Hormonal
Individual variability in hypertrophic response to resistance exercise is largely determined by endogenous variables such as basal satellite cell content, androgen receptor content, and gene expression profiles, rather than just exogenous training variables.
Accept that your genetic makeup (basal satellite cell count, androgen receptors) influences how much muscle you can build. While you cannot change your genetics, you can maximize your potential by optimizing the primary drivers: consistent resistance training and adequate protein intake. Do not blame your program for genetic ceilings.
individuals exhibiting greater hypertrophy in response to RET appear to have greater androgen receptor content at rest... enhanced satellite cell (SC) proliferation in response to loading differentiates higher from lower hypertrophic 'responders' to RET
Why this rating
Based on correlational studies and specific laboratory findings cited, though causality in humans is harder to prove than in rodents.
Source
Recent advances in understanding resistance exercise training-induced skeletal muscle hypertrophy in humans
Sophie Joanisse et al. · F1000Research · 2020
DOI 10.12688/f1000research.21588.1
More from this paper
- Resistance exercise training combined with sufficient dietary protein intake acts synergistically to maximize skeletal muscle hypertrophy, with protein intake saturating around 1.6 g/kg/day for general populations and potentially requiring 2.0-2.2 g/kg/day for resistance-trained individuals.Strong
- Muscle hypertrophy is driven by recurrent periods of positive net protein balance (NPB) resulting from resistance exercise coupled with protein feeding, rather than solely by transient increases in muscle protein synthesis (MPS) rates in the fasted state.Strong
Related findings · Hormonal
- Initial treatment for type 2 diabetes should be a combination of metformin and either an SGLT-2 inhibitor or a GLP-1 receptor agonist to achieve cardiorenal protection, rather than monotherapy or older agents like sulfonylureas.Strong
- For patients with specific monogenic obesity syndromes (leptin deficiency, POMC/PCSK1/LEPR mutations), targeted pharmacotherapy (recombinant leptin or setmelanotide) is highly effective and should be prioritized, unlike in polygenic obesity.Strong
- Continued weekly administration of 2.4 mg subcutaneous semaglutide prevents weight regain and promotes further weight loss in adults with overweight or obesity, whereas switching to placebo results in significant weight regain.Strong
This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →