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Single muscle fibre contractile properties differ between bodybuilders, power athletes and controls
Experimental Physiology
Abstract
New Findings
What is the central question of this study?
Do the contractile properties of single muscle fibres differ between body‐builders, power athletes and control subjects?
What is the main finding and its importance?
Peak power normalized for muscle fibre volume in power athletes is higher than in control subjects. Compared with control subjects, maximal isometric tension (normalized for muscle fibre cross‐sectional area) is lower in body‐builders. Although this difference may be caused in part by an apparent negative effect of hypertrophy, these results indicate that the training history of power athletes may increase muscle fibre quality, whereas body‐building may be detrimental.
We compared muscle fibre contractile properties of biopsies taken from the vastus lateralis of 12 body‐builders (BBs; low‐ to moderate‐intensity high‐volume resistance training), six power athletes (PAs; high‐intensity, low‐volume combined with aerobic training) and 14 control subjects (Cs). Maximal isotonic contractions were performed in single muscle fibres, typed with SDS‐PAGE. Fibre cross‐sectional area was 67 and 88% ( P < 0.01) larger in BBs than in PAs and Cs, respectively, with no significant difference in fibre cross‐sectional area between PAs and Cs. Fibres of BBs and PAs developed a higher maximal isometric tension (32 and 50%, respectively, P < 0.01) than those of Cs. The specific tension of BB fibres was 62 and 41% lower than that of PA and C fibres ( P < 0.05), respectively. Irrespective of fibre type, the peak power (PP) of PA fibres was 58% higher than that of BB fibres ( P < 0.05), whereas BB fibres, despite considerable hypertrophy, had similar PP to the C fibres. This work suggests that high‐intensity, low‐volume resistance training with aerobic exercise improves PP, while low‐ to moderate‐intensity high‐volume resistance training does not affect PP and results in a reduction in specific tension. We postulate that the decrease in specific tension is caused by differences in myofibrillar density and/or post‐translational modifications of contractile proteins.
... This technique is performed using a specialized force transducer, and can provide an indirect assessment of contractile material per muscle fiber cross-section (D'antona et al., 2007;Degens et al., 2010;Meijer et al., 2015). Readers interested in observing this technique can refer to an excellent visual methods article by Roche et al. (2015), as well as a comprehensive review on the topic by Canepari et al. (2010). ...
... A third, and significant, limitation to this technique includes the delicate and time-consuming steps involved with microdissections as well as the delicate nature of interfacing fibers with the force transducer. Because of the work required to perform this technique, it is common for less than 10 fibers per subject to be analyzed (Meijer et al., 2015). Finally, as with TEM, this technique is not widely performed due to the specialized equipment and expertise needed. ...
... Toth et al. (2012) used TEM to report that 18 weeks of resistance training decreased space occupied by myofibrils ∼15% in vastus lateralis muscle fibers from healthy individuals. Meijer et al. (2015) subsequently employed isolated fiber techniques and reported that body-builders, who possessed large vastus lateralis muscle fibers, presented specific tension values that were ∼40% lower than untrained participants. Our group used SDS-PAGE and Coomassie staining to determine 6 weeks of very high volume resistance training reduced relative abundances (per milligram dry tissue) of myosin heavy chain and actin by ∼30% in vastus lateralis muscle from 15 welltrained participants (Haun et al., 2019b). ...
Skeletal muscle fibers are multinucleated cells that contain mostly myofibrils suspended in an aqueous media termed the sarcoplasm. Select evidence suggests sarcoplasmic hypertrophy, or a disproportionate expansion of the sarcoplasm relative to myofibril protein accretion, coincides with muscle fiber or tissue growth during resistance training. There is also evidence to support other modes of hypertrophy occur during periods of resistance training including a proportional accretion of myofibril protein with fiber or tissue growth (i.e., conventional hypertrophy), or myofibril protein accretion preceding fiber or tissue growth (i.e., myofibril packing). In this review, we discuss methods that have been used to investigate these modes of hypertrophy. Particular attention is given to sarcoplasmic hypertrophy throughout. Thus, descriptions depicting this process as well as the broader implications of this phenomenon will be posited. Finally, we propose future human and rodent research that can further our understanding in this area of muscle physiology.
... Several studies have been commonly cited as providing support for the existence of sarcoplasmic hypertrophy [32,36,163,[171][172][173][174]. For instance, D'Antona et al. (2006) measured specific tension in single myofibers from recreationally active subjects, and from subjects that had engaged in bodybuilding for at least 2 years. ...
... However, it is important to point out that the same study also observed an increase in specific tension of the Type IIA and IIX myofibers from the same bodybuilders [163]. The work of Meijer et al. (2015) is another frequently cited study that measured specific tension in single myofibers. In this case, specific tension was measured in myofibers from control subjects, bodybuilders, and powerlifters. ...
... In this case, specific tension was measured in myofibers from control subjects, bodybuilders, and powerlifters. Importantly, it was concluded that specific tension was lower in the myofibers obtained from bodybuilders [172]. At first glance it would appear that this study provides clear support for the notion that bodybuilders experience sarcoplasmic hypertrophy; however, 9 of the 12 bodybuilders in the study admitted to recent use of anabolic steroids [172]. ...
The maintenance of skeletal muscle mass plays a critical role in health and quality of life. One of the most potent regulators of skeletal muscle mass is mechanical loading, and numerous studies have led to a reasonably clear understanding of the macroscopic and microscopic changes that occur when the mechanical environment is altered. For instance, an increase in mechanical loading induces a growth response that is mediated, at least in part, by an increase in the cross-sectional area of the myofibers (i.e., myofiber hypertrophy). However, very little is known about the ultrastructural adaptations that drive this response. Even the most basic questions, such as whether mechanical load-induced myofiber hypertrophy is mediated by an increase in the size of the pre-existing myofibrils and/or an increase in the number myofibrils, have not been resolved. In this review, we thoroughly summarize what is currently known about the macroscopic, microscopic and ultrastructural changes that drive mechanical load-induced growth and highlight the critical gaps in knowledge that need to be filled.
... However, select evidence has failed to confirm this relationship. For example, Meijer et al. (2015) have reported that lower specific tensions (N/cm 2 ) exist in single fibers isolated from bodybuilders with significantly larger fCSAs when compared to muscle fibers from controls and power athletes. Furthermore, in 1969 (although using a surgical ablation model in rodents) Rowe reported ∼25% decreases in specific tension although CSAs of muscle samples significantly increased (Rowe, 1969). ...
... Also, it stands to reason that some individuals may realize significant increases or decreases in myofibrillar protein content or myofibril number while others may not in response to the same training or unloading intervention. Research in humans in this regard seems equivocal (D'Antona et al., 2006;Trappe, 2009;Canepari et al., 2010;Meijer et al., 2015). ...
... In this regard, Tesch and Larsson (1982) found that muscle tissue from the medial deltoid and the VL obtained from high level bodybuilders exhibit larger slow twitch fiber fCSA values compared to recreationally trained individuals, although fibers exhibiting fast twitch properties yielded similar fCSA values between cohorts. Additionally, Meijer et al. (2015) reported that bodybuilders completing moderate to high volume training display greater mean fCSAs compared to untrained individuals and strength/power athletes. However, it is also important to note that while all fiber types were larger, there was a significant difference between type I fCSA of bodybuilders as compared to untrained individuals and strength/power athletes, yet no meaningful difference between type I fCSA of the untrained group and the strength/power group. ...
Skeletal muscle is highly adaptable and has consistently been shown to morphologically respond to exercise training. Skeletal muscle growth during periods of resistance training has traditionally been referred to as skeletal muscle hypertrophy, and this manifests as increases in muscle mass, muscle thickness, muscle area, muscle volume, and muscle fiber cross-sectional area (fCSA). Delicate electron microscopy and biochemical techniques have also been used to demonstrate that resistance exercise promotes ultrastructural adaptations within muscle fibers. Decades of research in this area of exercise physiology have promulgated a widespread hypothetical model of training-induced skeletal muscle hypertrophy; specifically, fCSA increases are accompanied by proportional increases in myofibrillar protein, leading to an expansion in the number of sarcomeres in parallel and/or an increase in myofibril number. However, there is ample evidence to suggest that myofibrillar protein concentration may be diluted through sarcoplasmic expansion as fCSA increases occur. Furthermore, and perhaps more problematic, are numerous investigations reporting that pre-to-post training change scores in macroscopic, microscopic, and molecular variables supporting this model are often poorly associated with one another. The current review first provides a brief description of skeletal muscle composition and structure. We then provide a historical overview of muscle hypertrophy assessment. Next, current-day methods commonly used to assess skeletal muscle hypertrophy at the biochemical, ultramicroscopic, microscopic, macroscopic, and whole-body levels in response to training are examined. Data from our laboratory, and others, demonstrating correlations (or the lack thereof) between these variables are also presented, and reasons for comparative discrepancies are discussed with particular attention directed to studies reporting ultrastructural and muscle protein concentration alterations. Finally, we critically evaluate the biological construct of skeletal muscle hypertrophy, propose potential operational definitions, and provide suggestions for consideration in hopes of guiding future research in this area.
... A. Maciejewska et al. (2012) продемонстрували, що роль окислювального метаболізму, індукованого PPARGC1A, полягає в комбінуванні пікової сили та потужності м'язових волокон і в підтримуванні зусиль високої інтенсивності протягом тривалих періодів під час змагань [28]. J. Meijer et al. (2015) у своїх напрацюваннях довели, що спортивні здібності бодібілдерів і силових атлетів пов'язані зі здатністю перемикання різних типів міоволокон скелетних м'язів, що включає перехід від гліколітичного типу IIb до багатих мітохондріями типів IIa та I. Саме кількість мітохондрій у залучених м'язових волокнах визначає максимальну стійку потужність і витривалість [30]. ...
... A. Maciejewska et al. (2012) продемонстрували, що роль окислювального метаболізму, індукованого PPARGC1A, полягає в комбінуванні пікової сили та потужності м'язових волокон і в підтримуванні зусиль високої інтенсивності протягом тривалих періодів під час змагань [28]. J. Meijer et al. (2015) у своїх напрацюваннях довели, що спортивні здібності бодібілдерів і силових атлетів пов'язані зі здатністю перемикання різних типів міоволокон скелетних м'язів, що включає перехід від гліколітичного типу IIb до багатих мітохондріями типів IIa та I. Саме кількість мітохондрій у залучених м'язових волокнах визначає максимальну стійку потужність і витривалість [30]. ...
Annotation. The impact of genetics on physiology and sports performance is one of the most controversial areas of sports medicine. Studies have shown that in addition to wild-type genes, almost 200 gene polymorphisms affect athletic performance, and more than 20 polymorphisms can determine the status of elite athletes. Sports results are manifested to a greater extent not only due to environmental factors, but also due to the athlete's own genotype, so the purpose of our review article is to study the effects of the PPARGC1A gene and its rs8192678 polymorphism on sports characteristics. For this purpose, we analyzed and processed the information known to date about a specific gene and the effects of its polymorphism, using the main databases. The PPARGC1A gene plays an important role in a number of physiological processes and is responsible for the metabolism of glucose and ATP, to a greater extent in muscle tissue; for oxidative processes in organs; and for switching one or another type of muscle fibers depending on the force load. It was proved that the expression of this gene can be induced under the influence of low temperatures. The PPARGC1A polymorphism has different effects on athletic performance, depending on its alleles. For example, the Gly allele, associated with muscle strength and endurance, favors athletic performance, while the Ser allele and the Ser-Gly genotype show no significant evidence. The results of our review are intended to help select a training strategy for each athlete in order to understand the role of environment and genotype in achieving athletic success.
... Our laboratory recently reported that 6 weeks of extremely HV resistance training decreased the relative abundances of myosin heavy chain and actin protein content per milligram of dry tissue (Haun et al., 2019a). Our findings, as well as those of others who have reported moderate-to-higher volume resistance training elicits similar molecular adaptations (MacDougall et al., 1982;Roth et al., 1999;Meijer et al., 2015), led us to postulate that a disproportionate increase in the sarcoplasmic space relative to myofibril protein accretion (i.e., sarcoplasmic hypertrophy) may be a training adaptation to HV resistance training (Roberts et al., 2020a). More recently, our laboratory demonstrated that lower volume, higher-load resistance training (3-5 sets of 2-6 repetitions at 65-90% 1RM) resulted in a maintenance of type I muscle fiber cross-sectional area (fCSA) while increasing type II fCSA. ...
... On the other hand, if values, and in particular the relative abundances of myofibril proteins decrease from pre-to-post training then this indicates a "dilution" effect wherein hypertrophy occurs in the midst of sarcoplasmic (or fluid) expansion. Although our data largely imply conventional hypertrophy occurred with HV training, a handful of studies exist showing that a disproportionate increase in non-contractile proteins and cellular spacing may occur following months to years of resistance training (Penman, 1969;MacDougall et al., 1982;Toth et al., 2012;Meijer et al., 2015). Recently, our laboratory has reported decreases in the relative abundances of MyHC and actin protein abundances per mg of dry tissue weight following 6 weeks of extremely high-volume resistance training in previously trained college-aged men (Haun et al., 2019a). ...
We evaluated the effects of higher-load (HL) versus (lower-load) higher-volume (HV) resistance training on skeletal muscle hypertrophy, strength, and muscle-level molecular adaptations. Trained men (n = 15, age: 23 ± 3 years; training experience: 7 ± 3 years) performed unilateral lower-body training for 6 weeks (3× weekly), where single legs were randomly assigned to HV and HL paradigms. Vastus lateralis (VL) biopsies were obtained prior to study initiation (PRE) as well as 3 days (POST) and 10 days following the last training bout (POSTPR). Body composition and strength tests were performed at each testing session, and biochemical assays were performed on muscle tissue after study completion. Two-way within-subject repeated measures ANOVAs were performed on most dependent variables, and tracer data were compared using dependent samples t-tests. A significant interaction existed for VL muscle cross-sectional area (assessed via magnetic resonance imaging; interaction p = 0.046), where HV increased this metric from PRE to POST (+3.2%, p = 0.018) whereas HL training did not (−0.1%, p = 0.475). Additionally, HL increased leg extensor strength more so than HV training (interaction p = 0.032; HV < HL at POST and POSTPR, p < 0.025 for each). Six-week integrated non-myofibrillar protein synthesis (iNon-MyoPS) rates were also higher in the HV versus HL condition, while no difference between conditions existed for iMyoPS rates. No interactions existed for other strength, VL morphology variables, or the relative abundances of major muscle proteins. Compared to HL training, 6 weeks of HV training in previously trained men optimizes VL hypertrophy in lieu of enhanced iNon-MyoPS rates, and this warrants future research.
... One of the possible factors is muscle force per cross-sectional area. Maximal force per cross-sectional area in muscle fibers was greater in power athletes, including track-and-field athletes, compared with bodybuilders with considerably hypertrophied muscle fibers, irrespective of fiber type (Meijer et al. 2015). The decreased force-generating capacity per cross-sectional area in bodybuilders is considered to be due, at least in part, to a reduction in the density of contractile protein following years of high volume resistance training (Haun et al. 2019;Meijer et al. 2015). ...
... Maximal force per cross-sectional area in muscle fibers was greater in power athletes, including track-and-field athletes, compared with bodybuilders with considerably hypertrophied muscle fibers, irrespective of fiber type (Meijer et al. 2015). The decreased force-generating capacity per cross-sectional area in bodybuilders is considered to be due, at least in part, to a reduction in the density of contractile protein following years of high volume resistance training (Haun et al. 2019;Meijer et al. 2015). Consequently, the individual differences in active muscle elasticity could be due to the changes in "muscle quality" induced by long-term training. ...
PurposeLimited information is available on the association between muscle material properties and sprint performance. We aimed to identify whether and how the elasticity of passive and active muscle of the medial gastrocnemius (MG) is related to sprint performance.MethodsMG shear wave speed was measured under passive and active (20%, 50%, 80% of maximal voluntary contraction [MVC]) conditions, with ultrasound shear wave elastography, in 18 male sprinters. Passive and active ankle joint stiffness was assessed by applying a short-range fast stretch during 0%, 20%, 50%, and 80% MVC of plantar flexion. Additionally, rate of torque development (RTD) during explosive plantar flexion was measured.ResultsPassive and active MG shear wave speed was negatively correlated with 100-m race time. Passive MG shear wave speed was positively correlated with RTD, and RTD was negatively correlated with 100-m race time. MG shear wave speed at 50% and 80% MVC showed a positive correlation with ankle joint stiffness at the corresponding contraction level, and ankle joint stiffness at 50% and 80% MVC showed negative correlations with 100-m race time. These correlations were significant even after controlling for MVC torque.Conclusion
Our findings indicate that passive and active muscle elasticity of plantar flexor is important to achieve superior sprint performance. Specifically, high elasticity of passive MG could be related to superior sprint performance through high explosive torque production. In contrast, high elasticity of active MG at moderate-to-high intensity is likely related to high sprint performance through high ankle joint stiffness.
... Type II fibers have a low content of mitochondria and oxidative enzymes and depend, to a greater extent, on glycolytic metabolism as the main source of energy. This type of fiber is associated with the high capabilities of an athlete in speed and power sports (sprint) [8]. ...
... The process of switching the type of muscle fibers is important, in particular the transition from glycolytic type IIb to types IIa and I rich in mitochondria, which is associated with high athletic capabilities of the individual in endurance sports. The number of mitochondria in the involved muscle fibers probably determines the power of the load at the level of MOC [8]. ...
All biological processes associated with high sports performance, including energy metabolism, are influenced by genetics. DNA sequence variations in such genes, single nucleotide variants (SNVs), could confer genetic advantages that can be exploited to achieve optimal athletic performance. Ignorance of these features can create genetic “barriers” that prevent professional athletes from pursuing a career in sports. Predictive Genomic DNA Profiling reveals single nucleotide variations (SNV) that may be associated with better suitability for endurance, strength and speed sports. (1) Background: To conduct a research on candidate genes associated with regulation of skeletal muscle energy metabolism among athletes. (2) Methods: We have searched for articles in SCOPUS, Web of Science, Google Scholar, Clinical keys, PubMed, e-LIBRARY databases for the period of 2010–2020 using keywords and keywords combinations; (4) Conclusions: Identification of genetic markers associated with the regulation of energy metabolism in skeletal muscles can help sports physicians and coaches develop personalized strategies for selecting children, teenagers and young adults for endurance, strength and speed sports (such as jogging, middle or long distance runs). However, the multifactorial aspect of sport performances, including impact of genetics, epigenetics, environment (training and etc.), is important for personalized strategies for selecting of athletes. This approach could improve sports performance and reduce the risk of sports injuries to the musculoskeletal system.
... Indirect evidence suggests it is also possible consistent bodybuilding type resistance training (high repetitions per set, training to failure) may result in greater SH [11,21]. Perhaps this hypertrophic difference partially explains observations indicating bodybuilders are not as strong or as powerful as other strength-power athletes in multi-joint absolute [22] relative [23] or single fiber [21] measures. ...
... Indirect evidence suggests it is also possible consistent bodybuilding type resistance training (high repetitions per set, training to failure) may result in greater SH [11,21]. Perhaps this hypertrophic difference partially explains observations indicating bodybuilders are not as strong or as powerful as other strength-power athletes in multi-joint absolute [22] relative [23] or single fiber [21] measures. ...
The block periodization training paradigm has been shown to produce enhanced gains in strength and power. The purpose of this study is to assess resistance training induced alterations in lean body mass and cross-sectional area using a block periodization training model among individuals (n = 15) of three differing strength levels (high, moderate and low) based on one repetition maximum back squat relative to body weight. A 3 × 5 mixed-design ANOVA was used to examine within-and between-subject changes in cross-sectional area (CSA), lean body mass (LBM), lean body mass adjusted (LBMadjusted) and total body water (TBW) over an 11-week resistance training program. LBMadjusted is total body water subtracted from lean body mass. The ANOVA revealed no statistically significant between-group differences in any independent variable (p > 0.05). Within-group effects showed statistically significant increases in cross-sectional area (p < 0.001), lean body mass (p < 0.001), lean body mass adjusted (p ˂ 0.001) and total body water (p < 0.001) from baseline to post intervention: CSA: 32.7 cm2 ± 8.6; 36.3 cm2 ± 7.2, LBM: 68.0 kg ± 9.5; 70.6 kg ± 9.4, LBMadjusted: 20.4 kg ± 3.1; 21.0 kg ± 3.3 and TBW: 49.8 kg ± 6.9; 51.7 kg ± 6.9. In conclusion, the results of this study suggest subjects experienced an increase in both lean body mass and total body water, regardless of strength level, over the course of the 11-week block periodized program. Gains in lean body mass and cross-sectional area may be due to edema at the early onset of training.
... Conversely, myofibrillar hypertrophy has been defined as the increase in the size or number of myofibrils accompanied by an increase in sarcomere number or protein abundance related to contractile force generation [179,181]. This has been demonstrated with bodybuilders as well as strength and power athletes [182,183]. It is important to make a distinction between these two modes of hypertrophy, as these variable changes may appear to be of a similar change in muscle hypertrophy via ultrasound (i.e., cellular swelling) [8]; however, the function within the muscle is likely different between these two separate alterations as a result of the training stimuli. ...
... However, the exact molecular mechanisms underpinning mCSA changes cannot be quantified using gross measurements alone that fail to detect the type of hypertrophy associated with altered cellular size. Considering that direct evidence for sarcoplasmic hypertrophy is expanding [145,182,188,189], albeit remaining controversial [29], a recent investigation demonstrated that after six weeks of high volume resistance training, the major contributor to the observed hypertrophic response was sarcoplasmic alterations [179]. Such adaptations may also increase fCSA while only promoting suboptimal strength improvements. ...
While strength is indeed a skill, most discussions have primarily considered structural adaptations rather than ultrastructural augmentation to improve performance. Altering the structural component of the muscle is often the aim of hypertrophic training, yet not all hypertrophy is equal; such alterations are dependent upon how the muscle adapts to the training stimuli and overall training stress. When comparing bodybuilders to strength and power athletes such as powerlifters, weightlifters, and throwers, while muscle size may be similar, the ability to produce force and power is often inequivalent. Thus, performance differences go beyond structural changes and may be due to the muscle's ultrastructural constituents and training induced adaptations. Relative to potentiating strength and power performances, eliciting specific ultrastructural changes should be a variable of interest during hypertrophic training phases. By focusing on task-specific hypertrophy, it may be possible to achieve an optimal amount of hypertrophy while deemphasizing metabolic and aerobic components that are often associated with high-volume training. Therefore, the purpose of this article is to briefly address different types of hypertrophy and provide directions for practitioners who are aiming to achieve optimal rather than maximal hypertrophy, as it relates to altering ultrastructural muscular components, to potentiate strength and power performance.
... Explosive resistance training results in specific neuromuscular adaptations, such as increased number of activated motor units (MUs), lower recruitment threshold of fast fibers, greater discharge rates of the fast MUs, longer fascicle lengths, increased propagation of action potentials along the sarcolemma, and higher type IIx fibers percentage area, which are associated with increase in power performance (Aagaard et al. 2002;Andersen et al. 2010;Hakkinen et al. 1985;Kyrolainen et al. 2005;Liu et al. 2013;Meijer et al. 2015;Oliveira et al. 2016;Peltonen et al. 2018;Rodríguez-Rosell et al. 2017;Stasinaki et al. 2019;Terzis et al. 2016;Vissing et al. 2008). Among these biological attributes type IIx and type IIa muscle fibers are of particular importance for muscle power. ...
... In power-trained participants the %CSA of type IIx fibers is strongly related to early RFD . Type IIx muscle fibers have faster conduction velocities , cross-bridge cycling rates (Bottinelli et al. 1996), shortening velocity (Widrick et al. 2002), and higher specific force (Meijer et al. 2015), rendering them proficient in rapid force development compared with type I and IIa fibers if they receive an adequate neural input Vecchio et al. 2019). The link between the %CSA of type IIx fibers and the training-induced changes in early and late RFD has been reported once before in response to heavy resistance training (Andersen et al. 2010), while here this relationship is revealed with power training. ...
This study aimed to investigate the effect of 3 different eccentric-only power training volumes on muscle fiber type composition and power performance. Twenty-nine females were assigned into 3 groups and performed 10 weeks of either 3 (low volume), 6 (moderate volume), or 9 (high volume) sets/session of 4 fast-velocity eccentric-only half-squats against 70% of concentric 1-repetition maximum (1RM), followed by 3 maximum countermovement jumps (CMJs) after each set. Half-squat 1RM, CMJ height/power, maximum isometric force, rate of force development (RFD) and muscle fiber cross-sectional area (CSA) were increased in all groups (p = 0.001). Low-volume training induced higher increases in CMJ height/power and early RFD, compared with the moderate- and high-volume training programs (p < 0.001). Significant reductions in type IIx muscle fiber percentages and %CSAs were found after moderate- and high-volume training, with concomitant increases in type IIa fibers (p = 0.001). Significant correlations were found between the changes in type IIa and type IIx percentages, fiber CSA, %CSA, and the changes in performance (r: –0.787 to 0.792; p < 0.05). These results suggest that relatively large eccentric power training volumes may result in detrimental neuromuscular adaptations, minimal changes in early RFD, and a reduction of type IIx muscle fiber percentage.
NoveltyLow but not high volume of power training maintains type IIx muscle fibers.
Early rate of force development increases after a low- or moderate-power training volume, but not after a high-power training volume.
Training-induced changes in type IIx muscle fiber percentage is related with changes in early rate of force development.
... MHC isoform content influences twitch forces (Meijer et al. 2015) and contractile speed (Bottinelli 2001;Pette et al. 1999) and is associated with the fatigability of the muscle fiber (Swallow et al. 2007;Taylor et al. 1997). Therefore, the MHC isoforms have been regarded as an important factor in the physical properties of the MU (Booth et al. 2010;Pette and Staron 2000) and are the most appropriate markers for fiber type delineation (Pette and Staron 2000). ...
... Thus it is plausible that the firing rates of the higherthreshold MUs are lower in individuals with greater percentages of type II MHC isoform content as a result of greater twitch forces generated by the MU. Therefore, MU force twitches, which are largely dictated by the physical properties (i.e., %MHC isoform content) of the MU pool (Meijer et al. 2015), play a significant factor in firing rate characteristics (Contessa and De Luca 2013). In addition, a principle of the onion skin control scheme is minimizing energy expenditure with greater reliance on lower-threshold MUs. ...
It is suggested that firing rate characteristics of motor units (MUs) are influenced by the physical properties of the muscle. However, no study has correlated MU firing rates at recruitment, targeted force, or derecruitment with the contractile properties of the muscle in vivo. Twelve participants (age=20.67±2.35) performed a 40% isometric maximal voluntary contraction of the leg extensors that included linearly increasing, steady force, and decreasing segments. Muscle biopsies were collected with myosin heavy chain (MHC) content quantified and surface electromyography (EMG) was recorded from the vastus lateralis. The EMG signal was decomposed into the firing events of single MUs. Slopes and y-intercepts were calculated for the (1) firing rates at recruitment versus recruitment threshold, (2) mean firing rates at steady force versus recruitment threshold, and (3) firing rates at derecruitment versus derecruitment threshold relationships for each subject. Correlations among type I %MHC isoform content and the slopes and y-intercepts from the three relationships were examined. Type I %MHC content was correlated with MU firing rates at recruitment (y-intercepts: r=-0.577; slopes: r=0.741) and targeted force (slopes: r=0.853) versus recruitment threshold, and MU firing rates at derecruitment (y-intercept: r=-0.597; slopes: r=0.701) versus derecruitment threshold relationships. However, the majority of the individual MU firing rates versus recruitment and derecruitment relationships were not significant (P>0.05) and, thus, revealed no systematic pattern. In contrast, MU firing rates during the steady force demonstrated a systematic pattern with higher firing rates for the lower- than higher-threshold MUs and was correlated with the physical properties of MUs in vivo.
... Since muscle represents a large portion of body mass, changes in mitochondrial content have a significant impact on whole body metabolism [19,29]. Strength/power athletes' performance is determined by the combination of both peak force/power and the ability to sustain and repeat high-intensity efforts for extended periods during a competition [5,30]. A main deciding factor of maximal sustainable power is the mitochondrial amount in the recruited muscle fibres. ...
... A main deciding factor of maximal sustainable power is the mitochondrial amount in the recruited muscle fibres. Ideally, an athlete strives to maximize both muscle power and endurance [30]. ...
The performance of professional strength and power athletes is influenced, at least partly, by genetic components. The main aim of this study was to investigate individually and in combination the association of ACE (I/D), ACTN3 (R577X) and PPARGC1A (Gly482Ser) gene polymorphisms with strength/power-oriented athletes' status in two cohorts of European athletes. A cohort of European Caucasians from Russia and Lithuania (161 athletes: by groups - weightlifters (87), powerlifters (60), throwers (14); by elite status - 'elite' (104), 'sub-elite' (57); and 1,202 controls) were genotyped for ACE, ACTN3 and PPARGC1A polymorphisms. Genotyping was performed by polymerase chain reaction and/or restriction fragment length polymorphism analysis. Statistically significant differences in ACTN3 (R577X) allele/genotype distribution were not observed in the whole cohort of athletes or between analysed groups separately when compared with controls. The odds ratio for athletes compared to controls of the ACE I/I genotype was 1.71 (95% CI 1.01-2.92) in the Russian cohort and for the ACE I/D genotype it was 2.35 (95% CI 1.10-5.06) in the Lithuanian cohort. The odds ratio of being a powerlifter in PPARGC1A Ser/Ser genotype carriers was 2.11 (95% CI: 1.09-4.09, P = 0.026). The ACTN3 (R577X) polymorphism is not associated with strength/power athletic status in two cohorts of European athletes. The ACE I/I genotype is probably the 'preferable genotype' for Russian athletes and the ACE I/D genotype for Lithuanian strength/power athletes. We found that the PPARGC1A (Gly482Ser) polymorphism is associated with strength/power athlete status. Specifically, the PPARGC1A Ser/Ser genotype is more favourable for powerlifters compared to controls.
... The fact that consistent physical activity modifies skeletal muscle morphology is widely accepted (Flück et al., 2019), but assessing and quantifying these modifications usually requires invasive techniques such as muscle biopsies. Biopsy-based studies have demonstrated significant adaptations of muscle tissue to long-term physical activity, including changes in muscle fiber type composition and size (Andersen and Aagaard, 2010;Meijer et al., 2015). They have also successfully shown distinct effects of different training regimens on metabolismand contraction-related cellular parameters (Terzis et al., 2010;Flück et al., 2019). ...
Adaptations in muscle physiology due to long-term physical training have been monitored using various methods: ranging from invasive techniques, such as biopsy, to less invasive approaches, such as electromyography (EMG), to various quantitative magnetic resonance imaging (qMRI) parameters. Typically, these latter parameters are assessed immediately after exercise. In contrast, this work assesses such adaptations in a set of qMRI parameters obtained at rest in the lumbar spine muscles of volunteers. To this end, we developed a multiparametric measurement protocol to extract quantitative values of (water) T2, fat fraction, T1, and Intra Voxel Incoherent Motion (IVIM) diffusion parameters in the lumbar back muscle. The protocol was applied to 31 healthy subjects divided into three differently trained cohorts: two groups of athletes (endurance athletes and powerlifters) and a control group with a sedentary lifestyle. Significant differences in muscle water T2, fat fraction, and pseudo-diffusion coefficient linked to microcirculatory blood flow in muscle tissue were found between the trained and untrained cohorts. At the same time, diffusion coefficients (resolved along different directions) provided additional differentiation between the two groups of athletes. Specifically, the strength-trained athletes showed lower axial and higher radial diffusion components compared to the endurance-trained cohort, which may indicate muscle hypertrophy. In conclusion, utilizing multiparametric information revealed new insights into the potential of quantitative MR parameters to detect and quantify long-term effects associated with training in differently trained cohorts, even at rest.
... Until recently, strength gains and muscle hypertrophy were thought to be two different training adaptations that required distinct training characteristics to be achieved (Suchomel, Nimphius, Bellon & Stone, 2018). With this background, bodybuilders -focused on muscle size gains and anthropometry changes-would train with lower loads, high number of repetitions, and shorter rest intervals between set with the aim of maximizing the gains in muscle hypertrophy (Meijer, Jaspers et al. 2015). In the other hand, weightlifters and powerlifters -focused in strength and power improvementswould train with higher loads and lower number of repetitions to maximize the gains in maximal strength induced by the training (Suchomel et al., 2018). ...
INTRODUCTION: Traditionally, it has been proposed that strength gains and muscle hypertrophy required distinct characteristics to be achieved with resistance training. However, current evidence shows that the obtaining of improvements of strength and hypertrophy can be obtained with a single resistance training protocol. The purpose of this systematic review was to examine the existing body of literature pertaining to association between load during resistance training and their effects on strength gains and muscle hypertrophy. METHODOLOGY: Searches were conducted on Web of Science, PubMed/Medline, and Embase with no year restriction applied to the search strategy. Selected studies met the following inclusion criteria: (a) studies that included a combination of young and old males and females, with no known medical conditions or injuries; (b) including a resistance training with high-loads (≥60% of one-repetition maximum, 1RM) or low-loads (<60% 1RM); (c) the duration and frequency of the resistance training protocols was equal; (d) measurement of hypertrophy and/or strength gains induced by the training; (e) in English and published in peer-reviewed journals. RESULTS: A total of 24 studies were included in the review. Overall, the increase in muscle mass were similar for both high-load and low-load resistance training protocols. However, in 10 out of 24 studies, the gains in strength were significantly higher with the high-load resistance training when compared to the low-load protocol. CONCLUSIONS: The use of loads above ≥60% of 1RM during a resistance training induces higher gains in muscle strength while muscle hypertrophy is similar to resistance training with lower loads. This suggests that the use of high loads is recommended during resistance training with the aim of maximizing training adaptations.
... Given that the mechanical tension of type II fibers is 1.4 times higher than the specific tension of type I fibers (Bottinelli et al., 1996;Widrick et al., 1996), at best, it could explain a 2% and not a 45% force reduction that was reported between these ages (Degens et al., 2009). It is also noteworthy that there are studies not observing tensional differences between fiber types (Ottenheijm et al., 2005;Degens and Larsson, 2007;Meijer et al., 2015). Hence, it is fair to conclude that fiber type shifting only minimally accounts for the age-associated force reduction seen during aging. ...
Muscle mass and force are key for movement, life quality, and health. It is well established that resistance exercise is a potent anabolic stimulus increasing muscle mass and force. The response of a physiological system to resistance exercise is composed of non-modifiable (i.e., age, gender, genetics) and modifiable factors (i.e., exercise, nutrition, training status, etc.). Both factors are integrated by systemic responses (i.e., molecular signaling, genetic responses, protein metabolism, etc.), consequently resulting in functional and physiological adaptations. Herein, we discuss the influence of non-modifiable factors on resistance exercise: age, gender, and genetics. A solid understanding of the role of non-modifiable factors might help to adjust training regimes towards optimal muscle mass maintenance and health.
... Hence, the quality of hypertrophy highly determines the relationship between RT-induced muscle growth and strength gains. In this context, studies using direct measurement techniques at the microscopic level (i.e., transmission electron microscopy) have shown that high-volume RT leads to increased sarcoplasmic component and decreased concentration of contractile proteins (actin and myosin) in both untrained subjects (Haun et al. 2019) and bodybuilders (Meijer et al. 2015). This model could explain the observed differences in correlation levels between our training groups, since faster eccentric contractions resulted in significantly higher training volume compared to slower ones (Kojić et al. 2021). ...
The aim of the study was to investigate how the relationship between resistance training-induced hypertrophy, strength, and
passive contractile adaptations is affected by contraction duration. Twenty university students (11 males) were randomly
assigned to either the fast eccentric/fast concentric phase group (F/F; 1 s both phases) or the slow eccentric/fast concentric
phase group (S/F; 4 s and 1 s, respectively). Both experimental groups completed a 7-week biceps curl training programme
with a total of 14 sessions (2 days/week). Elbow flexor muscle thickness (MT), one-repetition maximum (1RM), and tensiomyographic
(TMG) parameters (radial displacement—Dm and contraction time—Tc) were assessed. The percentage change
(Δ) in MT correlated significantly with the Δ1RM only in the S/F group (r = 0.712, p < 0.05). Both groups demonstrated
significant negative associations between ΔMT and ΔDm (r = 0.717–0.760, p < 0.01). Conversely, no significance was found
between ΔMT and ΔTc (F/F: r = -0.398, p = 0.255; S/F: r = 0.410, p = 0.239), Δ1RM and ΔTc (F/F: r = -0.278, p = 0.436;
S/F: r = 0.223, p = 0.536), nor Δ1RM and ΔDm (F/F: r = − 0.131, p = 0.719; S/F: r = − 0.351, p = 0.320). The main findings
indicate that the relationship between hypertrophy and strength gains is significantly stronger when resistance training was
paced with slower eccentric contractions comparing to fast ones. On the other hand, reduced Dm values indicate increase in
MT regardless of contraction duration, while strength gains are not correlated with corresponding TMG changes
... Furthermore, Kochanowicz et al. (2018b) reported no significant difference in elbow flexion strength between gymnasts and untrained individuals, whereas gymnasts had a greater lean tissue mass in the arms than untrained individuals. Cross-sectional studies have also provided evidence that dynamic strength normalized to the muscle size of body-builders, who are generally categorized as the practitioners of high-volume resistance exercises (Hackett, Johnson & Chow, 2013), is lower at the whole muscle (Alway et al., 1990;Sale et al., 1987) and single muscle fiber (Meijer et al., 2015) levels than in non-athletes or power athletes. Taken together, it is likely that long-term participation in gymnastics training produces a relatively higher muscle size gain than isometric or dynamic strength, and consequently causes the low F 0 /CSA index in gymnasts, i.e., muscle quality. ...
Background
The theoretical maximum force (F 0 ), velocity (V 0 ), and power (P max ) of athletes calculated from the relationship between force and velocity (F-V relationship) and the slope of the F-V relationship, reflect their competitive and training activity profiles. Evaluating the F-V relationship of athletes facilitates categorizing the profiles of dynamic muscle functions in relation to long-term sport-specific training. For gymnastics, however, no studies have tried to examine the profiles of F-V relation and power output for upper limb muscles in relation to the muscularity, while the use of the upper extremities in this sport is very unique as described earlier.
Purpose
It was hypothesized that the F-V relationship of the elbow flexion in gymnasts might be characterized by low capacity for generating explosive force, notably in terms of the force normalized to muscle size.
Methods
The F 0 , V 0 , and P max derived from the force-velocity relationship during explosive elbow flexion against six different loads (unloaded condition, 15, 30, 45, 60, and 75% of maximal voluntary isometric elbow flexion force (MVF EF )) for 16 gymnasts (GYM) and 22 judo athletes (JD). F 0 and P max were expressed as values relative to the cross-sectional area index (CSA index ) of elbow flexors (F 0 /CSA index and P max /CSA index , respectively), which was calculated from muscle thickness in the anterior upper arm. The electromyogram (EMG) activities of the biceps brachii (BB) during the maximal isometric and dynamic tasks were also determined.
Results
There were no significant differences in CSA index of elbow flexors between GYM and JD. MVF EF /CSA index for GYM was significantly lower than that for JD. Force was linearly associated with velocity in the dynamic elbow flexion for all the participants ( r = − 0.997 to −0.905 for GYM, r = − 0.998 to −0.840 for JD). F 0 , F 0 / CSA index , V 0 , P max , P max /CSA index , and MVF EF were significantly lower in GYM than in JD. The activity levels of BB during the dynamic tasks tended to be lower in GYM than in JD at load of <45%MVC.
Conclusion
Gymnasts cannot generate explosive elbow flexion force corresponding to their muscle size. This may be due to low neuromuscular activities during the maximal dynamic tasks against relatively low loads.
... It should also be noted that hypertrophy of muscle fibres may not always be synonymous with proportional increases in sarcomere components (i.e., actin and myosin), since high-volume resistance training in trained men reportedly resulted in fibre hypertrophy but dilution of contractile components (change in fibre size was not proportional to a change in myofibrillar proteins) (68). Hypertrophy of the sarcoplasm (but not contractile components) was previously reported in a cross-sectional study of contractile properties of untrained subjects, bodybuilders, and power athletes (115). Furthermore, the degree of fibre hypertrophy to a resistance training programme may be partially determined by the nature of the resistance training programme (50), and possibly the predominant fibre type and the size of those fibres prior to training (69). ...
... However, this works off the assumption that myostatin inhibition can induce both mass and function equally, or that mass increases always produce functional/strength improvements. It is well known that muscle strength and size are not increased in concert [41,42] and neither proportionate loss of mass, nor gain of mass arrest, can explain strength decline as humans age [43]. Indeed, studies of myostatin inhibitor drugs against age-related sarcopenic muscle wasting are consistent with data from the DMD clinical trials and support the lack of synergy between mass and strength, as well as the poor translation of murine myostatin inhibition in clinical trials. ...
Myostatin inhibition therapy has held much promise for the treatment of muscle wasting disorders. This is particularly true for the fatal myopathy, Duchenne Muscular Dystrophy (DMD). Following on from promising pre-clinical data in dystrophin-deficient mice and dogs, several clinical trials were initiated in DMD patients using different modality myostatin inhibition therapies. All failed to show modification of disease course as dictated by the primary and secondary outcome measures selected: the myostatin inhibition story, thus far, is a failed clinical story. These trials have recently been extensively reviewed and reasons why pre-clinical data collected in animal models have failed to translate into clinical benefit to patients have been purported. However, the biological mechanisms underlying translational failure need to be examined to ensure future myostatin inhibitor development endeavors do not meet with the same fate. Here, we explore the biology which could explain the failed translation of myostatin inhibitors in the treatment of DMD.
... In contrast with these results, two studies on isolated hypertrophic fibers of body builders, have shown that in well trained professional body builders increase in size and in force are dissociated, resulting in a lower specific tension for all fiber types, 24 or only for slow fibers. 25 Since determination of isometric force in single fibers ex vivo is carried out after sarcolemma permeabilization with a full supply of ATP and complete maximal calcium activation, the discrepancy likely finds a structural basis. ...
The question whether the muscle hypertrophy induced by resistance training, hormone administration or genetic manipulation is accompanied by a proportional increase in muscle strength is still open. This review summarizes and analyses data obtained in human and rodent muscles in studies that have monitored in parallel changes in muscle size and changes in muscle force, measured in isometric contractions in vivo, in isolated muscles ex vivo (in rodents) and in single muscle fibers. Although a general positive relation exists among the two variables, a number of studies show a clear dissociation with increase of muscle size with no change or even decrease in strength and, vice versa, increase in strength without increase in size. The possible mechanisms of such dissociation, which involves neural motor control and/or cellular and molecular adaptations of muscle fibers, are briefly discussed.
... However, this works off the assumption that myostatin inhibition can induce both mass and function equally, or that mass increases always produce functional/strength improvements. It is well known that muscle strength and size are not increased in concert [38,39] and neither proportionate loss of mass can explain, nor gain of mass arrest, strength decline as humans age [40]. Indeed, studies of myostatin inhibitor drugs against age-related sarcopenic muscle wasting are consistent with data from the DMD clinical trials and support the lack of synergy between mass and strength, as well as the poor translation of murine myostatin inhibition in clinical trials. ...
Myostatin inhibition therapy has held much promise for the treatment of muscle wasting disorders. This is particularly true for the fatal myopathy, Duchenne Muscular Dystrophy (DMD). Following on from promising pre-clinical data in dystrophin-deficient mice and dogs, several clinical trials were initiated in DMD patients using different modality myostatin inhibition therapies. All failed to show modification of disease course as dictated by the primary and secondary outcomes measures selected: the myostatin inhibition story thus far, is a failed clinical story. These trials have recently been extensively reviewed and reasons why pre-clinical data collected in animal models has failed to translate into clinical benefit to patients has been purported. However, the biological mechanisms underlying translational failure need to be examined to ensure future myostatin inhibitor development endeavors do not meet with the same fate. Here, we explore the biology which could explain the failed translation of myostatin inhibitors in the treatment of DMD.
... Power athletes, usually exercising with high intensity and lower volume, demonstrate a smaller muscle fibre CSA but a higher fibre specific tension compared to body builders training with high volume but low/moderate intensity (Meijer et al., 2015). The investigations of this thesis suggest that the muscle ECM might play an important role in respect to changes in strength following acute and chronic RE. ...
It is often observed that there is a high individual variability in the response to exercise-induced muscle damage (EIMD), even when tested in a homogeneous cohort accounting for age, sex, ethnicity and physical activity. The response to EIMD is very complex as several tissues, including skeletal muscle fibres, the extra-cellular matrix (ECM), and tendon, play a potential role in the damage response. Therefore, the overall aim of this PhD thesis was to investigate the physiological and genetic factors underpinning the response to muscle damaging exercise. For that, the following objectives were (i) to comprehensively assess the physiological mechanisms and recovery pattern of neuromuscular fatigue of the hamstring muscle group following an intermittent sprint (IS) intervention; (ii) to investigate inter-individual differences in skeletal muscle repair/recovery after an artificial wounding (scratch) assay using of primary human skeletal muscle cells in vitro; (iii) to ascertain whether multiple genetic variations, which are linked to varying tissues, forming a polygenic profile could distinguish between high and low responders following muscle damage in vivo and in vitro; and (iv) to assess whether a genetic profile is linked with the response to both EIMD and chronic resistance exercise. The methodological and analytical approaches utilised in this thesis identified a number of important, novel and impactful findings. Following IS, the impaired hamstring muscle function and delayed recovery is probably caused primarily by damage to the contractile tissue, and participants with a greater force generating capacity (larger physiological cross-sectional area) of the biceps femoris long head were less susceptible to hamstring strength loss immediately after IS, providing evidence that the structure of the muscle protects it against peripheral fatigue/damage. The in vitro study showed that skeletal muscles with an increased number of stem cells of the connective tissue (fibroblasts) might have a better capacity to reorganise the complex ECM, which results in a faster muscle strength recovery after muscle damaging exercise. However, a larger number of active muscle stem cells (myoblasts) seems to be important for the latter stage of muscle regeneration. Individuals possessing a non-preferential genetic profile demonstrated increased rate of muscle damage biomarkers than individuals with a preferential genetic profile. Lastly, we calculated a second polygenic profile which was linked with both the EIMD and the chronic resistance exercise response. These polygenic profiles may be used to anticipate an individual’s response/adaptation to EIMD and to chronic resistance exercise, thus enabling resistance exercise to be prescribed on a personalised level to improve muscle health and function.
... In contrast with these results, two studies on isolated hypertrophic fibers of body builders, have shown that in well trained professional body builders increase in size and in force are dissociated, resulting in a lower specific tension for all fiber types, 24 or only for slow fibers. 25 Since determination of isometric force in single fibers ex vivo is carried out after sarcolemma permeabilization with a full supply of ATP and complete maximal calcium activation, the discrepancy likely finds a structural basis. ...
The question whether the muscle hypertrophy induced by resistance training, hormone administration or genetic manipulation is accompanied by a proportional increase in muscle strength is still open. This review summarizes and analyses data obtained in human and rodent muscles in studies that have monitored in parallel changes in muscle size and changes in muscle force, measured in isometric contractions in vivo, in isolated muscles ex vivo (in rodents) and in single muscle fibers. Although a general positive relation exists among the two variables, a number of studies show a clear dissociation with increase of muscle size with no change or even decrease in strength and, vice versa, increase in strength without increase in size. The possible mechanisms of such dissociation, which involves neural motor control and/or cellular and molecular adaptations of muscle fibers, are briefly discussed.
... Our findings contrast other studies. For instance, long-term resistance training has been reported to reduce intramuscular myofibrillar volume [8], and another study indicated specific tensions are lower in muscle fibers isolated from bodybuilders compared to fibers isolated from power athletes and control subjects [23]. The latter study in particular suggests that years of training decreases myofibril density considering that the myofibril is the site of force production. ...
Resistance training generally increases skeletal muscle hypertrophy, whereas aging is associated with a loss in muscle mass. Interestingly, select studies suggest that aging, as well as resistance training, may lead to a reduction in the abundance of skeletal muscle myofibrillar (or contractile) protein (per mg tissue). Proteomic interrogations have also demonstrated that aging, as well as weeks to months of resistance training, lead to appreciable alterations in the muscle proteome. Given this evidence, the purpose of this small pilot study was to examine total myofibrillar as well as total sarcoplasmic protein concentrations (per mg wet muscle) from the vastus lateralis muscle of males who were younger and resistance-trained (denoted as YT, n = 6, 25 ± 4 years old, 10 ± 3 self-reported years of training), younger and untrained (denoted as YU, n = 6, 21 ± 1 years old), and older and untrained (denoted as OU, n = 6, 62 ± 8 years old). The relative abundances of actin and myosin heavy chain (per mg tissue) were also examined using SDS-PAGE and Coomassie staining, and shotgun proteomics was used to interrogate the abundances of individual sarcoplasmic and myofibrillar proteins between cohorts. Whole-body fat-free mass (YT > YU = OU), VL thickness (YT > YU = OU), and leg extensor peak torque (YT > YU = OU) differed between groups (p < 0.05). Total myofibrillar protein concentrations were greater in YT versus OU (p = 0.005), but were not different between YT versus YU (p = 0.325). The abundances of actin and myosin heavy chain were greater in YT versus YU (p < 0.05) and OU (p < 0.001). Total sarcoplasmic protein concentrations were not different between groups. While proteomics indicated that marginal differences existed for individual myofibrillar and sarcoplasmic proteins between YT versus other groups, age-related differences were more prominent for myofibrillar proteins (YT = YU > OU, p < 0.05: 7 proteins; OU > YT = YU, p < 0.05: 11 proteins) and sarcoplasmic proteins (YT = YU > OU, p < 0.05: 8 proteins; OU > YT&YU, p < 0.05: 29 proteins). In summary, our data suggest that modest (~9%) myofibrillar protein packing (on a per mg muscle basis) was evident in the YT group. This study also provides further evidence to suggest that notable skeletal muscle proteome differences exist between younger and older humans. However, given that our n-sizes are low, these results only provide a preliminary phenotyping of the reported protein and proteomic variables.
... Notwithstanding, and as discussed earlier, several studies suggest skeletal muscle myofibril protein density may actually decrease following weeks to years of higher volume resistance training in humans [16][17][18]. Furthermore, a recent study suggests that lower specific tensions are evident in single fibers isolated from bodybuilders with significantly larger fCSAs relative to control and power athlete fibers [36]. These authors explicitly stated "hypertrophy has a detrimental effect on specific tension", and noted that myofibril dilution through higher volume body building-style training may have been a driving factor for their observations. ...
Cellular adaptations that occur during skeletal muscle hypertrophy in response to high-volume resistance training are not well-characterized. Therefore, we sought to explore how actin, myosin, sarcoplasmic protein, mitochondrial, and glycogen concentrations were altered in individuals that exhibited mean skeletal muscle fiber cross-sectional area (fCSA) hypertrophy following 6 weeks of high-volume resistance training. Thirty previously resistance-trained, college-aged males (mean ± standard deviation: 21±2 years, 5±3 training years) had vastus lateralis (VL) muscle biopsies obtained prior to training (PRE), at week 3 (W3), and at week 6 (W6). Muscle tissue from 15 subjects exhibiting PRE to W6 VL mean fCSA increases ranging from 320–1600 μm² was further interrogated using various biochemical and histological assays as well as proteomic analysis. Seven of these individuals donated a VL biopsy after refraining from training 8 days following the last training session (W7) to determine how deloading affected biomarkers. The 15 fCSA hypertrophic responders experienced a +23% increase in mean fCSA from PRE to W6 (p<0.001) and, while muscle glycogen concentrations remained unaltered, citrate synthase activity levels decreased by 24% (p<0.001) suggesting mitochondrial volume decreased. Interestingly, repeated measures ANOVAs indicated that p-values approached statistical significance for both myosin and actin (p = 0.052 and p = 0.055, respectively), and forced post hoc tests indicated concentrations for both proteins decreased ~30% from PRE to W6 (p<0.05 for each target). Phalloidin-actin staining similarly revealed actin concentrations per fiber decreased from PRE to W6. Proteomic analysis of the sarcoplasmic fraction from PRE to W6 indicated 40 proteins were up-regulated (p<0.05), KEGG analysis indicated that the glycolysis/gluconeogenesis pathway was upregulated (FDR sig. <0.001), and DAVID indicated that the following functionally-annotated pathways were upregulated (FDR value <0.05): a) glycolysis (8 proteins), b) acetylation (23 proteins), c) gluconeogenesis (5 proteins) and d) cytoplasm (20 proteins). At W7, sarcoplasmic protein concentrations remained higher than PRE (+66%, p<0.05), and both actin and myosin concentrations remained lower than PRE (~-50%, p<0.05). These data suggest that short-term high-volume resistance training may: a) reduce muscle fiber actin and myosin protein concentrations in spite of increasing fCSA, and b) promote sarcoplasmic expansion coincident with a coordinated up-regulation of sarcoplasmic proteins involved in glycolysis and other metabolic processes related to ATP generation. Interestingly, these effects seem to persist up to 8 days following training.
... Skeletal muscle fiber type switching involves transition from glycolytic type IIb to mitochondria-rich types IIa and I which characterizes SP among power athletes. Mitochondrial amount in the recruited muscle fibers likely determines maximal sustainable power [47]. Not only has PPARGC1A been identified as master regulator of mitochondrial biogenesis, but it has also been shown to regulate proteins involved in angiogenesis and anti-oxidant defense as well as affect expression of inflammatory markers [19,48]. ...
Background
Genetics plays a role in determining potential for athletic ability (AA) and sports performance (SP). In this study, AA involves comparing sedentary controls with competitive athletes in power and endurance activities as well as a mix between the two (SP). However, variable results from genetic association studies warrant a meta-analysis to obtain more precise estimates of the association between PPARGC1A Gly482Ser polymorphism and AA/SP.
Methods
Multi-database literature search yielded 14 articles (16 studies) for inclusion. Pooled odds ratios (ORs) and 95% confidence intervals (CI) were used to estimate associations. Summary effects were modified based on statistical power. Subgroup analysis was based on SP (power, endurance and mixed) and race (Caucasians and Asians). Heterogeneity was assessed with the I² metric and its sources examined with outlier analysis which dichotomized our findings into pre- (PRO) and post-outlier (PSO).
Results
Gly allele effects significantly favoring AA/SP (OR > 1.0, P < 0.05) form the core of our findings in: (i) homogeneous overall effect at the post-modified, PSO level (OR 1.13, 95% CI 1.03–1.25, P = 0.01, I² = 0%); (ii) initially homogeneous power SP (ORs 1.22–1.25, 95% CI 1.05–1.44, P = 0.003–0.008, I² = 0%) which precluded outlier treatment; (iii) PRO Caucasian outcomes (ORs 1.29–1.32, 95% CI 1.12–1.54, P = 0.0005) over that of Asians with a pooled null effect (OR 0.99, 95% CI 0.72–1.99, P = 0.53–0.92) and (iv) homogeneous all > 80% (ORs 1.19–1.38, 95% CI 1.05–1.66, P = 0.0007–0.007, I² = 0%) on account of high statistical power (both study-specific and combined). In contrast, none of the Ser allele effects significantly favored AA/SP and no Ser-Gly genotype outcome favored AA/SP. The core significant outcomes were robust and showed no evidence of publication bias.
Conclusion
Meta-analytical applications in this study generated evidence that show association between the Gly allele and AA/SP. These were observed in the overall, Caucasians and statistically powered comparisons which exhibited consistent significance, stability, robustness, precision and lack of bias. Our central findings rest on association of the Gly allele with endurance and power, differentially favoring the latter over the former.
... Specific force was then calculated to be 29 N Á cm −2 in female and 32 N Á cm −2 in male rowers, which was slightly higher than that of male controls ( Narici, Landoni, & Minetti, 1992) and similar to the 30 N Á cm −2 reported for male controls after 9 weeks of strength training ( Erskine et al., 2010). Note that hypertrophied muscle fibres of body-builders demonstrated a lower fibre specific force than muscle fibres of power athletes and controls ( Meijer et al., 2015). Our Olympic rowers also demonstrated a large physiological cross-sectional area and muscle volume, though not at the cost of their specific force. ...
Rowers need to combine high sprint and endurance capacities. Muscle morphology largely explains muscle power generating capacity, however, little is known on how muscle morphology relates to rowing performance measures. The aim was to determine how muscle morphology of the vastus lateralis relates to rowing ergometer performance, sprint and endurance capacity of Olympic rowers. Eighteen rowers (12♂, 6♀, who competed at 2016 Olympics) performed an incremental rowing test to obtain maximal oxygen consumption, reflecting endurance capacity. Sprint capacity was assessed by Wingate cycling peak power. M. vastus lateralis morphology (volume, physiological cross-sectional area, fascicle length and pennation angle) was derived from 3-dimensional ultrasound imaging. Thirteen rowers (7♂, 6♀) completed a 2000-m rowing ergometer time trial. Muscle volume largely explained variance in 2000-m rowing performance (R² = 0.85), maximal oxygen consumption (R² = 0.65), and Wingate peak power (R² = 0.82). When normalized for differences in body size, maximal oxygen consumption and Wingate peak power were negatively related in males (r = −0.94). Fascicle length, not physiological cross-sectional area, attributed to normalized peak power. In conclusion, vastus lateralis volume largely explains variance in rowing ergometer performance, sprint and endurance capacity. For a high normalized sprint capacity, athletes may benefit from long fascicles rather than a large physiological cross-sectional area.
The interchangeable use of terms such as muscle mass, volume, cross-sectional area, and thickness in discussions on the physiology of muscle hypertrophy has led to misconceptions in research and practice. This review aims to highlight the improperness of this approach and highlights the overlooked parameter of muscular density (MD). The hypothesis is that muscle density acts as a mediator, leading to inevitable muscle enlargement in long-term strength training. It is proposed that research in muscular adaptations to training should implement measures of MD to complement measurements of muscle size. This article aims to refine the understanding of muscular adaptations and optimize training strategies for athletes and fitness enthusiasts.
Resistance training (RT) triggers diverse morphological and physiological adaptations that are broadly considered beneficial for performance enhancement as well as injury risk reduction. Some athletes and coaches therefore engage in, or prescribe, substantial amounts of RT under the assumption that continued increments in maximal strength capacity and/or muscle mass will lead to improved sports performance. In contrast, others employ minimal or no RT under the assumption that RT may impair endurance or sprint performances. However, the morphological and physiological adaptations by which RT might impair physical performance, the likelihood of these being evoked, and the training program specifications that might promote such impairments, remain largely undefined. Here, we discuss how selected adaptations to RT may enhance or impair speed and endurance performances while also addressing the RT program variables under which these adaptations are likely to occur. Specifically, we argue that while some myofibrillar (muscle) hypertrophy can be beneficial for increasing maximum strength, substantial hypertrophy can lead to macro- and microscopic adaptations such as increases in body (or limb) mass and internal moment arms that might, under some conditions, impair both sprint and endurance performances. Further, we discuss how changes in muscle architecture, fiber typology, microscopic muscle structure, and intra- and intermuscular coordination with RT may maximize speed at the expense of endurance, or maximize strength at the expense of speed. The beneficial effect of RT for sprint and endurance sports can be further improved by considering the adaptive trade-offs and practical implications discussed in this review.
Graphical abstract
Skeletal muscle, a highly heterogeneous tissue, is composed of a variety of cells and different muscle fiber types, mostly classified as slow and fast; the latter is divided into two subgroups, fast 2A and fast 2X. The functional properties of a muscle are determined not only by muscle fibers with their contractile and metabolic features but also by all cellular components. To appreciate the contribution of muscle fibers and, additionally, the specific contribution of each fiber type, single-fiber studies offer the most fruitful avenue. Single-fiber dissection from human muscle biopsy samples started 50 years ago in the 1970s and has generated a wealth of data on molecular, metabolic, and contractile characteristics of each fiber type in a variety of physiological conditions such as aging, and adaptive responses to training and disuse, and in pathological conditions. This chapter is aimed at presenting the analytical power of single-fiber studies and its impact on our knowledge of skeletal muscle in normal and pathological conditions. Special attention is given to the description and discussion of the methodologies and associated considerations for accurate analyses.Key wordsHuman skeletal muscleMuscle biopsySingle fiber dissectionEx vivo single-fiber physiologySingle-fiber biochemistry
This study examined relationships between percent myosin heavy chain (%MHC) expression and mechanomyographic amplitude (MMGRMS). Fifteen females (age ± SD=21.3 ± 5.3 yrs) completed isometric trapezoidal contractions at 30% and 70% maximal voluntary contraction (MVC). MMG was recorded from the vastus lateralis (VL). Participants gave a muscle biopsy of the VL post-testing. MMGRMS-torque relationships during the linearly varying segments were log-transformed and linear regressions were applied to calculate b terms (slopes). For the steady torque segment, MMGRMS was averaged. Correlations were performed for type I%MHC with the MMG variables. Multiple regression was utilized to examine prediction equations for type I%MHC. Type I%MHC was significantly correlated with the b terms during the increasing segment of the 70% MVC (p = 0.003; r = -0.718), and MMGRMS during steady torque at 30% (p = 0.008; r = -0.652) and 70% MVC (p = 0.040; r = -0.535). Type I% MHC reduced the linearity of the MMGRMS-torque relationship during the high-intensity linearly increasing segment, and MMGRMS at a low- and high-intensity steady torque. A combination of MMG variables estimated type I%MHC expression with 81.2% accuracy. MMG recorded during a low- and high-intensity isometric trapezoidal contraction may offer a simple, noninvasive test for estimating type I%MHC expression of the VL in sedentary females.
Skeletal muscle-related symptoms are common in both acute coronavirus disease (Covid)-19 and post-acute sequelae of Covid-19 (PASC). In this narrative review, we discuss cellular and molecular pathways that are affected and consider these in regard to skeletal muscle involvement in other conditions, such as acute respiratory distress syndrome, critical illness myopathy, and post-viral fatigue syndrome. Patients with severe Covid-19 and PASC suffer from skeletal muscle weakness and exercise intolerance. Histological sections present muscle fibre atrophy, metabolic alterations, and immune cell infiltration. Contributing factors to weakness and fatigue in patients with severe Covid-19 include systemic inflammation, disuse, hypoxaemia, and malnutrition. These factors also contribute to post-intensive care unit (ICU) syndrome and ICU-acquired weakness and likely explain a substantial part of Covid-19-acquired weakness. The skeletal muscle weakness and exercise intolerance associated with PASC are more obscure. Direct severe acute respiratory syndrome coronavirus (SARS-CoV)-2 viral infiltration into skeletal muscle or an aberrant immune system likely contribute. Similarities between skeletal muscle alterations in PASC and chronic fatigue syndrome deserve further study. Both SARS-CoV-2-specific factors and generic consequences of acute disease likely underlie the observed skeletal muscle alterations in both acute Covid-19 and PASC.
Chemically skinned fibres help study human muscle contractile function in vitro. A particularly important parameter is specific force (SF), i.e., maximal isometric force divided by cross‐sectional area, representing contractile quality. Although SF varies substantially between studies, the magnitude and cause of this variability remains puzzling. Here, we summarize and explore the cause of variability in SF between studies. A systematic search was conducted in Medline, Embase and Web of Science databases in June 2020, yielding 137 data sets. These are evaluated from 61 publications studying healthy, young adults. Reported data adjustment for key methodological differences allows between study comparisons. Five‐fold differences in mean SF data occur. Remarkably, adjustment for fibre shape, swelling and sarcomere length fails to reduce SF variance. However, grouping papers based on shared authorship reveal consistency within research groups. Lower SF is associated with higher phosphocreatine concentrations in the activating solution and using Triton X‐100 as a skinning agent. Whilst the analysis shows variance across the literature (I2 ≥96%), the ratio of SF in single fibres containing myosin heavy chain isoforms IIA or I is consistent across research groups. In conclusion, the skinned fibre technique is reliable for studying in vitro force generation of single fibres. Yet, solution composition used to activate fibres heavily influences SF values.
Periodization can be defined as a logical sequential, phasic method of manipulating fitness and recovery
phases to increase the potential for achieving specific performance goals while minimizing the potential for nonfunctional overreaching,
overtraining, and injury. Periodization deals with the micromanagement of timelines and fitness phases and is cyclic in
nature. On the other hand, programming deals with the micromanagement of the training process and deals with exercise selection,
volume, intensity, etc. Evidence indicates that a periodized training process coupled with appropriate programming can produce
superior athletic enhancement compared with nonperiodized process. There are 2 models of periodization, traditional and block.
Traditional can take different forms (i.e., reverse). Block periodization has 2 subtypes, single goal or factor (individual sports) and
multiple goals or factors (team sports). Both models have strengths and weaknesses but can be “tailored” through creative
programming to produce excellent results for specific sports.
Most pancreatic cancer patients are affected by cancer cachexia: a syndrome of severe weight loss, muscle wasting and adipose tissue loss. Several pathophysiological drivers including inflammation, altered protein, glucose, and lipid metabolism, anorexia, malabsorption, and neuro-endocrine changes are thought to underlie the development of cancer cachexia. Having cachexia in pancreatic cancer is associated with a mortality rate of up to 80%. Clinical assessment of body composition, nutritional status, physical fitness, and inflammation are important for (early) detection (and treatment) of cachexia. Many of these assessments can be performed using preoperative diagnostics used in routine care such as abdominal computer tomography scans and blood tests. High pre-operative C-reactive protein levels, increased skeletal muscle fat content (myosteatosis), and low peak oxygen consumption are among the strongest predictors of poor overall survival. Treatment of cancer cachexia remains a challenge as patients can present themselves with many different combinations of symptoms (phenotypes). Therefore, cancer cachexia should be addressed using a personalized multimodal approach, including at least nutritional support, anti-inflammatory drugs and/or immunonutrition, and exercise.
Skeletal muscle hypertrophy can be induced by hormones and growth factors acting directly as positive regulators of muscle growth or indirectly by neutralizing negative regulators, and by mechanical signals mediating the effect of resistance exercise. Muscle growth during hypertrophy is controlled at the translational level, through the stimulation of protein synthesis, and at the transcriptional level, through the activation of ribosomal RNAs and muscle-specific genes. mTORC1 has a central role in the regulation of both protein synthesis and ribosomal biogenesis. Several transcription factors and co-activators, including MEF2, SRF, PGC-1α4, and YAP promote the growth of the myofibers. Satellite cell proliferation and fusion is involved in some but not all muscle hypertrophy models.
Aim:
Skeletal muscles of Body Builders (BB) represent an interesting model to study muscle mass gains in response to high volume resistance training. It is debated whether muscle contractile performance improves in proportion to mass. Here we aim to assess whether muscle hypertrophy does not occur at the expense of performance.
Methods:
6 BB and 6 untrained controls (CTRL) were recruited. Cross Sectional Area (CSA) and maximum voluntary contraction (MVC) of quadriceps femoris muscle (QF) and CSA and architecture of vastus lateralis (VL) were determined. Moreover, a biopsy was taken from VL mid-portion and single fibres were analysed.
Results:
QF CSA and MVC were 32% (n.s., P=.052) and 58% (P=.009) higher in BB than in CTRL, respectively. VL CSA was 37% higher in BB (P=.030). Fast 2A fibres CSA was 24% (P=.048) greater in BB than in CTRL, when determined in immunostained sections of biopsy samples. Single permeabilized fast fibres CSA was 37% (n.s., P=.052) higher in BB than in CTRL, and their force was slightly higher in BB (n.s.), while specific tension (P0 ) was 19% (P=.024) lower. The lower P0 was not explained neither by lower myosin content nor by impaired calcium diffusion. Conversely, the swelling due to skinning-induced permeabilization was different and, when used to correct P0 , differences between populations disappeared.
Conclusions:
The results show that high degree of muscle hypertrophy is not detrimental for force generation capacity, as increases in fibre size and force are strictly proportional once the differential swelling response is accounted for.
Development and maintenance of sprint training adaptations: an uphill-downhill study. J Strength Cond Res 36(1): 90–98, 2022-We examined the development of performance adaptations resulting from an uphill-downhill training program and monitored the decline of adaptations during detraining. Twenty-eight men were randomly assigned to 1 of 2 sprint training groups who trained 3 times per week for 6 weeks and a control group (C). The uphill-downhill group (U+D) trained on an 80-m platform with 3° slopes, whereas the horizontal (H) group trained on flat track. Subjects were tested for maximal running speed (MRS), associated kinematics, and leg strength before and after training, with U+D subjects also tested after weeks 2 and 4 of training, and after a 3-week detraining period. The U+D group increased their MRS by 3.7% (from 8.75 ± 0.72 to 9.07 ± 0.64 m·s, p < 0.05), their stride rate by 3.1% (from 4.21 ± 0.21 to 4.34 ± 0.18 Hz, p < 0.05), and their knee extensors' maximum isometric force by 21% (from 2,242 ± 489 to 2,712 ± 498 N, p < 0.05) after training. The time course of changes showed declines for weeks 1-4 (1.4-5.1%), but an ascending trend of improvement compensated all losses by the end of week 6 (p < 0.05). During detraining, no decreases occurred. No changes were observed for the H and C groups. The minimum period to produce positive effects was 6 weeks, with a very good standard of performance maintained 3 weeks after training. U+D training will prove useful for all athletes requiring fast adaptations, and it can fit into training mesocycles because of its low time demands.
RESUMEN El presente estudio es cuantitativo de tipo correlacional el cual tuvo un diseño experimental puro y como objetivo el desarrollo de la hipertrofia en la masa muscular de miembros inferiores (MMMI) a través de un programa de musculación de 20 semanas, para el logro de este objetivo se realizó una intervención a 10 hombres sanos que se conformaron 2 grupos de 5 integrantes de manera aleatoria y se estimó la MMMI, posterior se empleó un test de laboratorio para conocer la potencia de miembros inferiores (PMI), el Grupo F1 (edad 17±1,52 años, talla(m) 1,73±0,05, MMMI (Kg) 11,19±1,39) aplicó un programa de entrenamiento con sobrecargas de frecuencia 1 mientras que el Grupo F2 (edad 18 ±2,86 años, talla(m) 1,71±0,07, MMMI (Kg) 10,7±1,04) efectuó un programa de entrenamiento de frecuencia 2, luego de finalizar las 20 semanas de entrenamiento se evaluó nuevamente la PMI y se estimó la MMMI. Después de analizar los resultados obtenidos se evidenciaron mejoras más significativas en el incremento de la MMMI en el Grupo F2 con respecto al Grupo F1, también se manifestó un mayor beneficio en el Grupo F2 en la mejora de la fuerza en los ejercicios efectuados, sin embargo ninguno de los grupos mejoró significativamente la PMI, por consiguiente se concluye que el entrenamiento con sobrecargas de frecuencia 2 permite obtener un incremento más significativo de la fuerza y MMMI comparado con el entrenamiento de frecuencia 1, no obstante no se encontraron mejoras significativas en la PMI con ninguno de los programas.
Introduction
Muscle hypertrophy is the main outcome of training for body building. Previous studies showed a discrepancy between the functional (force/tension) and structural (cross‐sectional area, CSA) proprieties of leg extensor muscles measured in vivo and the corresponding parameters measured in single muscle fibers [1] [2] . In particular, a puzzling finding from these studies was that of a lower specific tension of skinned fibers of body builders (BB) compared to a control (C) population.
In this study we aimed to investigate the possible reasons behind the alleged lower specific tension in single fibers of a strictly diet‐and‐training‐controlled BB population.
Methods
Five male body builders (26±4.7 yr; 87.2±9.7 kg; 178.4±7.5 cm) with a training history of at least 5 years were recruited for this study. Five age‐matched recreationally active males (24.6±3.6 yr; 84.4±14.9 kg; 186.4±4.4 cm) were recruited as controls. After ethical approval, biopsies from the vastus lateralis (VL) muscle were collected together with in‐vivo quadriceps maximum isometric voluntary contraction (MVC) and architecture and CSA. Data analysis included (i) single skinned fiber mechanics (n=200 fibers; maximum force, CSA, specific tension and calcium diffusion), (ii) single fiber myosin quantification (n=100 fibers), (iii) slow and fast fiber CSA via histological section analysis. In addition, swelling ratio (skinned fibers CSA/histological CSA) was calculated for each fiber type and for each subject. A general linear mixed model was used to assess statistically significant differences.
Results
Quadriceps MVC and CSA were 64% and 33% higher in BB than C (p<0.05), VL pennation angle (PA) and thickness (MT) were 16% and 15% higher in BB than C (p<0.05). Quadriceps specific force was 25% higher in BB than C (n.s.). Single skinned type 2 CSA and force were 48% and 28% higher in BB than C (p<0.05), while specific tension was 19% lower (p<0.05). Type 1 fibers specific tension was 32% higher in BB than C (p<0.05). Myosin content and calcium diffusion were similar among populations. CSA determined in histological sections was 10% and 27% higher in BB than C (p<0.05) for type1 and 2 fibers, respectively. When type 1 and type 2 fiber tensions were corrected for individual swelling ratio, the difference between BB and C disappeared.
Conclusions
Although at first sight these findings seem to confirm that in type 2 skinned fibers of BB specific tension is lower than in C, once accounting for fiber swelling, this difference disappears. This is further confirmed by the lack of difference in myosin concentration and calcium diffusion kinetics.
In contrast, the results point to the existence of a differential swelling response to the skinning process by BB and C fibers, possibly due to adaptations of the fiber cytoskeleton proteins or specific permeability of the membrane of slow and fast fibers.
ABSTRACT FOR DECADES, MOST SCIENTISTS AND PRACTITIONERS HAVE AGREED THAT MUSCLE HYPERTROPHY ALSO INDUCES STRENGTH GAINS. HOWEVER, A RECENT PUBLICATION “THE PROBLEM OF MUSCLE HYPERTROPHY: REVISITED,” BUCKNER, SL, DANKEL, SJ, MATTOCKS, KT, JESSEE, MB, MOUSER, JG, COUNTS, BR, ET AL. THE PROBLEM OF MUSCLE HYPERTROPHY: REVISITED. MUSCLE NERVE 54: 1012–1014, 2016, QUESTIONED THE MECHANISTIC ROLE THAT EXERCISE-INDUCED INCREASES IN MUSCLE SIZE HAVE ON THE EXERCISE-INDUCED INCREASES IN STRENGTH (OR FORCE PRODUCTION), AS WELL AS THE INFLUENCE THAT EXERCISE-INDUCED INCREASES IN STRENGTH HAVE ON SPORTS PERFORMANCE. SUCH SUGGESTIONS UNDERMINE THE IMPORTANCE OF CERTAIN ASPECTS OF STRENGTH AND CONDITIONING FOR SPORT. SPECIFICALLY, IF NOT ACTING AS A MECHANISM FOR STRENGTH ADAPTATION, IT IS UNCLEAR IF THERE IS A SPORTS-RELATED BENEFIT TO SKELETAL MUSCLE HYPERTROPHY. IN ADDITION, THE AUTHORS ARGUED THAT IF STRENGTH HAS LITTLE IMPACT ON SPORTS PERFORMANCE, STRENGTH AND CONDITIONING PROGRAMS MAY BE DOING LITTLE MORE THAN DELAYING RECOVERY FROM PRACTICING THE ACTUAL SPORT. THIS CONTENTION ALSO INDICATES THAT HYPERTROPHY SHOULD BE AVOIDED IN NEARLY ALL SCENARIOS BECAUSE INCREASED MUSCLE SIZE WOULD BE ADDITIONAL MASS THAT MUST BE OVERCOME. THE PURPOSE OF THIS SPECIAL DISCUSSION IS TO ALLOW FOR AN IN-DEPTH SCIENTIFIC DISCUSSION OF THE EXPERIMENTAL EVIDENCE FOR AND AGAINST THE POSITION OF BUCKNER ET AL. THAT EXERCISE-INDUCED INCREASES IN MUSCLE SIZE HAVE LITTLE RELEVANCE ON THE EXERCISE-INDUCED INCREASES IN STRENGTH, AND THUS, SPORT PERFORMANCE.
Previous investigations of strength have only focused on biomechanical or psychological determinants, while ignoring the potential interplay and relative contributions of these variables. The purpose of this study was to investigate the relative contributions of biomechanical, anthropometric, and psychological variables to the prediction of maximum parallel barbell back squat strength. Twenty-one college-aged participants (male = 14; female = 7; age = 23 ± 3 years) reported to the laboratory for two visits. The first visit consisted of anthropometric, psychometric, and parallel barbell back squat one-repetition maximum (1RM) testing. On the second visit, participants performed isometric dynamometry testing for the knee, hip, and spinal extensors in a sticking point position-specific manner. Multiple linear regression and correlations were used to investigate the combined and individual relationships between biomechanical, anthropometric, and psychological variables and squat 1RM. Multiple regression revealed only one statistically predictive determinant: fat free mass normalized to height (standardized estimate ± SE = 0.6 ± 0.3; t(16) = 2.28; p = 0.037). Correlation coefficients for individual variables and squat 1RM ranged from r = -0.79-0.83, with biomechanical, anthropometric, experiential, and sex predictors showing the strongest relationships, and psychological variables displaying the weakest relationships. These data suggest that back squat strength in a heterogeneous population is multifactorial and more related to physical rather than psychological variables.
The purpose of the present study was to evaluate muscular adaptations between heavy- and moderate-load resistance train-ing (RT) with all other variables controlled between conditions. Nineteen resistance-trained men were randomly assigned to either a strength-type RT routine (HEAVY) that trained in a loading range of 2-4 repetitions per set (n = 10) or a hypertro-phy-type RT routine (MODERATE) that trained in a loading range of 8-12 repetitions per set (n = 9). Training was carried out 3 days a week for 8 weeks. Both groups performed 3 sets of 7 exercises for the major muscle groups of the upper and lower body. Subjects were tested pre- and post-study for: 1 repetition maximum (RM) strength in the bench press and squat, upper body muscle endurance, and muscle thickness of the elbow flexors, elbow extensors, and lateral thigh. Results showed statistically greater increases in 1RM squat strength favoring HEAVY compared to MODERATE. Alternatively, statistically greater increases in lateral thigh muscle thickness were noted for MODERATE versus HEAVY. These findings indicate that heavy load training is superior for maximal strength goals while moderate load training is more suited to hypertrophy-related goals when an equal number of sets are performed between conditions.
Novel experimental methods, including a modified single fiber in vitro motility assay, X-ray diffraction experiments, and mass spectrometry analyses, have been performed to unravel the molecular events underlying the aging-related impairment in human skeletal muscle function at the motor protein level. The effects of old age on the function of specific myosin isoforms extracted from single human muscle fiber segments, demonstrated a significant slowing of motility speed (P < 0.001) in old age in both type I and IIa myosin heavy chain (MyHC) isoforms. The force-generating capacity of the type I and IIa MyHC isoforms was, on the other hand, not affected by old age. Similar effects were also observed when the myosin molecules extracted from muscle fibers were exposed to oxidative stress. X-ray diffraction experiments did not show any myofilament lattice spacing changes, but unraveled a more disordered filament organization in old age as shown by the greater widths of the 1, 0 equatorial reflections. Mass spectrometry (MS) analyses revealed eight age-specific myosin post-translational modifications (PTMs), in which two were located in the motor domain (carbonylation of Pro79 and Asn81) and six in the tail region (carbonylation of Asp900, Asp904, and Arg908; methylation of Glu1166; deamidation of Gln1164 and Asn1168). However, PTMs in the motor domain were only observed in the IIx MyHC isoform, suggesting PTMs in the rod region contributed to the observed disordering of myosin filaments and the slowing of motility speed. Hence, interventions that would specifically target these PTMs are warranted to reverse myosin dysfunction in old age.
In 2012 we will again see the impressive achievements of many athletes during the London Olympic Games. In particular for weightlifters success is dependent on the power- and force-generating capacity of their muscles, which in turn are strongly determined by muscle mass. Many athletes and bodybuilders therefore train intensively to develop as much muscle hypertrophy as possible. Unlimited hypertrophy, however, is impossible. Limitations may be imposed by the peak forces that the tendons, bones and joints can cope with, but also by factors within the muscles themselves. For instance, an increase in pennation angle, which accompanies hypertrophy, beyond 450 would result in a reduction in muscle strength even if muscle mass continuous to increase. There also is a trade-off between metabolism and diffusion, where highly oxidative fibers require shorter diffusion distances, and hence smaller fibers, for adequate
oxygen supply to the mitochondria, than glycolytic fibers. A similar situation applies to the myonuclei where transcripts are distributed over the cell mainly by diffusion and unbridled hypertrophy would, at least in theory, cause serious problems with fiber maintenance. Despite these limiting factors muscles in bodybuilders can be as much as 74% larger than in the normal population. Elderly people have a lower muscle mass that may cause problems with daily life activities and an increase in muscle strength would improve their quality of life. There are indications, however, that the maximal attainable hypertrophy is significantly reduced in the elderly. Here it is suggested that while individual fibers in the elderly may hypertrophy to a similar extent as their younger counterparts, the age-related loss of muscle fibers is an additional limiting factor of the whole muscle hypertrophy at old age.
Combined androgenic-anabolic steroids (AAS) and overloading affects tendon collagen metabolism and ultrastructure, and is often associated with a higher risk of injury. The aim of this prospective study was to investigate whether such effects would be reflected in the patellar tendon properties of individuals with a history of long-term resistance training and AAS abuse (RTS group), when compared to trained (RT) and untrained (CTRL) non-steroids users. Tendon cross-sectional area (CSA), stiffness, Young's modulus and toe-limit strain were measured in vivo, from synchronized ultrasonography and dynamometry data. The patellar tendon of RT and RTS subjects was much stiffer and larger than in the CTRL group. However, stiffness and modulus were higher in the RTS group (26%, P < 0.05 and 30%, P < 0.01, respectively) than in the RT group. Conversely, tendon CSA was 15% (P < 0.05) larger in the RT group than in RTS, although differences disappeared when this variable was normalized to quadriceps maximal isometric torque. Yet maximal tendon stress was higher in RTS than in RT (15%, P < 0.05), without any statistical difference in maximal strain and toe limit strain between groups. The present lack of difference in toe-limit strain does not substantiate the hypothesis of changes in collagen crimp pattern associated with AAS abuse. However, these findings indicate that tendon adaptations from years of heavy resistance training are different in AAS users, suggesting differences in collagen remodelling. Some of these adaptations (e.g. higher stress) could be linked to a higher risk of tendon injury.
Oxidative function during exercise was evaluated in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (RTA, body mass 102.6±7.3 kg, mean±SD) and 11 controls (CTRL, body mass 77.8±6.0). Pulmonary O2 uptake (V'O2) and vastus lateralis muscle fractional O2 extraction (by near-infrared spectroscopy) were determined during an incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers obtained by biopsy. Quadriceps femoris muscle cross sectional area, volume (determined by magnetic resonance imaging) and strength were greater in RTA vs. CTRL (by ~40%, ~33% and ~20%, respectively). V'O2peak during CE was higher in RTA vs. CTRL (4.05±0.64 L min(-1) vs. 3.56±0.30); no difference between groups was observed during KE. The O2 cost of CE exercise was not different between groups. When divided per muscle mass (for CE) or quadriceps muscle mass (for KE) V'O2peak was lower (by 15-20%) in RTA vs. CTRL. Vastus lateralis fractional O2 extraction was lower in RTA vs. CTRL at all work rates, both during CE and KE. RTA had higher ADP-stimulated mitochondrial respiration (56.7±23.7 pmolO2•s(-1)•mg(-1) ww) vs. CTRL (35.7±10.2), and a tighter coupling of oxidative phosphorylation. In RTA the greater muscle mass and maximal force, and the enhanced mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O2 diffusion. The net results are an enhanced whole body oxidative function at peak exercise, and unchanged efficiency and O2 cost at submaximal exercise, despite a much greater body mass.
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Muscle force is typically proportional to muscle size, resulting in constant force normalized to muscle fiber cross-sectional area (specific force). Mice overexpressing insulin-like growth factor-1 (IGF-1) exhibit a proportional gain in muscle force and size, but not the myostatin-deficient mice. In an attempt to explore the role of the cytoplasmic volume supported by individual myonuclei [myonuclear domain (MND) size] on functional capacity of skeletal muscle, we have investigated specific force in relation to MND and the content of the molecular motor protein, myosin, at the single muscle fiber level from myostatin-knockout (Mstn(-/-)) and IGF-1-overexpressing (mIgf1(+/+)) mice. We hypothesize that the addition of extra myonuclei is a prerequisite for maintenance of specific force during muscle hypertrophy. A novel algorithm was used to measure individual MNDs in 3 dimensions along the length of single muscle fibers from the fast-twitch extensor digitorum longus and the slow-twitch soleus muscle. A significant effect of the size of individual MNDs in hypertrophic muscle fibers on both specific force and myosin content was observed. This effect was muscle cell type specific and suggested there is a critical volume individual myonuclei can support efficiently. The large MNDs found in fast muscles of Mstn(-/-) mice were correlated with the decrement in specific force and myosin content in Mstn(-/-) muscles. Thus, myostatin inhibition may not be able to maintain the appropriate MND for optimal function.
The chemically skinned fibre is a suitable preparation to determine whether alterations in myofilament function contribute to muscle dysfunction during ageing and disorders such as chronic obstructive pulmonary disease (COPD). In this preparation the sarcolemma is chemically permeabilized and the myofilament lattice kept intact, functioning under controlled near-physiological conditions. As force generating capacity is an important determinant of muscle function and is related to fibre crosssectional area (FCSA), we compared several methods employed by researchers to determine FCSA. Specific tension, force divided by FCSA, has a co-efficient of variation of 27%, 37%, or 30% when the FCSA was measured from the width and depth assuming an elliptical circumference, the width assuming a circular circumference, and the width while the fibre was suspended in the air, respectively. The last method showed the closest relation with the FCSA in histological sections. The velocity of maximal unloaded shortening (V(0)) varied with fibre type, with fibres expressing the Beta/slow (type I) myosin heavy chain (MyHC) isoform being the slowest and fibres expressing the IIb MyHC isoform the fastest. While muscle weakness experienced after surgery could not be explained by changes in specific tension or FCSA of individual fibres, the preparation revealed significant changes in myofilament function during ageing and COPD.
We explored to which extent maximal velocity of shortening (Vmax), force per cross-sectional area (specific tension, Po) and curvature of the force–velocity relationship (a/Po in the Hill equation) contribute to differences in peak power of single, chemically skinned rat type I fibres. Force–velocity relationships were determined from isotonic contractions of 94 maximally activated fibres. Peak power (±SD) was 3.50 ± 1.64 W L−1. There was a tenfold range of peak power and five-, six- and fourfold ranges for Po, Vmax and a/Po, respectively. None of the differences between fibres was explicable by differences in myosin heavy or light chain composition. The inverse relationship between a/Po and Vmax suggests a similar underlying cause. Fitting the data to the Huxley (Progr Biophys Biophys Chem 7:255–318, 1957) cross-bridge model showed that the rate constant g
2 and the sum of the rate constants (f + g
1) co-varied, both being low in the slowest fibres. Approximately 16% of the variation in Po could be explained by variation in the proportion of attached cycling cross-bridges (f/(f + g
1)), but the origin of most of the variance in Po remains unknown.
The quest to increase lean body mass is widely pursued by those who lift weights. Research is lacking, however, as to the best approach for maximizing exercise-induced muscle growth. Bodybuilders generally train with moderate loads and fairly short rest intervals that induce high amounts of metabolic stress. Powerlifters, on the other hand, routinely train with high-intensity loads and lengthy rest periods between sets. Although both groups are known to display impressive muscularity, it is not clear which method is superior for hypertrophic gains. It has been shown that many factors mediate the hypertrophic process and that mechanical tension, muscle damage, and metabolic stress all can play a role in exercise-induced muscle growth. Therefore, the purpose of this paper is twofold: (a) to extensively review the literature as to the mechanisms of muscle hypertrophy and their application to exercise training and (b) to draw conclusions from the research as to the optimal protocol for maximizing muscle growth.
Hypoxia may be one of the factors underlying muscle dysfunction during ageing and chronic lung and heart failure. Here we tested the hypothesis that chronic hypoxia per se affects contractile properties of single fibres of the soleus and diaphragm muscle. To do this, the force–velocity relationship, rate of force redevelopment and calcium sensitivity of single skinned fibres from normoxic rats and rats exposed to 4 weeks of hypobaric hypoxia (410 mmHg) were investigated. The reduction in maximal force (P
0) after hypoxia (p = 0.031) was more pronounced in type IIa than type I fibres and was mainly attributable to a reduction in fibre cross-sectional area (p = 0.044). In type IIa fibres this was aggravated by a reduction in specific tension (p = 0.001). The maximal velocity of shortening (V
max) and shape of the force velocity relation (a/P
0), however, did not differ between normoxic and hypoxic muscle fibres and the reduction in maximal power of hypoxic fibres (p = 0.012) was mainly due to a reduction in P
0. In conclusion, chronic hypoxia causes muscle fibre dysfunction which is not only due to a loss of muscle mass, but also to a diminished force generating capacity of the remaining contractile material. These effects are similar in the soleus and diaphragm muscle, but more pronounced in type IIa than I fibres.
An inverse relationship exists between striated muscle fiber size and its oxidative capacity. This relationship implies that muscle fibers, which are triggered to simultaneously increase their mass/strength (hypertrophy) and fatigue resistance (oxidative capacity), increase these properties (strength or fatigue resistance) to a lesser extent compared to fibers increasing either of these alone. Muscle fiber size and oxidative capacity are determined by the balance between myofibrillar protein synthesis, mitochondrial biosynthesis and degradation. New experimental data and an inventory of critical stimuli and state of activation of the signaling pathways involved in regulating contractile and metabolic protein turnover reveal: (1) higher capacity for protein synthesis in high compared to low oxidative fibers; (2) competition between signaling pathways for synthesis of myofibrillar proteins and proteins associated with oxidative metabolism; i.e., increased mitochondrial biogenesis via AMP-activated protein kinase attenuates the rate of protein synthesis; (3) relatively higher expression levels of E3-ligases and proteasome-mediated protein degradation in high oxidative fibers. These observations could explain the fiber type–fiber size paradox that despite the high capacity for protein synthesis in high oxidative fibers, these fibers remain relatively small. However, it remains challenging to understand the mechanisms by which contractile activity, mechanical loading, cellular energy status and cellular oxygen tension affect regulation of fiber size. Therefore, one needs to know the relative contribution of the signaling pathways to protein turnover in high and low oxidative fibers. The outcome and ideas presented are relevant to optimizing treatment and training in the fields of sports, cardiology, oncology, pulmonology and rehabilitation medicine.
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Sarcopenia reflects a progressive withdrawal of anabolism and an increased catabolism, along with a reduced muscle regeneration capacity. Muscle force and power decline more than muscle dimensions: older muscle is intrinsically weak. Sarcopenic obesity (SO) among the elderly corroborates to the loss of muscle mass increasing the risk of metabolic syndrome development. Recent studies on the musculoskeletal adaptations with ageing and key papers on the mechanisms of muscle wasting, its functional repercussions and on SO are included. Neuropathic, hormonal, immunological, nutritional and physical activity factors contribute to sarcopenia. Selective fast fibre atrophy, loss of motor units and an increase in hybrid fibres are typical findings of ageing. Satellite cell number decreases reducing muscle regeneration capacity. SO promotes further muscle wasting and increases risk of metabolic syndrome development. The proportion of fast to slow fibres seems maintained in old age. In elderly humans, nuclear domain is maintained constant. Basal protein synthesis and breakdown show little changes in old age. Instead, blunting of the anabolic response to feeding and exercise and of the antiproteolytic effect of insulin is observed. Further understanding of the mechanisms of sarcopenia requires disentangling of the effects of ageing alone from those of disuse and disease. The causes of the greater anabolic resistance to feeding and exercise of elderly women need elucidating. The enhancement of muscle regeneration via satellite cell activation via the MAPK/notch molecular pathways seems particularly promising.
The ability of a muscle to shorten and produce force is crucial for locomotion, posture, balance and respiration. During a contraction, myosin heads on the myosin filament propel the actin filament via ATP hydrolysis, resulting in shortening of the muscle and/or force generation. The maximal shortening velocity of a muscle fibre is largely determined by the myosin ATPase activity, while maximal force is primarily determined by the cross-sectional area. Since most muscles are pennate rather than parallel-fibred and work at different lever ratios, muscle architecture and joint-tendon anatomy has to be taken into account to obtain the force and velocity characteristics of a muscle. Additionally, the recruitment of agonistic and antagonistic muscles will contribute to the torque generated during a contraction. Finally, tendon compliance may impact on the rate of force rise and force generated if it is such that the muscle contraction proceeds in the ascending limb of the length-tension relation. Even when magnetic resonance imaging and ultrasound, combined with EMG and/or electrical stimulation, have been applied to relate changes in muscle contractile properties to alterations in muscle size and architecture during ageing and resistance training, a disproportionate change in muscle strength and size remains to be explained.
The study of single muscle fibers has improved our understanding of muscle physiology and pathology. To compare three techniques for fiber preparation and storage, biopsies were obtained from the tibialis anterior and vastus lateralis muscles of a hemiparetic patient and a control subject. Single fibers were prepared with: (1) chemical skinning (CS) and storage at -20 degrees C; (2) chemical skinning followed by sucrose (SU) incubation and storage at -80 degrees C; or (3) freeze-drying (FD) and -80 degrees C storage. Cross-sectional area (CSA), resting, maximal (P0), and specific tension (P0/CSA), and maximum shortening velocity (V0) were determined in 189 cells. CSA was similar in all groups. Resting tension was higher and P0 and P0/CSA lower after FD. In general, V0 was the same in all groups. Our data suggest that CS and SU preserve the properties of single muscle fibers better than FD. SU may allow longer storage of fibers.
Whole muscle strength and cross-sectional area (WMCSA), and contractile properties of chemically skinned segments from single fibers of the quadriceps were studied in 7 young men (YM, 36.5 +/- 3. 0 yr), 12 older men (OM, 74.4 +/- 5.9 yr), and 12 older women (OW, 72.1 +/- 4.3 yr). WMCSA was smaller in OM compared with YM (56.1 +/- 10.1 vs. 79.7 +/- 13.1 cm(2); P = 0.031) and in OW (44.9 +/- 7.5; P < 0.003) compared with OM. Age-related, but not sex-related, differences in strength were eliminated after adjusting for WMCSA. Maximal force was measured in 552 type I and 230 type IIA fibers. Fibers from YM (type I = 725 +/- 221; type IIA = 792 +/- 271 microN) were stronger (P < 0.001) than fibers from OM (I = 505 +/- 179; IIA = 577 +/- 262 microN) even after correcting for size. Type IIA fibers were stronger (P < 0.005) than type I fibers in YM and OM but not in OW (I = 472 +/- 154; IIA = 422 +/- 97 microN). Sex-related differences in type I and IIA fibers were dependent on fiber size. In conclusion, differences in WMCSA explain age-related differences in strength. An intrinsic defect in contractile proteins could explain weakness in single fibers from OM. Sex-related differences exist at the whole muscle and single fiber levels.
The aim of this study was to assess the relationships between human muscle fiber hypertrophy, protein isoform content, and maximal Ca(2+)-activated contractile function following a short-term period of resistance exercise training. Six male subjects (age 27 +/- 2 yr) participated in a 12-wk progressive resistance exercise training program that increased voluntary lower limb extension strength by >60%. Single chemically skinned fibers were prepared from pre- and posttraining vastus lateralis muscle biopsies. Training increased the cross-sectional area (CSA) and peak Ca(2+)-activated force (P(o)) of fibers containing type I, IIa, or IIa/IIx myosin heavy chain by 30-40% without affecting fiber-specific force (P(o)/CSA) or unloaded shortening velocity (V(o)). Absolute fiber peak power rose as a result of the increase in P(o), whereas power normalized to fiber volume was unchanged. At the level of the cross bridge, the effects of short-term resistance training were quantitative (fiber hypertrophy and proportional increases in fiber P(o) and absolute power) rather than qualitative (no change in P(o)/CSA, V(o), or power/fiber volume).
The aim of this study was to investigate the modulation of satellite cell content and myonuclear number following 30 and 90 days of resistance training and 3, 10, 30, 60 and 90 days of detraining. Muscle biopsies were obtained from the vastus lateralis of 15 young men (mean age: 24 years; range: 20-32 years). Satellite cells and myonuclei were studied on muscle cross-sections stained with a monoclonal antibody against CD56 and counterstained with Mayer's haematoxylin. Cell cycle markers CyclinD1 and p21 mRNA levels were determined by Northern blotting. Satellite cell content increased by 19% (P= 0.02) at 30 days and by 31% (P= 0.0003) at 90 days of training. Compared to pre-training values, the number of satellite cells remained significantly elevated at 3, 10 and 60 days but not at 90 days of detraining. The two cell cycle markers CyclinD1 and p21 mRNA significantly increased at 30 days of training. At 90 days of training, p21 was still elevated whereas CyclinD1 returned to pre-training values. In the detraining period, p21 and CyclinD1 levels were similar to the pre-training values. There were no significant alterations in the number of myonuclei following the training and the detraining periods. The fibre area controlled by each myonucleus gradually increased throughout the training period and returned to pre-training values during detraining. In conclusion, these results demonstrate the high plasticity of satellite cells in response to training and detraining stimuli and clearly show that moderate changes in the size of skeletal muscle fibres can be achieved without the addition of new myonuclei.
The purpose of this investigation was to characterize the effects of marathon training on single muscle fiber contractile function in a group of recreational runners. Muscle biopsies were obtained from the gastrocnemius muscle of seven individuals (22 +/- 1 yr, 177 +/- 3 cm, and 68 +/- 2 kg) before, after 13 wk of run training, and after 3 wk of taper. Slow-twitch myosin heavy chain [(MHC) I] and fast-twitch (MHC IIa) muscle fibers were analyzed for size, strength (P(o)), speed (V(o)), and power. The run training program led to the successful completion of a marathon (range 3 h 56 min to 5 h 35 min). Oxygen uptake during submaximal running and citrate synthase activity were improved (P < 0.05) with the training program. Muscle fiber size declined (P < 0.05) by approximately 20% in both fiber types after training. P(o) was maintained in both fiber types with training and increased (P < 0.05) by 18% in the MHC IIa fibers after taper. This resulted in >60% increase (P < 0.05) in force per cross-sectional area in both fiber types. Fiber V(o) increased (P < 0.05) by 28% in MHC I fibers with training and was unchanged in MHC IIa fibers. Peak power increased (P < 0.05) in MHC I and IIa fibers after training with a further increase (P < 0.05) in MHC IIa fiber power after taper. These data show that marathon training decreased slow-twitch and fast-twitch muscle fiber size but that it maintained or improved the functional profile of these fibers. A taper period before the marathon further improved the functional profile of the muscle, which was targeted to the fast-twitch muscle fibers.
Unlabelled:
Bodybuilding is a sport in which competitors are judged on muscular appearance. This case study tracked a drug-free male bodybuilder (age 26-27 y) for the 6 mo before and after a competition.
Purpose:
The aim of this study was to provide the most comprehensive physiological profile of bodybuilding competition preparation and recovery ever compiled.
Methods:
Cardiovascular parameters, body composition, strength, aerobic capacity, critical power, mood state, resting energy expenditure, and hormonal and other blood parameters were evaluated.
Results:
Heart rate decreased from 53 to 27 beats/min during preparation and increased to 46 beats/min within 1 mo after competition. Brachial blood pressure dropped from 132/69 to 104/56 mmHg during preparation and returned to 116/64 mmHg at 6 mo after competition. Percent body fat declined from 14.8% to 4.5% during preparation and returned to 14.6% during recovery. Strength decreased during preparation and did not fully recover during 6 months of recovery. Testosterone declined from 9.22 to 2.27 ng/mL during preparation and returned back to the baseline level, 9.91 ng/mL, after competition. Total mood disturbance increased from 6 to 43 units during preparation and recovered to 4 units 6 mo after competition.
Conclusions:
This case study provides a thorough documentation of the physiological changes that occurred during natural bodybuilding competition and recovery.
We have investigated the relationship between cross-sectional area (CSA) and maximum rate of oxygen consumption (VO2max, in nmol .mm-3 .s-1) of heart and skeletal muscle cells from different species. VO2max and CSA were determined for single muscle fibres of Xenopus laevis at 20°C and for cardiomyocytes in thin trabeculae dissected from the right ventricle of rats at 38°C. Succinate dehydrogenase activity was determined using a quantitative histochemical method to estimate VO2max in mammalian skeletal muscle fibres. Literature values of volume density of mitochondria were used to estimate VO2max in some mammalian cardiomyocytes. We found that an inverse relationship exists between VO2max (range 1.5 to 0.024 nmol . mm-3 . s-1) and cross-sectional area (0.0002 to 0.018 mm2, respectively): VO2max = constant/CSA, where the value of the constant equals 0.39±0.18 pmol . mm-1 .s-1 (mean ± S.D., n = 14). Such a relationship is predicted by a simple Hill-type model for oxygen diffusion in cilindrical cells, if it is assumed that muscle cells are evolved so that anoxic cores in muscle cells are prevented. This indicates that the product of endurance of muscle cells (which is proportional to VO2max) and force production (which is proportional to cross-sectional area) is limited by oxygen diffusion, and that adaptation of heart and skeletal muscle cells to increased workload is limited by the interstitial oxygen tension.
It is not known why in vivo muscle specific tension increases following resistance training in humans but changes in muscle fibre-type composition, increased single-fibre specific tension or lateral force transmission might provide explanations. Lateral force transmission would increase specific tension but decrease contraction velocity, thus not affecting maximal power per unit muscle volume. In vivo muscle specific tension, power output and muscle volume were determined in the quadriceps femoris of 42 young men, while myosin heavy chain (MyHC) isoform composition, single-fibre (SF) specific tension, SF maximal shortening velocity (V(max)) and SF peak power (W(max)) of the vastus lateralis were established in a subsample (n = 17) before and after high-intensity leg-extension resistance training (3 sessions week(-1) for 9 weeks). Following training, in vivo muscle specific tension increased by 17% but the power output/muscle volume ratio remained unaltered. Furthermore, there was no relationship between the training-induced decrease in MyHC IIX and the change in specific tension in vivo. In addition, SF specific tension, V(max) and W(max) were unchanged following training. In conclusion, a change in fibre-type composition does not explain the increased in vivo specific tension, nor does it seem likely that increased myofilament packing occurred with resistance training. However, an unchanged in vivo power per unit muscle volume is in accordance with the notion of enhanced lateral force transmission after strength training.
We have explored the extent to which the maximal velocity of unloaded shortening (V(max)), the force generated per unit cross-sectional area (P(0)) and the curvature of the force-velocity relationship (a/P(0) in the Hill equation) contribute to differences in peak power of chemically skinned single fibres from the quadriceps muscle of healthy young male subjects. The analysis was restricted to type I and IIA fibres that contained a single type of myosin heavy chain on electrophoretic separation. Force-velocity relationships were determined from isotonic contractions of maximally activated fibres at 15 degrees C. Mean (+/- s.d.) peak powers were 1.99 +/- 0.72 watts per litre (W L(-1)) for type I fibres and 6.92 +/- 2.41 W L(-1), for type IIA fibres. The most notable feature, however, was the very large, sevenfold, range of power outputs within a single fibre type. This wide range was a consequence of variations in each of the three components determining power: P(0), V(max) and a/P(0). Within a single fibre type, P(0) varied threefold, and V(max) and a/P(0) two- to threefold. There were no obvious relationships between P(0) and V(max) or between P(0) and a/P(0). However, there was a suggestion of an inverse relationship between a/P(0) and V(max), the effect being to reduce, somewhat, the impact of differences in V(max) on peak power. In searching for the causes of variation in peak power of fibres of the same type, it appears likely that there are two factors, one that affects P(0) and another that leads to variation in both V(max) and a/P(0).
1. The force produced in single fibres isolated from the anterior tibialis muscle of the frog Rana temporaria has been measured in tetani near 4 degrees C, and then in calcium-activated contractures of segments of the same fibres after chemical demembranation. All measurements were made at a sarcomere length of 2.3 microns. Force was normalized for fibre cross-section by the dry weight per unit length of the segments, which is proportional to cross-sectional area (Elzinga, Howarth, Rall, Wilson & Woledge, 1989). 2. The ratio of the force developed by the skinned segments to that produced by the intact fibres was inversely related to segment cross-section (dry weight per unit length), falling from approximately 1.0 for the thinnest segments to 0.6 for the thickest segments. 3. It is calculated that the accumulation of orthophosphate ion within contracting segments can account for a significant part of the decline in relative force in thicker segments. 4. The absolute forces in intact fibres and their derived segments were strongly correlated, but normalization by segment cross-section removed the correlation. 5. It is concluded that the sources of the approximately twofold variation in normalized force in both intact and skinned preparations are different. The existence of diffusible, force-modulating factors in intact fibres, which may be removed during skinning, is considered.
Skeletal muscle was obtained from the vastus lateralis of three normal college male students. Two biopsies were obtained prior to a training period and one after the training period. Subjects participated in an intense weight training program involving isometric and isotonic exercises. The subjects participated in the exercise regimen five days in each week for a period of 10 weeks. Muscle tissue was processed immediately for electron microscope examination. The following parameters were measured from micrographs of longitudinal sections: sarcomere length, sarcomere width, intracellular fat, mitochondria number and mitochondria length. The following parameters were measured from micrographs of cross sections: myosin filament concentration, distance between myosin filaments, myosin filament diameter, the number of actin filaments in orbit around a myosin filament, and gross cell size. Major findings included significant changes in myosin filament concentration, distance between myosin filaments, and the number of actin filaments in orbit around a myosin filament.
1. Maximum velocity of shortening (Vmax) and compositions of myosin heavy chain (MHC) and myosin light chain (MLC) isoforms were determined in single fibres from the soleus or the lateral region of the quadriceps (vastus lateralis) muscles in man. Muscle samples were obtained by percutaneous biopsy, and membranes were permeabilized by glycerol treatment (chemical skinning) or by freeze-drying. 2. Types I, IIA and IIB MHCs were resolved from single fibre segments by 6% sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and five different fibre types were identified: fibres containing type I MHC, types I and IIA MHCs, type IIA MHC, types IIA and IIB MHCs, and type IIB MHC. Only a few fibres co-expressed types I and IIA MHCs but 28% of all quadriceps fibres expressed both IIA and IIB MHCs in variable proportions. Fibres co-expressing types I and IIB MHCs were not found. 3. Alkali (MLC1 and MLC3) and dithio nitrobenzoic acid (DTNB) (MLC2) myosin light chains were observed in all type II fibres in variable proportions. MLC (MLC1s and MLC2s) isoforms from type I fibres had lower migration rates than the corresponding isoforms from type II fibres (MLC1f and MLC2f). More than half of type I fibres in both soleus (65%) and quadriceps (68%) muscles also expressed 'fast' MLC3 and 36% of the type II fibres from quadriceps muscle expressed the slow isoform of MLC2. 4. Differences were observed in some mechanical characteristics of freeze-dried versus chemically skinned fibres. Maximum tension (P0) and specific tension were lower in freeze-dried types I and IIA fibres than in chemically skinned, while no differences were observed in the IIA/B fibres. The numbers of types I/IIA and IIB fibres were too low to allow statistical comparisons. In chemically skinned fibres, mean specific tension (0.20 +/- 0.01 N/mm2) did not vary with fibre type. In freeze-dried fibres, on the other hand, specific tensions varied according to MHC type: higher (P < 0.01) specific tensions were observed in types IIB (0.19 +/- 0.01 N/mm2) and type IIA/B fibres (0.18 +/- 0.04 N/mm2) than in type I fibres (0.12 +/- 0.02 N/mm2). The specific tension of type IIA fibres (0.12 +/- 0.05 N/mm2) did not differ significantly from the other fibre types. Cross-sectional areas and mean Vmax did not differ between freeze-dried and chemically skinned fibres, either when all fibres were pooled or within respective fibre types. Vmax data from all fibres of a given type, irrespective of membrane permeabilization technique, have therefore been pooled.(ABSTRACT TRUNCATED AT 400 WORDS)
Biopsy samples were taken from vastus lateralis muscle of seven young (YO, age 30.2 +/- 2.2 years), and seven elderly (EL, age 72.7 +/- 2.3 years) subjects and two elderly subjects whose right leg had been immobilized for 3.5 months (EL-IMM, ages 70 and 75). The following main parameters were studied: (1) myosin heavy chain (MHC) isoform distribution of the samples, determined by SDS-PAGE; (2) cross-sectional area (CSA), specific force (Po/CSA) and maximum shortening velocity (Vo) of a large population (n = 593) of single skinned muscle fibres, classified on the basis of MHC isoform composition determined by SDS-PAGE; (3) actin sliding velocity (Vf) on pure myosin isoforms determined by in vitro motility assays; (4) myosin concentration in single fibres determined by quantitative SDS-PAGE. MHC isoform distribution was shifted towards fast isoforms in EL and to a larger extent in EL-IMM. In EL and, more consistently, in EL-IMM we observed a higher percentage of hybrid fibres than in YO, and noted the presence of MHC-neonatal and of unusual hybrid fibres containing more than two MHC isoforms. Po/CSA significantly decreased in type 1 and 2A fibres in the order YO EL EL-IMM. Vo of type 1 and 2A fibres was significantly lower in EL and higher in EL-IMM than in YO, i.e. immobilization more than counteracted the age-dependent decrease in Vo. The latter phenomenon was not observed for Vf. Vf on myosin 1 was lower in both EL and EL-IMM than in YO. Vf on myosin 2X was lower in EL than in YO, and a similar trend was observed for myosin 2A. Myosin concentration decreased in type 1 and 2A fibres in the order YO EL EL-IMM and was linearly related to the Po/CSA values of corresponding fibre types from the same subjects. The experiments suggest that (1) myosin concentration is a major determinant of the lower Po/CSA of single fibres in ageing and especially following immobilization and (2) ageing is associated with lower Vo of single fibres due to changes in the properties of myosin itself, whereas immobilization is associated with higher Vo in the absence of a change in myosin function.
Needle biopsy samples were taken from vastus lateralis muscle (VL) of five male body builders (BB, age 27.4+/-0.93 years; mean+/-s.e.m.), who had being performing hypertrophic heavy resistance exercise (HHRE) for at least 2 years, and from five male active, but untrained control subjects (CTRL, age 29.9+/-2.01 years). The following determinations were performed: anatomical cross-sectional area and volume of the quadriceps and VL muscles in vivo by magnetic resonance imaging (MRI); myosin heavy chain isoform (MHC) distribution of the whole biopsy samples by SDS-PAGE; cross-sectional area (CSA), force (Po), specific force (Po/CSA) and maximum shortening velocity (Vo) of a large population (n=524) of single skinned muscle fibres classified on the basis of MHC isoform composition by SDS-PAGE; actin sliding velocity (Vf) on pure myosin isoforms by in vitro motility assays. In BB a preferential hypertrophy of fast and especially type 2X fibres was observed. The very large hypertrophy of VL in vivo could not be fully accounted for by single muscle fibre hypertrophy. CSA of VL in vivo was, in fact, 54% larger in BB than in CTRL, whereas mean fibre area was only 14% larger in BB than in CTRL. MHC isoform distribution was shifted towards 2X fibres in BB. Po/CSA was significantly lower in type 1 fibres from BB than in type 1 fibres from CTRL whereas both type 2A and type 2X fibres were significantly stronger in BB than in CTRL. Vo of type 1 fibres and Vf of myosin 1 were significantly lower in BB than in CTRL, whereas no difference was observed among fast fibres and myosin 2A. The findings indicate that skeletal muscle of BB was markedly adapted to HHRE through extreme hypertrophy, a shift towards the stronger and more powerful fibre types and an increase in specific force of muscle fibres. Such adaptations could not be fully accounted for by well known mechanisms of muscle plasticity, i.e. by the hypertrophy of single muscle fibre (quantitative mechanism) and by a regulation of contractile properties of muscle fibres based on MHC isoform content (qualitative mechanism). Two BB subjects took anabolic steroids and three BB subjects did not. The former BB differed from the latter BB mostly for the size of their muscles and muscle fibres.
The impact of ageing on force and velocity of human skeletal muscle fibres has been extensively studied. As discrepancies have been reported, it is still unclear whether or not a deterioration of the capacity of muscle fibres to develop force and shortening is involved in determining weakness and decrease in shortening velocity of skeletal muscle of elderly people. We compared myosin heavy chain (MHC) isoform distribution of vastus lateralis muscle, and specific force (Po/CSA) and maximum shortening velocity (Vo) of skeletal muscle fibres among one population of young controls (CTRL) and three populations of elderly (EL) subjects with very variable levels of physical activity: sedentary (EL-SED, n = 3); controls (EL-CTRL, n = 4); endurance trained (EL-END, n = 3). Muscle phenotype was progressively faster in the order EL-END --> CTRL --> EL-CTRL --> EL-SED. Po/CSA and Vo also varied among the different populations of elderly subjects generally showing a decreasing deterioration with increasing activity levels. The results suggest that discrepancies observed so far in age-induced deterioration of contractile properties of muscle fibres could depend on the different activity levels of the populations of elderly subjects enrolled in the studies.
Deterioration of contractile properties of muscle fibres in elderly subjects is modulated by the level of physical activity
- D Antona
- G Pellegrino
- M Carlizzi
- C Bottinelli
D'Antona G, Pellegrino M, Carlizzi C & Bottinelli R (2007). Deterioration of contractile properties of
muscle fibres in elderly subjects is modulated by the level of physical activity. European Journal
of Applied Physiology 100, 603-611.