Post Surgery Support - Need Advice.

Cashgarden

Bluelighter
Joined
Aug 11, 2013
Messages
62
So I tore my rotator cuff and surgery is the only option. After surgery which is coming up soon, what do you recommend to speed up recovery? I've been told recovery will take about a year from my doctor. I've hear longer from friends.

I've been completely off of AAS since the tear occurred about 2 months ago and was originally thinking of staying clean until I was fully recovered - for health reasons. Now I'm thinking I want to speed up my recovery.

I was thinking a low dose of Test and Deca. Also what about some peptides? Anyone here with some experience with this? Peptide research advice has been like a-holes. everyone has one and not necessarily the same. HGH is off the table due to cost - or is it? Anyway, I really appreciate the advice given here. Thanks in advance.
 
We've had a few posts up about injury healing recently. As mentioned in those threads, don't use AAS, they won't improve healing - they don't accelerate the growth of the type of collagen that you want, and make MTUs (muscle-tendon units) brittle and liable to tearing. Similarly with hGH - the continuous elevation of IGF-1 is not what you want. The only peptides I'd recommend would be GHRPs, 3-4 times daily.

Then you'll also want deep tissue massage work and stretching to help break up the little calcified adhesions and scarring tissue that forms around the tear and surgery.

And when you can train again, you'll want to focus exclusively on eccentric training in the area for the first 1-2 months, as this will strengthen the MTU much more effectively than peptides. Most of the other peptides currently being guinea-pig tested by guys (BPC, thymosin beta etc) have had mixed or negligible results.
 
Thanks CFC. I have been searching this site and the rest of the web for that matter but I've seen conflicting advice. Guess the hard way is the best way.
 
We've had a few posts up about injury healing recently. As mentioned in those threads, don't use AAS, they won't improve healing - they don't accelerate the growth of the type of collagen that you want, and make MTUs (muscle-tendon units) brittle and liable to tearing. Similarly with hGH - the continuous elevation of IGF-1 is not what you want. The only peptides I'd recommend would be GHRPs, 3-4 times daily.

Then you'll also want deep tissue massage work and stretching to help break up the little calcified adhesions and scarring tissue that forms around the tear and surgery.

And when you can train again, you'll want to focus exclusively on eccentric training in the area for the first 1-2 months, as this will strengthen the MTU much more effectively than peptides. Most of the other peptides currently being guinea-pig tested by guys (BPC, thymosin beta etc) have had mixed or negligible results.

To my understanding, the only problem with GH bleed was the risk of acromegaly. Are you suggesting it would also be counterproductive to healing?

Also, I've heard very good things about thymosin beta. BPC 157 I haven't heard much either way.
 
Here is an interesting study about cardio-regenerative activity associated with thymosin beta 4, also called TB-500.

Source- https://www.ncbi.nlm.nih.gov/pubmed/21654746

De novo cardiomyocytes from within the activated adult heart after injury.

Abstract

A significant bottleneck in cardiovascular regenerative medicine is the identification of a viable source of stem/progenitor cells that could contribute new muscle after ischaemic heart disease and acute myocardial infarction. A therapeutic ideal--relative to cell transplantation--would be to stimulate a resident source, thus avoiding the caveats of limited graft survival, restricted homing to the site of injury and host immune rejection. Here we demonstrate in mice that the adult heart contains a resident stem or progenitor cell population, which has the potential to contribute bona fide terminally differentiated cardiomyocytes after myocardial infarction. We reveal a novel genetic label of the activated adult progenitors via re-expression of a key embryonic epicardial gene, Wilm's tumour 1 (Wt1), through priming by thymosin β4, a peptide previously shown to restore vascular potential to adult epicardium-derived progenitor cells with injury. Cumulative evidence indicates an epicardial origin of the progenitor population, and embryonic reprogramming results in the mobilization of this population and concomitant differentiation to give rise to de novo cardiomyocytes. Cell transplantation confirmed a progenitor source and chromosome painting of labelled donor cells revealed transdifferentiation to a myocyte fate in the absence of cell fusion. Derived cardiomyocytes are shown here to structurally and functionally integrate with resident muscle; as such, stimulation of this adult progenitor pool represents a significant step towards resident-cell-based therapy in human ischaemic heart disease.
 
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To my understanding, the only problem with GH bleed was the risk of acromegaly. Are you suggesting it would also be counterproductive to healing?

There's quite a few problems with specifically synthetic hGH administration, from insulin resistance to organ overgrowth.

But with regards to injuries, there's not a true consensus yet. Actually there's surprisingly little research on humans given how potentially useful it might be expected to be.

However one picture that's begun to emerge is that continuously elevated GH appears to make tendons grow quickly and thick (thanks to more rapid collagen synthesis) but potentially more brittle, suggesting it detrimentally alters the matrix structure, possibly by reducing individual collagen fibril diameter.

There's also another strand of investigation that suggest GH doesn't increase collagen synthesis rates at all, however I'm generally more sceptical of those studies.

On balance, I'd rather use GHRPs to elevate GH frequently but without the continuous bleed effect.
 
There's also another strand of investigation that suggest GH doesn't increase collagen synthesis rates at all, however I'm generally more sceptical of those studies.

On balance, I'd rather use GHRPs to elevate GH frequently but without the continuous bleed effect.

I'd like to see the study describing GH's lack of collagen synthesis because it is notoriously labeled "facelift in a bottle" I agree with you on that one.

What dictates an elevated level per say? What if an individual was GH deficient due to an injury and the taxing nature of recovery from a disposition and one simply resumed the serum levels to natural concentrations via exogenous administration?
 
Here is an interesting study about cardio-regenerative activity associated with thymosin beta 4, also called TB-500.

Source- https://www.ncbi.nlm.nih.gov/pubmed/21654746

[h=1]De novo cardiomyocytes from within the activated adult heart after injury.[/h][h=3]Abstract[/h]A significant bottleneck in cardiovascular regenerative medicine is the identification of a viable source of stem/progenitor cells that could contribute new muscle after ischaemic heart disease and acute myocardial infarction. A therapeutic ideal--relative to cell transplantation--would be to stimulate a resident source, thus avoiding the caveats of limited graft survival, restricted homing to the site of injury and host immune rejection. Here we demonstrate in mice that the adult heart contains a resident stem or progenitor cell population, which has the potential to contribute bona fide terminally differentiated cardiomyocytes after myocardial infarction. We reveal a novel genetic label of the activated adult progenitors via re-expression of a key embryonic epicardial gene, Wilm's tumour 1 (Wt1), through priming by thymosin β4, a peptide previously shown to restore vascular potential to adult epicardium-derived progenitor cells with injury. Cumulative evidence indicates an epicardial origin of the progenitor population, and embryonic reprogramming results in the mobilization of this population and concomitant differentiation to give rise to de novo cardiomyocytes. Cell transplantation confirmed a progenitor source and chromosome painting of labelled donor cells revealed transdifferentiation to a myocyte fate in the absence of cell fusion. Derived cardiomyocytes are shown here to structurally and functionally integrate with resident muscle; as such, stimulation of this adult progenitor pool represents a significant step towards resident-cell-based therapy in human ischaemic heart disease.

There's quite a lot of promising research out there on it, and I'm still hopeful.

Maybe it's just the source of the stuff I've used on clients before, but it didn't seem to do anything special. I've also seen a lot of mixed reviews online, with a bit of hyperbole thrown in here and there.

I guess if you have money to burn it's worth a shot.
 
I'd like to see the study describing GH's lack of collagen synthesis because it is notoriously labeled "facelift in a bottle" I agree with you on that one.

What dictates an elevated level per say? What if an individual was GH deficient due to an injury and the taxing nature of recovery from a disposition and one simply resumed the serum levels to natural concentrations via exogenous administration?

Here's a few papers on the subject for you to peruse Grym.

When I say elevated, what I really mean is temporally - so over a non-physiological timespan.

It's believed that local IGF-1 is the main 'beneficial' upregulator of tendon collagen synthesis, but that exogenous continually elevated levels appear to interfere with correct physiological synthesis and produce smaller, weaker fibrils.


Int J Sports Med. 2012 Mar;33(3):240-3
Growth hormone does not stimulate early healing in rat tendons.
Andersson T1, Eliasson P, Aspenberg P.

http://www.ncbi.nlm.nih.gov/pubmed/22318558


J Bone Joint Surg Am. 2013 May 1;95(9):783-9.
Human growth hormone may be detrimental when used to accelerate recovery from acute tendon-bone interface injuries.
Baumgarten KM1, Oliver HA, Foley J, Chen DG, Autenried P, Duan S, Heiser P.

http://www.ncbi.nlm.nih.gov/pubmed/23636184


Muscles Ligaments Tendons J. 2014 Jul-Sep; 4(3): 329–332.
Cushing, acromegaly, GH deficiency and tendons
Mariano Galdiero,1 Renata S. Auriemma,2 Rosario Pivonello,1 and Annamaria Colao1

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4241424/#b45-329-332


GH and IGF1 levels are positively associated with musculotendinous collagen expression: experiments in acromegalic and GH deficiency patients
Simon Doessing, Lars Holm, Katja M Heinemeier, Ulla Feldt-Rasmussen1, Peter Schjerling, Klaus Qvortrup2, Jytte O Larsen3, Rie H Nielsen, Allan Flyvbjerg4 and Michael Kjaer

http://eje-online.org/content/163/6/853.long


J Physiol. 2010 Jan 15; 58 Pt 2): 341–351.
Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis
Simon Doessing,1 Katja M Heinemeier,1 Lars Holm,1 Abigail L Mackey,1 Peter Schjerling,1 Michael Rennie,3 Kenneth Smith,3 Søren Reitelseder,1 Anne-Marie Kappelgaard,4 Michael Højby Rasmussen,4 Allan Flyvbjerg,5 and Michael Kjaer1

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821728/
 
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