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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 -
Einstein (Sao Paulo, Brazil) 2021To compare the effects of different resistance training programs on measures of muscle strength and hypertrophy. (Randomized Controlled Trial)
Randomized Controlled Trial
OBJECTIVE
To compare the effects of different resistance training programs on measures of muscle strength and hypertrophy.
METHODS
Sixty-seven untrained subjects were randomized to one of two groups: Split Workout Routine (n=35), in which muscle groups were trained twice per week in an A/B split consisting of eight sets per session, or Full-Body Workout Routine (n=32), in which muscle groups were trained four times per week with four and eight sets per session. Both groups performed eight to 12 repetition maximum per set, with 60 seconds of rest between sets. Maximal strength and muscle thickness were assessed at baseline and after eight weeks of training.
RESULTS
A significant main effect of time (pre versus post) was observed for maximal strength in the bench press and squat exercises and thickness of the elbow extensor, elbow flexor and quadriceps femoris muscles. Selected variables did not differ significantly between groups.
CONCLUSION
Resistance training twice or four times per week has similar effects on neuromuscular adaptation, provided weekly set volume is equal.
Topics: Adaptation, Physiological; Humans; Hypertrophy; Muscle Strength; Muscle, Skeletal; Resistance Training
PubMed: 34468591
DOI: 10.31744/einstein_journal/2021AO5781 -
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 -
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 -
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 -
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 -
Nutrients Apr 2023The purpose of this paper was to carry out a systematic review with a meta-analysis of randomized controlled trials that examined the combined effects of resistance... (Meta-Analysis)
Meta-Analysis Review
The purpose of this paper was to carry out a systematic review with a meta-analysis of randomized controlled trials that examined the combined effects of resistance training (RT) and creatine supplementation on regional changes in muscle mass, with direct imaging measures of hypertrophy. Moreover, we performed regression analyses to determine the potential influence of covariates. We included trials that had a duration of at least 6 weeks and examined the combined effects of creatine supplementation and RT on site-specific direct measures of hypertrophy (magnetic resonance imaging (MRI), computed tomography (CT), or ultrasound) in healthy adults. A total of 44 outcomes were analyzed across 10 studies that met the inclusion criteria. A univariate analysis of all the standardized outcomes showed a pooled mean estimate of 0.11 (95% Credible Interval (CrI): -0.02 to 0.25), providing evidence for a very small effect favoring creatine supplementation when combined with RT compared to RT and a placebo. Multivariate analyses found similar small benefits for the combination of creatine supplementation and RT on changes in the upper and lower body muscle thickness (0.10-0.16 cm). Analyses of the moderating effects indicated a small superior benefit for creatine supplementation in younger compared to older adults (0.17 (95%CrI: -0.09 to 0.45)). In conclusion, the results suggest that creatine supplementation combined with RT promotes a small increase in the direct measures of skeletal muscle hypertrophy in both the upper and lower body.
Topics: Humans; Aged; Creatine; Resistance Training; Hypertrophy; Muscles; Dietary Supplements
PubMed: 37432300
DOI: 10.3390/nu15092116 -
International Journal of Environmental... Sep 2022This study aimed to conduct a meta-analysis of randomized controlled trials to examine the effects of the short-foot exercise (SFE) compared to foot orthosis or other... (Meta-Analysis)
Meta-Analysis Review
This study aimed to conduct a meta-analysis of randomized controlled trials to examine the effects of the short-foot exercise (SFE) compared to foot orthosis or other types of interventions. Eligibility criteria involved participants with flatfoot engaging in the SFE compared to other forms of intervention or control groups without specific intervention. Relevant studies published before the end of June 2022 were identified from databases. A meta-analysis was performed by calculating the mean differences (MD) and standard MD (SMD) using the random effects model. Six trials with 201 patients (out of 609 records) that met selection criteria were reviewed. Five of the six trials implemented distinct interventions in the control group such as shoe insoles and muscle strengthening exercises, while in the remaining trial, controls received no intervention. The SFE group significantly reduced the navicular drop test (NDT) values (MD: -0.23; 95% confidence interval: -0.45 to -0.02; = 0.04) and the foot posture index (FPI-6) score (MD: -0.67; 95% confidence interval: -0.98 to -0.36; < 0.0001) when compared to the control group. The muscle hypertrophy did not differ significantly between the groups. The SFE may contribute more benefits than other intervention as it affects flatfoot individuals' foot alignment. Hence, the SFE is recommended as a beneficial dynamic support when facing flatfoot problems.
Topics: Exercise Therapy; Flatfoot; Foot; Humans; Hypertrophy; Muscles
PubMed: 36231295
DOI: 10.3390/ijerph191911994 -
Journal of Strength and Conditioning... Feb 2022Hirono, T, Ikezoe, T, Taniguchi, M, Tanaka, H, Saeki, J, Yagi, M, Umehara, J, and Ichihashi, N. Relationship between muscle swelling and hypertrophy induced by...
Hirono, T, Ikezoe, T, Taniguchi, M, Tanaka, H, Saeki, J, Yagi, M, Umehara, J, and Ichihashi, N. Relationship between muscle swelling and hypertrophy induced by resistance training. J Strength Cond Res 36(2): 359-364, 2022-Muscle swelling immediately after resistance exercise may be induced by metabolic stress. The accumulation of metabolic stress is considered to promote muscle hypertrophy after several weeks of resistance training (RT). The purpose of this study was to determine the relationship between muscle swelling immediately after the first session of RT and muscle hypertrophy after a 6-week RT using ultrasonography. Twenty-two untrained young men performed knee extension resistance exercise consisting of 3 sets with 8 repetitions at a load of 80% of one repetition maximum for 6 weeks (3 d·wk-1). Muscle thickness of the quadriceps femoris was measured using ultrasonography device at 3 anatomical sites (proximal, medial, and distal sites) of the middle, lateral, and medial part of the anterior thigh. The sum of the muscle thickness at 9 measurement sites was used for analysis. Acute change in muscle thickness immediately after the first session of RT was used as an indicator of muscle swelling. Chronic change in muscle thickness after the 6-week RT was used as an indicator of muscle hypertrophy. A significant increase in muscle thickness was observed immediately after the first session of RT (8.3 ± 3.2%, p < 0.001). After the 6-week RT, muscle thickness increased significantly (2.9 ± 2.6%, p < 0.001). A significant positive correlation was found between muscle swelling and muscle hypertrophy (ρ = 0.443, p = 0.039). This study suggests that the greater the muscle swelling immediately after the first session of RT, the greater the muscle hypertrophy after RT.
Topics: Humans; Hypertrophy; Male; Muscle Strength; Muscle, Skeletal; Quadriceps Muscle; Resistance Training; Ultrasonography
PubMed: 31904714
DOI: 10.1519/JSC.0000000000003478 -
European Journal of Sport Science Jul 2023The biarticular triceps brachii long head (TB) is lengthened more in the overhead than neutral arm position. We compared triceps brachii hypertrophy after elbow...
The biarticular triceps brachii long head (TB) is lengthened more in the overhead than neutral arm position. We compared triceps brachii hypertrophy after elbow extension training performed in the overhead vs. neutral arm position. Using a cable machine, 21 adults conducted elbow extensions (90-0°) with one arm in the overhead (Overhead-Arm) and the other arm in the neutral (Neutral-Arm) position at 70% one-repetition maximum (1RM), 10 reps/set, 5 sets/session, 2 sessions/week for 12 weeks. Training load was gradually increased (+5% 1RM/session) when the preceding session was completed without repetition failure. 1RM of the assigned condition and MRI-measured muscle volume of the TB, monoarticular lateral and medial heads (TB), and whole triceps brachii (Whole-TB) were assessed pre- and post-training. Training load and 1RM increased in both arms similarly (+62-71% at post, = 0.285), while their absolute values/weights were always lower in Overhead-Arm (-34-39%, < 0.001). Changes in muscle volume in Overhead-Arm compared to Neutral-Arm were 1.5-fold greater for the TB (+28.5% vs. +19.6%, Cohen's = 0.61, < 0.001), 1.4-fold greater for the TB (+14.6% vs. +10.5%, = 0.39, = 0.002), and 1.4-fold greater for the Whole-TB (+19.9% vs. +13.9%, = 0.54, < 0.001). In conclusion, triceps brachii hypertrophy was substantially greater after elbow extension training performed in the overhead versus neutral arm position, even with lower absolute loads used during the training.Growing evidence suggests that resistance training at long muscle lengths promotes muscle hypertrophy, but its practical applications are yet to be explored.Triceps brachii muscle hypertrophy was substantially greater after cable elbow extension training performed in the overhead than neutral arm position, particularly in the biarticular triceps brachii long head, even with lower absolute loads lifted (i.e. lower mechanical stress to muscles/joints).Cable elbow extension training should be performed in the overhead rather than neutral arm position if one aims to maximise muscle hypertrophy of the triceps brachii or to prevent atrophy of this muscle.
Topics: Adult; Humans; Elbow; Elbow Joint; Muscle, Skeletal; Resistance Training; Hypertrophy
PubMed: 35819335
DOI: 10.1080/17461391.2022.2100279