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A key determinant of geriatric frailty is sarcopenia, the age-associated loss of skeletal muscle mass and strength (1,2). Although the etiology of sarcopenia is unknown, the correlation during aging between the loss of activity of satellite cells, which are endogenous muscle stem cells, and impaired muscle regenerative capacity has led to the hypothesis that the loss of satellite cell activity is also a cause of sarcopenia (3,4). We tested this hypothesis in male sedentary mice by experimentally depleting satellite cells in young adult animals to a degree sufficient to impair regeneration throughout the rest of their lives. A detailed analysis of multiple muscles harvested at various time points during aging in different cohorts of these mice showed that the muscles were of normal size, despite low regenerative capacity, but did have increased fibrosis. These results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of muscle size or fiber type composition during aging, but that their loss may contribute to age-related muscle fibrosis., Recent estimates indicate that up to one-third of elderly people suffer from frailty, characterized by a common set of symptoms including loss of muscle strength, increased fatigability, modest levels of [...]

McBride, JM, Skinner, JW, Schafer, PC, Haines, TL, and Kirby, TJ. Comparison of kinetic variables and muscle activity during a squat vs. a box squat. J Strength Cond Res 24(12): 3195-3199, 2010--The purpose of this investigation was to determine if there was a difference in kinetic variables and muscle activity when comparing a squat to a box squat. A box squat removes the stretch-shortening cycle component from the squat, and thus, the possible influence of the box squat on concentric phase performance is of interest. Eight resistance trained men (Height: 179.61 [+ or -] 13.43 cm; Body Mass: 107.65 [+ or -] 29.79 kg; Age: 24.77 [+ or -] 3.22 years; 1 repetition maximum [1RM]: 200.11 [+ or -] 58.91 kg) performed 1 repetition of squats and box squats using 60, 70, and 80% of their 1RM in a randomized fashion. Subjects completed the movement while standing on a force plate and with 2 linear position transducers attached to the bar. Force anal velocity were used to calculate power. Peak force and peak power were determined from the force--time and power--time curves during the concentric phase of the lift. Muscle activity (electromyography) was recorded from the vastus lateralis, vastus medialis, biceps femoris, anal longissimus. Results indicate that peak force and peak power are similar between the squat and box squat. However, during the 70% of 1 RM trials, the squat resulted in a significantly lower peak force in comparison to the box squat (squat = 3,269 [+ or -] 573 N, box squat = 3,364 [+ or -] 575 N). In addition, during the 80% of 1RM trials, the squat resulted in significantly lower peak power in comparison to the box squat (squat = 2,050 [+ or -] 486 W, box squat = 2,197 [+ or -] 544 W). Muscle activity was generally higher during the squat in comparison to the box squat. In conclusion, minimal differences were observed in kinetic variables and muscle activity between the squat and box squat. Removing the stretch-shortening cycle during the squat (using a box) appears to have limited negative consequences on performance. KEY WORDS force, power, stretch-shortening cycle, strength

The purpose of this investigation was to examine the relationship between maximal squat strength and sprinting times. Seventeen Division I-AA male football athletes (height = 1.78 [+ or -] 0.04 m, body mass [BM] = 85.9 [+ or -] 8.8 kg, body mass index [BMI] = 27.0 [+ or -] 2.6 kg/[m.sup.2], 1 repetition maximum [1RM] = 166.5 [+ or -] 34.1 kg, 1RM/BM = 1.94 [+ or -] 0.33) participated in this investigation. Height, weight, and squat strength (1RM) were assessed on day 1. Within 1 week, 5, 10, and 40 yard sprint times were assessed. Squats were performed to a 70[degrees] knee angle and values expressed relative to each subject's BM. Sprints were performed on a standard outdoor track surface with timing gates placed at the previously mentioned distances. Statistically significant (p [less than or equal to] 0.05) correlations were found between squat 1 RM/BM and 40 yard sprint times (r = -0.605, p = 0.010, power = 0.747) and 10 yard sprint times (r = -0.544, p = 0.024, power = 0.626). The correlation approached significance between 5 yard sprint times and 1RM/BM (r = -0.4502, p = 0.0698, power = 0.4421). Subjects were then divided into those above 1RM/BM of 2.10 and below 1RM/BM of 1.90. Subjects with a 1RM/BM above 2.10 had statistically significantly lower sprint times at 10 and 40 yards in comparison with those subjects with a 1RM/BM ratio below 1.90. This investigation provides additional evidence of the possible importance of maximal squat strength relative to BM concerning sprinting capabilities in competitive athletes. KEY WORDS power, running, football, athletes

The multinucleated nature of myofibres, coupled with the ability to add myonuclei through satellite cell fusion, led to the "myonuclear domain theory", which states that each myonucleus is responsible for the transcriptional output for a fixed amount of cytoplasm. Myonuclei positive for TUNEL are rare events and their presence in muscle has been questioned (Bruusgaard I et al i . 2012; Schwartz, 2019), warranting more robust and objective analysis approaches utilizing myonuclei-specific identification markers (Winje I et al i . 2018). However, technical challenges have hindered the ability to track satellite cell fusion on a per nucleus basis, as there can be translocation of genetic reporter proteins between neighbouring myonuclei (Masschelein I et al i . 2020). Keywords: ageing; apoptosis; myonuclei; skeletal muscle EN ageing apoptosis myonuclei skeletal muscle 2077 2080 4 05/02/22 20220501 NES 220501 The myonuclear domain hypothesis Adult muscle retains a population of muscle stem cells, termed satellite cells, that can be activated in response to muscle injury, but also participate in muscle adaptation and muscle homeostasis (Chen I et al i . 2020). [Extracted from the article]

Abstract Background The use of the Cre/loxP system for gene targeting has been proven to be a powerful tool for understanding gene function. The purpose of this study was to create and characterize an inducible, skeletal muscle-specific Cre transgenic mouse strain. Methods To achieve skeletal muscle-specific expression, the human α-skeletal actin promoter was used to drive expression of a chimeric Cre recombinase containing two mutated estrogen receptor ligand-binding domains. Results Western blot analysis, PCR and β-galactosidase staining confirmed that Cre-mediated recombination was restricted to limb and craniofacial skeletal muscles only after tamoxifen administration. Conclusions A transgenic mouse was created that allows inducible, gene targeting of floxed genes in adult skeletal muscle of different developmental origins. This new mouse will be of great utility to the skeletal muscle community.

The purpose of this investigation was to determine the relationship between relative net vertical impulse and jump height in a countermovement jump and static jump performed to varying squat depths. Ten college-aged males with 2 years of jumping experience participated in this investigation (age: 23.3 ± 1.5 years; height: 176.7 ± 4.5 cm; body mass: 84.4 ± 10.1 kg). Subjects performed a series of static jumps and countermovement jumps in a randomized fashion to a depth of 0.15, 0.30, 0.45, 0.60, and 0.75 m and a self-selected depth (static jump depth = 0.38 ± 0.08 m, countermovement jump depth = 0.49 ± 0.06 m). During the concentric phase of each jump, peak force, peak velocity, peak power, jump height, and net vertical impulse were recorded and analyzed. Net vertical impulse was divided by body mass to produce relative net vertical impulse. Increasing squat depth corresponded to a decrease in peak force and an increase in jump height and relative net vertical impulse for both static jump and countermovement jump. Across all depths, relative net vertical impulse was statistically significantly correlated to jump height in the static jump (r = .9337, p < .0001, power = 1.000) and countermovement jump (r = .925, p < .0001, power = 1.000). Across all depths, peak force was negatively correlated to jump height in the static jump (r = -0.3947, p = .0018, power = 0.8831) and countermovement jump (r = -0.4080, p = .0012, power = 0.9050). These results indicate that relative net vertical impulse can be used to assess vertical jump performance, regardless of initial squat depth, and that peak force may not be the best measure to assess vertical jump performance. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this investigation was to determine the effect of stable and unstable conditions on one repetition maximum strength and muscle activity during dynamic squatting using absolute and relative loading. Methods: Ten recreationally weight-trained males participated in this study (age = 24.1 ± 2.0 y, height = 178.0 ± 5.6 cm, body mass = 83.7 ± 13.4 kg, 1RM/body mass = 1.53 ± 0.31), which involved two laboratory sessions separated by 1 wk. Linear position transducers were used to track bar displacement while subjects stood on a force plate for all trials. Vastus lateralis (VL), biceps femoris (BF) and erector spinae (L1) muscle activity (average integrated EMG [IEMG]) was also recorded during all trials. During the first session subjects complete a one repetition maximum test in a stable dynamic squat (S1RM = 128.0 ± 31.4 kg) and an unstable dynamic squat (U1RM = 83.8 ± 17.3 kg) in a randomized order with a 30-min rest period between conditions. The second session consisted of the performance of three trials each for 12 different conditions (unstable and stable squats using three different absolute loads [six conditions] and unstable and stable squats using three different relative loads [six conditions]). Results: Results revealed a statistically significant difference between S1RM and U1RM values (P ≤ .05). The stable trials resulted in the same or a significantly higher value for VL, BF and L1 muscle activity in comparison with the unstable trials for all twelve conditions. Conclusions: Unstable squatting is of equal or less (depending on the loading condition) benefit to improving or maximizing muscle activity during resistance exercise. [ABSTRACT FROM AUTHOR]

The ability of myofibers to sense and respond appropriately to mechanical signals is one of the primary determinants of the skeletal muscle phenotype. In response to a change in mechanical load, muscle cells alter their protein metabolism, primarily through the regulation of protein synthesis rate. Protein synthesis rates are determined by both translation efficiency and translational capacity within the muscle. Translational capacity is strongly determined by the ribosome content of the muscle; thus the regulation of ribosomal biogenesis by mechanical inputs has been an area of recent interest. Despite the clear association between mechanical signals and changes in protein metabolism, the molecular pathways that link these events are still not fully elucidated. This review focuses on recent studies looking at how mechanosignaling impacts translational events. The role of impaired mechanotransduction in aging is discussed, as is the connection between age-dependent signaling defects and compromised ribosomal biogenesis during mechanical overload. Finally, emerging evidence suggests that the nucleus can act as a mechanosensitive element and that this mode of mechanotransduction may have an important role in skeletal muscle physiology and adaptation. [ABSTRACT FROM AUTHOR]

Recent loss-of-function studies show that satellite cell depletion does not promote sarcopenia or unloading-induced atrophy, and does not prevent regrowth. Although overload-induced muscle fiber hypertrophy is normally associated with satellite cell-mediated myonuclear accretion, hypertrophic adaptation proceeds in the absence of satellite cells in fully grown adult mice, but not in young growing mice. Emerging evidence also indicates that satellite cells play an important role in remodeling the extracellular matrix during hypertrophy. [ABSTRACT FROM AUTHOR]

Keywords: ageing; muscle atrophy; myonuclear apoptosis EN ageing muscle atrophy myonuclear apoptosis 2085 2086 2 05/02/22 20220501 NES 220501 In their Cross Talk article, Drs Schwartz and Gundersen (2022) argue that myonuclear apoptosis cannot occur, because it would not be possible to compartmentalize and restrict this event to individual myonuclei within the myofibre syncytium. Cross Talk opposing view: Myonuclei do not undergo apoptosis during skeletal muscle atrophy. We agree with the opposing authors that some early studies did not adequately identify apoptosis specifically in myonuclei during disuse atrophy; however, numerous recent studies have demonstrated myonuclear loss in isolated myofibres with appropriate myofibre delineation (Snijders et al., 2020). [Extracted from the article]

Although sarcopenia, age-associated loss of muscle mass and strength, is neither accelerated nor exacerbated by depletion of muscle stem cells, satellite cells, we hypothesized that adaptation in sarcopenic muscle would be compromised. To test this hypothesis, we depleted satellite cells with tamoxifen treatment of Pax7(CreER)-DTA mice at 4 months of age, and 20 months later subjected the plantaris muscle to 2 weeks of mechanical overload. We found myofiber hypertrophy was impaired in aged mice regardless of satellite cell content. Even in the absence of growth, vehicle-treated mice mounted a regenerative response, not apparent in tamoxifen-treated mice. Further, myonuclear accretion occurred in the absence of growth, which was prevented by satellite cell depletion, demonstrating that myonuclear addition is insufficient to drive myofiber hypertrophy. Satellite cell depletion increased extracellular matrix content of aged muscle that was exacerbated by overload, potentially limiting myofiber growth. These results support the idea that satellite cells regulate the muscle environment, and that their loss during aging may contribute to fibrosis, particularly during periods of remodeling. Overload induced a fiber-type composition improvement, independent of satellite cells, suggesting that aged muscle is very responsive to exercise-induced enhancement in oxidative capacity, even with an impaired hypertrophic response. [ABSTRACT FROM AUTHOR]

Adipose tissue has profound effects on whole-body insulin sensitivity. However, the underlying biological processes are quite complex and likely multifactorial. For instance, the adipose transcriptome is posttranscriptionally modulated by microRNAs, but the relationship between microRNAs and insulin sensitivity in humans remains to be determined. To this end, we utilized an integrative mRNA-microRNA microarray approach to identify putative molecular interactions that regulate the transcriptome in subcutaneous adipose tissue of insulinsensitive (IS) and insulin-resistant (IR) individuals. Using the Nano- String nCounter Human v1 microRNA Expression Assay, we show that 17 microRNAs are differentially expressed in IR vs. IS. Of these, 16 microRNAs (94%) are downregulated in IR vs. IS, including miR-26b, miR-30b, and miR-145. Using Agilent Human Whole Genome arrays, we identified genes that were predicted targets of miR-26b, miR-30b, and miR-145 and were upregulated in IR subjects. This analysis produced ADAM22, MYO5A, LOX, and GM2A as predicted gene targets of these microRNAs. We then validated that miR-145 and miR-30b regulate these mRNAs in differentiated human adipose stem cells. We suggest that use of bioinformatic integration of mRNA and microRNA arrays yields verifiable mRNA-microRNA pairs that are associated with insulin resistance and can be validated in vitro. [ABSTRACT FROM AUTHOR]

Background: Satellite cells, or muscle stem cells, have been thought to be responsible for all muscle plasticity, but recent studies using genetically modified mouse models that allow for the conditional ablation of satellite cells have challenged this dogma. Results have confirmed the absolute requirement of satellite cells for muscle regeneration but surprisingly also showed that they are not required for adult muscle growth. While the function of satellite cells in muscle growth and regeneration is becoming better defined, their role in the response to aerobic activity remains largely unexplored. The purpose of the current study was to assess the involvement of satellite cells in response to aerobic exercise by evaluating the effect of satellite cell depletion on wheel running performance. Results: Four-month-old female Pax7/DTA mice (n = 8-12 per group) were satellite cell depleted via tamoxifen administration; at 6 months of age, mice either remained sedentary or were provided with running wheels for 8 weeks. Plantaris muscles were significantly depleted of Pax7+cells (≥90% depleted), and 8 weeks of wheel running did not result in an increase in Pax7+ cells, or in myonuclear accretion. Interestingly, satellite cell-depleted animals ran ~27% less distance and were 23% slower than non-depleted animals. Wheel running was associated with elevated succinate dehydrogenase activity, muscle vascularization, lipid accumulation, and a significant shift toward more oxidative myosin heavy chain isoforms, as well as an increase in voltage dependent anion channel abundance, a marker of mitochondrial density. Importantly, these changes were independent of satellite cell content. Interestingly, depletion of Pax7+ cells from intra- as well as extrafusal muscle fibers resulted in atrophy of intrafusal fibers, thickening of muscle spindle-associated extracellular matrix, and a marked reduction of functional outcomes including grip strength, gait fluidity, and balance, which likely contributed to the impaired running performance. Conclusions: Depletion of Pax7-expressing cells in muscle resulted in reduced voluntary wheel running performance, without affecting markers of aerobic adaptation; however, their absence may perturb proprioception via disruption of muscle spindle fibers resulting in loss of gross motor coordination, indicating that satellite cells have a yet unexplored role in muscle function. [ABSTRACT FROM AUTHOR]

The ability of skeletal muscle to hypertrophy in response to a growth stimulus is known to be compromised in older individuals. We hypothesized that a change in the expression of protein-encoding genes in response to a hypertrophic stimulus contributes to the blunted hypertrophy observed with aging. To test this hypothesis, we determined gene expression by microarray analysis of plantaris muscle from 5- and 25-mo-old mice subjected to 1, 3, 5, 7, 10, and 14 days of synergist ablation to induce hypertrophy. Overall, 1,607 genes were identified as being differentially expressed across the time course between young and old groups; however, the difference in gene expression was modest, with cluster analysis showing a similar pattern of expression between the two groups. Despite ribosome protein gene expression being higher in the aged group, ribosome biogenesis was significantly blunted in the skeletal muscle of aged mice compared with mice young in response to the hypertrophic stimulus (50% vs. 2.5-fold, respectively). The failure to upregulate pre-47S ribosomal RNA (rRNA) expression in muscle undergoing hypertrophy of old mice indicated that rDNA transcription by RNA polymerase I was impaired. Contrary to our hypothesis, the findings of the study suggest that impaired ribosome biogenesis was a primary factor underlying the blunted hypertrophic response observed in skeletal muscle of old mice rather than dramatic differences in the expression of protein-encoding genes. The diminished increase in total RNA, pre-47S rRNA, and 28S rRNA expression in aged muscle suggest that the primary dysfunction in ribosome biogenesis occurs at the level of rRNA transcription and processing. [ABSTRACT FROM AUTHOR]

The purpose of this study was to compare the gene expression profile of mouse skeletal muscle undergoing two forms of growth (hypertrophy and regrowth) with the goal of identifying a conserved set of differentially expressed genes. Expression profiling by microarray was performed on the plantaris muscle subjected to 1, 3, 5, 7, 10, and 14 days of hypertrophy or regrowth following 2 wk of hind-limb suspension. We identified 97 differentially expressed genes (≥2-fold increase or ≥50% decrease compared with control muscle) that were conserved during the two forms of muscle growth. The vast majority (~90%) of the differentially expressed genes was upregulated and occurred at a single time point (64 out of 86 genes), which most often was on the first day of the time course. Microarray analysis from the conserved upregulated genes showed a set of genes related to contractile apparatus and stress response at day 1, including three genes involved in mechanotransduction and four genes encoding heat shock proteins. Our analysis further identified three cell cycle-related genes at day and several genes associated with extracellular matrix (ECM) at both days 3 and 10. In conclusion, we have identified a core set of genes commonly upregulated in two forms of muscle growth that could play a role in the maintenance of sarcomere stability, ECM remodeling, cell proliferation, fast-to-slow fiber type transition, and the regulation of skeletal muscle growth. These findings suggest conserved regulatory mechanisms involved in the adaptation of skeletal muscle to increased mechanical loading. [ABSTRACT FROM AUTHOR]

The ribosome is a supramolecular ribonucleoprotein complex that functions at the heart of the translation machinery to convert mRNA into protein. Ribosome biogenesis is the primary determinant of translational capacity of the cell and accordingly has an essential role in the control of cell growth in eukaryotes. Cumulative evidence supports the hypothesis that ribosome biogenesis has an important role in the regulation of skeletal muscle mass. The purpose of this review is to, first, summarize the main mechanisms known to regulate ribosome biogenesis and, second, put forth the hypothesis that ribosome biogenesis is a central mechanism used by skeletal muscle to regulate protein synthesis and control skeletal muscle mass in response to anabolic and catabolic stimuli. The mTORC1 and Wnt/β-catenin/c-myc signaling pathways are discussed as the major pathways that work in concert with each of the three RNA polymerases (RNA Pol I, II, and III) in regulating ribosome biogenesis. Consistent with our hypothesis, activation of these two pathways has been shown to be associated with ribosome biogenesis during skeletal muscle hypertrophy. Although further study is required, the finding that ribosome biogenesis is altered under catabolic states, in particular during disuse atrophy, suggests that its activation represents a novel therapeutic target to reduce or prevent muscle atrophy. Lastly, the emerging field of ribosome specialization is discussed and its potential role in the regulation of gene expression during periods of skeletal muscle plasticity. J. Cell. Physiol. 229: 1584-1594, 2014. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Our aim in the current study was to determine the necessity of satellite cells for long-term muscle growth and maintenance. We utilized a transgenic Pax7-DTA mouse model, allowing for the conditional depletion of > 90% of satellite cells with tamoxifen treatment. Synergist ablation surgery, where removal of synergist muscles places functional overload on the plantaris, was used to stimulate robust hypertrophy. Following 8 wk of overload, satellite celldepleted muscle demonstrated an accumulation of extracellular matrix (ECM) and fibroblast expansion that resulted in reduced specific force of the plantaris. Although the early growth response was normal, an attenuation of hypertrophy measured by both muscle wet weight and fiber cross-sectional area occurred in satellite cell-depleted muscle. Isolated primary myogenic progenitor cells (MPCs) negatively regulated fibroblast ECM mRNA expression in vitro, suggesting a novel role for activated satellite cells/MPCs in muscle adaptation. These results provide evidence that satellite cells regulate the muscle environment during growth.--Fry, C. S., Lee, J. D., Jackson, J. R., Kirby, T. J., Stasko, S. A., Liu, H., Dupont-Versteegden, E. E., McCarthy, J. J., Peterson, C. A. Regulation of the muscle fiber microenvironment by activated satellite cells during hypertrophy. [ABSTRACT FROM AUTHOR]

Resident muscle stem cells, known as satellite cells, are thought to be the main mediators of skeletal muscle plasticity. Satellite cells are activated, replicate, and fuse into existing muscle fibers in response to both muscle injury and mechanical load. It is generally well-accepted that satellite cells participate in postnatal growth, hypertrophy, and muscle regeneration following injury; however, their role in muscle regrowth following an atrophic stimulus remains equivocal. The current study employed a genetic mouse model (Pax7-DTA) that allowed for the effective depletion of >90% of satellite cells in adult muscle upon the administration of tamoxifen. Vehicle and tamoxifen-treated young adult female mice were either hindlimb suspended for 14 days to induce muscle atrophy or hindlimb suspended for 14 days followed by 14 days of reloading to allow regrowth, or they remained ambulatory for the duration of the experimental protocol. Additionally, 5-bromo-2=-deoxyuridine (BrdU) was added to the drinking water to track cell proliferation. Soleus muscle atrophy, as measured by whole muscle wet weight, fiber cross-sectional area, and single-fiber width, occurred in response to suspension and did not differ between satellite cell-depleted and control muscles. Furthermore, the depletion of satellite cells did not attenuate muscle mass or force recovery during the 14-day reloading period, suggesting that satellite cells are not required for muscle regrowth. Myonuclear number was not altered during either the suspension or the reloading period in soleus muscle fibers from vehicle-treated or satellite cell-depleted animals. Thus, myonuclear domain size was reduced following suspension due to decreased cytoplasmic volume and was completely restored following reloading, independent of the presence of satellite cells. These results provide convincing evidence that satellite cells are not required for muscle regrowth following atrophy and that, instead, the myonuclear domain size changes as myofibers adapt. [ABSTRACT FROM AUTHOR]

Studies have reported various results with respect the level of muscle activity present during the performance of exercises in stable and unstable conditions. Some of the contradictions may be due to the use of relative or absolute loading during the comparisons of the two conditions. The purpose of this investigation was to determine the effect of stable and unstable conditions on one repetition maximum strength and muscle activity during dynamic squatting using both relative and absolute loading. Ten recreationally weight trained males participated in this study (age = 24.1 ± 2.0 yrs, height = 178.0 ± 5.6 cm, body mass = 83.7 ± 13.4 kg, 1RM/body mass = 1.53 ± 0.31), which involved two laboratory sessions separated by one week. Linear position transducers were used to track bar displacement while subjects stood on a force plate for all trials. Vastus lateralis (VL), biceps femoris (BF) and erector spinae (L1) muscle activity (average integrated EMG (IEMG)) was also recorded during all trials. During the first session subjects complete a one repetition maximum test in a stable dynamic squat (S1 RM = 128.0 ± 31.4 kg) and an unstable dynamic squat (U1RM = 83.8 ± 17.3 kg) in a randomized order with a thirty minute rest period between conditions. The second session consisted of the performance of three trials each for twelve different conditions in a randomized order: 1) unstable squats using 70% of US1RM, 2) unstable squats using 80% of US1 RM, 3) unstable squats using 90% of US1RM, 4) stable squats using 70% of S1RM, 5) stable squat using 80% of S1RM 6) stable squats using 90% of S1RM, 7) unstable squats using 58.6 ± 12.1 kg, 8) unstable squats using 67.0 ± 13.9 kg, 9) unstable squats using 75.4 ± 15.6 kg, 10) stable squats using 58.6 ± 12.1 kg, 11) stable squats using 67.0 ± 13.9 kg, and 12) stable squats using 75.4 ± 15.6 kg. Results revealed a statistically significant difference between S1RM and US1RM values (p ≤ 0.05). The stable trials resulted in the same or a significantly higher value for VL, BF and L1 muscle activity in comparison to the unstable trials for all twelve conditions. It appears that an unstable condition during dynamic squatting results in the same or significantly lower values of muscle activity in comparison to stable squatting. Unstable exercises are not recommended for utilization by practitioners as they do not increase muscle activation in comparison to stable exercise modalities and may limit possible physiological adaptations. [ABSTRACT FROM AUTHOR]

Various methods of calculation can affect power output values in the power clean. This may be due to analysis of the bar, body and system using different kinetic and kinematic variables. The purpose of this study was to utilize the combination of a force plate and videography to determine power output of the bar, the body, and the system independent of one another. Seven college-aged males (height = 175.29 ± 5.47 cm, weight = 80.84 ± 7.18 kg, age = 24.7 ± 2.06 yr, 1RM = 97.14 ± 6.36 kg) with at least one year experience in the power clean performed two sets of one repetition each at 30, 40, 50, 60, 70, 80, and 90% of their 1 repetition maximum (1RM) in a randomized order. Force, power, and velocity were obtained for the bar, body and system independently. Peak power (PP) of the bar was found to be at 90% of 1RM (2308 ± 229.1 W), PP of the body at 90% of 1RM (1077 ± 538.7 W) and PP of the system at 80% of 1RM (1768 ± 470.7 W). Significant differences (p ≤ 0.05) in PP were found between the bar and body at 40%, 50%, 60%, and 70% of 1RM, while 60% of 1RM also showed significant differences between the system and body. Significant differences between the bar, body and system occurred at 80% and 90% of 1RM for PP. Peak velocity (PV) occurred for the bar, body and system at 30% of 1RM (Bar PV 30% = 2.38 ± 0.15 m/s), 30% of 1RM (Body PV 30% = 0.79 ± 0.21 m/s) and 60% of 1RM (System PV 60% = 0.90 ± 0.16 m/s), respectively. Every load displayed significant differences in PV between the bar and body and between the bar and system, except for 60% of 1RM, where a significant difference occurred between the bar, body, and system. Peak force (PF) was highest at 90% of 1RM for the bar (1291 ± 72.9 N), while both the body and system PF occurred at 80% of 1RM (Body PF 80% = 1505 ± 270.1 N, System PF 80% = 2797 ± 618.2 N). Significant differences in peak force were found between the bar, body and system at every load, except 90% of 1RM where significant differences were between the bar and body and between the bar and system. In conclusion, bar, body, and system values for PP, PV, and PF are influenced differently across the loading spectrum. Proper training loads for the power clean maybe influenced by whether PP of the bar, body or system is desired. [ABSTRACT FROM AUTHOR]

Prolonged duration in a weightless environment results in decreased neuromuscular function. In Earth's 1-g environment, resistance exercise helps prevent muscle atrophy and its subsequent attenuations in strength and power. Previous studies have attempted to apply findings of gravity-based research to a microgravity environment. Although it has been shown that the decrease in neuromuscular function from a weightless environment can be attenuated through resistance training in 1-g, studies have not been completely successful utilizing resistance training in a microgravity environment to completely counter these negative neuromuscular changes. To examine the effect of elastic band resistance training in a microgravity-simulated environment on muscle size, strength, power, and muscle activity pre- and post- training. Twenty college-age males were randomly assigned to a training (T) group (n = 13; age = 20.15 ± 1.34years; height = 178.85 ± 8.23 cm; mass = 77.47 ± 8.63 kg) or a control (C) group (n = 7; age = 21.71 ± 1.70 years; height = 174.8 ± 4.56 cm; mass = 73.90 ± 8.70 kg) that refrained from any training during the nine-week period. Kinetic and kinematic variables, as well as electromyography (EMG) of the vastus lateralis (VL), were collected and analyzed before and after the training period in which the T group completed a progressive resistance protocol consisting of six sets often dead lifts utilizing elastic bands while in the custom-made microgravity apparatus. Muscle size was obtained through a DEXA scan, strength was measured by one-repetition maximum (1RM) squat, power was assessed through a countermovement jump (CMJ) at body mass, and muscle activity was determined through EMG of the VL. Squat 1RM strength increased significantly in the T group (103.65 ± 26.94 kg to 115.38 ± 25.43 kg, p < 0.001) as compared to no change in the C group (121.43 ± 30.78 kg to 125.71 ± 21.62 kg). No statistically significant changes were observed in power during the CMJ (4738.61 ± 700.70 W to 4562.59 ± 971.31 W) after training. Changes in muscle size and activity were insignificant. This was the first study to examine the effectiveness of elastic resistance bands in a microgravity training environment. This model was effective in inducing strength gains. Utilizing resistance bands may be a viable exercise countermeasure to combat the negative neuromuscular effects experienced from prolonged exposure to microgravity. With the inefficacy of free weights in microgravity, it is necessary to find an alternative means of resistance training. Elastic resistance band training provides a practical and cost-effective method to increase strength in microgravity. Because this is the first study to utilize elastic resistance bands in a simulated microgravity environment, more research is warranted to determine the optimal training variables such as sets, reps, and rest periods needed to produce the greatest hypertrophy and strength gains. Additionally, future investigations should include this microgravity-simulated exercise protocol during a concurrent period of bed rest. Acknowledgment: This investigation was funded by a North Carolina Space Grant - New Investigations Program Grant. [ABSTRACT FROM AUTHOR]