Fact-checked by Grok 2 weeks ago

Muscle hypertrophy

Muscle hypertrophy is the enlargement of skeletal muscle fibers, resulting in an increase in muscle mass and cross-sectional area, primarily driven by an imbalance where muscle protein synthesis exceeds protein degradation. This process is most commonly induced through resistance training, which stimulates adaptive responses in muscle tissue, but can also be influenced by hormonal and growth factors such as insulin-like growth factor 1 (IGF-1) and testosterone. Muscle hypertrophy plays a critical role in enhancing physical strength, metabolic health, and overall locomotion, with implications for athletic performance and aging-related muscle preservation. The mechanisms underlying muscle hypertrophy involve multiple interconnected pathways, with three primary drivers identified in scientific literature: mechanical tension, muscle damage, and metabolic stress. Mechanical tension, generated by the force and stretch of muscle contractions during resistance exercise, is considered the dominant stimulus, activating signaling pathways like AKT/mTOR to promote protein synthesis and satellite cell proliferation. Muscle damage, arising from microtears in muscle fibers during intense eccentric contractions, triggers inflammatory responses and repair processes that contribute to fiber enlargement through satellite cell fusion and growth factor release. Metabolic stress, characterized by the accumulation of metabolites like lactate during high-repetition training, induces cell swelling, hormonal responses, and oxidative signaling that further support hypertrophic adaptations. Hypertrophy can manifest in two main forms: myofibrillar hypertrophy, which involves an increase in the size and number of contractile myofibrils for enhanced force production, and sarcoplasmic hypertrophy, which features expansion of the sarcoplasm (non-contractile elements like glycogen and fluid) often seen in endurance-oriented training. While myofibrillar changes are more directly linked to strength gains, sarcoplasmic alterations contribute to muscle endurance and volume, though the distinction remains a topic of ongoing research with evidence suggesting both occur concurrently in response to training variables like load, volume, and repetition range. Optimal hypertrophy requires progressive overload, adequate nutrition (particularly protein intake), and recovery, with resistance training protocols emphasizing 6–12 repetitions per set shown to maximize these outcomes across diverse populations.

Biological Foundations

Definition and Distinction from Hyperplasia

Muscle hypertrophy refers to the enlargement of existing skeletal muscle fibers, achieved primarily through an increase in myofibril number (myofibrillar hypertrophy) or sarcoplasmic volume (sarcoplasmic hypertrophy), which augments the muscle's cross-sectional area and enhances its force-producing capacity. The concept emerged in late 19th-century physiology research, notably through Bernhard Morpurgo's 1897 experiments on dogs, where treadmill training for two months led to hypertrophy in the sartorius muscle via increased fiber size without new fiber formation. This process is distinct from hyperplasia, the proliferation of new muscle fibers, which occurs rarely in adult humans but has been documented in certain animals, such as birds subjected to chronic mechanical overload like wing stretch, where fiber number can increase alongside size. In human skeletal muscle, adaptation to stimuli like resistance training overwhelmingly proceeds through hypertrophy rather than hyperplasia. Hypertrophy is typically measured non-invasively via ultrasound or MRI to track changes in muscle cross-sectional area, or through muscle biopsies to quantify fiber diameter increases, with representative training studies showing gains of 20-50% in fiber size over 10-16 weeks.

Relevant Muscle Anatomy and Physiology

Skeletal muscle fibers, also known as myocytes, are elongated, multinucleated cells that form the basic contractile units of skeletal muscle tissue. Each fiber is surrounded by a plasma membrane called the sarcolemma and contains numerous myofibrils, which are cylindrical organelles composed primarily of contractile proteins. Myofibrils occupy about 80% of the fiber's volume and are organized into repeating units called sarcomeres, the fundamental segments responsible for muscle contraction. The sarcomere extends from one Z-line to the next and consists of overlapping thin filaments made of actin and thick filaments composed of myosin, arranged in a precise lattice that gives muscle its striated appearance. Actin filaments anchor to Z-lines and extend toward the center of the sarcomere, while myosin filaments reside in the central A-band, with their globular heads projecting outward to interact with actin during contraction. The sarcoplasm, the cytoplasm within the muscle fiber, surrounds the myofibrils and includes organelles such as mitochondria, the sarcoplasmic reticulum for calcium storage, and a soluble protein fraction that supports metabolic functions; during hypertrophy, increases in sarcoplasmic volume contribute to overall fiber enlargement alongside myofibrillar additions. Skeletal muscle fibers are classified into distinct types based on their myosin heavy chain isoforms, contractile speed, and metabolic properties: Type I (slow-twitch, oxidative) fibers, which are fatigue-resistant and rely on aerobic metabolism for sustained activity; Type IIa (fast-twitch oxidative-glycolytic) fibers, which generate moderate force with both aerobic and anaerobic capacity; and Type IIx (fast-twitch glycolytic) fibers, which produce high force rapidly but fatigue quickly due to reliance on anaerobic glycolysis. The hypertrophy potential varies by fiber type, with Type II fibers, particularly IIa and IIx, exhibiting greater responsiveness to resistance training stimuli compared to Type I fibers, as evidenced by larger increases in cross-sectional area following high-load protocols. In physiological terms, skeletal muscle generates force through the cross-bridge cycling mechanism, where myosin heads bind to actin filaments, undergo a power stroke powered by ATP hydrolysis, and slide the filaments past each other to shorten the sarcomere and produce contraction. Approximately 20% of skeletal muscle mass consists of proteins, with myofibrillar proteins such as actin and myosin accounting for the majority of this protein content and forming the structural basis for force production. From an evolutionary perspective, human skeletal muscle has adapted for efficient bipedal locomotion and endurance activities, featuring a higher proportion of Type I fibers compared to other primates like chimpanzees, which possess greater fast-twitch fiber content and overall muscle power output; this endurance-oriented composition may limit the extent of extreme hypertrophy achievable in humans relative to our primate ancestors.

Cellular and Molecular Mechanisms

Protein Synthesis and Degradation Pathways

Muscle hypertrophy fundamentally arises from a positive net protein balance in skeletal muscle fibers, where the rate of protein synthesis exceeds the rate of protein degradation over time. This dynamic equilibrium can be expressed as ΔProtein = Synthesis Rate - Degradation Rate, with hypertrophy occurring when synthesis predominates. Following resistance exercise, muscle protein synthesis rates typically increase by approximately 50% above baseline levels for up to 24-48 hours, driven primarily by enhanced translation initiation and ribosomal biogenesis, while degradation rates remain relatively stable or slightly suppressed during the anabolic window. The mammalian target of rapamycin (mTOR) pathway serves as the central regulator of this anabolic response, integrating signals from mechanical tension, growth factors, and amino acids to promote protein accretion. Activation of mTOR complex 1 (mTORC1) by resistance exercise-induced mechanical load and essential amino acids, particularly leucine, leads to phosphorylation of downstream targets such as eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) and ribosomal protein S6 kinase 1 (S6K1), which facilitate translation initiation and elongation while supporting ribosomal biogenesis for sustained synthesis capacity. Seminal studies have demonstrated that mTORC1 inhibition via rapamycin blunts hypertrophy in response to overload, underscoring its necessity for load-mediated growth. Local production of insulin-like growth factor-1 (IGF-1) further amplifies mTOR signaling by activating the phosphoinositide 3-kinase (PI3K)/Akt pathway, enhancing translation efficiency and myonuclear transcriptional activity to support hypertrophy. Microtrauma from eccentric contractions can initiate this cascade as an upstream trigger. On the catabolic side, the ubiquitin-proteasome system (UPS) governs protein degradation, targeting myofibrillar components for breakdown via E3 ligases such as muscle RING-finger protein-1 (MuRF1) and muscle atrophy F-box (MAFbx/Atrogin-1). During hypertrophy, UPS activity is inhibited through mTORC1-mediated suppression of FoxO transcription factors, which otherwise upregulate these ligases in atrophy conditions, thereby shifting the balance toward net accretion. IGF-1 signaling contributes to this inhibition by phosphorylating FoxO, preventing its nuclear translocation and UPS induction. Recent advances highlight the role of epigenetic modifications, particularly histone acetylation, in sustaining long-term protein synthesis during chronic training. Increased histone acetyltransferase activity, such as p300/CBP, promotes acetylation of histones H3 and H4 at promoters of anabolic genes (e.g., those encoding IGF-1 and mTOR components), enhancing chromatin accessibility and transcriptional output for ribosomal proteins and translation factors.

Microtrauma, Inflammation, and Repair Processes

Muscle microtrauma, particularly during eccentric contractions where muscles lengthen under tension, induces structural disruptions such as Z-line streaming—disruptions in the sarcomere's Z-disks—and microtears in myofibrils, initiating the damage-repair cycle central to hypertrophy. These lesions occur due to the high mechanical stress on actin-myosin cross-bridges, exceeding their tensile strength and leading to localized fiber damage. Inflammation typically peaks 24-48 hours post-exercise, marked by edema, soreness, and elevated markers like creatine kinase, as the acute phase response mobilizes immune cells to the site. The inflammatory cascade begins with the release of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), from damaged muscle fibers and resident immune cells, which amplify the response and recruit circulating monocytes that differentiate into macrophages. Macrophages, initially pro-inflammatory (M1 phenotype), phagocytose cellular debris and necrotic material, transitioning to pro-reparative (M2) states that secrete anti-inflammatory factors and growth signals to resolve inflammation. Repair signaling involves fibroblast growth factor (FGF) pathways, where FGF2 promotes macrophage polarization toward tissue regeneration and stimulates myoblast proliferation for fiber reconstruction. Post-damage adaptive remodeling enhances muscle resilience through increased synthesis of extracellular matrix components, including collagen and other connective tissues, which provide structural support and force transmission. This remodeling, driven by transforming growth factor-beta (TGF-β) and mechanical cues, strengthens the perimysium and endomysium, reducing future susceptibility to injury while augmenting muscle size. A 2022 umbrella review of resistance training variables supports that moderate repetition schemes (6-12 reps per set at 60-80% of 1RM) optimize microtrauma-induced hypertrophy by balancing damage with recovery, whereas excessive damage from very high or low reps can impair net gains. This aligns with broader evidence that controlled eccentric loading in these ranges maximizes inflammatory and reparative responses without chronic overstress.

Role of Satellite Cells and Nuclei Addition

Satellite cells, which comprise approximately 2-10% of the total nuclei in adult skeletal muscle, serve as quiescent stem cells positioned between the basal lamina and the plasma membrane of muscle fibers. These cells activate in response to mechanical stimuli from resistance exercise, transitioning from quiescence to proliferation and eventual fusion with myofibers to donate new myonuclei. Activation is primarily mediated by hepatocyte growth factor (HGF), a key mitogen released from the extracellular matrix upon muscle loading or damage, which binds to the c-Met receptor on satellite cells to initiate their cell cycle entry. This process ensures that growing muscle fibers acquire sufficient transcriptional machinery to support expanded cytoplasmic volume, aligning with the myonuclear domain theory that posits each nucleus governs a finite cytoplasmic territory of roughly 1,000-2,000 μm³. The fusion of activated satellite cells with myofibers represents a critical step in hypertrophy, wherein progeny cells integrate into the fiber syncytium, increasing the myonuclear count. In the early stages of overload-induced hypertrophy, such as during the initial weeks of resistance training, myonuclear addition can be substantial (e.g., up to ~50% in animal models), preceding and facilitating fiber cross-sectional area gains. This accretion is most pronounced in untrained individuals, where satellite cell responsiveness is high, but it tends to plateau in chronically trained athletes, with subsequent hypertrophy relying more on domain expansion per existing nucleus rather than further fusions. Consequently, the added nuclei enhance the fiber's overall gene expression potential, enabling sustained protein accretion without diluting transcriptional efficiency. Adult satellite cell function exhibits notable limitations, particularly with aging and excessive training demands, which impair proliferation, fusion efficiency, and regenerative contributions to hypertrophy. In older individuals, the satellite cell pool diminishes in size and myogenic potency, resulting in blunted myonuclear addition and attenuated hypertrophic responses to exercise. Overtraining similarly disrupts satellite cell dynamics, reducing their activation and fusion rates due to chronic stress and inadequate recovery. Recent 2025 investigations using CRISPR/Cas9-mediated myostatin knockout in murine models have revealed enhanced satellite cell proliferation and fusion, with improved myogenic differentiation and greater myonuclear integration, highlighting myostatin inhibition as a strategy to bolster adult satellite cell efficacy. Each newly added myonucleus substantially augments the fiber's protein synthesis capacity through localized upregulation of ribosomal biogenesis and mRNA transcription within its domain. This nuclear scaling is complemented by insulin-like growth factor-1 (IGF-1), which further promotes satellite cell fusion to support hypertrophy-linked protein synthesis.

Training Stimuli for Hypertrophy

Resistance and Strength Training Protocols

Resistance training protocols for inducing muscle hypertrophy primarily revolve around the principle of progressive overload, which involves systematically increasing the demands placed on the muscles to drive adaptation. This is achieved through gradual increments in training load, volume, or intensity, such as using weights corresponding to 70-85% of one-repetition maximum (1RM) for 6-12 repetitions per set, thereby generating sufficient mechanical tension to stimulate protein synthesis and fiber growth. Seminal research emphasizes that without progressive overload, hypertrophic adaptations plateau, as the muscle requires escalating stress to continue enlarging. Key program variables optimized for hypertrophy include the number of sets, training frequency, rest intervals, and periodization strategies. Typically, 3-5 sets per exercise promote greater hypertrophy than single sets, with multiple sets yielding approximately 40% more muscle growth due to accumulated volume. Training each muscle group 2-3 times per week allows for adequate recovery while maximizing stimulus frequency, leading to superior outcomes compared to once-weekly sessions. Rest intervals of 60-90 seconds between sets are recommended to balance metabolic stress and recovery, enhancing hypertrophy without excessive fatigue. Periodization models, such as linear (gradual progression over weeks) or undulating (daily or weekly variations in volume and intensity), both effectively support hypertrophy when total volume is equated, though undulating may offer slight advantages in sustaining motivation and adaptation. Recent meta-analyses from 2021-2023 confirm the efficacy of these protocols, showing comparable hypertrophic gains across moderate (60-80% 1RM) and heavy (>80% 1RM) loads when effort and volume are matched, with typical increases of 8-12% in muscle cross-sectional area over 12 weeks in untrained individuals. For instance, a 2021 network meta-analysis found no significant differences in hypertrophy between load ranges, underscoring that proximity to failure and total work performed are more critical than absolute load. These findings hold across populations, with progressive overload via load or repetitions both yielding similar strength and size improvements in young adults. Regarding equipment and exercise variations, both free weights and machines elicit equivalent hypertrophic responses when volume is controlled, as demonstrated in a 2023 meta-analysis of 13 studies showing no differences in muscle thickness gains. Compound exercises, such as squats, engage multiple muscle groups for efficient overall hypertrophy, while isolation movements like bicep curls target specific areas for balanced development; integrating both maximizes regional growth without one superior to the other. As an adjunct, low-load protocols like blood flow restriction can enhance hypertrophy in traditional programs but are not essential for standard resistance training.

Blood Flow Restriction and Anaerobic Methods

Blood flow restriction (BFR) training involves the application of occlusion cuffs to the proximal portion of the limbs at 40-80% of arterial occlusion pressure during low-load resistance exercises, typically performed at 20-30% of one-repetition maximum (1RM). This technique restricts venous blood flow while allowing arterial inflow, leading to metabolite accumulation such as lactate and promoting muscle cell swelling, which contributes to hypertrophic signaling. Studies indicate that BFR training can elicit muscle hypertrophy gains comparable to those achieved with high-load resistance training (>70% 1RM), particularly in the quadriceps and other lower-body muscles. Anaerobic training protocols emphasize high-repetition sets (15-30 reps) taken to volitional fatigue, focusing on glycolytic energy pathways to induce metabolic stress and support hypertrophy. Techniques such as cluster sets, which involve brief intra-set rest intervals (e.g., 10-30 seconds) to accumulate more total repetitions without excessive fatigue, and drop sets, where load is progressively reduced within a set to extend time under tension, enhance anaerobic contributions by increasing lactate production and muscle pump. These methods promote similar hypertrophic outcomes to traditional moderate-rep schemes, with meta-analyses showing no significant differences in muscle thickness gains when volume is equated. For instance, one study reported approximately 10% increases in muscle cross-sectional area after 6 weeks with drop sets. Unique mechanisms in BFR and anaerobic methods include the upregulation of hypoxia-inducible factor 1-alpha (HIF-1α), which responds to localized hypoxia and metabolic byproducts like lactate to activate genes involved in angiogenesis, glucose metabolism, and protein synthesis pathways. This HIF-1α activation enhances anabolic signaling, including mammalian target of rapamycin (mTOR) pathway stimulation, distinct from primary mechanical tension in heavier loads, and contributes to satellite cell proliferation for long-term growth. Recent 2023 studies have demonstrated BFR's efficacy in rehabilitation populations, such as post-surgical patients, where low-load BFR protocols yielded 8-15% greater hypertrophy and strength improvements compared to non-restricted low-load training, facilitating recovery while minimizing joint stress. Safety guidelines for BFR and high-intensity anaerobic methods recommend avoiding implementation in individuals with hypertension due to potential acute blood pressure elevations and vascular strain. Sessions should be limited to under 20 minutes per limb to prevent excessive ischemia, with cuff pressures personalized via Doppler ultrasound to ensure partial but not complete occlusion, and immediate post-exercise monitoring for adverse effects like numbness or discoloration.

Aerobic Exercise Contributions

Aerobic exercise, particularly when incorporated into concurrent training programs alongside resistance work, can induce modest skeletal muscle hypertrophy, especially in untrained individuals and predominantly in Type I (slow-twitch) fibers. For instance, moderate-intensity cycling at 60-80% of VO2max over 12 weeks has been shown to increase Type I fiber cross-sectional area (CSA) by up to 20% and whole-muscle quadriceps volume by 6-12% in untrained adults, driven by overlapping adaptations in mitochondrial biogenesis that enhance oxidative capacity and support structural growth. This effect is more pronounced in the lower body, where endurance activities recruit a higher proportion of Type I fibers for sustained contractions, though impacts on Type II fibers remain minimal. At the molecular level, aerobic exercise activates AMP-activated protein kinase (AMPK) signaling, which promotes energy homeostasis and mitochondrial adaptations but intersects with the mammalian target of rapamycin (mTOR) pathway to facilitate balanced protein synthesis without fully suppressing hypertrophic signals. This interaction allows for modest growth in Type I fibers while having a less pronounced impact on Type II (fast-twitch) fibers, which are more responsive to anaerobic stimuli. Studies indicate that AMPK activation from aerobic bouts does not significantly interfere with mTOR-driven hypertrophy from concurrent resistance training, enabling additive effects in hybrid regimens. Recent longitudinal research has further demonstrated aerobic-only training's capacity for hypertrophy, challenging longstanding myths about an "interference effect" that purportedly negates muscle gains from endurance work. Similarly, concurrent protocols combining aerobic and resistance exercise have shown comparable or potentially greater overall quadriceps volume increases compared to resistance alone, underscoring aerobic contributions rather than hindrance. In practical applications, these findings support hybrid training programs for athletes requiring both strength and stamina, such as in team sports or triathlons, where aerobic sessions are sequenced to minimize any potential blunting of gains—often by separating modalities by at least 6 hours or prioritizing resistance on separate days. Systematic reviews confirm that well-structured concurrent training yields comparable hypertrophy to resistance-only protocols while enhancing endurance, making it ideal for multifaceted performance demands.

Acute and Temporary Responses

Intracellular Swelling and Fluid Shifts

During resistance exercise, the accumulation of metabolic byproducts such as lactate and hydrogen ions (H+) within muscle cells creates an osmotic gradient that draws water into the intracellular space, leading to acute cell swelling. This process is facilitated by water channel proteins known as aquaporins, particularly aquaporin-4 (AQP4), which are expressed in skeletal muscle fibers and enable rapid water influx to maintain osmotic balance during contraction-induced stress. Studies on isolated muscle fibers have shown that such osmotic swelling can increase cell volume by up to 15-20% within minutes of intense activity, contributing to the immediate sensation of muscle "pump" without altering the structural components of the myofibrils. A related mechanism involves glycogen supercompensation following exercise, where depleted glycogen stores are replenished at supraphysiological levels, accompanied by substantial water retention. Each gram of stored glycogen binds approximately 3-4 grams of water in the muscle, resulting in increased sarcoplasmic volume that peaks 24-48 hours post-exercise and enhances the apparent muscle size temporarily. This fluid shift is potassium-dependent and supports recovery but does not represent permanent hypertrophy, as the excess dissipates with normalized glycogen levels. Ultrasound imaging has been used to quantify these transient changes, revealing increases in muscle cross-sectional area (CSA) of 5-10% immediately after resistance exercise bouts, which gradually resolve within 72 hours as fluid dynamics normalize. These measurements highlight the non-structural nature of the swelling, distinguishing it from chronic adaptations. Research from 2022 indicates that this intracellular swelling acts as an anabolic signal, activating mechanosensitive pathways like mTORC1 to prime protein synthesis and support subsequent hypertrophic responses, though the effect is transient and does not directly cause long-term growth. Greater initial swelling has been correlated with enhanced hypertrophy over training periods, suggesting a facilitative role in adaptation signaling.

Metabolic Byproducts and Immediate Adaptations

During resistance exercise, the accumulation of metabolic byproducts such as lactate and reactive oxygen species (ROS) plays a key role in initiating signaling cascades that promote muscle hypertrophy. Lactate buildup inhibits the TSC1/2 complex, thereby indirectly activating the mTOR pathway to enhance protein synthesis. Concurrently, ROS generated from mitochondrial and enzymatic sources stimulates PGC-1α expression, driving mitochondrial biogenesis and oxidative adaptations that support sustained hypertrophic responses. These byproducts also contribute to secondary mTOR activation, bridging metabolic stress with anabolic signaling independent of structural damage. Acute hormonal responses further amplify these immediate adaptations by facilitating nutrient delivery and anabolic processes. Resistance training induces transient spikes in growth hormone (GH) and testosterone, with GH levels rising up to 400% immediately post-set and testosterone increasing by 15-40% in the acute phase, promoting enhanced glucose and amino acid uptake into muscle cells. These elevations, while not directly causative of hypertrophy, create a favorable environment for metabolite utilization and recovery signaling. Neural mechanisms provide the initial boost to strength before hypertrophic changes dominate, with early gains attributed to improved motor unit recruitment and firing rates. Within the first 4-6 weeks of training, these adaptations increase force output by enhancing neural drive to the muscle without significant myofiber growth. This transition underscores how immediate neuromuscular efficiency sets the stage for later metabolic and structural hypertrophy. Recent metabolomics research from 2025 highlights branched-chain amino acid (BCAA) oxidation as an early biomarker for hypertrophic potential following resistance exercise. Studies show that efficient BCAA catabolism in skeletal muscle correlates with greater hypertrophic responses, predicting individual variability in muscle growth through altered energy homeostasis and signaling.

Types and Functional Variations

Myofibrillar Hypertrophy Characteristics

Myofibrillar hypertrophy refers to the enlargement of muscle fibers through the addition of contractile elements, primarily an increase in myofibrillar proteins such as actin and myosin, which form the structural basis for force generation. This process involves the parallel addition of sarcomeres and myofibrils within existing muscle fibers, enhancing the muscle's capacity for tension development without significant expansion of non-contractile components. Research indicates that resistance training can lead to increases in myofibrillar protein content, as measured by techniques like muscle biopsy and protein synthesis assays, thereby directly contributing to improved mechanical properties of the muscle. This form of hypertrophy is most prominently induced by heavy-load, low-repetition training protocols, typically involving 1-6 repetitions at intensities of 80-100% of one-repetition maximum (1RM), which maximize mechanical tension on the muscle. Such regimens prioritize neural drive and fiber recruitment, resulting in functional adaptations like improvements in maximal strength over 8-12 weeks of training, as evidenced by longitudinal studies tracking one-repetition maximum lifts. These gains are particularly pronounced in power-oriented activities, where the enhanced density of contractile proteins translates to greater force output per unit of muscle volume. Myofibrillar adaptations disproportionately affect Type II (fast-twitch) fibers, which exhibit higher responsiveness to high-tension stimuli compared to Type I fibers. Biopsy analyses from resistance-trained individuals reveal greater increases in cross-sectional area specifically in fast-twitch fibers after 12-24 weeks of heavy loading, underscoring their role in explosive strength development. In contrast to sarcoplasmic hypertrophy, which focuses on metabolic volume for endurance, myofibrillar changes emphasize force-oriented structural enhancements.

Sarcoplasmic Hypertrophy Characteristics

Sarcoplasmic hypertrophy refers to the expansion of the sarcoplasm—the intracellular fluid and non-contractile components surrounding the myofibrils—leading to increased muscle fiber volume through accumulation of glycogen, mitochondria, and other organelles. This process typically contributes to 10-20% of overall hypertrophy volume via these elements, as evidenced by electron microscopy showing baseline sarcoplasmic occupancy of approximately 9% and mitochondrial volume of 5-6% that can expand disproportionately with training. Serial sarcomere addition may also occur in certain contexts, further supporting longitudinal muscle adaptations alongside volumetric growth. High-volume resistance training with moderate loads, often involving 10-20 repetitions per set, preferentially induces sarcoplasmic hypertrophy by promoting metabolic stress and fluid retention, which bodybuilders leverage for the temporary "pump" that enhances muscle fullness and vascularity during workouts. Such protocols, typically at 60-75% of one-repetition maximum, accumulate fatigue and stimulate non-contractile adaptations over several weeks. This form of hypertrophy predominantly affects type I (slow-twitch) and type IIa (fast-oxidative) muscle fibers, which possess higher mitochondrial density and glycogen storage capacity suited to endurance-oriented demands. Functionally, sarcoplasmic hypertrophy improves lactate buffering and energy substrate availability, enhancing muscle endurance and recovery between repetitions, but it can dilute myofibrillar density if unbalanced, potentially impairing maximal force production relative to muscle size. In contrast to myofibrillar hypertrophy, which prioritizes contractile protein accretion for strength, sarcoplasmic changes support metabolic resilience in repeated-effort scenarios. While training variables like load and volume may influence the relative contributions of myofibrillar and sarcoplasmic hypertrophy, evidence suggests both forms often occur concurrently in response to resistance training.

Influencing Factors

Hormonal and Nutritional Regulators

Hormonal regulators play a pivotal role in modulating muscle hypertrophy by influencing protein synthesis, degradation, and metabolic processes. Testosterone, a primary anabolic hormone, promotes muscle growth through androgen receptor activation, leading to increased satellite cell proliferation and myofibrillar protein accretion; variations in physiological testosterone levels can influence baseline muscle mass and responses to resistance training. In contrast, cortisol acts as a catabolic antagonist by elevating protein degradation via the ubiquitin-proteasome pathway and suppressing amino acid uptake, thereby counteracting anabolic signals and potentially attenuating hypertrophy gains during periods of elevated stress. Thyroid hormones, such as triiodothyronine (T3), regulate skeletal muscle metabolism by enhancing mitochondrial function and oxidative capacity, which supports energy availability for hypertrophic adaptations without directly driving protein synthesis. Nutritional factors are essential modulators of hypertrophy, primarily through their impact on muscle protein synthesis (MPS) and energy balance. Optimal protein intake for maximizing hypertrophy in resistance-trained individuals ranges from 1.6 to 2.2 g/kg body weight per day, as higher intakes yield diminishing returns beyond this threshold while supporting greater lean mass accrual compared to lower amounts. Within meals, achieving a leucine threshold of approximately 3 g activates the mTOR pathway, a key regulator of MPS, with intakes below this level resulting in suboptimal anabolic responses. A moderate calorie surplus of 300-500 kcal/day during bulking phases facilitates hypertrophy by providing the energetic substrate needed for net protein deposition, though excesses beyond this can promote fat gain without proportional muscle benefits. Nutrient timing and supplementation strategies further influence hypertrophy outcomes, though their effects are often context-dependent. The concept of a strict post-workout "anabolic window" for protein consumption—typically within 30-60 minutes—is debated, with evidence indicating that total daily intake outweighs precise timing for long-term muscle gains, though immediate post-exercise feeding may offer minor benefits in fasted states. Creatine supplementation at 5 g/day enhances intramuscular phosphocreatine stores, leading to small additional hypertrophy over resistance training alone, with meta-analyses showing modest increases in muscle thickness. Beta-alanine, at doses of 3.2-6.4 g/day, elevates muscle carnosine to buffer acidosis, potentially supporting higher training intensities and indirect hypertrophy benefits, particularly when combined with creatine, though direct effects on muscle size remain inconsistent. Recent advancements highlight emerging nutritional regulators of hypertrophy. Omega-3 fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), enhance insulin-like growth factor-1 (IGF-1) signaling and mTOR activation, promoting MPS and reducing inflammation to support greater muscle adaptations in older adults and athletes. Personalized nutrition approaches leveraging gut microbiome analysis, such as prebiotic interventions to modulate microbial composition, show promise in optimizing hypertrophy by improving nutrient absorption and reducing systemic inflammation, with 2024 studies linking specific taxa like Lactobacillus to enhanced muscle strength.

Genetic, Age, and Sex Influences

Muscle hypertrophy exhibits significant genetic influences, with heritability estimates for muscle mass and related traits ranging from 50% to 80% based on twin and family studies. These genetic factors determine baseline muscle size and the potential for adaptive growth in response to training stimuli. A prominent example is the ACTN3 R577X polymorphism, where the RR genotype (encoding functional alpha-actinin-3 protein) is associated with enhanced fast-twitch fiber performance and greater power-oriented hypertrophy, particularly in sprint and strength athletes, while the XX variant correlates with endurance adaptations and reduced fast-fiber hypertrophy potential. This polymorphism influences muscle fiber type distribution and strength gains, with RR carriers showing superior responses to resistance training in fast-velocity tasks. Age-related changes profoundly impact muscle hypertrophy capacity, with peak hypertrophic potential occurring in the 20s to 30s, after which skeletal muscle mass begins a progressive decline of approximately 3-8% per decade starting around age 30, accelerating to higher rates after 60. This sarcopenia is partly driven by satellite cell senescence, where the number and regenerative function of these muscle stem cells diminish, impairing myofiber repair and growth; by age 70, satellite cell content can drop by up to 50% compared to younger adults. However, resistance training can partially mitigate this decline in older individuals through enhanced satellite cell activation and myonuclear addition, preserving hypertrophic responsiveness despite age-related reductions. Sex differences in muscle hypertrophy stem from baseline physiological variations, with males typically possessing 30-50% greater skeletal muscle mass than females due to higher circulating testosterone levels, which promote myofiber hypertrophy and protein synthesis from puberty onward. Testosterone concentrations in males are 10-30 times higher than in females, contributing to larger absolute gains in muscle size following resistance training; for instance, meta-analyses show men achieving 1-2 kg more lean mass increase over similar training periods. Despite these absolute disparities, relative hypertrophic responses (percentage change in muscle cross-sectional area) are comparable between sexes when training volume and intensity are equated, indicating similar adaptive efficiency but scaled by starting mass. Recent genomic research has advanced understanding of these influences, including a 2024 genome-wide association study (GWAS) identifying 57 genetic variants associated with appendicular lean mass and fast-twitch muscle fiber size in humans, highlighting loci near genes involved in myogenesis and fiber composition. A 2025 eQTL meta-analysis identified 185 colocalizations with appendicular lean mass traits, implicating genes in the genetic architecture of muscular traits and integrating eQTL data to reveal regulatory mechanisms. Furthermore, epigenetic modifications induced by training, such as DNA methylation changes in metabolic and inflammatory genes, can persist lifelong, enhancing gene expression for hypertrophy even in later years and demonstrating training's role in altering inherited epigenetic landscapes.

Applications in Sports and Fitness

Strategies in Bodybuilding and Power Sports

In bodybuilding, athletes prioritize high-volume resistance training protocols to stimulate muscle hypertrophy, often utilizing split routines such as the bro-split, which dedicates specific days to individual muscle groups, typically training 5-6 days per week with 10-20 sets per muscle group to equate higher weekly volume. These approaches allow for concentrated stimulus on targeted muscles, leading to comparable hypertrophic outcomes to full-body routines when total volume is matched, though splits facilitate greater per-session volume without excessive fatigue. Posing practice is integral for developing symmetry and control, enhancing muscle presentation and definition during competitions by improving proprioception and visual balance, as evidenced by routines that emphasize bilateral alignment and aesthetic proportions. During contest preparation, carb cycling—alternating high- and low-carbohydrate intake phases—is employed to optimize glycogen replenishment and muscle fullness while minimizing fat, with studies showing increased muscular girth and reduced subcutaneous water retention in the final week. In powerlifting, hypertrophy phases are strategically incorporated into annual programming, typically lasting 8-12 weeks with moderate loads of 60-80% of one-repetition maximum (1RM) and 8-12 repetitions per set to build muscle mass as a foundation for maximal strength efforts. These phases precede peaking cycles, allowing athletes to accumulate volume for size gains before transitioning to heavier, lower-repetition work. Accessory exercises, such as variations of the main lifts (e.g., paused squats or triceps extensions), are used to address weak points like joint stability or secondary muscle contributions, promoting balanced hypertrophy and injury prevention through targeted overload. Block periodization models, which sequence distinct hypertrophy-focused blocks (higher volume, moderate intensity) with strength blocks (lower volume, higher intensity), are widely adopted in both disciplines to optimize adaptations over 12-24 weeks, with meta-analyses indicating superior strength gains and similar hypertrophy compared to non-periodized training. Studies indicate modest increases in muscle mass (typically 1-2 kg or 2-5%) in trained individuals following such programs over 12-24 weeks, with gains generally smaller in more advanced athletes due to training history. Historically, anabolic-androgenic steroids (AAS) have been used in bodybuilding and power sports to amplify hypertrophy, with supraphysiologic doses enabling 2-3 times greater lean mass gains than natural training alone, as demonstrated in controlled studies where testosterone administration combined with resistance exercise increased fat-free mass by 6 kg versus 2 kg in placebo groups over 10 weeks. However, AAS use carries substantial health risks, including cardiovascular toxicity such as left ventricular hypertrophy, hypertension, and elevated atherosclerosis, alongside liver damage and endocrine disruptions, contributing to higher mortality rates among users.

Endurance and General Athletic Contexts

In endurance sports such as cycling and rowing, muscle hypertrophy primarily targets the lower body to enhance force production and power output while maintaining aerobic efficiency, often resulting in modest increases in quadriceps cross-sectional area (CSA) of approximately 5% after a training season when combining high-repetition endurance work with targeted strength sessions. This selective leg hypertrophy, particularly in the vastus lateralis and biceps femoris, supports sustained performance without promoting upper body bulk that could impede aerodynamics or increase overall energy demands. Aerobic exercise contributions to these adaptations emphasize fiber type shifts toward greater oxidative capacity alongside size gains. In team sports like soccer, functional hypertrophy is achieved through concurrent training protocols that integrate plyometrics and moderate weightlifting, fostering balanced muscle development in the legs and core while minimizing interference with aerobic conditioning when strength sessions precede endurance work. These approaches yield improvements in explosive power and sprint performance without excessive mass accumulation, allowing athletes to maintain agility and recovery during match demands. General fitness programs, such as those in CrossFit-style training, promote balanced hypertrophy across major muscle groups through high-volume, varied-intensity circuits, typically resulting in 5-17% gains in overall strength and modest increases in lean body mass (approximately 1 kg) over 12 weeks in novice to intermediate participants. As of 2025, advancements in wearable technology, including smartwatches and EMG sensors, enable real-time tracking of training volume, muscle activation, and recovery metrics to optimize progress and prevent overtraining in these multifaceted routines. However, trade-offs exist, as excessive hypertrophy can elevate energy costs; adding muscle mass can increase submaximal VO2 requirements by 3-5% due to higher internal work, with the exact magnitude depending on the activity (e.g., greater in running than cycling). This underscores the need for moderated hypertrophy in endurance contexts to preserve performance economy.

Pathological and Clinical Aspects

Abnormal Hypertrophy in Diseases

Abnormal muscle hypertrophy in diseases manifests as pathological overgrowth or resistance to atrophy, often driven by underlying genetic, hemodynamic, or inflammatory mechanisms that disrupt normal muscle homeostasis. In cardiac muscle, pressure overload from conditions such as hypertension induces concentric hypertrophy, where the left ventricular wall thickens to compensate for increased afterload, thereby normalizing wall stress according to the Laplace law. This adaptive response can progress to maladaptive remodeling, characterized by interstitial fibrosis that impairs diastolic function and increases the risk of heart failure. In patients with left ventricular hypertrophy, echocardiographic assessments reveal increased left ventricular wall thickness in approximately 30-50% of cases, reflecting the extent of concentric remodeling, as observed in studies of heart failure cohorts. In skeletal muscle, abnormalities in myostatin signaling lead to excessive hypertrophy. Mutations in the myostatin gene (MSTN), a negative regulator of muscle growth, cause double muscling in Belgian Blue cattle, resulting in markedly increased muscle mass due to hyperplasia and hypertrophy of muscle fibers. Rare human mutations in MSTN similarly produce gross skeletal muscle hypertrophy, as observed in a child with a homozygous deletion leading to enhanced muscle strength and size without apparent pathology. In cancer-associated cachexia, dysregulation of myostatin contributes to muscle wasting, but inhibition of this pathway in preclinical models confers resistance to atrophy, preserving muscle mass through promoted hypertrophy and reduced proteolysis. Neuromuscular diseases like Duchenne muscular dystrophy (DMD) exhibit pseudohypertrophy due to dystrophin deficiencies, where the absence of this protein destabilizes the sarcolemma, leading to fiber necrosis, inflammation, and replacement by fat and connective tissue rather than true myofiber growth. In DMD, calf muscles often enlarge early in the disease, creating an illusion of hypertrophy, but histological analysis confirms infiltration by adipose tissue and fibrosis, correlating with progressive weakness.

Therapeutic Approaches to Modulate Hypertrophy

Therapeutic approaches to modulate muscle hypertrophy in clinical settings aim to either promote beneficial growth in cases of atrophy or inhibit excessive pathological enlargement, particularly in cardiac and skeletal muscle disorders. These strategies often integrate pharmacological, rehabilitative, and genetic interventions tailored to patient-specific needs, such as post-injury recovery or chronic disease management. Evidence from controlled trials supports their efficacy in altering muscle mass and function while minimizing adverse effects. In rehabilitation protocols following injury or immobilization, combining neuromuscular electrical stimulation (NMES) with resistance training effectively induces skeletal muscle hypertrophy to counteract atrophy. For instance, a 12-16 week NMES-resistance training program in individuals with spinal cord injury led to a 30% increase in knee extensor cross-sectional area, alongside improvements in strength and function, demonstrating its utility in restoring muscle mass in immobilized limbs. This approach leverages involuntary contractions to stimulate protein synthesis, offering a viable option when voluntary exercise is limited. To inhibit pathological cardiac hypertrophy, angiotensin-converting enzyme (ACE) inhibitors promote regression by reducing left ventricular mass independent of blood pressure lowering. Meta-analyses indicate that ACE inhibitors achieve an average 13% reduction in left ventricular mass index over 6-12 months in hypertensive patients with hypertrophy. Similarly, beta-blockers modulate excessive sympathetic drive, contributing to hypertrophy regression through attenuation of adrenergic signaling and prevention of ventricular remodeling. Clinical studies show beta-blockers induce approximately 6% regression in left ventricular mass, though less pronounced than ACE inhibitors, with benefits in heart failure patients by countering neurohormonal activation. Gene therapies targeting myostatin inhibition represent an emerging strategy to induce hypertrophy in conditions like sarcopenia. Follistatin-based approaches, which neutralize myostatin to enhance muscle growth, have shown promise in preclinical and early clinical models, with adeno-associated virus delivery increasing muscle mass and strength in aged animals. Recent phase II trials of myostatin inhibitors, such as bimagrumab (an activin type II receptor antibody), demonstrated lean body mass increases of up to 5-8% in sarcopenic patients over 24 weeks, supporting further investigation into follistatin gene therapies for age-related muscle loss. Pharmacological interventions like selective androgen receptor modulators (SARMs) provide targeted anabolic effects to promote muscle hypertrophy without the androgenic side effects of traditional steroids. In phase II trials, SARMs such as enobosarm increased lean body mass by 1-3 kg (approximately 3-5% in older adults) over 12-16 weeks in patients with muscle-wasting conditions, improving physical function with a favorable safety profile. Complementing these, nutritional therapy in malnourished patients supports hypertrophy by addressing deficits that exacerbate muscle loss. High-protein oral supplements combined with resistance training in sarcopenic or malnourished elderly individuals have been shown to increase skeletal muscle mass by 1-2% over 12 weeks, enhancing overall nutritional status and functional outcomes.

References

  1. [1]
    The Mechanisms of Muscle Hypertrophy and Their Application...
    Muscle hypertrophy occurs when protein synthesis exceeds protein breakdown. Hypertrophy is thought to be mediated by the activity of satellite cells, which ...Missing: definition review
  2. [2]
    Molecular Mechanisms of Skeletal Muscle Hypertrophy - PMC
    Nov 18, 2020 · Skeletal muscle hypertrophy can be induced by hormones and growth factors acting directly as positive regulators of muscle growth or indirectly by neutralizing ...
  3. [3]
    Mechanisms of muscle atrophy and hypertrophy - Nature
    Jan 12, 2021 · Consequently, the growth or the loss of muscle mass can influence general metabolism, locomotion, eating and respiration.
  4. [4]
    Sarcoplasmic Hypertrophy in Skeletal Muscle: A Scientific “Unicorn ...
    Jul 14, 2020 · Select evidence suggests sarcoplasmic hypertrophy, or a disproportionate expansion of the sarcoplasm relative to myofibril protein accretion, ...
  5. [5]
    Resistance Training Variables for Optimization of Muscle Hypertrophy
    Jul 3, 2022 · Hypertrophy is defined as an increase in muscular size, which can be achieved through exercise. Two main factors contribute to this ...
  6. [6]
    Different modes of hypertrophy in skeletal muscle fibers - PMC
    According to this definition, hypertrophy of skeletal muscle is an increase in the size of fibers without an increase in their number, irrespective of any ...
  7. [7]
    Resistance Training Variables for Optimization of Muscle Hypertrophy
    Jul 4, 2022 · Hypertrophy is defined as an increase in muscular size, which can be achieved through exercise. Two main factors contribute to this ...
  8. [8]
    Recent advances in understanding resistance exercise training ...
    Feb 24, 2020 · Skeletal muscle hypertrophy can be defined as an increase in muscle axial cross-sectional area (CSA), assessed via magnetic resonance ...
  9. [9]
    A Critical Evaluation of the Biological Construct Skeletal Muscle ...
    We propose that skeletal muscle hypertrophy be generally and simply defined as an increase in skeletal muscle size accompanied by an increase in mineral, ...
  10. [10]
    Exercise-induced skeletal muscle growth. Hypertrophy or hyperplasia?
    It was concluded that hyperplasia is not yet substantiated, and that new fibres, if present, may be the result of the development of satellite cells. Further ...
  11. [11]
    Mechanical overload and skeletal muscle fiber hyperplasia: a meta ...
    The results of this study suggest that in several animal species certain forms of mechanical overload increase muscle fiber number. Previous. Back to Top. Next.
  12. [12]
    Muscle thickness correlates to muscle cross‐sectional area in the ...
    The present study supports the use of ultrasound‐measured MT as a reliable tool for monitoring local long‐term hypertrophic responses (changes in VL skeletal ...
  13. [13]
    Methodological considerations for and validation of the ...
    Jan 6, 2021 · Our data suggest that B‐mode ultrasonography can be a suitable alternative to MRI for measuring changes in muscle size in response to increased ...
  14. [14]
    Functional properties of human muscle fibers after short-term ...
    The mean CSA of the type I, IIa, and IIa/IIx fibers all increased with resistance training. On an absolute basis, hypertrophy of the type IIa (+1,989 μm2) and ...Missing: typical | Show results with:typical
  15. [15]
    Physiology, Skeletal Muscle - StatPearls - NCBI Bookshelf
    Jul 30, 2023 · The arrangement of actin and myosin gives skeletal muscle its microscopic striated appearance and creates functional units called sarcomeres.
  16. [16]
    10.2 Skeletal Muscle – Anatomy & Physiology 2e
    A muscle fiber is composed of many myofibrils, which contain sarcomeres with light and dark regions that give the cell its striated appearance.
  17. [17]
    38.15: Muscle Contraction and Locomotion - Skeletal Muscle Fibers
    Nov 23, 2024 · Sarcomeres are composed of myofilaments of myosin and actin, which interact using the sliding filament model and cross-bridge cycle to contract.
  18. [18]
    Muscles and muscle tissue: Types and functions | Kenhub
    Myofibrils are essentially chained structures composed of repeating units of contractile units known as sarcomeres. These are primarily composed of two protein ...
  19. [19]
    Skeletal muscle fiber type: using insights from ... - PubMed Central
    Type 1 and 2A fibers primarily use oxidative metabolism, and type 2X and 2B fibers primarily rely upon glycolytic metabolism. However, even here there is ...
  20. [20]
    Fiber-Type-Specific Hypertrophy with the Use of Low-Load Blood ...
    Apr 27, 2023 · Although evidence indicates that the hypertrophic capacity of type II fibers is substantially greater than that of type I fibers [1], it is ...
  21. [21]
    The Cross-bridge Cycle - UCSD Muscle Physiology Homepage
    During the cross-bridge cycle, actin (A) combines with myosin (M) and ATP to produce force, adenosine diphosphate (ADP) and inorganic phosphate, Pi.
  22. [22]
    The evolution of human fatigue resistance - PMC - PubMed Central
    May 12, 2022 · Chimpanzee muscle fibers were also longer, enabling them to shorten with higher intrinsic velocity and thus generate more power. These findings, ...
  23. [23]
    Daily resistance-type exercise stimulates muscle protein synthesis in ...
    Whereas acute studies have shown that resistance-type exercise increases muscle protein synthesis rates by 50–100%, we observed a lower impact of resistance- ...
  24. [24]
    Mechanisms regulating skeletal muscle growth and atrophy
    Mar 21, 2013 · Muscle hypertrophy occurs when the overall rates of protein synthesis exceed the rates of protein degradation. Two major signaling pathways ...Muscle Growth · Satellite Cell Fusion And... · Muscle Atrophy
  25. [25]
    mTOR as a Key Regulator in Maintaining Skeletal Muscle Mass
    mTOR controls the anabolic and catabolic signaling of skeletal muscle mass, resulting in the modulation of muscle hypertrophy and muscle wastage.Abstract · Introduction · mTOR Signaling Regulates... · mTOR Regulation Signals...Missing: seminal | Show results with:seminal
  26. [26]
    The epigenetic regulatory effect of histone acetylation and ...
    Dec 8, 2023 · This comprehensive review aims to elucidate the epigenetic regulatory impact of histone acetylation modification on skeletal muscle metabolism.2 Histone Acetylation · 2.1 Histone... · 3.2. 1 Class I HdacsMissing: 2024 | Show results with:2024
  27. [27]
    Genome-wide epigenetic dynamics during postnatal skeletal muscle ...
    Oct 23, 2023 · This process largely determines the efficiency of protein synthesis and the potential of hypertrophy. Furthermore, it has been reported that ...
  28. [28]
    Pathophysiology of Exercise-Induced Muscle Damage and Its ...
    At the cellular level, EIMD encompasses damage of myofibrils and Z-line streaming, membrane damage of T-tubules and sarcoplasmic reticulum, disrupted ...
  29. [29]
    Muscle damage from eccentric exercise: mechanism ... - NIH
    In eccentric exercise the contracting muscle is forcibly lengthened; in concentric exercise it shortens. While concentric contractions initiate movements, ...Missing: hypertrophy microtrauma
  30. [30]
    Temporal Pattern of the Repeated Bout Effect of Eccentric Exercise ...
    The pain typically peaks between 24 and 72 hours postexercise when the muscles are tender and swollen.– The severity and distribution of pain associated with ...
  31. [31]
    Divergent Roles of Inflammation in Skeletal Muscle Recovery From ...
    Feb 13, 2020 · Classical muscle wasting cytokines include TWEAK, TNFα, and IL-6. High concentrations of these cytokines may down-regulate mRNA translation and ...
  32. [32]
    Aberrant repair and fibrosis development in skeletal muscle
    May 4, 2011 · M1 macrophages also produce high levels of pro-inflammatory cytokines, such as TNFα and interleukin (IL)-1β and IL-12. In addition, they can be ...
  33. [33]
    Fibroblast growth factor signaling in macrophage polarization
    Jun 19, 2024 · FGF/FGFR signaling play a crucial role in tissue repair, a complex physiological process involving various cell types such as fibroblasts, ...
  34. [34]
    CCN2 participates in overload-induced skeletal muscle hypertrophy
    Jan 16, 2022 · CCN2, also known as connective tissue growth factor (CTGF), is induced during a time course of overload-driven skeletal muscle hypertrophy in mice.
  35. [35]
    Loading Recommendations for Muscle Strength, Hypertrophy ... - NIH
    A moderate repetition scheme with moderate loads (from 8 to 12 repetitions per set with 60% to 80% of 1RM) optimizes hypertrophic gains. A high repetition ...
  36. [36]
    Satellite Cells Contribution to Exercise Mediated Muscle ...
    Satellite cell involvement in muscle hypertrophy​​ It is suggested that SC addition to skeletal muscle fibers positively promotes muscle hypertrophy (36).
  37. [37]
    Satellite cells in human skeletal muscle plasticity - Frontiers
    Skeletal muscle satellite cells are considered to play a crucial role in muscle fiber maintenance, repair and remodeling.Abstract · Introduction · Satellite Cell Identification in... · Satellite Cells and Muscle...Missing: seminal | Show results with:seminal
  38. [38]
    Hepatocyte growth factor affects satellite cell activation ... - PubMed
    Hepatocyte growth factor (HGF) is the only known growth factor that activates quiescent satellite cells in skeletal muscle.
  39. [39]
    Myonuclear Domain Flexibility Challenges Rigid Assumptions on ...
    May 29, 2018 · Satellite cell-mediated myonuclear accretion is thought to be required for skeletal muscle fiber hypertrophy, and even drive hypertrophy by preceding growth.
  40. [40]
    Role of satellite cells versus myofibers in muscle hypertrophy ...
    Aug 6, 2012 · Here, we show that myofibers are the primary target for signaling by myostatin/activin and that satellite cells, which are stem cells resident ...
  41. [41]
    Myonuclei acquired by overload exercise precede hypertrophy and ...
    We show that the increase in fiber size during overload hypertrophy is preceded by addition of nuclei; thus, the increase in size could be causally related ...
  42. [42]
    Myonuclear accretion is a determinant of exercise-induced ... - eLife
    Apr 23, 2019 · (2018b) Myonuclear domain flexibility challenges rigid assumptions on satellite cell contribution to skeletal muscle fiber hypertrophy.
  43. [43]
    Satellite cells in ageing: use it or lose it | Open Biology - Journals
    May 20, 2020 · This review examines how periodic activation and cycling of satellite cells through exercise can mitigate senescence acquisition and myogenic decline.Missing: overtraining | Show results with:overtraining
  44. [44]
    Restoring Mitochondrial Function and Muscle Satellite Cell Signaling
    Notable changes include a reduced number and function of muscle satellite cells, reorganization of motor units, fiber loss and/or atrophy, and increased ...Missing: overtraining | Show results with:overtraining
  45. [45]
    Role of damage and management in muscle hypertrophy
    In this review, we summarize recent findings concerning the relationship between MuSCs and hypertrophy, and discuss what remains to be discovered.Missing: seminal | Show results with:seminal
  46. [46]
    CRISPR/Cas9 Myostatin Deletion Improves Muscle Stem Cells in Mice
    The present study examines the impact of myostatin deletion using CRISPR/Cas9 editing on the myogenic differentiation (MD) of C2C12 muscle stem cells.
  47. [47]
    Muscle memory and a new cellular model for muscle atrophy and ...
    Jan 1, 2016 · The higher number of nuclei should contribute to the increase in protein synthesis because total protein synthesis is the product of synthesis ...
  48. [48]
    The Role of Satellite Cells in Muscle Hypertrophy - PubMed
    Feb 7, 2014 · Satellite cells are not only responsible for muscle repair and regeneration, but also for hypertrophic growth.
  49. [49]
    Maximizing Muscle Hypertrophy: A Systematic Review of Advanced ...
    Dec 4, 2019 · Muscle hypertrophy occurs when muscle protein synthesis exceeds muscle protein breakdown and results in positive net protein balance in ...Maximizing Muscle... · 3. Discussion · 3.7. Drop Sets And...
  50. [50]
    Resistance Training Recommendations to Maximize Muscle ...
    Aug 16, 2021 · This position stand of leading experts in the field synthesizes the current body of research to provide guidelines for maximizing skeletal muscle hypertrophy ...<|control11|><|separator|>
  51. [51]
    Effects of linear and daily undulating periodized resistance training ...
    Aug 22, 2017 · The meta-analysis comparing LP and DUP indicated that the effects of the two periodization models on muscle hypertrophy are likely to be similar.
  52. [52]
    Resistance Training Load Effects on Muscle Hypertrophy ... - PubMed
    Jun 1, 2021 · Although muscle hypertrophy improvements seem to be load independent, increases in muscle strength are superior in high-load RT programs.
  53. [53]
    a systematic review and Bayesian network meta-analysis
    Jul 5, 2023 · All RTxs were superior to CTRL for muscle strength and hypertrophy. Higher-load (>80% of single repetition maximum) prescriptions maximised strength gains.
  54. [54]
    Effects of Resistance Training Overload Progression Protocols on ...
    Our findings indicate that the progression of overload through load or repetitions can be used to promote gains in strength and muscle hypertrophy in young men ...
  55. [55]
    Effect of free-weight vs. machine-based strength training on maximal ...
    Aug 15, 2023 · The effect of free-weight- versus machine-based training on hypertrophy. The meta-analysis revealed no significant differences in hypertrophy ...
  56. [56]
    Blood Flow Restriction Training - Physiopedia
    As a result of the hypoxia hypoxia-inducible factor (HIF-1α) is activated. This leads to an increase in anaerobic lactic metabolism and the production of ...Introduction · Blood Flow Restriction (BFR... · BFR and Strength Training
  57. [57]
    Blood Flow Restriction Training in Rehabilitation: A Useful Adjunct ...
    Apr 30, 2019 · Training pressures need to be at least 40% of limb occlusion pressure, and can be up to 80% (lower in the arm than in the leg). Wider cuffs ...Skip main navigation · Abstract · Hypertrophy Is Possible With...
  58. [58]
    A Review on the Mechanisms of Blood-Flow Restriction Resistance ...
    Sep 24, 2014 · Metabolic stress may play the dominant role in mediating the potent hypertrophic effects seen with blood-flow restriction (BFR) resistance ...Missing: paper | Show results with:paper
  59. [59]
    Effects of Blood Flow Restriction Training on Muscular Strength and ...
    Oct 10, 2018 · Studies that combined walking with and without BFR showed percentage changes of 13.3 ± 8.5% and 0.4 ± 3.9% in muscular strength, respectively.<|separator|>
  60. [60]
    Potential Moderators of the Effects of Blood Flow Restriction Training ...
    May 22, 2024 · In the meta-analysis by Lixandrão et al., they observed that BFR-RT and HL-RT have similar gains in muscle hypertrophy, while HL-RT is more ...
  61. [61]
    Effects of Drop Sets on Skeletal Muscle Hypertrophy - NIH
    Jul 31, 2023 · Drop sets are often used to enhance muscle hypertrophy because decreasing the load may be an effective strategy to fully fatigue the muscle ...Missing: cluster anaerobic
  62. [62]
    (PDF) Effects of Drop Sets on Skeletal Muscle Hypertrophy
    Jul 31, 2023 · The purpose of this systematic review and meta-analysis was to compare the effects of drop sets over traditional sets on skeletal muscle hypertrophy.
  63. [63]
    Can You Drop (Set) Weight for Gains? - Stronger by Science
    Drop sets are enjoyable, time efficient, and according to a new meta-analysis, lead to similar hypertrophy and strength gains as traditional sets.
  64. [64]
    Rest-pause and drop-set training elicit similar strength and ...
    Crescent pyramid and drop-set systems do not promote greater strength gains, muscle hypertrophy, and changes on muscle architecture compared with traditional ...
  65. [65]
    Effects of Blood Flow Restriction Exercise and Possible Applications ...
    During BFRT, HGF release is induced by NO and leads to activation of SCs. Hypoxia-inducible factor 1α (HIF-1α) ... 1 may promote muscle hypertrophy by aiding ...
  66. [66]
    Low-Load Resistance Exercise with Blood Flow Restriction ...
    Nov 8, 2022 · The results reported herein showed that the HIF (isoforms 1α and 1β) mRNA level was significantly increased in all training groups; however, ...
  67. [67]
    Effects of blood flow restriction combined with high-load training on ...
    This activates the HIF-1α/mTORC1 signaling axis, enhancing protein synthesis rates (Hughes et al., 2019; DePhillipo et al., 2018). Clinical trials confirm BFR's ...
  68. [68]
    Impact of exercise with blood flow restriction on muscle hypertrophy ...
    Moreover, BFRT significantly increased muscle strength and power for males and females. However, males increase muscle strength and power to a greater extent ...
  69. [69]
    Effects of blood-flow restricted exercise versus conventional ...
    Oct 25, 2023 · Objective. To compare the effect of low-load blood flow restricted resistance training (BFR-RT) versus high-load resistance training (HL-RT) ...<|separator|>
  70. [70]
    Overall Safety and Risks Associated with Blood Flow Restriction ...
    Mar 12, 2022 · BFRT has effects on endovascular and muscular growth hormones, and as such, those with hypertension or other vascular disease should be warned ...ABSTRACT · INTRODUCTION · RESULTS · DISCUSSION
  71. [71]
    A Useful Blood Flow Restriction Training Risk Stratification for ...
    Some studies have shown the safety of the BFRT at various time intervals as early as 2 days post-surgery (Iversen et al., 2016). A previous study demonstrated ...Introduction · Hypertension, Blood Pressure... · Cardiovascular Disease and...
  72. [72]
    Blood Flow Restriction Training - PMC - NIH
    Specifically, we will discuss proposed mechanisms of effectiveness, safety considerations, application guidelines, and clinical recommendations. The ...
  73. [73]
    Skeletal Muscle Hypertrophy after Aerobic Exercise Training - NIH
    We and others have demonstrated that aerobic exercise acutely and chronically alters protein metabolism and induces skeletal muscle hypertrophy.
  74. [74]
    RaceRunning training improves stamina and promotes skeletal ...
    Mar 27, 2020 · Our data support the use of RaceRunning to increase cardiorespiratory fitness and promote skeletal muscle hypertrophy in affected limbs in ...
  75. [75]
    Concurrent Strength and Endurance Training: A Systematic Review ...
    Oct 17, 2023 · Concurrent training results in small interference for lower-body strength adaptations in males, but not in females.<|control11|><|separator|>
  76. [76]
    The influence of intracellular lactate and H+ on cell volume in ... - NIH
    Intracellular lactate and H+ concentrations were simultaneously increased by exposing resting muscle fibres to extracellular solutions that contained 20–80 mm ...Missing: aquaporins | Show results with:aquaporins
  77. [77]
    Aquaporins in skeletal muscle: reassessment of the functional role of ...
    Mar 19, 2004 · Thus, rapid water transport seems to have a physiological role in contraction-induced muscle swelling.
  78. [78]
    Fundamentals of glycogen metabolism for coaches and athletes - PMC
    Each gram of glycogen is stored with at least 3 g of water,14,15 making weight gain a noticeable response to glycogen super-compensation in many athletes.Missing: 4g | Show results with:4g
  79. [79]
    Peak week recommendations for bodybuilders: an evidence based ...
    Jun 13, 2021 · Additionally, since each gram of glycogen draws ~ 3–4 g water into the muscle [31] and this is a potassium dependent process (see above), a ...Missing: 4g | Show results with:4g
  80. [80]
    pQCT- and Ultrasound-based Muscle and Fat Estimate Errors after ...
    Unaccustomed resistance exercise can cause errors in pQCT- and ultrasound-based muscle and adipose estimates for at least 72 h.Missing: 5-10% resolving hours
  81. [81]
    pQCT- and Ultrasound-based Muscle and Fat Estimate Errors...
    It was hypothesized that pQCT estimates of CSA and muscle area would be increased 24, 48, and 72 h after the resistance exercise, and these changes would be ...Missing: transient | Show results with:transient
  82. [82]
    Relationship Between Muscle Swelling and Hypertrophy Induced by ...
    Feb 1, 2022 · This study suggests that the greater the muscle swelling immediately after the first session of RT, the greater the muscle hypertrophy after RT.
  83. [83]
    The Physiology of Resistance Exercise and Skeletal Muscle Growth
    Sep 1, 2022 · Resistance exercise stimulates calcium mobilization, AMPK and Wnt signaling, and growth hormone release while also causing metabolic stress, ...<|control11|><|separator|>
  84. [84]
    Strength gains and distinct acute blood lactate responses induced ...
    Sep 3, 2025 · Firstly, lactate is believed to inhibit the activity of the TSC1/2 complex, indirectly activating the mTOR signaling pathway. This process ...
  85. [85]
    Reactive Oxygen Species in Skeletal Muscle Signaling - PMC
    Low levels of ROS activate specific key signaling molecules such as PGC-1α, AMPK, and MAPK, which control cellular mechanisms for muscle adaptation (oxidative ...
  86. [86]
    Dual roles of mTOR in skeletal muscle adaptation - Frontiers
    Resistance training causes muscle hypertrophic remodeling, primarily through mammalian target of rapamycin (mTOR)-mediated protein synthesis (1).
  87. [87]
    Effects of heavy-resistance training on hormonal response patterns ...
    Heavy-resistance exercise has been shown to be a potent stimulus for acute increases in circulating hormones in younger men (5, 23, 24, 30,36-38, 40, 41, 59).Missing: spikes nutrient uptake
  88. [88]
    Associations of exercise-induced hormone profiles and gains ... - NIH
    Acute elevations in endogenous hormones (e.g., growth hormone—GH, testosterone, and insulin-like growth factor—IGF-1) are proposed to contribute to resistance ...Missing: nutrient | Show results with:nutrient
  89. [89]
    Hormones, Hypertrophy, and Hype: An Evidence-Guided Primer...
    In summary, the acute postexercise rises in systemic testosterone, growth hormone, and IGF-1 are neither sufficient nor necessary for stimulating a rise in ...Missing: uptake | Show results with:uptake
  90. [90]
    The increase in muscle force after 4 weeks of strength training is ...
    Previous studies have indicated that several weeks of strength training is sufficient to elicit significant adaptations in the neural drive sent to the muscles.
  91. [91]
    Neuromuscular adaptations to resistance training in elite versus ...
    Jun 8, 2025 · This critical review synthesized evidence on neuromuscular adaptations to resistance training, focusing on muscle hypertrophy, architectural changes, motor ...
  92. [92]
    Global Skeletal Muscle Metabolomics Reveals Mechanisms Behind ...
    Mar 15, 2025 · We also propose that HighR individuals may possess more efficient BCAA metabolism, facilitating the conversion of BCAAs into branched-chain keto ...
  93. [93]
    Amino Acid Metabolite Profiling for Predicting and Understanding ...
    Aug 14, 2025 · Recent metabolomics research highlights amino acid metabolites—branched-chain amino acids, aromatic amino acids, and tryptophan-derived ...Missing: hypertrophy | Show results with:hypertrophy
  94. [94]
    The Role of Dietary Protein Intake and Resistance Training on ...
    Dec 1, 2004 · Myofibrillar hypertrophy occurs due to increases in the number of myosin/actin filaments inside each sarcomere. This leads to increased strength ...
  95. [95]
    Resistance training‐induced changes in integrated myofibrillar ... - NIH
    We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive attenuation of muscle damage.
  96. [96]
    (PDF) The Role of Fiber Types in Muscle Hypertrophy - ResearchGate
    Aug 6, 2025 · The purpose of this article will be to review the research regarding fiber type-specific hypertrophy and draw evidence-based conclusions as to their ...<|control11|><|separator|>
  97. [97]
    Exercise-Induced Myofibrillar Hypertrophy is a Contributory Cause ...
    Apr 23, 2019 · The primary focus of this commentary is to discuss the relationship between training-induced increases in muscle size (ie, hypertrophy) and changes in strength.Missing: running | Show results with:running
  98. [98]
    Does Muscle Growth Plateau Faster Than We Think? (16 Studies)
    Aug 22, 2022 · Some studies suggest muscle growth plateaus within 3 months, but others show no plateau, and trained individuals can still experience growth.Missing: myofibrillar | Show results with:myofibrillar
  99. [99]
    Sarcoplasmic Hypertrophy in Skeletal Muscle: A Scientific “Unicorn ...
    Jul 13, 2020 · Around a century earlier, Morpurgo reported results from the first training-induced hypertrophy study in an animal model, and the author ...
  100. [100]
    Muscle fiber hypertrophy in response to 6 weeks of high-volume ...
    Muscle fiber hypertrophy in response to 6 weeks of high-volume resistance training in trained young men is largely attributed to sarcoplasmic hypertrophy.
  101. [101]
    Effects of High-Volume Versus High-Load Resistance Training on ...
    We evaluated the effects of higher-load (HL) versus (lower-load) higher-volume (HV) resistance training on skeletal muscle hypertrophy, strength, and muscle- ...Missing: experiment | Show results with:experiment
  102. [102]
    (PDF) The Effect of Myofibril and Sarcoplasmic Hypertrophy Training ...
    Oct 7, 2025 · Conclusion Myofibrillar hypertrophy training resulted in greater hypertrophy compared to sarcoplasmic training according to muscle ...
  103. [103]
    A Critical Evaluation of the Biological Construct Skeletal Muscle ...
    Myofibrillar hypertrophy can be defined as an increase in the size and/or number of myofibrils accompanied by an increase in sarcomere number or sarcomeric ...
  104. [104]
    Various Factors May Modulate the Effect of Exercise on ... - NIH
    Nov 7, 2020 · Although exercise increases plasma testosterone concentrations, this effect depends on many factors, including the aforementioned ones.Missing: variance | Show results with:variance
  105. [105]
    How Much Do Variations in Physiological Testosterone Matter To ...
    Cross-sectional data, dose-response studies, and TRT studies all support variations within the normal range as having an impact on fat-free mass and muscle.
  106. [106]
    The regulation of muscle mass by endogenous glucocorticoids - PMC
    Feb 3, 2015 · Glucocorticoids elicit the atrophy of muscle by increasing the rate of protein degradation by the ubiquitin-proteasome system and autophagy lysosome system.Glucocorticoids As Mediators... · Glucocorticoid-Mediated... · Glucocorticoids In DiseaseMissing: hypertrophy | Show results with:hypertrophy
  107. [107]
    Role of thyroid hormone in skeletal muscle physiology in
    Thyroid hormone affects skeletal muscle metabolism. T3 treatment increases maximal oxygen consumption, which is more than two times bigger in the soleus than ...Introduction · Thyroid hormone affects... · Influence of illness on skeletal...
  108. [108]
    Systematic review and meta-analysis of protein intake to support ...
    Feb 20, 2022 · In conclusion, increasing daily protein ingestion results in small additional gains in LBM and lower body muscle strength gains in healthy ...Missing: 1.6-2.2g/kg leucine 3g/ mTOR calorie surplus 300-500 kcal
  109. [109]
    Protein timing and its effects on muscular hypertrophy and strength ...
    Dec 14, 2012 · Protein supplementation pre- and post-workout increases physical performance, training session recovery, lean body mass, muscle hypertrophy, and strength.Protein And Calorie Intake · Leucine And Muscle Protein... · Types Of Protein
  110. [110]
    Is an Energy Surplus Required to Maximize Skeletal Muscle ...
    Skeletal muscle hypertrophy requires the further remodeling of muscle, ensuring it is an energy intensive process. As such, there has been much discussion ...
  111. [111]
    Is There a Postworkout Anabolic Window of Opportunity for Nutrient ...
    Nov 30, 2018 · Based on current evidence, it appears clear that any effect of protein timing on muscle hypertrophy, if in fact there is one, is relatively ...
  112. [112]
    The Effects of Creatine Supplementation Combined with Resistance ...
    Apr 28, 2023 · A pooled analysis of the current data suggests that creatine supplementation promotes a small increase in skeletal muscle hypertrophy in both ...
  113. [113]
    Effects of Creatine and β-Alanine Co-Supplementation on Exercise ...
    Chronic β-alanine supplementation (typically 3.2–6.4 g/day for 2–10 weeks) increases muscle carnosine content by approximately 10% after 2 weeks and up to 80% ...Missing: window debated
  114. [114]
    (PDF) The Role of Omega-3 Polyunsaturated Fatty Acids in Muscle ...
    Jul 30, 2024 · Studies demonstrate that omega-3 PUFAs enhance muscle protein synthesis via the mTOR pathway and possess anti-inflammatory properties that may reduce muscle ...
  115. [115]
    Effect of gut microbiome modulation on muscle function and cognition
    Feb 29, 2024 · This study aims to assess whether the modulation of the gut microbiome using a prebiotic improves muscle function (as measured by 5× chair rise ...
  116. [116]
    Scientists link gut microbes to stronger muscles and healthier aging
    Aug 19, 2025 · Researchers discovered that gut microbes, including Lactobacillus reuteri and L. johnsonii, can enhance muscle strength in aging mice.
  117. [117]
    Genetic influences on muscle strength, lean body mass, and bone ...
    All three muscle variables have a moderate genetic component with heritability estimates of 0.52 for lean body mass, 0.46 for leg extensor strength, and ...Missing: hypertrophy | Show results with:hypertrophy
  118. [118]
    A Systematic Review and Meta-analysis of the Association Between ...
    Apr 12, 2024 · This systematic review with meta-analysis assessed ACTN3 R577X genotype frequencies in power versus endurance athletes and non-athletes.
  119. [119]
    ACTN3 (R577X) genotype is associated with fiber type distribution
    The aim of this study was to quantify the association between the polymorphism and muscle fiber type distribution and fast-velocity knee extension strength.
  120. [120]
    Muscle tissue changes with aging - PMC - PubMed Central
    Muscle mass decreases approximately 3–8% per decade after the age of 30 and this rate of decline is even higher after the age of 60 [4,5].Missing: peak | Show results with:peak
  121. [121]
    Senescence atlas reveals an aged-like inflamed niche that blunts ...
    Dec 21, 2022 · During ageing, tissue regenerative functions decline, in part due to stem cell-intrinsic accumulation of damage (for example, DNA damage, loss ...Missing: hypertrophy | Show results with:hypertrophy
  122. [122]
    (PDF) Effects of Resistance Training on Older Adults - ResearchGate
    Aug 5, 2025 · This review highlights the benefits of resistance training toward improvements in functional status, health and quality of life among older adults.
  123. [123]
    Physiological and molecular sex differences in human skeletal ...
    Nov 11, 2021 · On average, males are taller, heavier, have greater lean body mass and lower fat mass, and have a higher proportion of fast-twitch (type II) ...Abstract · Biographies · References
  124. [124]
    Circulating Testosterone as the Hormonal Basis of Sex Differences ...
    A clear sex difference in athletic performance emerges as circulating testosterone concentrations rise in men because testes produce 30 times more testosterone ...
  125. [125]
    Sex differences in absolute and relative changes in muscle size ...
    Feb 25, 2025 · Sex differences in absolute and relative changes in muscle size following resistance training in healthy adults: a systematic review with Bayesian meta-analysis
  126. [126]
    Identification of Genomic Predictors of Muscle Fiber Size - PMC - NIH
    The aim of our study was to determine whether 1535 genetic variants previously identified in a genome-wide association study of appendicular lean mass are ...
  127. [127]
    Skeletal muscle eQTL meta-analysis implicates genes in the genetic ...
    Sep 23, 2025 · A stepwise analysis identified 18,818 conditionally distinct signals for 12,283 genes, and 35% of these genes contained two or more signals.
  128. [128]
    Physical exercise and epigenetic modifications in skeletal muscle ...
    Mar 21, 2025 · The most prevalent types of histone modifications include acetylation, phosphorylation, methylation, and ubiquitination. These modifications are ...
  129. [129]
    Effect of heavy strength training on thigh muscle cross ... - PubMed
    The purpose of this study was to investigate the effect of heavy strength training on thigh muscle cross-sectional area (CSA), determinants of cycling ...Missing: quadriceps | Show results with:quadriceps
  130. [130]
    Selective training-induced thigh muscles hypertrophy in ... - PubMed
    We have reported, for the first time, a selective hypertrophy of Vastus lateralis and Biceps femoris in professional road cyclists confirming their involvement ...
  131. [131]
    Sequencing Effects of Concurrent Strength and Endurance Training ...
    May 23, 2024 · There is evidence that plyometric training has the potential to induce muscle hypertrophy in healthy individuals, irrespective of age, sex or ...
  132. [132]
    Strength training in soccer with a specific focus on highly trained ...
    This review examines the extent to which distinct modes of strength training improve soccer players' performance, as well as the effects of concurrent strength ...
  133. [133]
    The Effects of CrossFit® Practice on Physical Fitness and Overall ...
    Dec 28, 2024 · In fact, it has been demonstrated that 12 weeks of regular CrossFit® training can elicit a significant increase in maximal strength (~9 to 17%) ...
  134. [134]
    Wearable Technology Named Top Fitness Trend for 2024 - ACSM
    Here are the top 10 trends for 2024: Wearable Technology. Think fitness trackers, smart watches, heart rate monitors, and GPS tracking devices, including ...
  135. [135]
    Myocardial stress and hypertrophy: a complex interface between ...
    Pressure overload usually elicits concentric hypertrophy, with a high ratio of LV wall thickness to radius (h/R). In contrast, volume overload triggers ...Missing: paper | Show results with:paper
  136. [136]
    Left Ventricular Hypertrophy: Major Risk Factor in Patients with ...
    Left ventricular hypertrophy is both a major maladaptive response to chronic pressure overload and an important risk factor in patients with hypertension.
  137. [137]
    Left ventricular hypertrophy, wall thickness, and histological myocyte ...
    Oct 28, 2024 · 2D-derived echocardiographic increased LVWT in patients with LVH defined by increased LVM index was present in approximately 30-50%. Furthermore ...
  138. [138]
    Double muscling in cattle due to mutations in the myostatin gene
    Two breeds of double-muscled cattle, Belgian Blue and Piedmontese, which are known to have an increase in muscle mass relative to conventional cattle.
  139. [139]
    Myostatin Mutation Causes Gross Muscle Hypertrophy in Child
    Jun 24, 2004 · We report the identification of a myostatin mutation in a child with muscle hypertrophy, thereby providing strong evidence that myostatin does play an ...Missing: source | Show results with:source
  140. [140]
    Cancer cachexia: molecular mechanisms and treatment strategies
    May 22, 2023 · The inhibition of myostatin leads to muscle hypertrophy and hence promotes its potency in preventing muscle loss [173,174,175]. Several ...
  141. [141]
    The Paradox of Muscle Hypertrophy in Muscular Dystrophy - PMC
    Muscle hypertrophy in humans has generally been attributed to deposition of fat and connective tissue (pseudohypertrophy), but recent imaging studies suggest ...
  142. [142]
    Duchenne Muscular Dystrophy - StatPearls - NCBI Bookshelf
    In DMD, both dystrophin and DGC proteins are missing, leading to excessive membrane fragility and permeability, dysregulation of calcium homeostasis, and ...
  143. [143]
    Physical therapy for muscle strengthening in individuals with ...
    Jul 22, 2024 · ... hypertrophy in individuals with ALS [16]. Recent studies have shown ... denervation [17]. Therefore, the development of treatment ...
  144. [144]
    The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis
    Jul 9, 2025 · Muscle tissue in ALS patients and in animal models demonstrates severe regenerative deficits, including impaired myogenesis and impaired ...
  145. [145]
    Neuromuscular electrical stimulation resistance training enhances ...
    Furthermore, NMES-RT resulted in a 30% increase (P = 0.0001; η2p= 0.37) in absolute knee extensor muscle CSA, with a significant interaction between groups (P ...
  146. [146]
    Enhancing Adaptations to Neuromuscular Electrical Stimulation ...
    NMES reduces muscle atrophy and weakness after immobilization by increasing or maintaining muscle protein synthesis (5), although suppression of protein ...Missing: percentage | Show results with:percentage
  147. [147]
    ACE Inhibitors Best for Left Ventricular Hyptertrophy
    Aug 1, 1996 · ACE inhibitors appeared to be the most effective, on average lowering left ventricular mass index by 13%, compared with 7% for diuretics, 6% for beta-blockers, ...
  148. [148]
    Mechanisms of the beneficial effects of beta-adrenoceptor ...
    These agents attenuate the effects of sympathetic activation during the development of heart failure, prevent ventricular remodelling and improve cardiac ...
  149. [149]
    Therapeutic applications and challenges in myostatin inhibition for ...
    This follistatin AAV has shown promising results in mice, with a single injection significantly increasing long-term muscle mass and strength in wild-type, aged ...
  150. [150]
    Advances in research on pharmacotherapy of sarcopenia - PMC
    In its phase II trial in patients with sarcopenia (NCT01604408, completed in 2013), landogrozumab treatment significantly increased muscle mass and partially ...
  151. [151]
    GSK2881078, a SARM, Produces Dose-Dependent Increases in ...
    Jul 2, 2018 · GSK2881078 yielded dose-dependent increases in lean mass with evidence of enhanced sensitivity in women. The compound was well tolerated.Abstract · Methods · Results · Discussion
  152. [152]
    Effectiveness of Nutritional Supplementation on Muscle Mass in ...
    Sep 17, 2012 · Nutritional supplementation is effective in the treatment of sarcopenia in old age, and its positive effects increase when associated with ...