This is completely false, look up the concept of competitive inhibitors. A higher affinity compound (or the natural one that is a "perfect fit") being present does not somehow prevent the lower affinity one from binding at all. If this was true almost no drugs at all in existence would work, only giving people the natural substances (like testosterone) would work... any relative difference in affinities, even massive ones, can be overcome through one substance outcompeting another.
I've got a degree in molecular cell biology, basics of competitive inhibition is a first year subject. Let me try explain to you where your misunderstanding here.
A drug works to competitively inhibit via binding the active binding site on a given receptor, this prevents the normal hormone substrate from binding it's active site, simple enough. What I think you are trying to argue is that in drug use etc when the concentration of the drug (inhibitor) is greater than that of the normal substrate it will bind at a greater rate therefore achieving greater levels of inhibition.
What you miss here is that chemical inhibitors (your average drug) are very small chemical molecules much much smaller than a protein, with a very basic one dimensional structure, that align electrochemically to only to a small specific area of the protein receptor at the active site, thus they can have a great affinity to that site and outcompete the much larger more complex natural protein hormone.
In the case we are speaking of here we are talking about much larger more complex molecules, proteins (insulin and igf proteins) Protein structure is much more complex with four stages of structure (you have probably covered tertiary quaternary etc) this means that these molecules affinity for each other's receptors active sites is much more regulated by their structures, much more than a tiny chemical (typical drug) that can bind freely to a receptor active site and easily outcompete the natural hormone due to its simplicity in structure, an advantage that the less than optimised insulin does not have over igf proteins when binding the igf receptors.
So as I said the structural optimisation of the igf hormone for its receptor in addition to its very high concentrations in pro bodybuilders will likely negate the great majority off target binding of insulin to igf receptors, there will still be some binding but the degree to which this occurs will likely be drastically reduced for these reasons.
