduced (P<0.05). In PostExh, time to exhaustion was 21% greater than PreExh (P<0.001); however, muscle Lac(-) accumulation was unchanged; muscle H(+) concentration, ATP degradation, IMP accumulation, and anaerobic ATP production rate were reduced; and plasma Lac(-), norepinephrine, and H(+) concentrations were higher (P<0.05). Sprint training resulted in reduced anaerobic ATP generation during intense exercise, suggesting that aerobic metabolism was enhanced, which may allow increased time to fatigue.

This study investigated the effects of electrical stimulation (ES) leg cycle training on muscle performance and oxidative capacity in individuals with severe disuse atrophy following spinal cord injury (n=6). ES-cycling comprised 3 sessions per week, at 30-min per session, over 10 weeks using a commercial recumbent cycle ergometer. Total work during a graded incremental ES-cycling test increased from 51.8 ± 39.3kJ to 112.9 ± 33.5kJ(p<.05). Oxidative capacity of the trained muscles demonstrated an augmented citrate synthase activity from 6.9 ± 1.4 mU·mg-1 protein to 16.0 ± 3.1 mU·mg-1 protein (p<.05). Serial sections of muscle biopsies from the r. vastus lateralis taken before and after ES training were stained using standard histochemical stains for the determination of fibre type composition and capillary density. (*p<.05)Table These data suggest that severely atrophied leg muscles in individuals with paraplegia have the ability to improve total work performance concomitant with an increase in oxidative capacity, improved microcirculation and an overall alteration of fibre type from IIB→IIA→IIC→I, after ES-induced cycle training.

Conference Abstract| January 01 1994 Effects of Neuromuscular Electrical Stimulation upon Performance and Fibre Type Composition of Paralysed Muscle RM Crameri; RM Crameri 1Dept. of Biological Sciences, The University of Sydney, Australia Search for other works by this author on: This Site PubMed Google Scholar GM Davis; GM Davis 1Dept. of Biological Sciences, The University of Sydney, Australia Search for other works by this author on: This Site PubMed Google Scholar MJ McKenna; MJ McKenna #Dept. of Physical Education and Recreation, Victorian University of Technology, Victoria, Australia Search for other works by this author on: This Site PubMed Google Scholar M Climstein; M Climstein 1Dept. of Biological Sciences, The University of Sydney, Australia Search for other works by this author on: This Site PubMed Google Scholar JR Sutton JR Sutton 1Dept. of Biological Sciences, The University of Sydney, Australia Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1994) 87 (s1): 11–12. https://doi.org/10.1042/cs087s011a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation RM Crameri, GM Davis, MJ McKenna, M Climstein, JR Sutton; Effects of Neuromuscular Electrical Stimulation upon Performance and Fibre Type Composition of Paralysed Muscle. Clin Sci (Lond) 1 January 1994; 87 (s1): 11–12. doi: https://doi.org/10.1042/cs087s011a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search nav search search input Search input auto suggest search filter All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1994 The Biochemical Society and the Medical Research Society1994 Article PDF first page preview Close Modal You do not currently have access to this content.