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Peter Kazakov
Peter Kazakov

Muscle Mature

However, the cells in our bones, muscles and connective tissues are always turning over as they mature, die, and are replaced with new cells. As such, our muscles are living, dynamic structures that mature and evolve with training over time.

muscle mature

Muscle maturity does not refer to your muscular build when you finish puberty and have grown into your adult build. Rather, muscle maturity occurs much later on in adulthood as a product of years of strength training.

Even once you reach muscle maturity, your individual muscle fibers are still in a dynamic state of repairing and renewing, but your muscles have basically reached peak form and strength, having adapted and developed to their maximum capacity after years of training.

Moreover, meat from younger animals (veal vs. beef or lamb vs. mutton, for example) tends to be more tender and fattier than meat from mature animals. This is due to a lower muscle density and a higher percentage of intramuscular fat.

When you achieve muscle maturity, your muscles are compact, firm, and formed from toughened muscle fibers with thickened myofibrils (the structural proteins that compose the muscle fibers) at the microscopic level.

Most bodybuilding experts say that most people achieve muscle maturity somewhere between the ages of 25-40 years old, depending on how old you were when you first started serious or formal strength training.

Heavier loads trigger muscle hypertrophy, which refers to muscle building or the increase in muscle mass triggered by a cascade of various hormones and RNA factors that control protein synthesis. Through hypertrophy, your muscle fibers get bigger, stronger, and denser.

Along with carbohydrates and fat, protein provides energy (4 kcals per gram), but it also aids in muscle recovery after strength training, helping heal any microscopic damage and building new muscle fibers to adapt to your training loads.

Background: Pax7+ satellite cells are required for skeletal muscle fiber growth during post-natal development in mice. Satellite cell-mediated myonuclear accretion also appears to persist into early adulthood. Given the important role of satellite cells during muscle development, we hypothesized that the necessity of satellite cells for adaptation to an imposed hypertrophic stimulus depends on maturational age.

Methods: Pax7CreER-R26RDTA mice were treated for 5 days with vehicle (satellite cell-replete, SC+) or tamoxifen (satellite cell-depleted, SC-) at 2 months (young) and 4 months (mature) of age. Following a 2-week washout, mice were subjected to sham surgery or 10 day synergist ablation overload of the plantaris (n = 6-9 per group). The surgical approach minimized regeneration, de novo fiber formation, and fiber splitting while promoting muscle fiber growth. Satellite cell density (Pax7+ cells/fiber), embryonic myosin heavy chain expression (eMyHC), and muscle fiber cross sectional area (CSA) were evaluated via immunohistochemistry. Myonuclei (myonuclei/100 mm) were counted on isolated single muscle fibers.

Generally speaking, athletes with solid muscle maturity will have a harder, more grainy look to their physique, with deeper striations, more apparent dryness, and potentially sharper or more clearly defined angles.

Things that pass as sage advice from coach to athlete across generations may not stand up to scientific scrutiny. As a concept, muscle maturity is hard to pin down and study in a laboratory setting. Research on the idea in actual bodybuilders is sparse to nonexistent.

Fortunately, the effects of exercise (specifically weight lifting) on your muscles is far more clear. Anyone who has hit the iron and maintained a proper diet long enough will notice that their body grows and responds in kind.

Notably, training also affects your muscle tone. (4) While tone has the colloquial definition of shaping or defining a tissue in fitness circles, its scientific definition refers to the level of resting tension or tightness in a tissue. Your muscles do become more taut as you acclimate to regular lifting.

However, fat is also stored (in much smaller quantities) within your muscle tissue. Engaging in an effective hypocaloric diet will reduce your fat stores throughout your body, helping to define and emphasize your muscles themselves.

Though in the past believed to be a rare phenomenon, endothelial-mesenchymal transdifferentiation has been described with increasing frequency in recent years. It is believed to be important in embryonic vascular development, yet less is known regarding its role in the adult vasculature. Using FACS and immunomagnetic (Dynabeads) purification techniques (based on uptake of DiI-acetylated low-density lipoproteins and/or PECAM-1 expression) and double-label indirect immunostaining (for endothelial and smooth muscle [SM] markers), we demonstrate that mature bovine vascular endothelium contains cells of an endothelial phenotype (defined by VE-cadherin, von Willebrand factor, PECAM-1, and elevated uptake of acetylated low-density lipoproteins) that can undergo endothelial-mesenchymal transdifferentiation and further differentiate into SM cells (as defined by expression of alpha-SM-actin, SM22alpha, calponin, and SM-myosin). "Transitional" cells, coexpressing both endothelial markers and alpha-SM-actin, were consistently observed. The percentage of cells capable of endothelial-mesenchymal transdifferentiation within primary endothelial cultures was estimated as 0.01% to 0.03%. Acquisition of a SM phenotype occurred even in the absence of proliferation, in gamma-irradiated (30 Gy) and/or mitomycin C-treated primary cell cultures. Initiation of transdifferentiation correlated with disruption of cell-cell contacts (marked by loss of VE-cadherin expression) within endothelial monolayers, as well as with the action of transforming growth factor-beta(1). In conclusion, our in vitro data show that mature bovine systemic and pulmonary endothelium contains cells that can acquire a SM phenotype via a transdifferentiation process that is transforming growth factor-beta(1)- and cell-cell contact-dependent, but proliferation-independent.

There is something out there that you may have heard of called muscle maturity. It is your secret weapon and hidden gem to looking your best. This notion of muscle maturity serves even more true with people in fitness and bodybuilding. Through years of physical activity and work, the muscles mature and are able to contract more intensely. This then leads to deeper striations and thicker more dense fibers. The skin thins as well as people age, so the muscles are therefore revealed even more (along with some vascularity).

A person in high school could weigh 180 pounds and be 8% body fat. This would be an ideal look for most people in their 30s, 40s, and even 50s. Already marking it up for something that will never be, many people as they age just go to the weight room and lift to get bigger muscles and try to maintain as much youth as possible through achieving a sense of size. However, if a person was to take advantage of their muscle maturity by being active, eating healthy, and hitting the weight room, they would see that the 180-pound, 8% body fat frame would look much better on them now than it ever did in high school. This is because the muscles look more pleasing and aesthetic due to their maturity.

(A) 3-month-old male mice were treated with vehicle, 50 mg/kg/day chloroquine, 0.4 mg/kg/day colchicine or 2 mg/kg/day vinblastine for two days and tibialis anterior (TA) muscle lysates were evaluated by LC3 immunoblot. Actin is shown as a loading control. Blot is representative of 3 independent experiments. (B) TA from similarly treated mice as in (A) was subjected to immunofluorescence using an LC3 antibody. Colchicine treated mice had an increase in LC3 positive puncta. Images were taken at the same camera setting and exposure time. Scale is 40 µM. (C) The TA muscle from 3-month-old male mice was electroporated with a tandemly tagged mCherry-GFP-LC3 reporter construct. Mice were either treated for two days with vehicle or 0.4 mg/kg/day colchicine. Vehicle treated mice had diffuse LC3 fluorescence while colchicine treated mice generated GFP and mCherry positive co-localizing puncta consistent with colchicine impairing autophagosome maturation to an acidic organelle. Scale is 25 µM.

(A) Similar mice were treated with vehicle, 0.4 mg/kg/day colchicine, nutrient deprivation (starvation) or nutrient deprivation plus 0.4 mg/kg/day colchicine for two days. TA muscle lysates were evaluated by LC3 and p62 immunoblot. Note that colchicine treatment significantly increases LC3-II levels. These levels are augmented by nutrient deprivation. Blot is representative of three independent experiments. (B) LC3-II/actin ratios were quantitated via densitometry from six mice per treatment condition. Error bars represent standard error and **denote p values of

To confirm that colchicine treatment did indeed block autophagosome degradation (i.e., fusion of the autophagosome with the lysosome), we utilized a tandemly tagged mCherry-GFP-LC3 reporter construct.6 This reporter fluoresces green and red in the neutral environment of an autophagosome and red in the acidic environment of an autolysosome or other acidic organelle. This construct was electroporated into the TA muscle of 3-month-old male mice and allowed to express for seven days. On day 5, mice were treated with saline or 0.4 mg/kg i.p. colchicine for two days. TA muscle was harvested and sectioned. Untreated mouse muscle had diffuse green and red fluorescence throughout the myofiber with no visible puncta as would be expected for an LC3 protein that is not present on an autophagic structure (Fig. 1C). In contrast, two days of colchicine treatment generated myofibers with multiple dual fluorescing GFP and mCherry positive puncta consistent with autophagosomes that have not matured to autolysosomes and become acidified (Fig. 1C). In nonelectroporated myofibers, colchicine induced more LC3 positive puncta than Lamp2 positive puncta and LC3 and Lamp2 did not co-localize (not shown). These data further support that two days of 0.4 mg/kg i.p. colchicine is able to block autophagosome degradation in mouse skeletal muscle and this dose was employed for all subsequent experiments. 041b061a72


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