como entrenar fibras blancas o rojas?

alex1312

New member
hola es mi primer post y tenia una duda de como entrenar las fibras blancas y las fibras rojas
gracias de antemano
 
hola es mi primer post y tenia una duda de como entrenar las fibras blancas y las fibras rojas
gracias de antemano

Estaras de broma no? No creo ni k sepas cuales son las blancas y cuales las rojas ni el porque.
Documentate hazme el favor, que esto es un foro.
 
pues hablales y diles a unas que trabajen mas que otras ya esta
eso me va de lujo
 
hola es mi primer post y tenia una duda de como entrenar las fibras blancas y las fibras rojas
gracias de antemano

Información

Cada uno tiene una genética distinta, entonces, te puede venir mejor entrenar resistencia o velocidad en función de la proporción de fibras musculares que tengas. Pero no puedes convertir un tipo de fibras en otras.
 
yo lo decia por k e estado buscando informacion y encontre k trabajando mas series rapidas se trabajan las fibras blancas y trabajando menos series se trabajaban las rojas
 
si pero que no es correcto de lo que e mencionado???

Que las fibras explosivas son las responsables de la fuerza y la hipertrofia.
No sé si sabes inglés, pero este estudio es muy bueno
This URL has been removed!

Ahí dice, comparando la musculatura de culturistas (BB) con un grupo de control (ctrl)
Among fast fibres, hypertrophy was significantly more pronounced in type 2X and type 2AX fibres than in type 2A fibres. Type 2X and 2AX fibres were
92% and 61% larger in BB than in CTRL, respectively


Entre las fibras rápidas la hipertrofia era singificativvamente mayor en las de tipo 2X y 2AX que en las 2A. Las de tipo 2X y 2AX eran respectivamente mayores en un 92% y en un 61% en BB que en CTRL.



Yo creo que eso es un mito. Hipertrofia sólo hay una.
En ese mismo estudio que cito lo que se incrementa es la fibra.
Vamos, que eso de que hay un músculo puro y uno que es el resultado de incremento de glucógeno y agua me parece un cuento chino

Aquí se habla de eso:
https://es.fitness.com/forum/cultur...fia-no-funcional-por-kelly-baggett-90782.html
 
entonces segun tu para que sirve entrenar fuerza??? y por ej como explicas que gente con menos musculatura levante mas???

El entrenamiento de fuerza sirve para ganar fuerza.
Y el de hipertrofia para ganar hipertrofia.
Son fines diferentes y métodos diferentes.
Y, en la vida real, la mayor parte de los aficionados hacen híbridos.
O sea, rutinas en las que se busca progresar en cargas trabajando en rangos bajos de reps combinados con volumen más alto.

La fuerza no es sólo cuestión muscular, si no de adaptación neural, que viene dada por la práctica de la técnica. Aparte, viene determinada por la genética. Hay gente más fuerte que otra.

Pero entre un culturista y un powerlifter de peso máximo las diferencias en hipertrofia son mínimas.
Mira este video. Centopani entrenando con el strongman Poundstone:
This URL has been removed!

Lo de gente con menos musculatura que levanta mucho me parece otra leyenda urbana.
Busca videos de powerlifters y a ver si encuentras a uno así.
 
eso no es leyenda, hay halterofilos que siendo mas pequeños levantan mas que culter por ej

Levantan ¿en qué?
¿En sus movimientos específicos?
No creo que Cutler haga enviones y arrancadas.
Los otros son especialistas que entrenan esos movimientos desde la infancia.
En press banca cualquier culturista ganaría a un halterófilo. Más que nada porque estos no practican ese movimiento.

Y no os liéis, la fuerza es importante en culturismo, pero no es el fin de esta actividad.
Además, hay variaciones individuales. Hay gente que responde muy bien a entrenamientos muy pesados con fines culturistas, gente que no.

Yo lo único que sé es que eso de la hipertrofia sarcomérica y sarcoplásmática sólo se lee en foros de culturismo.
Me harté de buscar artículos científicos y deportivos y no encontré ni uno.
Sólo un texto de This URL has been removed! en el que lo despachaban como un mito.

Y buscando, sólo encontré estudios como el que postée en el que no usan jamás esos términos.
vamos, que ppara mí hipertrofia hay una.
Luego hay trabajo específico que es el que determina el nivel de fuerza.
 
y yo desde luego he experimentado una cosa curiosa, te cuento yo mis dos primeros años entrene solo volumen puro weider, y quitando los primeros meses de ganancias por se novato creci relativamente poco, acave cojiendo mania a esas rutinas y me dedique ala fuerza con la que subi, pero muxo mas aun de fuerza en los basicos y me puse mas duro en general, pero con muuuucha diferencia te hablo almenos en mi claro, cuando mas he crecido ha sido altenando 6 semanas fuerza 6 semanas hipertrofia, y casualmente las semanas de fuerza casi no subo, pero luego cuando paso a volumen si suvo y muxo, pero por otra parte es normal que que ese aumento de fuerza que tuve en la rutina de fuerza, lo sigo notando en la de volumen, y tiro mas en todos lso ejercicios tipicos de rutina dividida, y otra cosa cuando hago fuerza jamas tengo ni media agujeta, cosa que en volumen no me puedo ni mover, con lo cual creo que si que hay algo por ahi......y yo desde luego creo que en la union esta la fuerza, y entenar haciendo periodos de fuerza periodos de fuerza hipertrofia y periodos de hipertrofia es lo ideal, me parece muy dificil cuando superas los 80 90 k dar buena forma a toooodos los musculos de cuerpo solo son sentadillas y peso muerto, por otra parte me parece que en volumen si no subes los pesos antes o despues sin esteroides te estancas, y ahi es donde entra el papel importante de hacer rutinas tipo full body de fuerza 5x5 por poner un ej (solo es mi opinion y experiencia)

Tu caso no es raro. Es lo que nos pasa a la mayoría de la gente.
ya te he dicho antes que hay casos raros de gente que coge hipertofia trabajando a bajas reps con pesos altos.
Pero es poco común.

Lo habitual es lo tuyo.

La hipertrofia se basa en
- Porgresión de cargas
- Volumen de entrenamiento

Subir de fuerza con una weider es extremadamente diifícil. Por eso viene bien alternar esos períodos de fuerza si buscas hipertofia.
Hacer rutinas de fuerza exclusivamente es interesante si vas a competir en power.
Aún así, los powerlifters hacen períodos de hipertrofia.

Entre otras cosas les viene bien para descansar las articulaciones que se castigan mucho con el tipo de entrenamiento que hacen.
 
Joder pues yo subo de puta madre entrenando fuerza,soy un rarito de esos.
El mito de la hipertrofia no funcional ya lo lei, y si no me equivoco afirmaba que la cantidad de sarcoplasma era proporcional al volumen de fibra muscular.

Una pregunta, en teoria deberia poderse vaciar por casi completo ese sarcoplasma y quedarte con lo que viene siendo esa "fuerza", no? lo digo porque en deportes en los que es necesario regular el peso seria lo perfecto.
De hecho,yo ahora mismo me siento descargado de glucogeno por completo,sin embargo la fuerza la he aumentado en grandes proporciones (tengo mucha mas fuerza relativa).

saludos
 
Joder pues yo subo de puta madre entrenando fuerza,soy un rarito de esos.
El mito de la hipertrofia no funcional ya lo lei, y si no me equivoco afirmaba que la cantidad de sarcoplasma era proporcional al volumen de fibra muscular.

Una pregunta, en teoria deberia poderse vaciar por casi completo ese sarcoplasma y quedarte con lo que viene siendo esa "fuerza", no? lo digo porque en deportes en los que es necesario regular el peso seria lo perfecto.
De hecho,yo ahora mismo me siento descargado de glucogeno por completo,sin embargo la fuerza la he aumentado en grandes proporciones (tengo mucha mas fuerza relativa).

saludos

No se puede vaciar el sarcoplasma. El músculo es agua en su mayor parte.
Cuando le quitas el agua queda la mojama, o la cecina. Pero eso es carne muerta y desecada.

¿Te sientes descargado de glucógeno?
¿Qué pasa, no comes hidratos?
No entiendo, Explosivo.
 
hola xplosivo dices que subes de puta madre entrenando solo fuerza? si no recuerdo mal en un post tullo pesas 72 k o asi no??

Ahora si,tras una deficion un poco a lo bestia y porque me interesa para competir en mi deporte.
Pero me he puesto en 80 solo entrenando fuerza.

Pureta,me refiero a que he bajado la ingesta de hidratos en gran medida y con ello he bajado mucho peso (aunque no tanto volumen),pero que subiendo los hidratos un mes vuelvo a subir el peso segurisimo, comprobado al 100%
 
me pasa igual.......... si me contestas la pregunta que te hize te lo agradeceria_porro_

¿Qué pregunta?
No te entiendo.

Lo que dice Explosivo de vaciar el sarcoplasma no tiene ni pies ni cabeza.
Tendrás poco glucógeno si entrenas y no ingieres hcs. Pero según que entrenamientos eso te afecta la performance.
Por eso hacen cargas de hidratos los que hacen cetogénicas.
Porque sin glucógeno malamente se entrena.
 
¿Qué pregunta?
No te entiendo.

Lo que dice Explosivo de vaciar el sarcoplasma no tiene ni pies ni cabeza.
Tendrás poco glucógeno si entrenas y no ingieres hcs. Pero según que entrenamientos eso te afecta la performance.
Por eso hacen cargas de hidratos los que hacen cetogénicas.
Porque sin glucógeno malamente se entrena.

En eso estoy completamente deacuerdo,hay que comer hidratos para rendir.Yo los he recortado porque en verano no estaba preparandome para competicion,ahora las cosas se ponen muy cuesta arriba si no se come a lo grande.
Lo del sarcoplasma simplemente era una pregunta.

Entrenando fuerza tambien crece el sarcoplasma por asi decirlo?
 
no se si lo quieres para un deporte en concreto de puta madre, pero yo cuando pesava 72 k me veia anorexico(me lo sigo viendo) y creo que apartir de cierto tamaño, es necesario periorizar, no se eslo que dije antes veo deificil dar forma a todos los musculos de un tio de 100k solo con 3 ejercicios

A ver, obviamente no estoy igual de grande con 80 kilos que con 72,pero yo ahora me veo mucho mas versatil en todo, antes tambien estaba funcional, pero hay que adaptarse en funcion de las necesidades, y para competir en deportes de contacto, hay una gran diferencia en hacerlo en la categoria 80-85 que 70-75,a demas que mover mas musculo es un mayor gasto y te cansas un poco antes.
Una vez cumpla mis objetivos pues seguramente vuelva a ponerme grandecillo, aunque como ya te he dicho entrenando fuerza subo bien.
 
Última edición:
Yo lo único que sé es que eso de la hipertrofia sarcomérica y sarcoplásmática sólo se lee en foros de culturismo.
Me harté de buscar artículos científicos y deportivos y no encontré ni uno.
Sólo un texto de This URL has been removed! en el que lo despachaban como un mito.

Este es un buen artículos sobre Hipertrofia Sarcoplasmica

Sarcoplasmic Hypertrophy and Rep Range

By Dan Moore​

One of the issues I still see when reading training articles is how the rep range dictates whether any hypertrophic response predominantly influences changes in size of the contractile components of muscle cells or the sarcoplasmic volume. The intent of this article is not to dispute that sarcoplasmic hypertrophy exists but to clarify if the rep range used will dictate which protein fraction will increase and whether or not the rep range specifically induces different changes to the nuclear domain of muscle fibers.

There may very well be other factors such as metabolite accumulation and osmolality shifts within the cell that would give temporary changes to the muscle cell volume and size but since these are mostly temporary I did not feel they should be included in this article.


What is the Sarcoplasm?

Within the sarcoplasm there are soluble (or aqueous) components (making up 80 percent of it); composed of ions and soluble macromolecules like enzymes, carbohydrates, different salts and proteins, as well as a great proportion of RNA. This watery component can be more or less gel-like or liquid depending on the condition and the activity phases of the cell. In general, margin regions of the cell are gel-like and the cell's interior is liquid.

The insoluble constituents of the sarcoplasm are organelles (such as the mitochondria, the chloroplast, lysosomes, peroxysomes, ribosomes), several vacuoles, cytoskeletons as well as complex membrane structures (e.g. sarcoplasmic reticulum).

The muscle protein fraction that makes up the cytoplasm (sarcoplasm in a muscle cell) is made up of mostly enzymes participating in cell metabolism, such as the anaerobic energy conversion from glycogen to ATP, intracellular transport, and several other enzyme functions. This fraction adds up to about 25 or 30% of the total muscle protein versus the larger and more talked about structural protein (myofibril protein) makes up about 40%.

Skeletal muscle protein
When speaking of protein synthesis one of the things that first must be identified is which fraction of protein we are talking about.

Whole body protein synthesis is an average of the synthesis rates of various proteins in different tissues of the body, skin, muscle, organs, and plasma.

Mixed muscle protein is an average of the synthesis rates of total muscle proteins and includes mitochondrial, sarcoplasmic, structural components and connective tissue proteins.

Myofibrillar protein is comprised of individual proteins such as myosin, actin, titin, tropomyosin, troponin, protein C, and some components of mitochondrial proteins.

Sarcoplasmic proteins are mostly enzymes participating in cell metabolism. However, if the organelles within the muscle cells are broken, this protein fraction may also contain the metabolic enzymes localized inside the sarcoplasmic reticulum, mitochondria and lysosomes.

Fractional Protein Synthesis
It has now been known for some time that chronic elevation in protein synthesis above that of breakdown is of prime importance in skeletal muscle hypertrophy (1,2). It is this basis of understanding that we start this article off by looking into how feeding and exercise impacts fractional protein turnover.

Years ago David Millward and Peter Bates identified that protein synthesis had a direct relationship to both feeding and fasting (3). They also noted that during tissue growth (from feeding) the maintenance of a constant composition necessitates the same absolute increase in synthesis for all proteins, both contractile (myofibril) and soluble (sarcoplasmic). This would mean that the increase in the synthesis rate for each protein will be an increasing proportion of the overall rate for the slower-turning-over proteins or in more simpler terms, the increase of both fractions are held within a ratio.

Resistance training has shown very strong shifts in protein turnover (4,5) and most of the studies have used mixed muscle protein turnover as the gauge of effectiveness. Unfortunately this method does not show how resistance or dynamic exercise training differently affects each fraction.

In a study looking at age affects of Protein Synthesis (6) it was noted that by the end of 2 weeks of weight-lifting exercise, MHC and mixed protein synthesis rates increased in both younger and older participants. The actin protein synthesis rate was increased after exercise in only the younger group. The magnitude of the exercise-induced increase in MHC and mixed protein synthesis rates was similar in the younger and older groups. In the younger group, the MHC and Actin (contractile) protein synthesis rate increased 83% and 78% respectively while the mixed muscle protein synthesis rate increased (102%). This study points to the identification that, as with feeding, all proteins are up regulated with resistance exercise. Now the interesting point was that the exercise protocol used seven weight-lifting exercises (Nautilus equipment) that included the chest press, inclined chest press, latissimus pull-down (wide and narrow grip), leg press, knee extension, knee flexion, and two free weight-lifting exercises that included seated overhead press and overhead triceps extension. Each participant completed ten weight-lifting exercise sessions: 2–3 sets/day of the nine exercises listed above, 8–12 repetitions/set, 60–90% of maximum voluntary muscle strength. This was a pretty broad range of intensity and easily points out that the rep range itself isn’t the determining factor.

To further illustrate that the intensity or rep range utilized does not change this ratio all too dramatically we can look at more recent work looking into the synthetic rates of fractional proteins with dynamic or resistance type exercise.

Atherton et al. (7) used electrical stimulation with high frequency (HFS; 6x10 repetitions of 3 s-bursts at 100 Hz to mimic resistance training) to identify signalling present during increased protein synthesis. What he noted, significant to this article and discussion, was that HFS significantly increased myofibrillar and sarcoplasmic protein synthesis 3 h after stimulation 5.3 and 2.7 fold, respectively.

Interestingly Bowtell (8) found that when the same total amount of ATP is turned over, exercise at 60, 75 and 90% of the one-repetition-maximum force results in exactly the same stimulation of muscle protein synthesis, suggesting that once all muscle fibers are recruited increases in tension above 65% cause no further stimulation in muscle protein synthesis. Even though I am not aware if the specific fractions were measured in the Bowtell study it would stand to reason that in light of the previous both fractions would be up regulated.

In another study, Louis (9) subjects carried out 20 series of 10 repetitions (with a rest of 80 s after each series) on an isokinetic dynometer to evaluate if Creatine has an impact on anabolic signalling and protein synthesis. Again, in the realm of this article, what was found interesting was that this exercise increased the synthetic rates of myofibrillar and sarcoplasmic proteins by 2- 3 fold.

Looking at dynamic exercise (one legged kicking), Miller (10) saw that the rates of protein synthesis in the exercised leg increased substantially by 6 h and peaked within 24 h in both myofibrillar and sarcoplasmic fractions, i.e. increases of 2.8 and 2-fold, respectively. The rates of myofibrillar and sarcoplasmic protein synthesis in the exercised muscle had fallen slightly by 48 h but were still significantly above the rates in the rested leg. By 72 h, the rates of both fractions had decreased.

Our last look at fractional elevations will look at whether or not there is a fiber type dependency. In many animals the rate of protein synthesis is higher in slow-twitch, oxidative than fast-twitch, glycolytic muscles. To find if this held true for muscles in the human body a recent study (11) recruited nine healthy, young men and with a constant infusion looked at synthetic rates in the soleus, vastus lateralis and tricep. Type-1 fibers contributed 83 +/- 4% (mean +/-s.e.m.) of total fibers in soleus, 59 +/- 3% in vastus lateralis and 22 +/- 2% in triceps. The basal myofibrillar and sarcoplasmic protein fractional synthetic rates (FSR, % h(-1)) were 0.034 +/- 0.001 and 0.064 +/- 0.001 (soleus), 0.031 +/- 0.001 and 0.060 +/- 0.001 (vastus), and 0.027 +/- 0.001 and 0.055 +/- 0.001 (triceps). During amino acid infusion, myofibrillar protein FSR increased to 3-fold, and sarcoplasmic to 2-fold above basal values (P < 0.001), again showing that even within differing types of muscle tissue the ratio remains.

What can be seen when reviewing these and many other papers on the subject is the response to resistance training of fractional elevation remains in line with the results of feeding, both are elevated but the slower turnover proteins (myofibrillar) generally show a larger magnitude in increase. Since these studies show that this holds true with resistance training, dynamic exercise and HFES, all utilizing differing intensities and work output, it seems unlikely that the rep range is the sole cause of any increase in sarcoplasmic fraction up-regulation.

Nuclear Domains
It is well established that satellite cell contribution is a very important factor in muscle hypertrophy (12,13). As a cell grows and increases it’s cytoplasmic volume the nucleus must maintain mRNA production for the entire area of increased size of cytoplasm (14). Since muscle cells are multi-nucleic, each nucleus controls mRNA over a finite area or its domain (14,15), hence the term nuclear domain.

Skeletal muscle hypertrophy has shown to induce increases in myonuclei and or increases in domain size (16). Resistance training has reported a very broad range of increases in fiber hypertrophy (17). In several hypertrophy studies it appears that there is a limit that needs to be reached before domain size increases necessitates increased nuclei donation. Studies that have shown significant increase in hypertrophy, above 26%, also showed large additions of myonuclei in animals (18-20) and in humans (21).

Work in humans is rather limited but what can be seen in this smaller body of work is very interesting. Acutely, resistance training and resistance type training do not exert the same magnitude of response in humans as what is seen in smaller animals.

A recent study (22) examining the acute effect of training showed less significant changes in donated nuclei and in fact after an acute bout of (a) fifty one legged ‘drop down’ jumps were performed from a stable platform of 45 cm, (b) eight sets of ten maximal eccentric knee extensions at –30 degree/s using an isokinetic dynamometer and (c) eight sets of ten maximal eccentric knee extensions at –180 degree/s using an isokinetic dynamometer, satellite cell proliferation did occur but there was no increased satellite cell donation. Apparently a single bout in humans is not enough to induce the same changes seen in smaller animals.

Kadi looked at chronic application in a very interesting and telling look at training and detraining. (23). In this study he subjected 15 subjects to 3 months of progressive resistance training using a 6-12 RM. The various exercises were conducted in 4–5 sets, in the first weeks (training sessions 0–5) exercises involved 10–12 RM loads, followed by 10 RM loads in early weeks (training sessions 6–15), heavier loads of 6–10 RM in the later weeks (training sessions 16–30), and very heavy loads of 6–8 RM in the final weeks (training sessions 31–38). The subjects then detrained for 3 months. Satellite cell activity increased significantly over the entire training period. Reaching significance at around 30 and again at the 90-day marks. Hypertrophy of fiber increased at 30 days and 90 days, 6.7% and 17% respectively. Interestingly though was the observation that the area controlled by each nuclei was virtually unchanged over the entire training period. This clearly illustrates that the rep range was not the primary inducer of hypertrophy or domain volume changes since the fiber size and satellite cell count increased no matter the rep range. It also clearly indicates that the duration of chronic training is a key element in both hypertrophy and satellite cell activity.

An earlier study by the same researcher (24) saw a concomitant increase in satellite cell count and an increase in myonuclei donation over a 10-week training protocol in female athletes. The muscle examined in this study was the trapezius so it could be that the increase could be muscle specific, as it’s been shown that the trapezius has a higher androgen receptor content (25). This may have also been another reason why the previously cited work by Kadi showed such a difference as the biopsies were taken from the vastus lateralis.

In summary it is very common to see studies reflecting both increased protein synthesis and hypertrophy with a myriad of rep ranges and resistance training protocols. The extent of hypertrophy may be a direct reflection in increased translational efficiency or an increase in pre-translational abundance of mRNA. The differences may be owing to the training status of the individual and not necessarily the rep range used in the resistance training routine. Although it appears that the rep range will have an impact on metabolic shifts in isoform content this does not change the sarcoplasmic vs. contractile protein synthesis ratio but merely dictates which fiber type will experience the greater amount of hypertrophy.

As stated in Rennie’s 2004 review (26), it may take 20 weeks of resistance training to increase hypertrophy by 20%. This coincides very well with the research presented in this article, as it appears that the change in fiber size has a direct correlation to when satellite cells donate their nuclei for continued domain regulation. Therefore moderate increases in nuclear domain are very possible without the aided donation of nuclei from satellite cells and this does not appear to be rep range dependant. A statement can also be made that the results seen in small animals and humans may be very different. This may be owing to the extent of damage that is seen and how hypertrophy and necrotic damage stimulate the satellite pool differently but that is beyond the scope of this article.



Dan Moore
Hypertrophy-Research.com


(1)Changes in rates of protein synthesis breakdown during hypertrophy of the anterior and posterior latissimus dorsi muscles. Biochem. J. 176:407–17

(2)Protein turnover during skeletal muscle hypertrophy.Fed. Proc. 39:42–47

(3)Synthesis rates of myofibrillar and sarcoplasmic protein fractions in different muscles and the changes observed during postnatal development and in response to feeding and starvation Biochem. J. (1983) 214,587-592

(4)Increased rates of muscle protein turnover and amino acid transport after resistance exercise in humans. Am J Physiol Endocrinol Metab 268: E514–E520, 1995.

(5)Changes in human muscle protein synthesis following resistance exercise. J Appl Physiol 73: 1383–1388,1992.

(6)Resistance exercise acutely increases MHC and mixed muscle protein synthesis rates in 78–84 and 23–32 yr olds Am J Physiol Endocrinol Metab 278: E620–E626, 2000.

(7) Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signaling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation. FASEB J. 2005 May;19(7):786-8. Epub 2005 Feb 16.

(8) Stimulation of human quadriceps protein synthesis after strenuous exercise: no effects of varying intensity between 60 and 90% of one repetition maximum (1RM). J Physiol 547.P, P16.

(9) No effect of creatine supplementation on human myofibrillar and sarcoplasmic protein synthesis after resistance exercise. Am J Physiol Endocrinol Metab. 2003 Nov;285(5):E1089-94.

(10)Coordinated collagen and muscle protein synthesis in human patella tendon and quadriceps muscle after exercise.J Physiol. 2005 Sep 15;567(Pt 3):1021-33.


(11)Protein synthesis rates in human muscles: neither anatomical location nor fibre-type composition are major determinants. J Physiol. 2005 Feb 15;563(Pt 1):203-11. Epub 2004 Dec 20.

(12)Gamma irradiation prevents compensatory hypertrophy of overloaded mouse extensor digitorum longus muscle. J. Appl. Physiol. 73:2538–43

(13)Cellular molecular responses to increased skeletal muscle loading after irradiation. Am. J. Physiol.
Cell Physiol. 283:C1182–95

(14)The control of cell mass and replication. The DNA unit-a personal 20 year study. Early Hum Dev 12, 211-239.

(15) Nuclear Domains in Muscle Cells. Cell 59, 771-772

(16)Regulation of Skeletal muscle fiber size, shape and function. J Biochem (Suppl. 1), 123-133

(17) Exercise, protein metabolism, and muscle growth. Int J Sport Nutr Exerc Metab. 2001 Mar;11(1):109-32. Review.

(18)Morphometric analyses on the muscles of exercise trained and untrained dogs. Am J Anat. 1983 Mar;166(3):359-68.

(19)Plasticity of myonuclear number in hypertrophied and atrophied mammalian skeletal muscle fibers. J Appl Physiol. 1995 May;78(5):1969-76.

(20)Modulation of myonuclear number in functionally overloaded and exercised rat plantaris fibers.J Appl Physiol. 1999 Aug;87(2):634-42.

(21)Is Hypertrophy limited in elderly muscle fibers? A comparison in elderly and young strength-trained men. Basic Appl Myol 1998; 8, 419-427

(22)Changes in satellite cells in human skeletal muscle after a single bout of high intensity exercise. J Physiol. 2004 Jul 1;558(Pt 1):333-40.

(23)The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol. 2004 Aug 1;558(Pt 3):1005-12.

(24)Concomitant increases in myonuclear and satellite cell content in female trapezius muscle following strength training. Histochem Cell Biol 2000; 113, 99-103.

(25)The expression of androgen receptors in human neck and limb muscles: effects of training and self-administration of androgenic-anabolic steroids. Histochem Cell Biol. 2000 Jan;113(1):25-9.

(26)Control of the Size of the Human Muscle Mass Annu. Rev. Physiol. 2004. 66:799–828
 
A mi me pasa igual, entrenando a fuerza ke es lo unico ke entreno subo de peso mas d lo que me gustaría.
Ahora rondo los 81 kilos para 1,76.
En un post recuerdo que explosivo puso sus medidas y por curiosidad me medi. Recuerdo que tenia lo mismo de brazo.Tenia 2 cm mas de pierna y dos mas de gemelos. dos mas de espalda (Normal pesando 11 kilos mas ke el). Igual de pecho. PERO de cintura explosivo tenia 71cm (ke no se me olvida) y yo 92. (Lo flipo).
Esa va a ser la diferencia explosivo que mi almacen esta en la zona media jejejej. Y me tengo ke controlar mucho para subir xq mi cuerpo tiende a subir de peso pero sin cortarse en guardar grasas el cabron. saludos
 
Última edición:
Este es un buen artículos sobre Hipertrofia Sarcoplasmica

Le he echado un ojo a varios de los estudios que cita y lo único que he visto claro es que el ejercicio produce un incremente de la hipertrofia. Y que la hipertrofia es tanto aumento de los filamentos de actina y miosina como del contenido proteico del sarcoplasma celular.
Vamos, que no veo en parte alguna que digan que aumenta una cosa y no la otra.

Yo creo que los de las dos hipertrofias lo inventó Verhokansky. Y normalmente por lo que leo en los foros parece que la gente cree que una de las dos hipertofias es crecimiento del músculo de verdad y la otra hinchazón de líquido y glucógeno.

Y, por lo que veo, las dos cosas son simultáneas e inseparables: más contenido proteico del sarcoplasma e incremento de tamaño de los filamentos de actina y miosina.
 
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