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Medicine and Science in Sports and... Sep 2022Skeletal muscle plays a critical role in physical function and metabolic health. Muscle is a highly adaptable tissue that responds to resistance exercise (RE; loading)... (Review)
Review
Skeletal muscle plays a critical role in physical function and metabolic health. Muscle is a highly adaptable tissue that responds to resistance exercise (RE; loading) by hypertrophying, or during muscle disuse, RE mitigates muscle loss. Resistance exercise training (RET)-induced skeletal muscle hypertrophy is a product of external (e.g., RE programming, diet, some supplements) and internal variables (e.g., mechanotransduction, ribosomes, gene expression, satellite cells activity). RE is undeniably the most potent nonpharmacological external variable to stimulate the activation/suppression of internal variables linked to muscular hypertrophy or countering disuse-induced muscle loss. Here, we posit that despite considerable research on the impact of external variables on RET and hypertrophy, internal variables (i.e., inherent skeletal muscle biology) are dominant in regulating the extent of hypertrophy in response to external stimuli. Thus, identifying the key internal skeletal muscle-derived variables that mediate the translation of external RE variables will be pivotal to determining the most effective strategies for skeletal muscle hypertrophy in healthy persons. Such work will aid in enhancing function in clinical populations, slowing functional decline, and promoting physical mobility. We provide up-to-date, evidence-based perspectives of the mechanisms regulating RET-induced skeletal muscle hypertrophy.
Topics: Exercise; Humans; Hypertrophy; Mechanotransduction, Cellular; Muscle, Skeletal; Resistance Training
PubMed: 35389932
DOI: 10.1249/MSS.0000000000002929 -
Sports Medicine (Auckland, N.Z.) Oct 2021Lack of time is among the more commonly reported barriers for abstention from exercise programs. The aim of this review was to determine how strength training can be... (Review)
Review
Lack of time is among the more commonly reported barriers for abstention from exercise programs. The aim of this review was to determine how strength training can be most effectively carried out in a time-efficient manner by critically evaluating research on acute training variables, advanced training techniques, and the need for warm-up and stretching. When programming strength training for optimum time-efficiency we recommend prioritizing bilateral, multi-joint exercises that include full dynamic movements (i.e. both eccentric and concentric muscle actions), and to perform a minimum of one leg pressing exercise (e.g. squats), one upper-body pulling exercise (e.g. pull-up) and one upper-body pushing exercise (e.g. bench press). Exercises can be performed with machines and/or free weights based on training goals, availability, and personal preferences. Weekly training volume is more important than training frequency and we recommend performing a minimum of 4 weekly sets per muscle group using a 6-15 RM loading range (15-40 repetitions can be used if training is performed to volitional failure). Advanced training techniques, such as supersets, drop sets and rest-pause training roughly halves training time compared to traditional training, while maintaining training volume. However, these methods are probably better at inducing hypertrophy than muscular strength, and more research is needed on longitudinal training effects. Finally, we advise restricting the warm-up to exercise-specific warm-ups, and only prioritize stretching if the goal of training is to increase flexibility. This review shows how acute training variables can be manipulated, and how specific training techniques can be used to optimize the training response: time ratio in regard to improvements in strength and hypertrophy.
Topics: Exercise; Humans; Hypertrophy; Muscle Strength; Muscle, Skeletal; Resistance Training
PubMed: 34125411
DOI: 10.1007/s40279-021-01490-1 -
Journal of Sport and Health Science Mar 2022We aimed to perform a systematic review and meta-analysis of the effects of training to muscle failure or non-failure on muscular strength and hypertrophy. (Meta-Analysis)
Meta-Analysis Review
PURPOSE
We aimed to perform a systematic review and meta-analysis of the effects of training to muscle failure or non-failure on muscular strength and hypertrophy.
METHODS
Meta-analyses of effect sizes (ESs) explored the effects of training to failure vs. non-failure on strength and hypertrophy. Subgroup meta-analyses explored potential moderating effects of variables such as training status (trained vs. untrained), training volume (volume equated vs. volume non-equated), body region (upper vs. lower), exercise selection (multi- vs. single-joint exercises (only for strength)), and study design (independent vs. dependent groups).
RESULTS
Fifteen studies were included in the review. All studies included young adults as participants. Meta-analysis indicated no significant difference between the training conditions for muscular strength (ES = -0.09, 95% confidence interval (95%CI): -0.22 to 0.05) and for hypertrophy (ES = 0.22, 95%CI: -0.11 to 0.55). Subgroup analyses that stratified the studies according to body region, exercise selection, or study design showed no significant differences between training conditions. In studies that did not equate training volume between the groups, the analysis showed significant favoring of non-failure training on strength gains (ES = -0.32, 95%CI: -0.57 to -0.07). In the subgroup analysis for resistance-trained individuals, the analysis showed a significant effect of training to failure for muscle hypertrophy (ES = 0.15, 95%CI: 0.03-0.26).
CONCLUSION
Training to muscle failure does not seem to be required for gains in strength and muscle size. However, training in this manner does not seem to have detrimental effects on these adaptations, either. More studies should be conducted among older adults and highly trained individuals to improve the generalizability of these findings.
Topics: Adaptation, Physiological; Aged; Humans; Hypertrophy; Muscle Strength; Muscle, Skeletal; Resistance Training; Young Adult
PubMed: 33497853
DOI: 10.1016/j.jshs.2021.01.007 -
Journal of Neuromuscular Diseases 2021Skeletal muscle hypertrophy can be induced by hormones and growth factors acting directly as positive regulators of muscle growth or indirectly by neutralizing negative... (Review)
Review
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.
Topics: Humans; Hypertrophy; Muscle, Skeletal; Protein Biosynthesis; Signal Transduction
PubMed: 33216041
DOI: 10.3233/JND-200568 -
Journal of Applied Physiology... Jan 2019One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a... (Review)
Review
One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as "hypertrophy stimulus," and the sensor of such a signal as "hypertrophy sensor." In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.
Topics: Animals; Humans; Hypertrophy; Mechanotransduction, Cellular; Muscle, Skeletal; Resistance Training; Stress, Physiological; Weight-Bearing
PubMed: 30335577
DOI: 10.1152/japplphysiol.00685.2018 -
Physiological Reviews Oct 2023Mechanisms underlying mechanical overload-induced skeletal muscle hypertrophy have been extensively researched since the landmark report by Morpurgo (1897) of... (Review)
Review
Mechanisms underlying mechanical overload-induced skeletal muscle hypertrophy have been extensively researched since the landmark report by Morpurgo (1897) of "work-induced hypertrophy" in dogs that were treadmill trained. Much of the preclinical rodent and human resistance training research to date supports that involved mechanisms include enhanced mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling, an expansion in translational capacity through ribosome biogenesis, increased satellite cell abundance and myonuclear accretion, and postexercise elevations in muscle protein synthesis rates. However, several lines of past and emerging evidence suggest that additional mechanisms that feed into or are independent of these processes are also involved. This review first provides a historical account of how mechanistic research into skeletal muscle hypertrophy has progressed. A comprehensive list of mechanisms associated with skeletal muscle hypertrophy is then outlined, and areas of disagreement involving these mechanisms are presented. Finally, future research directions involving many of the discussed mechanisms are proposed.
Topics: Humans; Animals; Dogs; Muscle, Skeletal; Signal Transduction; Mechanistic Target of Rapamycin Complex 1; Protein Biosynthesis; Hypertrophy; Mammals
PubMed: 37382939
DOI: 10.1152/physrev.00039.2022 -
Cells Aug 2020Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle... (Review)
Review
Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence has suggested that IGF-1/Akt can inhibit muscle atrophy-inducing cytokine and myostatin signaling via inhibition of the NF-κΒ and Smad pathways, respectively. Several miRNAs have been found to regulate IGF-1 signaling in skeletal muscle, and these miRs are likely regulated in different pathological conditions and contribute to the development of muscle atrophy. IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. Importantly, IGF-1 levels and IGF-1R downstream signaling are suppressed in many chronic disease conditions and likely result in muscle atrophy via the combined effects of altered protein synthesis, UPS activity, autophagy, and muscle regeneration.
Topics: Humans; Hypertrophy; Insulin-Like Growth Factor I; Muscle, Skeletal; Muscular Atrophy; Signal Transduction
PubMed: 32858949
DOI: 10.3390/cells9091970 -
Biomedica : Revista Del Instituto... Mar 2019Altitude and simulated-hypoxia training produces different physiological and/or biochemical adaptations in the skeletal muscle. These are: oxidative capacity,... (Review)
Review
Altitude and simulated-hypoxia training produces different physiological and/or biochemical adaptations in the skeletal muscle. These are: oxidative capacity, mitochondrial activity modifications, aerobic metabolism changes and myoglobin content. The purpose of this review was to analyze the adaptations of skeletal muscle in response to the combination of strength-resistance exercise and hypoxia. In general terms, the structural adaptations of the muscle are similar in hypoxia and normoxia except that hypoxia training produces an increase of the volume and cross-sectional area of the muscle fiber. In conclusion, the synergic effect of the combination of strength resistance training with normobaric hypoxia produces better and greater adaptations and beneficial physiological changes of the muscle tissue, which shows favorable phenotypic changes in skeletal muscle hypertrophy.
Topics: Acclimatization; Humans; Hypertrophy; Hypoxia; Muscle, Skeletal; Resistance Training
PubMed: 31021559
DOI: 10.7705/biomedica.v39i1.4084 -
International Journal of Environmental... Dec 2019Effective hypertrophy-oriented resistance training (RT) should comprise a combination of mechanical tension and metabolic stress. Regarding training variables, the most...
BACKGROUND
Effective hypertrophy-oriented resistance training (RT) should comprise a combination of mechanical tension and metabolic stress. Regarding training variables, the most effective values are widely described in the literature. However, there is still a lack of consensus regarding the efficiency of advanced RT techniques and methods in comparison to traditional approaches.
METHODS
MEDLINE and SPORTDiscus databases were searched from 1996 to September 2019 for all studies investigating the effects of advanced RT techniques and methods on muscle hypertrophy and training variables. Thirty articles met the inclusion criteria and were consequently included for the quality assessment and data extraction.
RESULTS
Concerning the time-efficiency of training, the use of agonist-antagonist, upper-lower body supersets, drop and cluster sets, sarcoplasma stimulating training, employment of fast, but controlled duration of eccentric contractions (~2s), and high-load RT supplemented with low-load RT under blood flow restriction may provide an additional stimulus and an advantage to traditional training protocols. With regard to the higher degree of mechanical tension, the use of accentuated eccentric loading in RT should be considered. Implementation of drop sets, sarcoplasma stimulating training, low-load RT in conjunction with low-load RT under blood flow restriction could provide time-efficient solutions to increased metabolic stress.
CONCLUSIONS
Due to insufficient evidence, it is difficult to provide specific guidelines for volume, intensity of effort, and frequency of previously mentioned RT techniques and methods. However, well-trained athletes may integrate advanced RT techniques and methods into their routines as an additional stimulus to break through plateaus and to prevent training monotony.
Topics: Humans; Hypertrophy; Muscle Strength; Muscle, Skeletal; Resistance Training
PubMed: 31817252
DOI: 10.3390/ijerph16244897 -
Acta Physiologica Hungarica Mar 2015Cycle training is widely performed as a major part of any exercise program seeking to improve aerobic capacity and cardiovascular health. However, the effect of cycle... (Review)
Review
Cycle training is widely performed as a major part of any exercise program seeking to improve aerobic capacity and cardiovascular health. However, the effect of cycle training on muscle size and strength gain still requires further insight, even though it is known that professional cyclists display larger muscle size compared to controls. Therefore, the purpose of this review is to discuss the effects of cycle training on muscle size and strength of the lower extremity and the possible mechanisms for increasing muscle size with cycle training. It is plausible that cycle training requires a longer period to significantly increase muscle size compared to typical resistance training due to a much slower hypertrophy rate. Cycle training induces muscle hypertrophy similarly between young and older age groups, while strength gain seems to favor older adults, which suggests that the probability for improving in muscle quality appears to be higher in older adults compared to young adults. For young adults, higher-intensity intermittent cycling may be required to achieve strength gains. It also appears that muscle hypertrophy induced by cycle training results from the positive changes in muscle protein net balance.
Topics: Adolescent; Adult; Bicycling; Female; Humans; Hypertrophy; Male; Middle Aged; Muscle Strength; Muscle, Skeletal; Organ Size; Physical Conditioning, Human; Young Adult
PubMed: 25804386
DOI: 10.1556/APhysiol.102.2015.1.1