Article

Is Postexercise Muscle Soreness a Valid Indicator of Muscular Adaptations?

Authors:
To read the full-text of this research, you can request a copy directly from the author.

Abstract

DELAYED ONSET MUSCLE SORENESS (DOMS) IS A COMMON SIDE EFFECT OF PHYSICAL ACTIVITY, PARTICULARLY OF A VIGOROUS NATURE. MANY EXERCISERS WHO REGULARLY PERFORM RESISTANCE TRAINING CONSIDER DOMS TO BE ONE OF THE BEST INDICATORS OF TRAINING EFFECTIVENESS, WITH SOME RELYING UPON THIS SOURCE AS A PRIMARY GAUGE. THIS ARTICLE DISCUSSES THE RELEVANCE OF USING DOMS TO ASSESS WORKOUT QUALITY.

No full-text available

Request Full-text Paper PDF

To read the full-text of this research,
you can request a copy directly from the author.

... The treasurer of the Victorian Rowing Association, Walter B. House, had already provided a good basis for discussion with a five-page letter. 56 The second commission, which initially attracted only 17 delegates, was concerned with the possibility of reintroducing of the Olympic Games. In addition Coubertin wanted to clarify two more points, which he had added to the programme in May. ...
... У першій, під головуванням президента Гоночного Клубу де Франс Мішеля Гондінета, обговорювалася проблема аматорства. Скарбник Вікторіанської асоціації веслування Уолтер Б. Хаус, вже дав глибоке обґрунтування для обговорення в листі з п'яти сторінок [56]. ...
... Значение EIMD в формировании мышечной гипертрофии при физических нагрузках. В современных работах отмечается, что EIMD и DOMS возникают в результате выполнения непривычных или неадекватно интенсивных в данный момент времени (не соответствующих существующим адаптационным возможностям организма спортсмена) физических нагрузок, а их выраженность модулируется типом, интенсивностью и продолжительностью упражнений [55,56]. Многие спортсмены и тренеры, к сожалению, продолжают считать DOMS хорошим индикатором эффективности тренировок и показателем будущего позитивного ремоделирования скелетной мускулатуры. ...
Article
Full-text available
Objective. The article is aimed to define the content and the components of e-learning system in Olympic education based on the generalization of international experience of applying modern information and communication technologies at the Centers for Olympic studies and education. Methods: Theoretical analysis and analytical review of literature, materials of the Internet, web-sites of the Olympic study centers, system analysis, questionnaires, SWOT-analysis, methods of mathematical statistics. Results: The content, organizational structure and the impact of external and internal factors of the informational-educational environment of the distance learning in the Olympic studies center were determined to reveal the effectiveness of the implementation of distance learning technologies into the Olympic education system. Conclusions. Results of the research showed that proposed module of distance education ‘Olympic Legacy’ in the International centre for Olympic studies and education at the Olympic Educational and Scientific Institute of National University of Ukraine on Physical Education and Sports should be considered as an instrument for raising the level of professional education in the field of physical culture and sports. Keywords: distance learning, Olympic education, center for Olympic research and education.
... However, lengthening contractions, particularly when high forces are generated, precipitate temporary exercise-induced muscle damage (EIMD) that can last for several days after the initial bout [7]. This EIMD manifests as a reduction in neuromuscular function, reduced range of motion, increased muscle soreness, limb swelling and the elevation of intramuscular proteins in blood [21,25]. These signs and symptoms impair muscle function and inhibit the potential to engage in high intensity exercise on subsequent days, which is often required by athletic populations. ...
... Excess concentration of lactic acid; Local spasm of motor units [6,25]. ...
... For example, reduction in whole body protein breakdown following resistance training sessions has been demonstrated by the consumption of a meal high in protein [2]. Exercise-induced muscle damage that results in muscle soreness, reduces the ability to train and is potentially detrimental for the performance of a strength athlete [3]. Additionally, enhanced recovery is associated with a lower level of serum muscle damage and inflammation markers, such as creatine kinase and tumor necrosis factor alpha (TNF-α; [4][5][6]). ...
... Minimising nutrient deprivation pre-exercise, and acute refeeding post exercise may therefore be required for maximal recovery gains (particularly when training frequency is considered). A possible reason why a recent meta-analysis [3] on this subject did not find any beneficial effect of nutrient timing is that the majority of included studies were performed on untrained individuals. The anabolic 'window' for untrained individuals may be prolonged for >2 days following resistance exercise in contrast to strength-trained individuals [1]. ...
Article
Full-text available
Background Dietary protein intakes up to 2.9 g.kg−1.d−1 and protein consumption before and after resistance training may enhance recovery, resulting in hypertrophy and strength gains. However, it remains unclear whether protein quantity or nutrient timing is central to positive adaptations. This study investigated the effect of total dietary protein content, whilst controlling for protein timing, on recovery in resistance trainees. Methods Fourteen resistance-trained individuals underwent two 10-day isocaloric dietary regimes with a protein content of 1.8 g.kg−1.d−1 (PROMOD) or 2.9 g.kg−1.d−1 (PROHIGH) in a randomised, counterbalanced, crossover design. On days 8–10 (T1-T3), participants undertook resistance exercise under controlled conditions, performing 3 sets of squat, bench press and bent-over rows at 80% 1 repetition maximum until volitional exhaustion. Additionally, participants consumed a 0.4 g.kg−1 whey protein concentrate/isolate mix 30 min before and after exercise sessions to standardise protein timing specific to training. Recovery was assessed via daily repetition performance, muscle soreness, bioelectrical impedance phase angle, plasma creatine kinase (CK) and tumor necrosis factor-α (TNF-α). ResultsNo significant differences were reported between conditions for any of the performance repetition count variables (p > 0.05). However, within PROMOD only, squat performance total repetition count was significantly lower at T3 (19.7 ± 6.8) compared to T1 (23.0 ± 7.5; p = 0.006). Pre and post-exercise CK concentrations significantly increased across test days (p ≤ 0.003), although no differences were reported between conditions. No differences for TNF-α or muscle soreness were reported between dietary conditions. Phase angle was significantly greater at T3 for PROHIGH (8.26 ± 0.82°) compared with PROMOD (8.08 ± 0.80°; p = 0.012). Conclusions When energy intake and peri-exercise protein intake was controlled for, a short term PROHIGH diet did not improve markers of muscle damage or soreness in comparison to a PROMOD approach following repeated days of intensive training. Whilst it is therefore likely that moderate protein intakes (1.8 g.kg−1.d−1) may be sufficient for resistance-trained individuals, it is noteworthy that both lower body exercise performance and bioelectrical phase angle were maintained with PROHIGH. Longer term interventions are warranted to determine whether PROMOD intakes are sufficient during prolonged training periods or when extensive exercise (e.g. training twice daily) is undertaken.
... Reports of pain were similar to those experienced in people who had not previously been riding horses and required no medical intervention. Schoenfeld & Contreras (2013) reported that muscle soreness is common following a novel physical activity. None of our participants had engaged in THR before the study nor had they been riding horses. ...
Article
Posttraumatic stress disorder commonly occurs among U.S. military veterans. Therapeutic horseback riding (THR) has emerged as an adjunct therapy. We explored 20 veterans’ perceived benefits, drawbacks and views of a 6-week THR program. Participants had confirmed diagnoses of posttraumatic stress disorder, traumatic brain injury, or both. Veterans rode the same horse weekly, the same day, at the same time. Data were collected as part of a randomized clinical trial testing the effects of THR on Post-Traumatic Stress Disorder. Veterans responded to an open-ended questionnaire. Content analysis was used for data analysis. Benefits were “Connection to the Horse,” “Relaxing,” “180 Degree Change,” and “Meeting New People.” Drawbacks were “None,” “Struggle to Get There,” “Pain,” “Too Short,” and “It is Structured.” Overall perceptions were “I Absolutely Loved It,” “Feel Again,” “The Horse,” “The People,” and “No Worries.” Participants viewed THR as positive. Findings may elucidate why THR may be clinically beneficial.
... As dores surgidas de diferentes tipos de periodização de treinamentos, geralmente estão presentes nas pré-temporadas, onde a intensidade e volume de trabalho são maiores, proporcionando um suporte necessário para as competições futuras. Outro fator causal da dor, é ocasionado por uma lesão que mudará completamente o cotidiano do atleta, afastando-o dos treinamentos e competições, para viver um período em um ambiente voltado para a reabilitação (RUBIO, 2007;SCHOENFELD, 2013;HENRIQUES, 2015). ...
Article
O futebol é o esporte mais praticado no mundo e, paralelamente à expansão desta atividade, cresceram também as lesões traumáticas, do sistema músculo esquelético, uma vez que, com a modernização evoluiu principalmente na questão física, caracterizada por mudanças rápidas de direção, aceleração, desaceleração, resistência, força, agilidade, flexibilidade e pelo contato físico entre os praticantes. O objetivo deste trabalho foi caracterizar os tipos e quantidade de lesões de atletas de futebol profissional de uma equipe do interior do Estado de São Paulo no período de de 2009 à 2015. Foi realizado um levantamento dos tipos e número de lesões dos atletas por meio de avaliação funcional do fisioterapeuta da referida equipe e análise dos resultados dos exames de diagnóstico por imagem. Os resultados apontam um total de 201 lesões: muscular (64%), joelho (18%), tornozelo/pé (8%), ombro/punho/mão/coluna (2%) e face/costela/púbis/perna (1%). Em relação ao período estudado observou-se diminuição das lesões musculares da ordem de 8%. Quanto ao total de lesões ocorreu pequeno aumento em 2013 e um decréscimo de 22% nas temporadas de 2014 e 2015. Estes resultados indicam que as lesões musculares predominam em relação às demais corroborando com a evolução do futebol no que se refere ao aumento do contato e exigência física dos atletas nos treinos e jogos. Entretanto, constatou-se que as lesões individuais e coletiva da equipe diminuíram em cada temporada à medida que o clube investiu na estrutura clínica e física para prevenção e reabilitação deste atletas.
... DOMS becomes evident about 6-8 hours after an intense exercise bout and peaks at approximately 24-72 hours post-exercise [77]. The DOMS pattern of the subject is in agreement with the literature, but the magnitude was much lower. ...
Article
Full-text available
Increases in strength and muscle mass can be achieved with weight training and adequate recovery (including nutrition and sleep). The time course of recovery and adaptation (super-compensation) for different number of sets has not been adequately investigated in the literature. A 40-year-old well-trained male exercised the chest with (a) 3 sets of bench press, (b) 5 sets of bench press, (c) 5 sets of bench press and 4 sets of dips, all to momentary concentric muscular failure during a 6 months body split program. The recovery was assessed by comparing the number of repetitions of the first bench press set to the previous training session. The results showed that with 3 and 5 sets to failure adaptation (+1 repetition) took place after 5 days. 9 sets needed 7 days for recovery and no adaptation took place. The adaptation was faster when exercising the chest without training the back and/or legs, indicating that Selye's adaptation energy (resources potential) might be applicable to weight training as well. Delayed onset muscle soreness (DOMS) and motivation (mood) were found to be useful indexes of recovery. Implications on training volume and frequency and how the findings can be applied in practice are discussed.
... However dynamic strength tests could induce additional fatigue (Halson, 2014). Another option used by coaches is to assess recovery through perceived pain, like delayed onset muscle soreness (DOMS), which is widely used to monitor fatigue and predict cellular damage (Schoenfeld & Contreras, 2013). ...
Article
Full-text available
Here we demonstrated that a single resistance exercise session causes muscle damage, delayed onset muscle soreness (DOMS), higher creatine kinase (CK) and lactate dehydrogenase (LDH) activity, and increased IL-6 concentration without changes in muscle strength. Sixteen healthy untrained subjects performed five exercises consisting of three sets of 10 maximum repetitions for each exercise and 1 minute rest period between sets and exercises. Blood samples were taken after 30 minutes, 24, 48 and 72 hours and before exercise. Muscular performance was assessed by maximum isometric strength (MIS) before, 24h, 48h and 72h exercise session. We have concluded that the single resistance exercise session, performed on this study, led to muscle damage and this variable cannot be evaluated through maximal isometric strength. Among those markers, CK was more sensitive to muscle damage. This information might be important for adequate recovery between training sessions.
... However, the testing for this study was performed 48 hours after baseline measurements of calf musculature strength was established, which is when delayed onset muscle sorness can peak, possibly skewing their results (Schoenfeld & Contreras, 2013). While PCr recovery rates are important for recovery from bouts of anaerobic work, muscle reoxygenation rates are another important factor in recovery (Tomlin & Wenger, 2001). ...
Thesis
Full-text available
There is debate if a high aerobic capacity will improve recovery from repeated bouts of sprinting, which primarily taxes the anaerobic energy systems. The relationship between aerobic capacity and repeat sprint ability in ice hockey players is not well established; moreover, the relationships that have been examined involved off-ice testing protocols, which lack specificity to the ice hockey. Purpose: The purpose of this study was to examine the relationship between on-ice aerobic capacity (VO2peak and VIIT) and repeated on-ice sprint ability (RISA) via percentage of power output decrement (%DPO), and other measurements of on-ice power output (OPO). Methods: 11 male professional ice hockey players, recruited from an American Hockey League team, participated in two maximal effort on-ice tests. Aerobic capacity was tested via the 30-15 Intermittent Ice Test. Gas exchange was measured directly measured via an Oxycon portable O2 analyzer in four of the participants. OPO was measured via the Repeat Ice Skating Test. The relationship between these variables for nine of the participants was then analyzed via Pearson’s correlational testing. Results: There was no significant relationship between VIIT or VO2peak to %DPO (r =-.036 and .197 respectively; p > .05) or any other measurement of RISA. Discussion: The results from this study suggest that aerobic capacity was not related to RISA. While the results were not statistically significant, likely due to a small sample size, the effect size for %DPO and aerobic capacity (VIIT and VO2peak) was small, indicating that the relationship was nearly negligible. Elite level ice hockey players may not have a better RISA resultant from a higher aerobic capacity.
Article
Full-text available
Background: Due to the lack of consensus definition of running-related injuries, the prevalence and incidence of running-related injuries had been reported to vary between 19% and 92%. Moreover, the epidemiology of running-related injuries in Asian populations has been rarely investigated. The purpose of this study was to use the consensus definition of running related injuries and investigate the epidemiology of running-related injuries in a Korean population. Methods: Using the cross-sectional design, an online survey was circulated among various running communities in Korea. The questionnaire contained information on the presence and location of pain attributed to running, demographic characteristics, weekly running mileage, participation in high-intensity training, running pace, the longest running event participated, the type of shoes, foot strike, the reason for running, and exercise experience prior to running. Results: Among 1046 runners (male = 624, female = 422) who responded, 94.7% experienced pain while running, but only 37% were categorized as having running-related injuries. Themost common site of injury was the knee followed by the ankle. Exercise experience prior to running (OR = 1.57 95% CI: 1.13 - 2.21), setting specific running goals (OR = 1.57 95% CI:1.08 - 2.27), increases in weekly running mileage (p = 0.03), and the longest running event participated (p = 0.01) were associated with significant increases in running-related injuries. Conclusions: To avoid running-related injuries, runners should be careful when increasing weekly mileage. Moreover, runners with previous exercise experience may need to approach running more cautiously. Setting goals and pursuing longer-distance running events may be motivating, but at the same time, can increase the risk of running-related injuries.
Article
The aim of this study was compare changes in upper body muscle strength and size in trained men performing resistance training (RT) programs involving multi-joint plus single-joint (MJ+SJ) or only multi-joint (MJ) exercises. Twenty young men with at least two years of experience in RT were randomized in two groups: MJ+SJ (n = 10, 27.7 + 6.6 years) and MJ (n = 10, 29.4 + 4.6 years). Both groups trained for 8 weeks following a linear periodization model. Measures of elbow flexors and extensors 1RM, flexed arm circumference (FAC) and arm muscle circumference (AMC) were taken pre and post training period. Both groups significantly increased 1RM for elbow flexion (4.99 and 6.42% for MJ and MJ+SJ, respectively), extension (10.60 vs 9.79%, for MJ and MJ+SJ, respectively), FAC (1.72 vs 1.45%, for MJ and MJ+SJ, respectively) and AMC (1.33 vs 3.17% for MJ and MJ+SJ, respectively). Comparison between groups revealed no significant difference in any variable. In conclusion, eight weeks of RT involving MJ or MJ+SJ resulted in similar alterations in muscle strength and size in trained participants. Therefore, the addition of SJ exercises to a RT program involving MJ exercises does not seem to promote additional benefits to trained men suggesting MJ only RT to be a time efficient approach.
Article
Full-text available
Eccentric exercise continues to receive attention as a productive means of exercise. Coupled with this has been the heightened study of the damage that occurs in early stages of exposure to eccentric exercise. This is commonly referred to as delayed onset muscle soreness (DOMS). To date, a sound and consistent treatment for DOMS has not been established. Although multiple practices exist for the treatment of DOMS, few have scientific support. Suggested treatments for DOMS are numerous and include pharmaceuticals, herbal remedies, stretching, massage, nutritional supplements, and many more. DOMS is particularly prevalent in resistance training; hence, this article may be of particular interest to the coach, trainer, or physical therapist to aid in selection of efficient treatments. First, we briefly review eccentric exercise and its characteristics and then proceed to a scientific and systematic overview and evaluation of treatments for DOMS. We have classified treatments into 3 sections, namely, pharmacological, conventional rehabilitation approaches, and a third section that collectively evaluates multiple additional practiced treatments. Literature that addresses most directly the question regarding the effectiveness of a particular treatment has been selected. The reader will note that selected treatments such as anti-inflammatory drugs and antioxidants appear to have a potential in the treatment of DOMS. Other conventional approaches, such as massage, ultrasound, and stretching appear less promising.
Article
Full-text available
TARGETED HIP EXTENSION EXERCISES ARE OFTEN PERFORMED TO DEVELOP STRENGTH, POWER, AND ENDURANCE IN THE HIP EXTENSORS. ALTHOUGH THESE EXERCISES CAN POSSESS SIMILAR MOVEMENT PATTERNS, BIOMECHANICALLY THE INSTANTANEOUS TORQUE AT DIFFERENT RANGES OF HIP EXTENSION VARIES DEPENDING ON BODY POSITION RELATIVE TO SPACE. FOR THESE REASONS, IT IS PROPOSED THAT: (A) HIP EXTENSION EXERCISES MIGHT TRANSFER BETTER TO SPORT ACTIONS WHERE THE REGION OF FORCE ACCENTUATION IS MOST SPECIFIC; (B) HIP EXTENSION EXERCISES MAY LEAD TO UNIQUE STRUCTURAL ADAPTATIONS; AND (C) A VARIETY OF EXERCISES MIGHT BE NECESSARY TO MAXIMIZE HIP EXTENSION STRENGTH AND POWER THROUGHOUT THE ENTIRE RANGE OF MOTION.
Article
Full-text available
Exercise-induced muscle damage is an important topic in exercise physiology. However several aspects of our understanding of how muscles respond to highly stressful exercise remain unclear In the first section of this review we address the evidence that exercise can cause muscle damage and inflammation in otherwise healthy human skeletal muscles. We approach this concept by comparing changes in muscle function (i.e., the force-generating capacity) with the degree of leucocyte accumulation in muscle following exercise. In the second section, we explore the cytokine response to 'muscle-damaging exercise', primarily eccentric exercise. We review the evidence for the notion that the degree of muscle damage is related to the magnitude of the cytokine response. In the third and final section, we look at the satellite cell response to a single bout of eccentric exercise, as well as the role of the cyclooxygenase enzymes (COX1 and 2). In summary, we propose that muscle damage as evaluated by changes in muscle function is related to leucocyte accumulation in the exercised muscles. 'Extreme' exercise protocols, encompassing unaccustomed maximal eccentric exercise across a large range of motion, generally inflict severe muscle damage, inflammation and prolonged recovery (> 1 week). By contrast, exercise resembling regular athletic training (resistance exercise and downhill running) typically causes mild muscle damage (myofibrillar disruptions) and full recovery normally occurs within a few days. Large variation in individual responses to a given exercise should, however be expected. The link between cytokine and satellite cell responses and exercise-induced muscle damage is not so clear The systemic cytokine response may be linked more closely to the metabolic demands of exercise rather than muscle damage. With the exception of IL-6, the sources of systemic cytokines following exercise remain unclear The satellite cell response to severe muscle damage is related to regeneration, whereas the biological significance of satellite cell proliferation after mild damage or non-damaging exercise remains uncertain. The COX enzymes regulate satellite cell activity, as demonstrated in animal models; however the roles of the COX enzymes in human skeletal muscle need further investigation. We suggest using the term 'muscle damage' with care. Comparisons between studies and individuals must consider changes in and recovery of muscle force-generating capacity.
Article
Full-text available
Exercise-induced muscle damage (EIMD) occurs primarily from the performance of unaccustomed exercise, and its severity is modulated by the type, intensity, and duration of training. Although concentric and isometric actions contribute to EIMD, the greatest damage to muscle tissue is seen with eccentric exercise, where muscles are forcibly lengthened. Damage can be specific to just a few macromolecules of tissue or result in large tears in the sarcolemma, basal lamina, and supportive connective tissue, and inducing injury to contractile elements and the cytoskeleton. Although EIMD can have detrimental short-term effects on markers of performance and pain, it has been hypothesized that the associated skeletal muscle inflammation and increased protein turnover are necessary for long-term hypertrophic adaptations. A theoretical basis for this belief has been proposed, whereby the structural changes associated with EIMD influence gene expression, resulting in a strengthening of the tissue and thus protection of the muscle against further injury. Other researchers, however, have questioned this hypothesis, noting that hypertrophy can occur in the relative absence of muscle damage. Therefore, the purpose of this article will be twofold: (a) to extensively review the literature and attempt to determine what, if any, role EIMD plays in promoting skeletal muscle hypertrophy and (b) to make applicable recommendations for resistance training program design.
Article
Full-text available
This study aims to review the main aspects that induce muscle damage, and to discuss the adaptations of this phenomenon, applications and limitations of this study area. Damage induced by strength training has been utilized for two purposes: 1) verification of the recovery period required between training sessions, which has a direct influence on designing exercise programs; and 2) as indication for higher training intensity, mainly in studies on the "repeated bout effect". There is some speculation about the role of muscle damage in inducing hypertrophy. However, studies demonstrate that exercise-induced muscle damage may not be a consistent indicator of higher chronic hypertrophic response, because hypertrophy also occurs in training strategies with very low mechanical overloads. In addition, aerobic exercise, also induces muscle damage, exhibits no hypertrophic response after training. The remodeling process induced bay muscle damage promotes alterations to strength x length relationship for stretched positions, indicating an increased number of sarcomeres in series, due to strength exercises. Therefore, the study on strength exercise-induced damage seems to be adequate for implementing adequate rest periods to recovery from different sessions of strength training, and not to suggest chronic hypertrophy.
Article
Full-text available
Skeletal muscle is a dynamic tissue that responds adaptively to both the nature and intensity of muscle use. This phenotypic plasticity ensures that muscle structure is linked to patterns of muscle use throughout the lifetime of an animal. The cascade of events that result in muscle restructuring - for example, in response to resistance exercise training - is often thought to be initiated by muscle damage. We designed this study to test the hypothesis that symptomatic (i.e. detectable) damage is a necessary precursor for muscle remodeling. Subjects were divided into two experimental populations: pre-trained (PT) and naive (NA). Demonstrable muscle damage was avoided in the PT group by a three-week gradual 'ramp-up' protocol. By contrast, the NA group was subjected to an initial damaging bout of exercise. Both groups participated in an eight-week high-force eccentric-cycle ergometry program (20 min, three times per week) designed to equate the total work done during training between the groups. The NA group experienced signs of damage, absent in the PT group, as indicated by greater than five times higher levels of plasma creatine kinase (CK) and self-reporting of initial perceived soreness and exertion, yet muscle size and strength gains were not different for the two groups. RT-PCR analysis revealed similar increases in levels of the growth factor IGF-1Ea mRNA in both groups. Likewise, the significant (P<0.01) increases in mean cross-sectional area (and total muscle volume) were equal in both groups. Finally, strength increases were identical for both groups (PT=25% and NA=26% improvement). The results of this study suggest that muscle rebuilding - for example, hypertrophy - can be initiated independent of any discernible damage to the muscle.
Article
Full-text available
Temporary muscle damage precipitated by downhill walking affects muscle function and potentially exposes muscle to further musculoskeletal injury. We hypothesized that the use of trekking poles would help maintain muscle function and reduce indices of muscle damage after a day's mountain trekking. Thirty-seven physically active males (n = 26) and females (n = 11) volunteered to participate and were divided into either a trekking pole (TP) or no pole (NP) group. Participants carried a day sack (5.6 ± 1.5 kg) and made the ascent and descent of the highest peak in England and Wales (Mount Snowdon). HR and RPE were recorded during the ascent and descent. Indices of muscle damage, namely, maximal voluntary contraction, muscle soreness, creatine kinase (CK), and vertical jump performance, were measured before, immediately after (except CK), and 24, 48, and 72 h after trek. HR was not different between groups, although RPE was significantly lower in TP during the ascent. The TP group showed attenuation of reductions in maximal voluntary contraction immediately after and 24 and 48 h after the trek; muscle soreness was significantly lower at 24 and 48 h after the trek, and CK was also lower at 24 h after the trek in the TP group. No differences in vertical jump were found. Trekking poles reduce RPE on mountain ascents, reduce indices of muscle damage, assist in maintaining muscle function in the days after a mountain trek, and reduce the potential for subsequent injury.
Article
Full-text available
The high forces undergone during repetitive eccentric, or lengthening, contractions place skeletal muscle under considerable stress, in particular if unaccustomed. Although muscle is highly adaptive, the responses to stress may not be optimally regulated by the body. Reactive oxygen species (ROS) are one component of the stress response that may contribute to muscle damage after eccentric exercise. Antioxidants may in turn scavenge ROS, thereby preventing or attenuating muscle damage. The antioxidant vitamins C (ascorbic acid) and E (tocopherol) are among the most commonly used sport supplements, and are often taken in large doses by athletes and other sportspersons because of their potential protective effect against muscle damage. This review assesses studies that have investigated the effects of these two antioxidants, alone or in combination, on muscle damage and oxidative stress. Studies have used a variety of supplementation strategies, with variations in dosage, timing and duration of supplementation. Although there is some evidence to show that both antioxidants can reduce indices of oxidative stress, there is little evidence to support a role for vitamin C and/or vitamin E in protecting against muscle damage. Indeed, antioxidant supplementation may actually interfere with the cellular signalling functions of ROS, thereby adversely affecting muscle performance. Furthermore, recent studies have cast doubt on the benign effects of long-term, high-dosage antioxidant supplementation. High doses of vitamin E, in particular, may increase all-cause mortality. Although some equivocation remains in the extant literature regarding the beneficial effects of antioxidant vitamin supplementation on muscle damage, there is little evidence to support such a role. Since the potential for long-term harm does exist, the casual use of high doses of antioxidants by athletes and others should perhaps be curtailed.
Article
Full-text available
Most research on muscle hypertrophy has focused on the responses of muscle cells to mechanical loading; however, a number of studies also suggest that inflammatory cells may influence muscle hypertrophy. Neutrophils and macrophages accumulate in skeletal muscle following increased mechanical loading, and we have demonstrated that macrophages are essential for hypertrophy following synergist ablation. Whether neutrophils are required remains to be determined. Non-steroidal anti-inflammatory drugs impair adaptive responses of skeletal muscle in both human and animal experiments suggesting that the routine use of such drugs could impair muscle performance. Much remains to be learned about the role of inflammatory cells in muscle hypertrophy, including the molecular signals involved in calling neutrophils and macrophages to skeletal muscle as well as those that regulate their function in muscle. In addition, although we have demonstrated that macrophages produce growth promoting factors during muscle hypertrophy, the full range of functional activities involved in muscle hypertrophy remains to be determined. Further investigation should provide insight into the intriguing hypothesis that inflammatory cells play integral roles in regulating muscle hypertrophy.
Article
Full-text available
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.
Article
Full-text available
We review cellular and molecular processes involved in injury and repair of skeletal muscle with regard to the amount and location of damage produced. Discussion is based on advances made by use of newer techniques, including immunochemistry, in situ hybridization, molecular biology, ultrastructural analysis, and cell culture. Damage and repair processes after eccentric work, stretch, overload, chronic stimulation, cold injury, and other models are discussed for cellular and molecular components. Hypertrophy or hyperplasia can occur under certain conditions. After injury, satellite cells are activated by growth factors. These cells can also be activated during fiber-type transformation, probably to provide necessary DNA content rather than to supply cells of a new lineage. Emphasis is given to myosin mRNA studied by in situ hybridization to localize subcellular distribution. Increases in mRNA concentration are found near nuclei in damaged regions and at the subcellular sites being repaired in the middle of skeletal muscle fibers or near the myotendon junction. The activation of genes for muscle regulatory factors during development is compared with their activation in regeneration and response to injury.
Article
Full-text available
Pain, stiffness, and indicators of muscle damage occur at different times after eccentric muscle action. After a single bout of maximal resisted lengthening of the elbow flexors, elbow position, pain perception, and indicators of cellular damage were measured. Immediately postexercise, a significant decrease in resting muscle length was observed that continued to 48 h. At this time, an increase in perceived muscle soreness was noted (P less than 0.05), and a biopsy of the biceps brachii revealed mast cell degranulation, separations of the extracellular matrix from myofibers, and increased plasma constituents in the extracellular space. It is proposed that myofiber disruption allows intracellular proteins to escape and extracellular proteins and ions to enter, causing swelling, whereas the disrupted extracellular matrix initiates the inflammatory response, which includes the release of mast cell granules seen at 48 h postexercise. Thus the delayed sensation of pain (soreness) after repeated eccentric muscle actions probably results from inflammation in response to extracellular matrix disruption.
Article
Full-text available
The transduction mechanism (or mechanisms) responsible for converting a mechanical load into a skeletal muscle growth response are unclear. In this study we have used a mechanically active tissue culture model of differentiated human skeletal muscle cells to investigate the relationship between mechanical load, sarcolemma wounding, fibroblast growth factor release, and skeletal muscle cell growth. Using the Flexcell Strain Unit we demonstrate that as mechanical load increases, so too does the amount of sarcolemma wounding. A similar relationship was also observed between the level of mechanical load inflicted on the cells and the amount of bFGF (FGF2) released into the surrounding medium. In addition, we demonstrate that the muscle cell growth response induced by chronic mechanical loading in culture can be inhibited by the presence of an antibody capable of neutralizing the biological activity of FGF. This study provides direct evidence that mechanically induced, sarcolemma wound-mediated FGF release is an important autocrine mechanism for transducing the stimulus of mechanical load into a skeletal muscle growth response.
Article
Full-text available
Skeletal muscle glutamine uptake via the transport system Nm is subject to rapid (t(1/2) = approximately 1 min) regulation after changes in cell volume by mechanisms that remain to be elucidated. Wortmannin (phosphatidylinositol 3-kinase inhibitor) but not rapamycin (inhibitor of p70S6 kinase activation) prevents both hypo-osmotic swelling-induced stimulation and hyperosmotic shrinkage-induced inhibition of Na+-dependent glutamine uptake in primary culture of rat skeletal muscle. G-protein inhibitors (cholera, pertussis toxins) also abolished responses of glutamine transport to cell volume changes whereas these responses were sustained in the presence of G-protein activators (MAS 7, lysophosphatidic acid). Swelling-induced activation of glutamine transport does not seem to involve release of autocrine factors because "conditioned" medium from swollen cells has no effect on previously unstimulated cells. System A amino acid transport exhibits responses to cell volume change that are opposite to those of system Nm, but these are also blocked by wortmannin. Active phosphatidylinositol 3-kinase appears to be required to enable muscle cells to exhibit rapid, volume-induced changes in amino acid transport when suitably stimulated.
Article
Full-text available
Repair and regeneration of adult skeletal muscle are mediated by satellite cells. In healthy muscle these rare mononucleate muscle precursor cells are mitotically quiescent. Upon muscle injury or degeneration, members of this self-renewing pool are activated to proliferate and then differentiate. Here we analyzed in single satellite cells the expression of a set of regulatory genes that are candidates for causal roles in satellite cell activation, maturation, and differentiation. Individual cells were identified as satellite cells and selected for analysis based on their physical association with single explanted myofibers or their position beneath the basal lamina in unperturbed muscle tissue. Using a multiplex single-cell RT-PCR assay we simultaneously monitored expression of all four MyoD family regulators of muscle determination and differentiation (MRFs) together with two candidate markers of satellite cell identity, c-met and m-cadherin. By making these measurements on large numbers of individual cells during the time course of satellite cell activation, we were able to define which expression states (possible combinations of the six genes) were represented and to specify how the representation of each state changed with time. Activated satellite cells began to express either MyoD or myf5 first among the MRFs; most cells then expressed both myf-5 and MyoD simultaneously; myogenin came on later in cells expressing both MyoD and myf5; and many cells ultimately expressed all four MRFs simultaneously. The results for fiber-associated satellite cells from either predominantly fast or slow muscles were indistinguishable from each other. The c-met receptor tyrosine kinase was also monitored because it is a candidate for mediating activation of quiescent satellite cells (Allen et al., 1995) and because it might also be a candidate molecular marker for satellite cells. A significant difficulty in studying mouse satellite cells has been the absence of molecular markers that could identify them in the quiescent state before expression of MRFs or desmin and distinguish them from fibroblasts. We show here that c-met receptor is present beneath the basal lamina on presumptive satellite cells in intact muscle and that c-met mRNA and protein are expressed by all myofiber-associated satellite cells from the time of explant through the course of activation, proliferation, and differentiation. c-met was not detected in muscle-derived fibroblasts or in other mononucleate cells from healthy muscle explants. When compared directly with m-cadherin, which has previously been suggested as a marker for quiescent satellite cells, m-cadherin mRNA was detected only in a small subset of satellite cells at early times after myofiber explant. However, at late times following activation (by 96 hr in this fiber culture system), c-met and m-cadherin were uniformly coexpressed. From the individual satellite cell expression types observed, a model of the satellite cell population at rest and during the time course of activation was generated.
Article
Full-text available
Hormonal and inflammatory responses to low-intensity resistance exercise with vascular occlusion were studied. Subjects (n = 6) performed bilateral leg extension exercise in the seated position, with the proximal end of their thigh compressed at 214 +/- 7.7 (SE) mmHg throughout the session of exercise by means of a pressure tourniquet. Mean intensity and quantity of the exercise were 20% of 1 repetition maximum and 14 repetitions x 5 sets, respectively. In each set, the subjects repeated the movement until exhaustion. Plasma concentrations of growth hormone (GH), norepinephrine (NE), lacate (La), lipid peroxide (LP), interleukin-6 (IL-6), and activity of creatine phosphokinase (CPK) were measured before and after the exercise was finished and the tourniquet was released. Concentrations of GH, NE, and La consistently showed marked, transient increases after the exercise with occlusion, whereas they did not change a great deal after the exercise without occlusion (control) done at the same intensity and quantity. Notably, concentration of GH reached a level approximately 290 times as high as that of the resting level 15 min after the exercise. IL-6 concentration showed a much more gradual increase and was maintained at a slightly higher level than in the control even 24 h after exercise. Concentrations of LP and CPK showed no significant change. The results suggest that extremely light resistance exercise combined with occlusion greatly stimulates the secretion of GH through regional accumulation of metabolites without considerable tissue damage.
Article
Full-text available
In eccentric exercise the contracting muscle is forcibly lengthened; in concentric exercise it shortens. While concentric contractions initiate movements, eccentric contractions slow or stop them. A unique feature of eccentric exercise is that untrained subjects become stiff and sore the day afterwards because of damage to muscle fibres. This review considers two possible initial events as responsible for the subsequent damage, damage to the excitation-contraction coupling system and disruption at the level of the sarcomeres. Other changes seen after eccentric exercise, a fall in active tension, shift in optimum length for active tension, and rise in passive tension, are seen, on balance, to favour sarcomere disruption as the starting point for the damage. As well as damage to muscle fibres there is evidence of disturbance of muscle sense organs and of proprioception. A second period of exercise, a week after the first, produces much less damage. This is the result of an adaptation process. One proposed mechanism for the adaptation is an increase in sarcomere number in muscle fibres. This leads to a secondary shift in the muscle's optimum length for active tension. The ability of muscle to rapidly adapt following the damage from eccentric exercise raises the possibility of clinical applications of mild eccentric exercise, such as for protecting a muscle against more major injuries.
Article
Full-text available
High force eccentric muscle contractions can result in delayed onset muscle soreness (DOMS), prolonged loss of muscle strength, decreased range of motion, muscle swelling and an increase of muscle proteins in the blood. At the ultrastructural level Z-line streaming and myofibrillar disruptions have been taken as evidence for muscle damage. In animal models of eccentric exercise-induced injury, disruption of the cytoskeleton and the sarcolemma of muscle fibres occurs within the first hour after the exercise, since a rapid loss of staining of desmin, a cytoskeletal protein, and the presence of fibronectin, a plasma and extracellular protein, are observed within the muscle fibres. In the present study, biopsies from subjects who had performed different eccentric exercises and had developed DOMS were examined. Our aim was to determine whether eccentric exercise leading to DOMS causes sarcolemmal disruption and loss of desmin in humans. Our study shows that even though the subjects had DOMS, muscle fibres had neither lost staining for desmin nor contained plasma fibronectin. This study therefore does not support previous conclusions that there is muscle fibre degeneration and necrosis in human skeletal muscle after eccentric exercise leading to DOMS. Our data are in agreement with the recent findings that there is no inflammatory response in skeletal muscle following eccentric exercise in humans. In combination, these findings should stimulate the search for other mechanisms explaining the functional and structural alterations in human skeletal muscle after eccentric exercise.
Article
Full-text available
The repeated bout effect refers to the adaptation whereby a single bout of eccentric exercise protects against muscle damage from subsequent eccentric bouts. While the mechanism for this adaptation is poorly understood there have been significant recent advances in the understanding of this phenomenon. The purpose of this review is to provide an update on previously proposed theories and address new theories that have been advanced. The potential adaptations have been categorized as neural, mechanical and cellular. There is some evidence to suggest that the repeated bout effect is associated with a shift toward greater recruitment of slow twitch motor units. However, the repeated bout effect has been demonstrated with electrically stimulated contractions, indicating that a peripheral, non-neural adaptation predominates. With respect to mechanical adaptations there is evidence that both dynamic and passive muscle stiffness increase with eccentric training but there are no studies on passive or dynamic stiffness adaptations to a single eccentric bout. The role of the cytoskeleton in regulating dynamic stiffness is a possible area for future research. With respect to cellular adaptations there is evidence of longitudinal addition of sarcomeres and adaptations in the inflammatory response following an initial bout of eccentric exercise. Addition of sarcomeres is thought to reduce sarcomere strain during eccentric contractions thereby avoiding sarcomere disruption. Inflammatory adaptations are thought to limit the proliferation of damage that typically occurs in the days following eccentric exercise. In conclusion, there have been significant advances in the understanding of the repeated bout effect, however, a unified theory explaining the mechanism or mechanisms for this protective adaptation remains elusive.
Article
Full-text available
This study examined the fatigue effects of stretch-shortening cycle exercises of different intensity and duration on stretch reflex EMG and mechanical responses of the triceps surae muscle. Twelve subjects performed either a 10-km run ( n=6) or short but exhaustive rebound exercise on a sledge apparatus ( n=6). Passive reflex tests (mechanically induced ankle dorsiflexions) were examined before, after as well as 2 h, 2 and 7 days after exercise. Mechanical reflex responses were recorded from the ergometer torque signal. An acute contractile failure was observed as large reductions in twitch responses, especially in the sledge subgroup who showed high post-exercise peak blood lactate and an increased EMG/torque ratio. Independently of the exercise, the delayed fatigue analysis revealed strong relationships between the reflex-induced EMG and mechanical changes. In addition to muscle damage, these results may be explained by inhibitory effects via the sensitisation of small muscle afferents particularly during the exercise-induced delayed recovery process.
Article
Full-text available
Modified muscle use or injury can produce a stereotypic inflammatory response in which neutrophils rapidly invade, followed by macrophages. This inflammatory response coincides with muscle repair, regeneration, and growth, which involve activation and proliferation of satellite cells, followed by their terminal differentiation. Recent investigations have begun to explore the relationship between inflammatory cell functions and skeletal muscle injury and repair by using genetically modified animal models, antibody depletions of specific inflammatory cell populations, or expression profiling of inflamed muscle after injury. These studies have contributed to a complex picture in which inflammatory cells promote both injury and repair, through the combined actions of free radicals, growth factors, and chemokines. In this review, recent discoveries concerning the interactions between skeletal muscle and inflammatory cells are presented. New findings clearly show a role for neutrophils in promoting muscle damage soon after muscle injury or modified use. No direct evidence is yet available to show that neutrophils play a beneficial role in muscle repair or regeneration. Macrophages have also been shown capable of promoting muscle damage in vivo and in vitro through the release of free radicals, although other findings indicate that they may also play a role in muscle repair and regeneration through growth factors and cytokine-mediated signaling. However, this role for macrophages in muscle regeneration is still not definitive; other cells present in muscle can also produce the potentially regenerative factors, and it remains to be proven whether macrophage-derived factors are essential for muscle repair or regeneration in vivo. New evidence also shows that muscle cells can release positive and negative regulators of inflammatory cell invasion, and thereby play an active role in modulating the inflammatory process. In particular, muscle-derived nitric oxide can inhibit inflammatory cell invasion of healthy muscle and protect muscle from lysis by inflammatory cells in vivo and in vitro. On the other hand, muscle-derived cytokines can signal for inflammatory cell invasion, at least in vitro. The immediate challenge for advancing our current understanding of the relationships between muscle and inflammatory cells during muscle injury and repair is to place what has been learned in vitro into the complex and dynamic in vivo environment.
Article
The objectives of this review are to delineate muscle damage induced in resistance training, discuss how muscle damage is associated with increases in strength and/or muscle cross-sectional area, and clarify whether “pain” is necessary for “gain” in muscle function and muscle volume in resistance training. Resistance training induces muscle damage, especially in the initial phase of training when unaccustomed eccentric actions are performed. Muscle damage is best indicated by loss of muscle strength and range of motion, and delayed onset muscle soreness does not necessarily reflect the magnitude of muscle damage. Resistance training employing eccentric biased exercises has potential for increasing not only eccentric strength but also isometric strength, and seems to be superior to exercise based solely on concentric actions. Since muscle damage and soreness are induced to a greater extent in eccentric muscle actions than with isometric or concentric actions, it is believed that muscle damage is necessary for size and strength gain. However, it appears that muscles become less susceptible to muscle damage as training progresses. We concluded that muscle damage and/or muscle soreness are not necessarily indispensable for exercise-induced muscle adaptation.
Article
Currently no research has investigated the relationship between muscle damage, hormonal status, and perceived recovery scale (PRS). Therefore, the purpose of this study was to determine the effects of a high volume training session on PRS and to determine the relationship between levels of testosterone, cortisol and creatine kinase (CK) and PRS. Thirty-five trained subjects (21.3 ± 1.9 years) were recruited. All subjects participated in a high volume resistance training session consisting of 3 sets of full squats, bench press, deadlifts, pullups, dips, bent over rows, shoulder press, and barbell curls and extensions. Pre and post PRS scale measurements (0-10), soreness, creatine kinase (CK), cortisol, and testosterone were measured prior to and 48 hours following training. PRS declined from 8.6 ± 2.3 to 4.2 ± 1.85 (p < 0.05). Leg, chest, and arm soreness increased from pre to post exercise. Creatine kinase significantly increased from pre to post workout (189.4 ± 100.2 to 512 ± 222.7 U/L). Cortisol, testosterone, and free testosterone did not change. There was an inverse relationship between CK and PRS (r=0.58, p < 0.05). When muscle damage was low prior to training, cortisol, free and total testosterone were not correlated to PRS. However, when damage peaked at 48 hours post exercise, free, but not total testosterone, showed a low, direct relationship with PRS (r=0.2, p < 0.05). High volume resistance exercise lowers PRS scores. These changes are partly explained by a rise in serum indices of muscle damage. Moreover, free testosterone appears to have a positive relationship to PRS.
Article
The current study examined the prospective relationship between pain-related fear and altered motor behavior, as well as perceived interference, among 51 healthy participants following induction of delayed-onset muscle soreness (DOMS) to the trunk extensor muscles. Healthy participants without history of back pain completed standardized reaches to high and low targets at self-paced and rapid speeds before and after induction of acute low back pain using a DOMS paradigm. Pain-related fear was assessed prior to DOMS induction. Three-dimensional joint motions of the thoracic spine, lumbar spine, and hip were recorded using an electromagnetic tracking device. DOMS-induced differences between high- and low-fear participants were observed for lumbar spine flexion, but not for thoracic or hip flexion. Pain-related fear scores were not predictive of lumbar flexion during baseline, but predicted reduced lumbar flexion during self- and fast-paced trials to low target locations once DOMS was induced. Pain-related fear was likewise predictive of perceived interference in life activities following DOMS induction. The findings suggest that initially pain-free individuals with high pain-related fear adopt avoidant spinal strategies during common reaching movements shortly after injury is sustained, which may comprise a risk factor for future pain and disability.
Article
The purpose of this study was to examine the time course of adaptation through 20 days of eccentric training and 5 days of detraining. A total of 22 untrained subjects trained one arm every 2nd day for 20 days. Subjects performed maximal isokinetic eccentric biceps brachii training at 90 degrees /s (six sets of eight reps). Muscle thickness (reported in cm) via ultrasound, strength (reported in Nm) and muscle activation (electromyography) were measured before, during, and after training (nine time points). Strength in the trained arm decreased after 8 days of training (65.6 +/- 4.1 to 57.5 +/- 3.5; p < 0.05) and remained decreased throughout the study. Agonist muscle activation amplitude of the trained arm increased after 14 days of training (p < 0.05) and remained elevated throughout the study. Antagonist muscle activation decreased after 20 days of training (p < 0.05). Muscle thickness increased after 8 days of training (3.66 +/- 0.11 to 3.90 +/- 0.12; p < 0.05) and remained above baseline until the end of training (3.97 +/- 0.12). After 5 days of detraining, muscle thickness decreased (3.97 +/- 0.12 vs. 3.85 +/- 0.11; p < 0.05), but remained higher than baseline (p < 0.05). Muscle thickness did not change significantly in the untrained arm at any time point. In conclusion, the early increase in biceps brachii muscle thickness coupled with a significant decrease in strength is an indicator of muscle damage leading to swelling and impaired muscle function. The persistent decrease in strength, despite an increase in muscle activation, suggests that the recovery interval was inadequate to allow complete repair of muscle damage. Intense eccentric training performed every 2nd day leads to a prolonged impairment of muscle strength in previously untrained individuals.
Article
Exercise-induced muscle damage (EIMD) is a popular area of investigation; however, many of the existing methods to induce muscle damage lack specificity to a sporting context. The aim of this investigation was to examine the extent of damage precipitated from a sport-specific, repeated sprint protocol and therefore elucidate its suitability as an appropriate model to investigate EIMD. Twenty male subjects (age 22 +/- 2 years, height 178 +/- 6.6 cm, mass 84.6 +/- 13.6 kg in mean +/- SD) volunteered. Following a standardized warm-up, they conducted 15 x 30 m sprints with a 10-m deceleration zone in which subjects were required to come to a complete halt; each repetition was separated by 60 seconds of rest. Maximum isometric force (MVC), serum creatine kinase activity (CK), muscle soreness (DOMS), and limb girth were taken immediately before and at 24 hours, 48 hours, and 72 hours after exercise to elucidate the extent of muscle damage. There were significant time effects for all dependent variables. CK and DOMS were significantly elevated above baseline for 72 hours postexercise (p < 0.05), whereas MVC was significantly lower and limb girth remained significantly elevated for 48 hours postexercise (p < 0.05). These data show that the repeated sprint protocol with a rapid deceleration precipitates significant levels of damage in the days following the exercise bout and therefore may be used as a suitable alternative to examine the damage response from a sport specific repeated sprint mode of exercise.
Article
A role of the immune system in muscular adaptation to physical exercise has been suggested but data from controlled human studies are scarce. The present study investigated immunological events in human blood and skeletal muscle by immunohistochemistry and flow cytometry after eccentric cycling exercise and multiple biopsies.Immunohistochemical detection of neutrophil- (CD11b, CD15), macrophage- (CD163), satellite cell- (CD56) and IL-1β-specific antigens increased similarly in human skeletal muscle after eccentric cycling exercise together with multiple muscle biopsies, or multiple biopsies only.Changes in immunological variables in blood and muscle were related, and monocytes and natural killer (NK) cells appeared to have governing functions over immunological events in human skeletal muscle.Delayed onset muscle soreness, serum creatine kinase activity and C-reactive protein concentration were not related to leukocyte infiltration in human skeletal muscle.Eccentric cycling and/or muscle biopsies did not result in T cell infiltration in human skeletal muscle. Modes of stress other than eccentric cycling should therefore be evaluated as a myositis model in human.Based on results from the present study, and in the light of previously published data, it appears plausible that muscular adaptation to physical exercise occurs without preceding muscle inflammation. Nevertheless, leukocytes seem important for repair, regeneration and adaptation of human skeletal muscle.
Article
Skeletal muscle is an accessible adult stem-cell model in which differentiated myofibres are maintained and repaired by a self-renewing stem-cell compartment. These resident stem cells, which are known as satellite cells, lie on the surface of the muscle fibre, between the plasmalemma and overlying basal lamina. Although they are normally mitotically quiescent in adult muscle, satellite cells can be activated when needed to generate myoblasts, which eventually differentiate to provide new myonuclei for the homeostasis, hypertrophy and repair of muscle fibres, or fuse together to form new myofibres for regeneration. Satellite cells also self-renew in order to maintain a viable stem-cell pool that is able to respond to repeated demand. The study of the control of self-renewal has led to the idea that the satellite-cell pool might be heterogeneous: that is it might contain both self-renewing satellite ;stem' cells and myogenic precursors with limited replicative potential in the same anatomical location. The regulatory circuits that control satellite-cell self-renewal are beginning to be deciphered, with Pax7, and Notch and Wnt signalling being clearly implicated. This Commentary seeks to integrate these interesting new findings into the wider context of satellite-cell biology, and to highlight some of the many outstanding questions.
Article
Rhabdomyolysis and myoglobinuric acute renal failure may occur following strenuous exercise and may be more common in less physically conditioned persons. A case of moderately severe acute renal failure after the exercise involved in a routine Army Physical Fitness Test (APFT) is described. This level of exertion, which is universally applied to Army personnel, should be recognized as a potential etiology of rhabdomyolysis. Prospective studies may help define the exact risk to renal function provided by the APFT.
Article
1. The influence of three mechanical factors, force, muscle length and passive lengthening, on long-lasting changes in voluntary force generation, the force:frequency relationship and the development of tenderness has been studied in healthy human skeletal muscle. The elbow flexors were used in all studies. The effect of muscle length was also investigated in the quadriceps and adductor pollicis muscles. Eighty maximal voluntary contractions (MVCs) were performed: one contraction, lasting approximately 2 s, every 15 s. The MVC and force:frequency relationships were measured before and immediately after the exercise and, together with an assessment of tenderness, at 24 h intervals thereafter. 2. In a series of experiments designed to investigate the effects of force, eccentric (lengthening) contractions were found to cause greater fatique and delayed-onset muscle pain than either isometric or concentric (shortening) contractions. There were, however, no substantial differences between the effects of isometric and concentric contractions. Changes in MVC took 24-48 h to return to normal while the low-frequency fatigue required 3-4 days to recover. 3. Passive lengthening with a comparable number of movements over the full range had no effect on the force generation of the muscle, nor did it cause any muscle pain. 4. In the series of experiments designed to investigate the effects of length, isometric MVCs were performed at either short or long length and the muscles subsequently tested at an intermediate length. The contractions at long length resulted in greater low-frequency fatigue and pain, despite the fact that they generated less force than those at the short length. 5. The results demonstrate that there is no simple relationship between the force generated during exercise and the development of long-lasting muscle fatigue and pain. Furthermore, there is a length-dependent component in the generation of low-frequency fatigue and muscle pain.
Article
The perception of muscle soreness is probably due to the activation of free nerve endings around muscle fibers. These nerve endings serve as receptors of noxious stimuli associated with muscle damage. Modulation of soreness may take place at the peripheral receptor sites or at a central or spinal level. This multilevel modulation may explain the large intersubject variation in the perception of muscle soreness. The type of exercise that produces the greatest degree of soreness is eccentric exercise, although isometric exercise may also result in soreness. Eccentric exercise has been shown to produce muscle cellular damage and decrements in motor performance as well. Although training is considered to prevent muscle soreness, even trained individuals will become sore following a novel or unaccustomed exercise bout. Thus, training is specific to the type of exercise performed. Our laboratories have shown that the performance of a single exercise bout will have an effect on a subsequent similar bout given up to 6 weeks later. Thus, when a second bout of downhill running was given to subjects 6 weeks after the first bout, with no intervening exercise, less soreness developed, and muscle damage was estimated to be reduced. The explanation for this long-lasting prophylactic or "training effect" is currently under investigation in our laboratories.
Article
The time course and pattern of the initiation of satellite cell mitoses was studied following a crush injury of the distal third of the 30-day-old rat extensor digitorum longus, a muscle in which myofibers run the entire length of the belly. Satellite cell mitotic activity was monitored using autoradiography after injection of 3H-thymidine. Satellite cell labeling rose above control values by 15 hours post injury at the injured site and by 20 hours in the middle third or adjacent undamaged portion of the muscle. Labeling decreased in the proximal third of the muscle, so that by 25 hours post injury, a gradient of labeling was established along the muscle length. Electron microscopy (EM) quantitation showed that the reduced labeling in the proximal third resulted from a reduction in satellite cell numbers. The results suggest that mitotic activity of satellite cells after localized injury occurs mainly at or near the site of injury, but that many of the dividing cells have migrated from undamaged areas distant from the lesion site.
Article
The source of the new nuclei appearing during the growth of muscle fibers was examined in the tibialis anterior muscle of young Sherman rats (14–17 days of age) using radioautography at various intervals after a single injection of a small, non-toxic dose of 3H-thymidine (2 μCi/g body weight). Two techniques were employed: (1) labeled nuclei were detected in 1 μ thick radioautographs examined in the light microscope, and identified by simultaneous electron microscope examination of an adjacent section. The nuclei were then classified either as “true” muscle nuclei (within the plasmalemma of the fibers) or as belonging to “satellite cells” (which are mononucleated cells with scanty cytoplasm wedged between plasmalemma and basement membrane). (2) Muscle fibers freed by collagenase digestion were radioautographed one hour after 3H-thymidine injection in order to determine the total number of labeled nuclei (true muscle nuclei plus those of satellite cells) per unit length of fiber.Certain nuclei within the basement membrane of muscle fibers are labeled one hour after 3H-thymidine and, therefore, synthesize DNA. The electron microscope demonstrates that these nuclei invariably belong to satellite cells, never to true muscle nuclei. Furthermore, the total number of labeled nuclei per unit length of fiber doubles between 1 and 24 hours; and, therefore, the labeled satellite cell nuclei undergo mitosis.Following mitosis, half of the daughters of satellite cells are incorporated into the fibers to become true muscle nuclei. The remaining half divides again later; and half of their daughter cells are incorporated. Thus, satellite cells in young rats divide repeatedly and function as a source of true muscle nuclei.
Article
The effect of cell-volume pertubations on mammary tissue protein synthesis has been examined. Cell-swelling, induced by a hyposmotic shock, increased the rate of incorporation of radiolabelled leucine and methionine into trichloroacetic acid precipitable material. The incorporation of radiolabel under both isosmotic and hyposmotic conditions was inhibited by cycloheximide. The increases in mammary protein synthesis as a result of cell-swelling may be attributable to an increase in casein synthesis. Conversely, cell-shrinking, as a consequence of a hyperosmotic challenge, almost abolished mammary protein (casein) synthesis. The finding that cell-volume pertubations had no significant effect on steady-state casein mRNA levels suggests that the regulation, within the time course of the experiments, is at the level of translation. The results strongly suggest that mammary cell volume may be an important cellular signal in the control of mammary protein synthesis in general and casein synthesis in particular.
Article
In addition to the well-known property of reactive oxygen species (ROS) to cause non-specific cellular damage, the potential role of ROS in regulation of signal transduction has been recognized. Studies of vascular smooth muscle cells strongly suggest that ROS are required for cell growth signaling. The IP3-induced Ca2+ release from vascular smooth muscle can be selectively stimulated by ROS which may enhance signal transduction for muscle contraction and gene expression. The subunit-subunit contact within the ryanodine receptor complex, as well as intermolecular interactions between the ryanodine receptor and triadin, are redox sensitive, suggesting that ROS may regulate cardiac muscle Ca(2+)-signaling events. The biochemistry of ROS and thiol regulation may allow for specific interactions between ROS and target molecules during redox regulation.
Article
Insulin-like growth factor I (IGF-I) is critical in promoting growth of skeletal muscle. When IGF-I is introduced into mouse hindlimb muscles by viral-mediated gene transfer, local overexpression of IGF-I produces significant increases in muscle mass and strength compared with untreated controls (Barton-Davis et al. 1998). We have proposed that this functional hypertrophy is primarily owing to the activation of satellite cells which leads to increased muscle regeneration. In order to test if satellite cells are essential in mediating the hypertrophic effects of IGF-I, we used gamma radiation to destroy the proliferative capacity of satellite cells. The right hindlimbs of adult C57BL/6 male mice were subjected to one of the following treatments: (1) 2,500 rad gamma radiation only, (2) viral-mediated gene transfer of IGF-I only, (3) 2,500 rad gamma radiation plus viral-mediated gene transfer of IGF-I, or (4) no intervention as a control. Approximately 4 months after treatment, the extensor digitorum longus muscles (EDL) from both hindlimbs were removed for mechanical and morphological measurements. Treatment with gamma radiation significantly prevented normal growth of the muscle. When combined with IGF-I treatment, approximately half of the IGF-I effect was prevented by gamma radiation treatment. This suggests that the remaining half of IGF-I induced hypertrophy is owing to paracrine/autocrine effects on the adult myofibres. Thus, these data are consistent with a mechanism by which IGF-I induced muscle hypertrophy via a combination of satellite cell activation and increasing protein synthesis in differentiated myofibres.
Article
The effect of changing cell volume on rat mammary protein synthesis has been examined. Cell swelling, induced by a hyposmotic challenge, markedly increased the incorporation of radiolabelled amino acids (leucine and methionine) into trichloroacetic acid (TCA)-precipitable material: reducing the osmolality by 47% increased leucine and methionine incorporation into mammary protein by 147 and 126% respectively. Conversely, cell shrinking, induced by a hyperosmotic shock, almost abolished the incorporation of radiolabelled amino acids into mammary protein: increasing the osmolality by 70% reduced leucine and methionine incorporation into mammary protein by 86 and 93% respectively. The effects of cell swelling and shrinking were fully reversible. Volume-sensitive mammary tissue protein synthesis was dependent upon the extent of the osmotic challenge. Isosmotic swelling of mammary tissue, using a buffer containing urea (160 mM), increased the incorporation of radiolabelled leucine into TCA-precipitable material by 106%. Swelling-induced mammary protein synthesis was dependent upon calcium: removing extracellular calcium together with the addition of EGTA markedly reduced volume-activated protein synthesis. Cell swelling-induced protein synthesis was inhibited by the Ca(2+) ATPase blocker thapsigargin suggesting that volume-sensitive protein synthesis is dependent upon luminal calcium.
Article
It has previously been shown that females incur less muscle damage than males after strenuous exercise, but limited data are available for humans. To determine possible differences between the sexes in humans, the response to high-force eccentric exercise was examined in a large sample of women (n = 83) and men (n = 82). The participants performed a bout of eccentric exercise of the elbow flexors consisting of 70 maximal repetitions. Isometric strength, resting elbow angle and muscle soreness were measured before, immediately after (except soreness) and then daily for 7 days after exercise. There was a significant loss in strength among both groups (69% for women and 63% for men) (P < 0.01) immediately after exercise; at 168 h post-exercise, women still had a 27% strength loss and men had a 24% strength loss. No significant difference in strength loss or recovery rate was found between men and women. Soreness reached peak values 32-48 h post-exercise (P < 0.01), with no significant difference between men and women. Range of motion decreased significantly until 3 days after exercise (14.6 degrees or 0.255 rad loss for women; 12.2 degrees or 0.213 rad loss for men) (P < 0.01); at 168 h post-exercise, the women and men still showed a loss of 4.8 degrees (0.084 rad) and 4.0 degrees (0.07 rad), respectively. There was a significant interaction of sex x time (P < 0.01); a post-hoc test indicated that the women experienced a greater loss in range of motion at 72 h than men and this difference was maintained to 168 h post-exercise (P < 0.01). Thus, our results do not support the contention that women have a lower response to eccentric exercise than men.
Article
Reactive oxygen species (ROS) are generated as by-products of cellular metabolism, primarily in the mitochondria. When cellular production of ROS overwhelms its antioxidant capacity, damage to cellular macromolecules such as lipids, protein, and DNA may ensue. Such a state of "oxidative stress" is thought to contribute to the pathogenesis of a number of human diseases including those of the lung. Recent studies have also implicated ROS that are generated by specialized plasma membrane oxidases in normal physiological signaling by growth factors and cytokines. In this review, we examine the evidence for ligand-induced generation of ROS, its cellular sources, and the signaling pathways that are activated. Emerging concepts on the mechanisms of signal transduction by ROS that involve alterations in cellular redox state and oxidative modifications of proteins are also discussed.
Article
In this study we investigated force loss and recovery after eccentric exercise, and further characterized profound losses in muscle function (n = 192 subjects--98 males, 94 females; population A). Maximal voluntary contractile force (MVC) was assessed before, immediately after, and at 36 and 132 h after eccentric exercise. Two groups were then established (A1 and A2). Group A1 demonstrated a > 70% reduction in MVC immediately after exercise, but were recovering at 132 h after exercise. These subjects performed a follow-up MVC 26 days later (n = 32). Group A2 demonstrated a > 70% reduction in MVC immediately post-exercise, but still exhibited a > 65% reduction in force at 132 h post-exercise; these subjects also performed a follow-up MVC every 7 days until full recovery was established (n = 9). In population A, there was a 57% reduction in MVC immediately post-exercise and a 67% recovery by 132 h post-exercise (P < 0.01), with no significant gender differences (P > 0.05). In group A1, although more females (two-thirds) showed large force losses after exercise, these females demonstrated greater %MVC recovery at 132 h post-exercise (59% vs 44%) and at 26 days post-exercise (93% vs 81%) compared to the males. In group A2, MVC recovery occurred between 33 and 47 days post-exercise. In conclusion, 21% of all subjects showed a delayed recovery in MVC after high-force eccentric exercise. Although there were no significant gender differences in force loss, a disproportionately larger number of females demonstrated force reductions of > 70%. However, their recovery of force was more rapid than that observed for the males who also demonstrated a > 70% force loss.
Article
Physical exercise is necessary for maintaining normal function of skeletal muscle. The mechanisms governing normal muscle function and maintenance are vastly unknown but synergistic function of hormones, neurosignalling, growth factors, cytokines and other factors, is undoubtedly important. Because of the complex interaction among these systems the lack of complete understanding of muscle function is not surprising. The purpose of exercise-induced changes in muscle cell function is to adapt the tissue to a demand of increased physical work capacity. Some of the approaches used to investigate changes in skeletal muscle cell function are exercise and electrical stimulation in animals and human models and isolated animal muscle. From these models, it has been concluded that during physical exercise, in an intensity and duration dependent manner, skeletal muscle is damaged and subsequently inflamed. The purpose of the inflammation would be to repair the exercise-induced damage. Because of the design and methods used in a majority of these studies, concerns must be raised, and the question asked whether the paradigm of exercise-induced muscle inflammation in fact is fiction. In a majority of conducted studies, a non-exercising control group is lacking and because of the invasive nature of the sampling methods used to study inflammation it does not appear impossible that observed inflammatory events in human skeletal muscle after physical exercise are methodological artefacts.
Article
To examine the plasma interleukin (IL)-6 response in elderly (E) and young (Y) humans, 10 E and 10 Y subjects completed 60 min of eccentric lower limb exercise at the same relative oxygen uptake. Plasma IL-6 was measured before, immediately after, and 5 days into recovery from exercise, as were the biochemical markers of muscle damage, creatine kinase (CK), and myoglobin. In both groups, IL-6 increased (P < 0.05) immediately after exercise and peaked 4 h after exercise at 4.35 +/- 1.7 vs. 5.05 +/- 3.17 pg/ml for E and Y subjects, respectively. However, the increase in IL-6 in both groups was modest relative to the increases in CK peaking at 539 +/- 413 vs. 10,301 +/- 5,863 U/l for E and Y subjects, respectively. In addition, the increase in IL-6 was less pronounced (P < 0.05) in E subjects compared with Y subjects. These results suggest that IL-6 increases progressively after eccentric exercise, suggesting that this increase is related to muscle damage. However, the modest increase in IL-6, despite large increases in CK, suggests that the IL-6 response to muscle damage does not make an important contribution to the large increase in IL-6 observed during concentric exercise of long duration. Our data also suggest that aging may be associated with impaired repair mechanisms for exercise-induced muscle damage.
Article
This study investigated the relationship between delayed-onset muscle soreness and other indicators of muscle damage following eccentric exercise. Male students (n = 110) performed 12 (12ECC), 24 (24ECC), or 60 maximal eccentric actions of the elbow flexors (60ECC). Maximal isometric force, relaxed and flexed elbow joint angles, upper arm circumference, and plasma creatine kinase activity were assessed immediately before and after, and for 4 days after exercise. Muscle soreness (SOR) was evaluated by a visual analog scale (a 50-mm line, 0: no pain, 50: extremely painful) when the elbow flexors were palpated (SOR-Pal), flexed (SOR-Flx) and stretched (SOR-Ext). Although 24ECC and 60ECC resulted in significantly (P <; 0.05) larger changes in all indicators and slower recovery compared to 12ECC, no significant differences were evident for SOR-Pal and SOR-Flx between 12ECC and 24ECC, or 12ECC and 60ECC. In contrast, SOR-Ext was significantly (P <; 0.05) lower for 12ECC compared to 24ECC and 60ECC. A Pearson product-moment correlation showed SOR-Pal did not correlate significantly with any indicators, however, SOR-Ext and SOR-Flx showed weak (r <; 0.32) but significant (P <; 0.05) correlations with other indicators. Because of generally poor correlations between DOMS and other indicators, we conclude that use of DOMS is a poor reflector of eccentric exercise-induced muscle damage and inflammation, and changes in indirect markers of muscle damage and inflammation are not necessarily accompanied with DOMS.
Article
This placebo-controlled, double-blind crossover study assessed whether exclusive activation of peripheral opioid receptors results in significant pain reduction. To achieve opioid activity restricted to the periphery, we used a short-term (2 h) low dose infusion of morphine-6-beta-glucuronide (M6G) because M6G does not pass the blood-brain barrier during this time in amounts sufficient to induce CNS effects. The lack of central opioid effects of M6G was confirmed by a lack of change of the pupil size and absence of other opioid-related CNS effects. As a positive control, morphine was infused at a dosage that definitely produced CNS effects. This was evident by a rapid decrease of the pupil size and by other typical opioid-related side effects including nausea, vomiting, itchiness, hiccup and sedation. Three different pain models were employed to evaluate the analgesic effects: (i) cutaneous inflammatory hyperalgesia induced by briefly freezing a small skin area to -30 degrees C ('freeze lesion'); (ii) muscle hyperalgesia induced by a series of concentric and eccentric muscle contractions (DOMS model; delayed onset of muscle soreness); and (iii) pain induced by electrical current (5 Hz sinus stimuli of 0-10 mA). M6G significantly reduced cutaneous hyperalgesia in the 'freeze lesion' model as assessed with von Frey hairs. It also reduced muscle hyperalgesia in the DOMS model. Electrical pain, however, was not affected by M6G. Morphine was significantly more active in the 'freeze lesion' and DOMS model, and also significantly increased the electrical pain threshold and tolerance. Subcutaneous tissue concentrations of M6G and morphine as assessed with microdialysis were about half those of the respective plasma concentrations. The results of the study indicate that M6G has antihyperalgesic effects in inflammatory pain through activation of peripheral opioid receptors. Since this occurs at concentrations that do not cause central opioid effects, M6G might be useful as a peripheral opioid analgesic.
Article
Eccentric contractions (ECs), in which a muscle is forced to lengthen while activated, result in muscle injury and, eventually, muscle strengthening and prevention of further injury. Although the mechanical basis of EC-induced injury has been studied in detail, the biological response of muscle is less well characterized. This study presents the development of a minimally invasive model of EC injury in the mouse, follows the time course of torque recovery after an injurious bout of ECs, and uses Affymetrix microarrays to compare the gene expression profile 48 h after ECs to both isometrically stimulated muscles and contralateral muscles. Torque dropped by approximately 55% immediately after the exercise bout and recovered to initial levels 7 days later. Thirty-six known genes were upregulated after ECs compared with contralateral and isometrically stimulated muscles, including five muscle-specific genes: muscle LIM protein (MLP), muscle ankyrin repeat proteins (MARP1 and -2; also known as cardiac ankyrin repeat protein and Arpp/Ankrd2, respectively), Xin, and myosin binding protein H. The time courses of MLP and MARP expression after the injury bout (determined by quantitative real-time polymerase chain reaction) indicate that these genes are rapidly induced, reaching a peak expression level of 6-11 times contralateral values 12-24 h after the EC bout and returning to baseline within 72 h. Very little gene induction was seen after either isometric activation or passive stretch, indicating that the MLP and MARP genes may play an important and specific role in the biological response of muscle to EC-induced injury.
Article
Muscular adaptation to physical exercise has previously been described as a repair process following tissue damage. Recently, evidence has been published to question this hypothesis. The purpose of this study was to investigate inflammatory processes in human skeletal muscle and epimysium after acute physical exercise with large eccentric components. Three groups of subjects (n= 19) performed 45 min treadmill running at either 4 deg (n= 5) or 8 deg (n= 9) downhill or 4 deg uphill (n= 5) and one group served as control (n= 9). One biopsy was taken from each subject 48 h post exercise. Blood samples were taken up to 7 days post exercise. Compared to the control group, none of the markers of inflammation in muscle and epimysium samples was different in any exercised group. Only subjects in the Downhill groups experienced delayed onset of muscle soreness (DOMS) and increased serum creatine kinase activity (CK). The detected levels of immunohistochemical markers for T cells (CD3), granulocytes (CD11b), leukaemia inhibitory factor (LIF) and hypoxia-inducible factor 1beta (HIF-1beta) were greater in epimysium from exercised subjects with DOMS ratings >3 (0-10 scale) compared to exercised subjects without DOMS but not higher than controls. Eccentric physical exercise (downhill running) did not result in skeletal muscle inflammation 48 h post exercise, despite DOMS and increased CK. It is suggested that exercise can induce DOMS by activating inflammatory factors present in the epimysium before exercise. Repeated physical training may alter the content of inflammatory factors in the epimysium and thus reduce DOMS.
Article
In contrast to the research using typical experimental pain stimuli, there is no consensus that women are more sensitive to delayed onset muscle pain than men. The purpose of this study was to examine sex differences in delayed onset muscle pain with use of a quantified stimulus intensity and multidimensional and valid pain measures. Ninety-five participants (49.5% women) completed eccentric exercise and then returned to the laboratory at 24 and 48 hours postexercise. The same relative intensity of the eccentric exercise was administered to women and men based on their eccentric strength. The occurrence of muscle pain was confirmed by increases in intensity, F2, 182 = 162.28, P<0.01, eta = 0.64, and unpleasantness, F2, 182 = 204.03, P < 0.01, eta = 0.69, and standardized pain ratings, F2, 180 = 67.44, P < 0.01, eta = 0.43. The affective ratios indicated that the muscle pain was more unpleasant than intense. No sex differences were detected except that men reported higher affective ratios than women, F1, 92 = 4.06, P < 0.05, eta = 0.04. The absence of higher muscle pain ratings in women than men in this investigation resembles a review of the delayed onset muscle soreness and pain literature. However, the findings contradict a few other acute muscle pain investigations, in which actual muscle tissue damage was not induced by eccentric contractions. Additional research is required to identify the parameters that influence the detection of sex differences.