Muscle quality (MQ), defined as the amount of strength and/or power per unit of muscle mass, is a novel index of functional capacity that is increasingly relied upon as a critical biomarker of muscle ...health in low functioning aging and pathophysiological adult populations. Understanding the phenotypical attributes of MQ and how to use it as an assessment tool to explore the efficacy of resistance exercise training interventions that prioritize functional enhancement over increases in muscle size may have implications for populations beyond compromised adults, including healthy young adults who routinely perform physically demanding tasks for competitive or occupational purposes. However, MQ has received far less attention in healthy young populations than it has in compromised adults. Researchers and practitioners continue to rely upon static measures of lean mass or isolated measures of strength and power, rather than using MQ, to assess integrated functional responses to resistance exercise training and physical stress. Therefore, this review will critically examine MQ and the evidence base to establish this metric as a practical and important biomarker for functional capacity and performance in healthy, young populations. Interventions that enhance MQ, such as high-intensity stretch shortening contraction resistance exercise training, will be highlighted. Finally, we will explore the potential to leverage MQ as a practical assessment tool to evaluate function and enhance performance in young populations in non-traditional research settings.
Vascular blood flow restriction (BFR) training stimulates muscle hypertrophy by increasing muscle activation and muscle swelling. Previous studies used expensive pneumatic cuffs, which may not be ...practical for regular use. The aim was to investigate the acute effects of low-intensity practical BFR (LI-pBFR) on muscle activation, muscle swelling, and damage. Twelve trained male participants completed a 30-, 15-, 15-, 15-repetition scheme at 30% of their leg press 1-repetition maximum under control and LI-BFR conditions. Under the LI-BFR trial, knee wraps were applied to the thighs at a pressure that resulted in venous, not arterial, occlusion. In the control trial, wraps were applied with zero pressure. Ultrasound-determined muscle thickness was recorded at baseline; 0 minutes post with wraps; 0, 5, and 10 minutes post without wraps. Muscle activation was recorded during warm-ups and on the final set of 15 repetitions. Indices of muscle damage (soreness, power, and muscle swelling) were also recorded. There was a condition by time effect for muscle thickness (p < 0.0001, effect size ES = 0.5), in which muscle thickness increased in the LI-pBFR condition 0 minutes post with wraps and through 5 minutes post without wraps. No changes occurred in the control. There was a condition by time effect for muscle activation (p < 0.05, ES = 0.2). The LI-pBFR had greater activation than the control did. There were no condition by time effects on indices of muscle damage. Our data indicate that practical BFR significantly increases muscle activation and muscle thickness without increasing indices of damage.
Previous research has established the role of resistance training (RT) on muscle function in adolescents, but a lack of evidence to optimize RT for enhancing muscle quality (MQ) exists. This study ...examined whether RT frequency is associated with MQ in a nationally representative adolescent cohort. A total of 605 adolescents (12−15 year) in NHANES were stratified based on RT frequency. MQ was calculated as combined handgrip strength divided by arm lean mass (via dual-energy X-ray absorptiometry). Analysis of covariance was adjusted for sex, race/ethnicity, and arm fat percentage; p < 0.05 was considered significant. RT frequency was associated with MQ for 2−7 day/week but not 1 day/week. When no RT was compared to 1−2 and 3−7 day/week, associations were present for 3−7 day/week but not 1−2 day/week. When comparing no RT to 1−4 and 5−7 day/week, associations existed for 5−7 day/week but not 1−4 day/week. Next, no RT was compared to 1, 2−3, and 4−7 day/week; associations were found for 4−7 day/week, while 2−3 day/week had a borderline association (p = 0.06); there were no associations for 1 day/week. Finally, no RT was compared to 1, 2, 3, 4, and 5−7 day/week; associations were present for all except 1 and 3 day/week. These prospective data suggest a minimum RT frequency of 2 day/week is associated with MQ in adolescents as indicated by the lack of differences in MQ between 1 day/week RT versus no RT.
Introduction
Studies utilizing beta-hydroxy-beta-methylbutyrate (HMB) supplementation in trained populations are limited. No long-term studies utilizing HMB free acid (HMB-FA) have been conducted. ...Therefore, we investigated the effects of 12 weeks of HMB-FA supplementation on skeletal muscle hypertrophy, body composition, strength, and power in trained individuals. We also determined the effects of HMB-FA on muscle damage and performance during an overreaching cycle.
Methods
A three-phase double-blind, placebo- and diet-controlled randomized intervention study was conducted. Phase 1 was an 8-week-periodized resistance-training program; Phase 2 was a 2-week overreaching cycle; and Phase 3 was a 2-week taper. Muscle mass, strength, and power were examined at weeks 0, 4, 8, and 12 to assess the chronic effects of HMB-FA; and assessment of these, as well as cortisol, testosterone, and creatine kinase (CK) was performed at weeks 9 and 10 of the overreaching cycle.
Results
HMB-FA resulted in increased total strength (bench press, squat, and deadlift combined) over the 12-week training (77.1 ± 18.4 vs. 25.3 ± 22.0 kg,
p
< 0.001); a greater increase in vertical jump power (991 ± 168 vs. 630 ± 167 W,
p
< 0.001); and increased lean body mass gain (7.4 ± 4.2 vs. 2.1 ± 6.1 kg,
p
< 0.001) in HMB-FA- and placebo-supplemented groups, respectively. During the overreaching cycle, HMB-FA attenuated increases in CK (−6 ± 91 vs. 277 ± 229 IU/l,
p
< 0.001) and cortisol (−0.2 ± 2.9 vs. 4.5 ± 1.7 μg/dl,
p
< 0.003) in the HMB-FA- and placebo-supplemented groups, respectively.
Conclusions
These results suggest that HMB-FA enhances hypertrophy, strength, and power following chronic resistance training, and prevents decrements in performance following the overreaching.
Snell dwarf mice (Pit1dw/dw) exhibit deficiencies in growth hormone, prolactin, and thyroid stimulating hormone. Besides being an experimental model of hypopituitarism, these mice are long‐lived ...(>40% lifespan extension) and utilized as a model of slowed/delayed aging. Whether this longevity is accompanied by a compromised quality of life in terms of muscular performance has not yet been characterized. In this study, we investigated nontrained and trained muscles 1 month following a general validated resistance‐type exercise protocol in 3‐month‐old Snell dwarf mice and control littermates. Nontrained Snell dwarf gastrocnemius muscles exhibited a 1.3‐fold greater muscle mass to body weight ratio than control values although muscle quality, maximum isometric torque normalized to muscle mass, and fatigue recovery were compromised. For control mice, training increased isometric torque (17%) without altering muscle mass. For Snell dwarf mice, isometric torque was unaltered by training despite decreased muscle mass that rendered muscle mass to body weight ratio comparable to control values. Muscle quality and fatigue recovery improved twofold and threefold, respectively, for Snell dwarf mice. This accompanied a fourfold increase in levels of vascular cell adhesion molecule‐1 (VCAM‐1), a mediator of progenitor cell recruitment, and muscle remodeling in the form of increased number of central nuclei, additional muscle fibers per unit area, and altered fiber type distribution. These results reveal a trade‐off between muscle quality and longevity in the context of anterior pituitary hormone deficiency and that resistance‐type training can diminish this trade‐off by improving muscle quality concomitant with VCAM‐1 upregulation and muscle remodeling.
Utilization of high-intensity resistance training to counter age-related sarcopenia is currently debated because of the potential for maladaptation when training design is inappropriate. Training ...design is problematic because the influence of various loading variables (e.g. contraction mode, repetition number, and training frequency) is still not well characterized at old age. To address this in a precisely controlled manner, we developed a rodent model of high-intensity training consisting of maximally-activated stretch-shortening contractions (SSCs), contractions typical during resistance training. With this model, we determined that at old age, high-repetition SSC training (80 SSCs: 8 sets of 10 repetitions) performed frequently (i.e. 3 days per week) for 4.5 weeks induced strength deficits with no muscle mass gain while decreasing frequency to 2 days per week promoted increases in muscle mass and muscle quality (i.e. performance normalized to muscle mass). This finding confirmed the popular notion that decreasing training frequency has a robust effect with age. Meanwhile, the influence of other loading variables remains contentious. The aim of the present study was to assess muscle adaptation following modulation of contraction mode and repetition number during high-intensity SSC training. Muscles of young (3 month old) and old (30 month old) male rats were exposed to 4.5 weeks of low-repetition static training of 4 (i.e. 4 sets of one repetition) isometric (ISO) contractions 3 days per week or a more moderate-repetition dynamic training of 40 SSCs (i.e. 4 sets of 10 repetitions) 3 days per week. For young rats, performance and muscle mass increased regardless of training protocol. For old rats, no muscle mass adaptation was observed for 4 ISO training while 40 SSC training induced muscle mass gain without improvement in muscle quality, an outcome distinct from modulating training frequency. Muscle mass gain for old rats was accompanied by decreased protein levels of tumor necrosis factor alpha, a mediator of age-related chronic inflammatory signaling, to young levels. These findings suggest that while dynamic high-intensity training with a moderate number of repetitions has a limited capacity for altering muscle quality, such training is a viable strategy for countering age-related inflammatory signaling and modifying muscle mass.
•At young age, muscle adapted to a variety of high-activation training protocols.•At old age, muscle mass responded to moderate repetitions in dynamic training.•Tumor necrosis factor alpha levels returned to young levels.•Muscle quality did not improve unlike the case for training frequency modulation.•Moderate repetition number is a viable strategy with dynamic training at old age.
Acetaminophen (ACE) is a widely used analgesic and antipyretic drug with various applications, from pain relief to fever reduction. Recent studies have reported equivocal effects of habitual ACE ...intake on exercise performance, muscle growth, and risks to bone health. Thus, this study aimed to assess the impact of a 6‐week, low‐dose ACE regimen on muscle and bone adaptations in exercising and non‐exercising rats. Nine‐week‐old Wistar rats (n = 40) were randomized to an exercise or control (no exercise) condition with ACE or without (placebo). For the exercise condition, rats ran 5 days per week for 6 weeks at a 5% incline for 2 min at 15 cm/s, 2 min at 20 cm/s, and 26 min at 25 cm/s. A human equivalent dose of ACE was administered (379 mg/kg body weight) in drinking water and adjusted each week based on body weight. Food, water intake, and body weight were measured daily. At the beginning of week 6, animals in the exercise group completed a maximal treadmill test. At the end of week 6, rats were euthanized, and muscle cross‐sectional area (CSA), fiber type, and signaling pathways were measured. Additionally, three‐point bending and microcomputer tomography were measured in the femur. Follow‐up experiments in human primary muscle cells were used to explore supra‐physiological effects of ACE. Data were analyzed using a two‐way ANOVA for treatment (ACE or placebo) and condition (exercise or non‐exercise) for all animal outcomes. Data for cell culture experiments were analyzed via ANOVA. If omnibus significance was found in either ANOVA, a post hoc analysis was completed, and a Tukey's adjustment was used. ACE did not alter body weight, water intake, food intake, or treadmill performance (p > .05). There was a treatment‐by‐condition effect for Young's Modulus where placebo exercise was significantly lower than placebo control (p < .05). There was no treatment by condition effects for microCT measures, muscle CSA, fiber type, or mRNA expression. Phosphorylated‐AMPK was significantly increased with exercise (p < .05) and this was attenuated with ACE treatment. Furthermore, phospho‐4EBP1 was depressed in the exercise group compared to the control (p < .05) and increased in the ACE control and ACE exercise group compared to placebo exercise (p < .05). A low dose of ACE did not influence chronic musculoskeletal adaptations in exercising rodents but acutely attenuated AMPK phosphorylation and 4EBP1 dephosphorylation post‐exercise.
Acetaminophen, a common pain reliever and fever reducer, has been studied for its effects on exercise performance, muscle growth, and bone health, with mixed results. This study determined how a low dose of acetaminophen affected rats over 6 weeks, comparing those who exercised to those who did not. We measured the rats' body weight, food and water intake, exercise ability, and the biostructural and biochemical properties of muscle and bone. We found that acetaminophen did not change how much the rats ate, drank, weighed, or how well they performed on a treadmill. However, in rats that exercised, acetaminophen seemed to change cellular signals related to muscle adaptation after exercise suggesting that while the drug does not impact the overall growth of muscle and bone, it might alter how muscles respond to exercise at the cellular level. To determine how high doses of acetaminophen affect muscle, we conducted experiments with human muscle cells. We exposed the muscle cells to various levels of acetaminophen, some doses mirroring what we see in human blood and some much higher, to see if it would impact the growth, fusion, or size of muscle cells. Interestingly, we found that only the very high doses of acetaminophen led to less merging of muscle cells, a result that aligns with previous research on different NSAIDs. Taken together, our study indicates that low doses of acetaminophen taken for 6 weeks are unlikely to affect musculoskeletal adaptations.
Cellular inflammatory response, mediated by arachidonic acid (AA) and cyclooxygenase, is a highly regulated process that leads to the repair of damaged tissue. Recent studies on murine C2C12 cells ...have demonstrated that AA supplementation leads to myotube hypertrophy. However, AA has not been tested on primary human muscle cells. Therefore, the purpose of this study was to determine whether AA supplementation has similar effects on human muscle cells.
Proliferating and differentiating human myoblasts were exposed to AA in a dose-dependent manner (50-0.80 µM) for 48 (myoblasts) or 72 (myotubes) hours. Cell viability was tested using a 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and cell counting; myotube area was determined by immunocytochemistry and confocal microscopy; and anabolic signaling pathways were evaluated by western blot and RT-PCR.
Our data show that the treatment of primary human myoblasts treated with 50 µM and 25 µM of AA led to the release of PGE
and PGF
at levels higher than those of control-treated cells (
< 0.001 for all concentrations). Additionally, 50 µM and 25 µM of AA suppressed myoblast proliferation, myotube area, and myotube fusion. Anabolic signaling indicated reductions in total and phosphorylated TSC2, AKT, S6, and 4EBP1 in myoblasts at 50 µM of AA (
< 0.01 for all), but not in myotubes. These changes were not affected by COX-2 inhibition with celecoxib.
Together, our data demonstrate that high concentrations of AA inhibit myoblast proliferation, myotube fusion, and myotube hypertrophy, thus revealing potential deleterious effects of AA on human skeletal muscle cell health and viability.
Snell dwarf mice with the
mutation are deficient in growth hormone, prolactin, and thyroid stimulating hormone and exhibit >40% lifespan extension. This longevity is accompanied by compromised ...muscular performance. However, research regarding young (3-month-old) Snell dwarf mice demonstrate exceptional responsivity to resistance-type training especially in terms of a shifted fiber type distribution and increased protein levels of vascular cell adhesion molecule-1 (VCAM-1), a possible mediator of such remodeling. In the present study, we investigated whether this responsiveness persists at 12 months of age. Unlike 12-month-old control mice, age-matched Snell dwarf mice remained resistant to training-induced maladaptive decreases in performance and muscle mass. This was accompanied by retainment of the remodeling capacity in muscles of Snell dwarf mice to increase VCAM-1 protein levels and a shift in myosin heavy chain (MHC) isoform distribution with training. Even decreasing training frequency for control mice, an alteration which protected muscles from maladaptation at 12 months of age, did not result in the overt remodeling observed for Snell dwarf mice. The results demonstrate a distinct remodeling response to resistance-type exercise operative in the context of the
mutation of long-lived Snell dwarf mice.
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