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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 -
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 -
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 -
Current Opinion in Clinical Nutrition... Jul 2023Highlight contemporary evidence examining the effects of carbohydrate restriction on the intracellular regulation of muscle mass and anaerobic performance. (Review)
Review
PURPOSE OF REVIEW
Highlight contemporary evidence examining the effects of carbohydrate restriction on the intracellular regulation of muscle mass and anaerobic performance.
RECENT FINDINGS
Low carbohydrate diets increase fat oxidation and decrease fat mass. Emerging evidence suggests that dietary carbohydrate restriction increases protein oxidation, thereby limiting essential amino acid availability necessary to stimulate optimal muscle protein synthesis and promote muscle recovery. Low carbohydrate feeding for 24 h increases branched-chain amino acid (BCAA) oxidation and reduces myogenic regulator factor transcription compared to mixed-macronutrient feeding. When carbohydrate restriction is maintained for 8 to 12 weeks, the alterations in anabolic signaling, protein synthesis, and myogenesis likely contribute to limited hypertrophic responses to resistance training. The blunted hypertrophic response to resistance training when carbohydrate availability is low does not affect muscle strength, whereas persistently low muscle glycogen does impair anaerobic output during high-intensity sprint and time to exhaustion tests.
SUMMARY
Dietary carbohydrate restriction increases BCAA oxidation and impairs muscle hypertrophy and anaerobic performance, suggesting athletes who need to perform high-intensity exercise should consider avoiding dietary strategies that restrict carbohydrate.
Topics: Humans; Physical Endurance; Anaerobiosis; Dietary Carbohydrates; Diet, Carbohydrate-Restricted; Amino Acids, Branched-Chain; Hypertrophy; Muscle, Skeletal
PubMed: 37057671
DOI: 10.1097/MCO.0000000000000934 -
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 Strength and Conditioning... Sep 2023Kassiano, W, Costa, B, Kunevaliki, G, Soares, D, Zacarias, G, Manske, I, Takaki, Y, Ruggiero, MF, Stavinski, N, Francsuel, J, Tricoli, I, Carneiro, MAS, and Cyrino, ES.... (Randomized Controlled Trial)
Randomized Controlled Trial
Kassiano, W, Costa, B, Kunevaliki, G, Soares, D, Zacarias, G, Manske, I, Takaki, Y, Ruggiero, MF, Stavinski, N, Francsuel, J, Tricoli, I, Carneiro, MAS, and Cyrino, ES. Greater gastrocnemius muscle hypertrophy after partial range of motion training performed at long muscle lengths. J Strength Cond Res 37(9): 1746-1753, 2023-Whether there is an optimal range of motion (ROM) to induce muscle hypertrophy remains elusive, especially for gastrocnemius. This study aimed to compare the changes in gastrocnemius muscle thickness between calf raise exercise performed with full ROM (FULL ROM ), partial ROM performed in the initial (INITIAL ROM ), and final (FINAL ROM ) portions of the ROM. Forty-two young women performed a calf training program for 8 weeks, 3 days·week -1 , with differences in the calf raise ROM configuration. The calf raise exercise was performed in a pin-loaded, horizontal, leg-press machine, in 3 sets of 15-20 repetition maximum. The subjects were randomly assigned to 1 of the 3 groups: FULL ROM (ankle: -25° to +25°), INITIAL ROM (ankle: -25° to 0°), and FINAL ROM (ankle: 0° to +25°), where 0° was defined as an angle of 90° of the foot with the tibia. The muscle thickness measurements of medial and lateral gastrocnemius were taken by means of B-mode ultrasound. INITIAL ROM elicited greater medial gastrocnemius increases than FULL ROM and FINAL ROM (INITIAL ROM = +15.2% vs. FULL ROM = +6.7% and FINAL ROM = +3.4%; p ≤ 0.009). Furthermore, INITIAL ROM elicited greater lateral gastrocnemius increases than FINAL ROM (INITIAL ROM = +14.9% vs. FINAL ROM = +6.2%; p < 0.024) but did not significantly differ from FULL ROM (FULL ROM = +7.3%; p = 0.060). The current results suggest that calf training performed at longer muscle lengths may optimize gastrocnemius muscle hypertrophy in young women. Therefore, when prescribing hypertrophy-oriented training, the inclusion of the calf raise exercise performed with partial ROM in the initial portion of the excursion should be considered.
Topics: Humans; Female; Muscle, Skeletal; Leg; Ankle; Range of Motion, Articular; Hypertrophy; Muscle Strength
PubMed: 37015016
DOI: 10.1519/JSC.0000000000004460