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Llwellyn's protocol is supported by evidence of β₂-adrenergic downregulation. Later evidence (Abo et al.) supports a view that 3 weeks of clen treatment is marked by an increased myostatin gene expression, suggesting myostatin functions as a negative regulator of hypertrophy in the latter stages of clen treatment. Follistatin is upregulated in the near term and is associated with the hypertrophy response in humans (Hostrup et al.) with β₂-adrenergic agonists.
Treatment with rhGH does make sense as β₂-adrenergic agonism inhibits GH secretion. Considerations for yohimbine: α₂-adrenergic antagonists can completely block the stimulatory effects on GH secretion of enhancing cholinergic tone with cholinesterase inhibitors versus the α₂-adrenergic agonist clonidine which stimulates GH secretion.
Treatment with rhGH does make sense as β₂-adrenergic agonism inhibits GH secretion. Considerations for yohimbine: α₂-adrenergic antagonists can completely block the stimulatory effects on GH secretion of enhancing cholinergic tone with cholinesterase inhibitors versus the α₂-adrenergic agonist clonidine which stimulates GH secretion.