Getbig.com: American Bodybuilding, Fitness and Figure
Getbig Main Boards => Gossip & Opinions => Topic started by: Rmj11 on March 01, 2025, 11:39:35 PM
-
i=8cjU-E2bthygIRKE
Diet
Breakfast - Egg and cheese (cottage) omelette cooked in organic butter
Lunch - Beef patty and eggs
Dinner - Chicken salad
-
what!
No cream of rice and almond butter?
-
??? 3 meals a day on a bulk diet?
-
??? 3 meals a day on a bulk diet?
his offseason meant no drugs, why would he load himself up with loads of food
Back then Arnold grew into shows by upping the drugs and food
These days they juice heavily year round and eat like fucking babies.
Arnold knew it wasnt about creating new tissue, it was about artificially stretching what he had
(https://external-preview.redd.it/3lehLqbGTdpZEx7mULBr-fLJ2i29kje-tVOQVFP-Egk.png?width=640&crop=smart&auto=webp&s=c695c5b45b922b4a29c3c598da02e3b54961ed99)
-
Arnold was slim off drugs.
-
Back then when he was a Alpha male eating steak ,
now vegan Beta.
-
Back then when he was a Alpha male eating steak ,
now vegan Beta.
Big soy boy.
-
Back then when he was a Alpha male eating steak ,
now vegan Beta.
He`s my all time favorite bodybuilder.......now I can`t stand him. :(
-
He`s my all time favorite bodybuilder.......now I can`t stand him. :(
Same here Tim .I’ve watched Pumping Iron and Dorian's training videos all the time .This is why I like his 80’s action movie rival Sly more .Sly stays away from political BS.
-
Same here Tim .I’ve watched Pumping Iron and Dorian's training videos all the time .This is why I like his 80’s action movie rival Sly more .Sly stays away from political BS.
Sly is smart..................A rnold lost the ball at the goal line. :(
-
He`s my all time favorite bodybuilder.......now I can`t stand him. :(
X2, unfortunately, a once great alpha is now an old fool holding on to the final flickering moments of his fame.... and life. Embarrassing and sad. Oh well, history will always show him as winner of the 1980 Olympia :D.
-
X2, unfortunately, a once great alpha is now an old fool holding on to the final flickering moments of his fame.... and life. Embarrassing and sad. Oh well, history will always show him as winner of the 1980 Olympia :D.
Contrary to some peoples opinion on here.........I won`t mention any names though!! ;D
-
??? 3 meals a day on a bulk diet?
Arnold has stated he never had a huge appetite. He actually consumed more when training for a contest.
Breakfast
Half a pound burger patty
3 to 4 scrambled eggs
Bacon
Lunch
Steak and eggs with salad
Afternoon snack
2 cans of tuna
Salad
Dinner
3 and a quarter pound of steak, chicken or fish
Salad
Fruit
-
https://www.tiktok.com/t/ZT2XeS4ej/
-
https://www.tiktok.com/t/ZT2XeS4ej/
he went from 190 to 235 due to glycogen and water retention in his previously stretched muscle fibres..
-
Back then when he was a Alpha male eating steak ,
now vegan Beta.
At his age (77) it would be unwise to eat like a 25 year old who does heavy lifting. Especially with his heart problems, his approach is smart and follows common sense.
-
Arnold was slim off drugs.
He looked great, lean, healthy and athletic.
Builders now often do not come off drugs. That's the only reason they look bigger than the bodybuilders from the Golden Era. And they use way more chemicals than in the past.
Bodybuilders who do come 100% clean usually are less muscular than Arnold was on that photo. Levrone, Platz, Tom Prince etc etc. Look at Dennis Wolf. He's now full of ugly tattoos but otherwise a similar build to Arnold off gear.
-
he went from 190 to 235 due to glycogen and water retention in his previously stretched muscle fibres..
If that was the case he would have looked like all glycogen and water retention.
-
Sly is smart..................A rnold lost the ball at the goal line. :(
It might look like that to some. But consider Arnold's past. Austrian, son of a SS member. This was used against Arnold for decades. Lots of hate, false accusations of "racism", fascism etc.
Arnold is very smart. By staying away from MAGA and seemingly embracing communist Kamala nobody comes up with the usual Third Reich accusations and bs anymore. He has positioned himself on the safe side. Which is in his interest, and that of his children and grandchildren.
Arnold is a family man, and financially very shrewd. Well, apart from his divorce. But even that seems to have been handled in a positive way. Beneficial to both parties.
I understand the criticism, but perhaps Arnold has no choice, considering his background and the hate and distrust against him personally and his Austrian family.
Being seen as a relatively woke and liberal guy is a smart move.
Even in 2025 people still underestimate his intelligence.
-
his offseason meant no drugs, why would he load himself up with loads of food
Back then Arnold grew into shows by upping the drugs and food
These days they juice heavily year round and eat like fucking babies.
Arnold knew it wasnt about creating new tissue, it was about artificially stretching what he had
(https://external-preview.redd.it/3lehLqbGTdpZEx7mULBr-fLJ2i29kje-tVOQVFP-Egk.png?width=640&crop=smart&auto=webp&s=c695c5b45b922b4a29c3c598da02e3b54961ed99)
(https://i.pinimg.com/736x/f3/54/51/f3545109bac72c407758bbf8f46400e9.jpg)
-
If that was the case he would have looked like all glycogen and water retention.
are you saying he created all new muscle in 9 weeks?
You have the same amount of muscle fibres in your body when you start training to when you finish.
You dont grow new muscles, you just stretch and expand the ones you have
Even Basile knows that.
-
Arnold has stated he never had a huge appetite. He actually consumed more when training for a contest.
Breakfast
Half a pound burger patty
3 to 4 scrambled eggs
Bacon
Lunch
Steak and eggs with salad
Afternoon snack
2 cans of tuna
Salad
Dinner
3 and a quarter pound of steak, chicken or fish
Salad
Fruit
Paco Arse's meaty gay caulk
Mouthful of Semen
Anal remnants from tonging Paco's grommet
(https://thumbs.dreamstime.com/z/bsuinessman-awe-points-up-looks-to-side-curious-businessman-standing-white-background-portrait-picture-128109939.jpg)
-
Arnold is a man dedicated to his family and he f*cked the maid and created his clone.
-
are you saying he created all new muscle in 9 weeks?
You have the same amount of muscle fibres in your body when you start training to when you finish.
You dont grow new muscles, you just stretch and expand the ones you have
Even Basile knows that.
I'm too lazy to look it up now but some newer study said bodybuilders had an abnormal amount of fibers of average size, contradicting all previous research where hyperplasia has never been shown, and have shown that training causes hypertrophy of existing fibers. Maybe good bodybuilders have more than average number of fibers from birth? You are of course likely right, but otoh you look at these bodybuilders like Lunsford and his evolution and it's almost unbelievable how much he's grown, is it all just hypertrophy? Maybe they haven't looked at enhanced bodybuilders from start to finish to definitely rule it out? I don't know, maybe they have looked at how much a fiber can hypertrophy by percentage, then you might be able get a clue if it's just hypertrophy?
-
I'm too lazy to look it up now but some newer study said bodybuilders had an abnormal amount of fibers of average size, contradicting all previous research where hyperplasia has never been shown, and have shown that training causes hypertrophy of existing fibers. Maybe good bodybuilders have more than average number of fibers from birth? You are of course likely right, but otoh you look at these bodybuilders like Lunsford and his evolution and it's almost unbelievable how much he's grown, is it all just hypertrophy? Maybe they haven't looked at enhanced bodybuilders from start to finish to definitely rule it out? I don't know, maybe they have looked at how much a fiber can hypertrophy by percentage, then you might be able get a clue if it's just hypertrophy?
Yes, hyperplasia does not occur in humans, cats rats and birds yes, people , no.
-
(https://i.pinimg.com/736x/f3/54/51/f3545109bac72c407758bbf8f46400e9.jpg)
Man he looks like his son, (Patrick maybe?) in that running pic.
-
Arnold is a man dedicated to his family and he f*cked the maid and created his clone.
(https://www.getbig.com/boards/index.php?action=dlattach;topic=698987.0;attach=1559811;image)
(https://www.etonline.com/sites/default/files/styles/640xh/public/images/2016-05/embed_joseph_baena_FFN_JDFF_051616_52059475.jpg?width=1024&quality=80)
-
Man he looks like his son, (Patrick maybe?) in that running pic.
Yup.
(https://i.pinimg.com/736x/f3/54/51/f3545109bac72c407758bbf8f46400e9.jpg)
(https://static0.thethingsimages.com/wordpress/wp-content/uploads/2023/10/what-growing-up-with-arnold-was-really-like-for-patrick-schwarzenegger.jpg)
(https://i.dailymail.co.uk/i/pix/2011/11/06/article-2058380-0EAF262900000578-980_468x594.jpg)
(https://akns-images.eonline.com/eol_images/Entire_Site/2013510/rs_634x1024-130610055927-634.PatrickS.jc.shirtless.jc.jpg)
-
Yes, hyperplasia does not occur in humans, cats rats and birds yes, people , no.
Hyperplasia absolutely does occur, but not with Arnold. You’re suggesting it’s all glycogen and water, again, if it’s just glycogen and water he would have looked like it that suggestion would indicate his diet would have been high in carbs when in fact it was just the opposite but probably higher than most since he grew into the show. Zane did the same thing. So, of course not hyperplasia but rather hypertrophy.
Back in the 80’s (and I’ve mentioned this before) myself, Rory Liedelmeyer, Jonny Aranita, Bob Paris, Scott Livingstone and Tom Touchstone were involved in a training experiment put on by Jeff Feliciano with the “100’s” system of training with hopes of creating hyperplasia using the steroid “ Bolasterone”. We were the first in the country to do this. Now, since there was no muscle biopsy taken we couldn’t say for sure if it actually worked, but all of us got big and hard AF in our own rights within a 5-7 week period if I recall. Anyway, there are plenty of studies that show hyperplasia does in fact occur.
-
Yup.
(https://i.pinimg.com/736x/f3/54/51/f3545109bac72c407758bbf8f46400e9.jpg)
(https://static0.thethingsimages.com/wordpress/wp-content/uploads/2023/10/what-growing-up-with-arnold-was-really-like-for-patrick-schwarzenegger.jpg)
(https://i.dailymail.co.uk/i/pix/2011/11/06/article-2058380-0EAF262900000578-980_468x594.jpg)
(https://akns-images.eonline.com/eol_images/Entire_Site/2013510/rs_634x1024-130610055927-634.PatrickS.jc.shirtless.jc.jpg)
That bottom pic. He sure does have his dads ab structure
-
Hyperplasia absolutely does occur, but not with Arnold. You’re suggesting it’s all glycogen and water, again, if it’s just glycogen and water he would have looked like it that suggestion would indicate his diet would have been high in carbs when in fact it was just the opposite but probably higher than most since he grew into the show. Zane did the same thing. So, of course not hyperplasia but rather hypertrophy.
Back in the 80’s (and I’ve mentioned this before) myself, Rory Liedelmeyer, Jonny Aranita, Bob Paris, Scott Livingstone and Tom Touchstone were involved in a training experiment put on by Jeff Feliciano with the “100’s” system of training with hopes of creating hyperplasia using the steroid “ Bolasterone”. We were the first in the country to do this. Now, since there was no muscle biopsy taken we couldn’t say for sure if it actually worked, but all of us got big and hard AF in our own rights within a 5-7 week period if I recall. Anyway, there are plenty of studies that show hyperplasia does in fact occur.
I remember that article and I tried that program but didn't last very long. It was pure misery.
-
Hyperplasia absolutely does occur, but not with Arnold. You’re suggesting it’s all glycogen and water, again, if it’s just glycogen and water he would have looked like it that suggestion would indicate his diet would have been high in carbs when in fact it was just the opposite but probably higher than most since he grew into the show. Zane did the same thing. So, of course not hyperplasia but rather hypertrophy.
Back in the 80’s (and I’ve mentioned this before) myself, Rory Liedelmeyer, Jonny Aranita, Bob Paris, Scott Livingstone and Tom Touchstone were involved in a training experiment put on by Jeff Feliciano with the “100’s” system of training with hopes of creating hyperplasia using the steroid “ Bolasterone”. We were the first in the country to do this. Now, since there was no muscle biopsy taken we couldn’t say for sure if it actually worked, but all of us got big and hard AF in our own rights within a 5-7 week period if I recall. Anyway, there are plenty of studies that show hyperplasia does in fact occur.
great, show me a scientific study showing definitive proof.
Not one suggesting in "may occur"
-
Yes, hyperplasia does not occur in humans, cats rats and birds yes, people , no.
Actually...it does.
-
Actually...it does.
evidence please...
-
evidence please...
Hyperplasia occurs through an increase in cell number within a tissue or organ, typically as a response to a stimulus that drives cell proliferation. Below, I’ll break down the process and cite relevant studies to ground the explanation in scientific evidence.
How Hyperplasia Occurs
1 Trigger or Stimulus:
Hyperplasia begins with a signal that pushes cells to divide. This can be hormonal, mechanical, compensatory, or pathological. For instance, hormones like estrogen stimulate endometrial hyperplasia during the menstrual cycle, while chronic irritation (e.g., from injury) can trigger skin hyperplasia.
◦ Study: A 2001 review by Cheung and Hamilton in Endocrine Reviews (“Endometrial hyperplasia and carcinoma: Molecular mechanisms”) details how estrogen excess, unopposed by progesterone, drives endometrial cell proliferation via estrogen receptor activation, increasing mitotic activity (DOI: 10.1210/edrv.22.2.0427).
2 Cell Proliferation:
Once triggered, cells ramp up their division rate through the cell cycle (G1, S, G2, mitosis). This involves DNA replication and mitosis, regulated by growth factors, cytokines, and genetic pathways like cyclins and cyclin-dependent kinases (CDKs). Proto-oncogenes (e.g., c-Myc) promote division, while tumor suppressors (e.g., p53) keep it in check.
◦ Study: A 1997 paper by Sherr in Science (“Cancer Cell Cycles”) explains how growth factors bind to receptors, activating signaling cascades (e.g., MAPK pathway) that push cells into the S-phase for DNA synthesis, a key step in hyperplasia (DOI: 10.1126/science.278.5340.1670).
◦ Example: In liver regeneration (compensatory hyperplasia), hepatocyte proliferation is driven by hepatocyte growth factor (HGF) and interleukin-6 (IL-6). A 2003 study by Taub in Journal of Clinical Investigation (“Liver regeneration: from myth to mechanism”) highlights how HGF triggers cyclin D expression, initiating mitosis (DOI: 10.1172/JCI200318012).
3 Tissue Expansion:
The increased cell division leads to more cells, expanding the tissue. These cells typically remain differentiated and functional, distinguishing hyperplasia from neoplasia (cancer). The extent depends on the stimulus duration and tissue type.
◦ Study: In benign prostatic hyperplasia (BPH), a 2011 study by Roehrborn in European Urology (“Etiology, pathophysiology, and natural history of benign prostatic hyperplasia”) shows how androgen-driven epithelial and stromal cell proliferation thickens the prostate, supported by histological evidence of increased cell counts (DOI: 10.1016/j.eururo.2011.03.013).
Types of Hyperplasia
• Physiological: Normal adaptation, e.g., mammary gland hyperplasia in pregnancy driven by prolactin and estrogen (see Zwick et al., 1999, Molecular and Cellular Endocrinology, DOI: 10.1016/S0303-7207(99)00056-5).
• Pathological: Excessive growth, e.g., BPH or endometrial hyperplasia from hormonal imbalance.
• Compensatory: Tissue repair, e.g., liver regeneration post-hepatectomy.
Key Distinction
Hyperplasia differs from hypertrophy (cell size increase). A 2015 review by Vander Heiden in Nature Reviews Molecular Cell Biology (“Cell growth versus cell proliferation”) clarifies that hyperplasia involves mitosis, while hypertrophy involves protein synthesis without division (DOI: 10.1038/nrm4040).
Wrap-Up
Hyperplasia is a controlled, stimulus-driven process where cells divide to meet a demand, backed by molecular mechanisms like growth factor signaling and cell cycle regulation. The studies cited provide experimental and clinical evidence—
-
1. Trigger or Stimulus: What Sets It Off?
Hyperplasia doesn’t just happen randomly; it’s a response to a specific need or stress. The triggers vary widely, and the body’s signaling systems are finely tuned to detect and respond to them.
• Hormonal Triggers: Hormones are classic drivers. For example, in endometrial hyperplasia, estrogen stimulates uterine lining growth during the proliferative phase of the menstrual cycle. If unopposed by progesterone (e.g., in anovulatory cycles), this can become excessive.
◦ Study: A 2006 paper by Shang in Nature Reviews Cancer (“Molecular origins of endometrioid endometrial cancer”) elaborates on how estrogen activates estrogen receptor-alpha (ERα), upregulating genes like IGF-1 (insulin-like growth factor-1), which promotes mitosis (DOI: 10.1038/nrc1746).
◦ Mechanism: ERα binds DNA at estrogen response elements, increasing transcription of proliferation genes—think of it as flipping an “on” switch for cell division.
• Mechanical or Injury-Related Triggers: Physical stress, like constant friction, triggers epidermal hyperplasia (e.g., callus formation). The skin senses pressure via mechanoreceptors, sparking keratinocyte division.
◦ Study: A 1998 study by Fuchs and Raghavan in Current Opinion in Genetics & Development (“Getting under the skin of epidermal morphogenesis”) shows how integrins (cell-matrix adhesion proteins) sense mechanical stress, activating the MAPK/ERK pathway to boost cell division (DOI: 10.1016/S0959-437X(98)80059-6).
• Compensatory Triggers: When part of an organ is lost or damaged, hyperplasia kicks in to regenerate it. The liver is a poster child for this—remove up to 70% of it, and hepatocytes divide to restore mass within weeks.
◦ Study: Michalopoulos and DeFrances, in a 2007 Science review (“Liver regeneration”), detail how partial hepatectomy triggers a cytokine storm (TNF-α, IL-6) and growth factors (HGF, EGF), priming quiescent hepatocytes to re-enter the cell cycle (DOI: 10.1126/science.1132614).
• Pathological Triggers: Chronic inflammation or irritation can overstimulate hyperplasia. In bronchial hyperplasia (e.g., from smoking), inflammatory cytokines like IL-1β drive epithelial cell division.
◦ Study: A 2010 study by Grivennikov et al. in Cell (“Immunity, inflammation, and cancer”) links chronic inflammation to hyperplasia via NF-κB signaling, which upregulates proliferation genes (DOI: 10.1016/j.cell.2010.01.025).
2. Cell Proliferation: The Engine Room
Once triggered, cells shift from a resting state (G0) into the cell cycle. This is where the magic happens—DNA gets copied, and cells split. It’s a tightly choreographed dance involving signaling pathways, gene expression, and checkpoints.
• Signaling Pathways:
◦ Growth factors (e.g., HGF, EGF) bind receptors, activating cascades like MAPK/ERK or PI3K/AKT. These pathways converge on the nucleus, turning on genes like cyclin D.
◦ Study: A 2004 paper by Blume-Jensen and Hunter in Nature (“Oncogenic kinase signalling”) maps how receptor tyrosine kinases (RTKs) amplify proliferation signals in hyperplasia and cancer (DOI: 10.1038/nature02585).
◦ Example: In muscle injury-induced hyperplasia, IGF-1 activates PI3K/AKT, boosting satellite cell division (Adams, 2002, Journal of Applied Physiology, DOI: 10.1152/japplphysiol.00832.2001).
• Cell Cycle Machinery:
◦ Cyclin D pairs with CDKs (e.g., CDK4/6) to push cells past the G1 checkpoint into S-phase, where DNA replication occurs. Later, cyclin B and CDK1 drive mitosis.
◦ Study: Sherr and Roberts, in a 2004 Genes & Development review (“CDK inhibitors: positive and negative regulators of G1-phase progression”), explain how mitogens (e.g., growth factors) override inhibitors like p27 to sustain hyperplasia (DOI: 10.1101/gad.1226404).
◦ Checkpoints ensure fidelity—e.g., p53 halts the cycle if DNA damage is detected, preventing hyperplasia from becoming neoplasia.
• Genetic Regulation:
◦ Proto-oncogenes (e.g., c-Myc, c-Jun) amplify proliferation, while tumor suppressors (e.g., Rb, p53) apply the brakes. In hyperplasia, this balance keeps growth functional, not chaotic.
◦ Study: A 1999 paper by Evan and Vousden in Nature (“Proliferation, cell cycle and apoptosis in cancer”) highlights how c-Myc overexpression drives hyperplasia but requires apoptotic safeguards to avoid malignancy (DOI: 10.1038/20972).
3. Tissue Expansion: Building the Outcome
As cells multiply, the tissue grows. The new cells integrate into the existing structure, maintaining function (unlike cancer, where architecture goes haywire). The extent and pattern depend on the tissue’s biology.
• Examples:
◦ Endometrium: Estrogen-driven hyperplasia thickens the lining with more glandular cells, preparing for potential pregnancy (Cheung, 2001).
◦ Liver: Hepatocytes proliferate in a zonal pattern post-injury, restoring mass and function (Michalopoulos, 2007).
◦ Prostate (BPH): Androgens (DHT) stimulate stromal and epithelial hyperplasia, enlarging the gland and compressing the urethra (Roehrborn, 2011).
◦ Skin: Keratinocyte hyperplasia from friction adds layers to the epidermis, forming a protective callus (Fuchs, 1998).
• Regulation: Feedback loops often halt hyperplasia once the stimulus fades—e.g., progesterone curbs endometrial growth mid-cycle, or liver regeneration stops when mass is restored.
◦ Study: A 2013 review by Campisi in Annual Review of Physiology (“Aging, cellular senescence, and cancer”) notes how senescence (cells stopping division) limits hyperplasia in aging tissues, preventing overgrowth (DOI: 10.1146/annurev-physiol-030212-183653).
Nuances and Variations
• Physiological vs. Pathological: Physiological hyperplasia (e.g., pregnancy-induced breast growth) is temporary and adaptive. Pathological hyperplasia (e.g., BPH) persists and disrupts function.
◦ Study: Zwick et al. (1999) show prolactin and estrogen synergize in mammary hyperplasia, a reversible process post-lactation.
• Hyperplasia vs. Hypertrophy: Hyperplasia adds cells; hypertrophy enlarges them. Muscle growth often blends both, though human muscle hyperplasia is controversial (Adams, 2002).
• Risk of Malignancy: Prolonged hyperplasia (e.g., endometrial) can precede cancer if mutations accumulate, shifting from regulated to uncontrolled growth (Shang, 2006).
Conclusion
Hyperplasia is a dynamic, stimulus-driven process where cells divide to expand tissue, guided by intricate signaling, cell cycle machinery, and genetic controls. Studies from hormonal (Cheung, Shang), regenerative (Michalopoulos, Taub), and pathological (Roehrborn) contexts paint a clear picture: it’s adaptive, regulated, and context-specific. Want me to zoom in on a particular type or mechanism further?
-
1. Trigger or Stimulus: What Sets It Off?
Hyperplasia doesn’t just happen randomly; it’s a response to a specific need or stress. The triggers vary widely, and the body’s signaling systems are finely tuned to detect and respond to them.
• Hormonal Triggers: Hormones are classic drivers. For example, in endometrial hyperplasia, estrogen stimulates uterine lining growth during the proliferative phase of the menstrual cycle. If unopposed by progesterone (e.g., in anovulatory cycles), this can become excessive.
◦ Study: A 2006 paper by Shang in Nature Reviews Cancer (“Molecular origins of endometrioid endometrial cancer”) elaborates on how estrogen activates estrogen receptor-alpha (ERα), upregulating genes like IGF-1 (insulin-like growth factor-1), which promotes mitosis (DOI: 10.1038/nrc1746).
◦ Mechanism: ERα binds DNA at estrogen response elements, increasing transcription of proliferation genes—think of it as flipping an “on” switch for cell division.
• Mechanical or Injury-Related Triggers: Physical stress, like constant friction, triggers epidermal hyperplasia (e.g., callus formation). The skin senses pressure via mechanoreceptors, sparking keratinocyte division.
◦ Study: A 1998 study by Fuchs and Raghavan in Current Opinion in Genetics & Development (“Getting under the skin of epidermal morphogenesis”) shows how integrins (cell-matrix adhesion proteins) sense mechanical stress, activating the MAPK/ERK pathway to boost cell division (DOI: 10.1016/S0959-437X(98)80059-6).
• Compensatory Triggers: When part of an organ is lost or damaged, hyperplasia kicks in to regenerate it. The liver is a poster child for this—remove up to 70% of it, and hepatocytes divide to restore mass within weeks.
◦ Study: Michalopoulos and DeFrances, in a 2007 Science review (“Liver regeneration”), detail how partial hepatectomy triggers a cytokine storm (TNF-α, IL-6) and growth factors (HGF, EGF), priming quiescent hepatocytes to re-enter the cell cycle (DOI: 10.1126/science.1132614).
• Pathological Triggers: Chronic inflammation or irritation can overstimulate hyperplasia. In bronchial hyperplasia (e.g., from smoking), inflammatory cytokines like IL-1β drive epithelial cell division.
◦ Study: A 2010 study by Grivennikov et al. in Cell (“Immunity, inflammation, and cancer”) links chronic inflammation to hyperplasia via NF-κB signaling, which upregulates proliferation genes (DOI: 10.1016/j.cell.2010.01.025).
2. Cell Proliferation: The Engine Room
Once triggered, cells shift from a resting state (G0) into the cell cycle. This is where the magic happens—DNA gets copied, and cells split. It’s a tightly choreographed dance involving signaling pathways, gene expression, and checkpoints.
• Signaling Pathways:
◦ Growth factors (e.g., HGF, EGF) bind receptors, activating cascades like MAPK/ERK or PI3K/AKT. These pathways converge on the nucleus, turning on genes like cyclin D.
◦ Study: A 2004 paper by Blume-Jensen and Hunter in Nature (“Oncogenic kinase signalling”) maps how receptor tyrosine kinases (RTKs) amplify proliferation signals in hyperplasia and cancer (DOI: 10.1038/nature02585).
◦ Example: In muscle injury-induced hyperplasia, IGF-1 activates PI3K/AKT, boosting satellite cell division (Adams, 2002, Journal of Applied Physiology, DOI: 10.1152/japplphysiol.00832.2001).
• Cell Cycle Machinery:
◦ Cyclin D pairs with CDKs (e.g., CDK4/6) to push cells past the G1 checkpoint into S-phase, where DNA replication occurs. Later, cyclin B and CDK1 drive mitosis.
◦ Study: Sherr and Roberts, in a 2004 Genes & Development review (“CDK inhibitors: positive and negative regulators of G1-phase progression”), explain how mitogens (e.g., growth factors) override inhibitors like p27 to sustain hyperplasia (DOI: 10.1101/gad.1226404).
◦ Checkpoints ensure fidelity—e.g., p53 halts the cycle if DNA damage is detected, preventing hyperplasia from becoming neoplasia.
• Genetic Regulation:
◦ Proto-oncogenes (e.g., c-Myc, c-Jun) amplify proliferation, while tumor suppressors (e.g., Rb, p53) apply the brakes. In hyperplasia, this balance keeps growth functional, not chaotic.
◦ Study: A 1999 paper by Evan and Vousden in Nature (“Proliferation, cell cycle and apoptosis in cancer”) highlights how c-Myc overexpression drives hyperplasia but requires apoptotic safeguards to avoid malignancy (DOI: 10.1038/20972).
3. Tissue Expansion: Building the Outcome
As cells multiply, the tissue grows. The new cells integrate into the existing structure, maintaining function (unlike cancer, where architecture goes haywire). The extent and pattern depend on the tissue’s biology.
• Examples:
◦ Endometrium: Estrogen-driven hyperplasia thickens the lining with more glandular cells, preparing for potential pregnancy (Cheung, 2001).
◦ Liver: Hepatocytes proliferate in a zonal pattern post-injury, restoring mass and function (Michalopoulos, 2007).
◦ Prostate (BPH): Androgens (DHT) stimulate stromal and epithelial hyperplasia, enlarging the gland and compressing the urethra (Roehrborn, 2011).
◦ Skin: Keratinocyte hyperplasia from friction adds layers to the epidermis, forming a protective callus (Fuchs, 1998).
• Regulation: Feedback loops often halt hyperplasia once the stimulus fades—e.g., progesterone curbs endometrial growth mid-cycle, or liver regeneration stops when mass is restored.
◦ Study: A 2013 review by Campisi in Annual Review of Physiology (“Aging, cellular senescence, and cancer”) notes how senescence (cells stopping division) limits hyperplasia in aging tissues, preventing overgrowth (DOI: 10.1146/annurev-physiol-030212-183653).
Nuances and Variations
• Physiological vs. Pathological: Physiological hyperplasia (e.g., pregnancy-induced breast growth) is temporary and adaptive. Pathological hyperplasia (e.g., BPH) persists and disrupts function.
◦ Study: Zwick et al. (1999) show prolactin and estrogen synergize in mammary hyperplasia, a reversible process post-lactation.
• Hyperplasia vs. Hypertrophy: Hyperplasia adds cells; hypertrophy enlarges them. Muscle growth often blends both, though human muscle hyperplasia is controversial (Adams, 2002).
• Risk of Malignancy: Prolonged hyperplasia (e.g., endometrial) can precede cancer if mutations accumulate, shifting from regulated to uncontrolled growth (Shang, 2006).
Conclusion
Hyperplasia is a dynamic, stimulus-driven process where cells divide to expand tissue, guided by intricate signaling, cell cycle machinery, and genetic controls. Studies from hormonal (Cheung, Shang), regenerative (Michalopoulos, Taub), and pathological (Roehrborn) contexts paint a clear picture: it’s adaptive, regulated, and context-specific. Want me to zoom in on a particular type or mechanism further?
Great, lets hope you dont get that type of hyperplasia, its cancer FFS
Now try and find one that specifies muscle growth and not just cell generation
-
(https://www.getbig.com/boards/index.php?action=dlattach;topic=698987.0;attach=1559811;image)
(https://www.etonline.com/sites/default/files/styles/640xh/public/images/2016-05/embed_joseph_baena_FFN_JDFF_051616_52059475.jpg?width=1024&quality=80)
Looks like a twink without the drugs... hankinsesque...
-
Gh, igf1 create more muscle fibers
-
Gh, igf1 create more muscle fibers
Great, so show me the evidence...
As discussed previously, biopsy data in humans do not provide evidence that GH increases the number of oxidative type I muscle fibres. However, studies uniformly show that the increase in muscle mass is associated with an increase in oxygen consumption during GH replacement (Whitehead et al.
https://jme.bioscientifica.com/view/journals/jme/52/1/R107.xml#:~:text=As%20discussed%20previously%2C%20biopsy%20data,GH%20replacement%20(Whitehead%20et%20al.