It is generally assumed that because insulin is an anabolic hormone, more insulin means equals muscle mass. If we look at the research we will find that insulin effects have been misunderstood (or overstated).
Insulin and skeletal muscle anabolism
Insulin has a role in muscle hypertrophy because it stimulates muscle protein synthesis (MPS) and inhibits muscle protein breakdown (MPB). But insulin’s effect on MPS is dependent on blood amino acid availability and it is achieved at minimal concentrations. For instance, ingestion of 100g of carbohydrates after resistance exercise has failed to show a positive net protein balance compared to placebo and the changes were minor compared to ingestion of amino acids. Accordingly, postprandial stimulation of MPS is independent of changes in insulin.
With an adequate supply of amino acids, insulin’s maximal effects on MPS and MPB are achieved at 30mU/L. Further stimulation doesn’t increase MPS nor decrease MPB to a greater extent. When an ample amount of protein is ingested, the addition of carbohydrates in the post exercise environment doesn’t further increase MPS. After 60 min of resistance exercise, with the ingestion of only 0.3g/kg/h of protein insulin levels averaged 16.5 uU/mL during the 6 hour recovery period. This seems to support the findings by Rennie et al., who showed that increasing levels of insulin above 10-15uU/mL does not further enhance MPS nor reduce MPB.
A positive net protein balance is achieved by an adequate extracellular concentration of amino acids, a minimal amount of insulin and an energy surplus (approximately 0.7kcal/g of protein synthesized or 240kcal/day for an average person).
Insulin as a lipogenic hormone
Insulin is probably the most lipogenic hormone, so every diet must focus on insulin control. Some people argue that fat intake, independent of changes of insulin can inhibit HSL and lipolysis, so insulin’s role on body fat accretion isn’t that important. Nevertheless, this is just one part of the story. Insulin, besides strongly inhibiting HSL, also increases glucose uptake and glycolisis in adypocites, FFA uptake by LPL, has long-term effects on the expression of lipogenic genes and possibly stimulates de novo fatty acid synthesis.
Fat loss/accretion is determined by the net balance between lipolysis and reesterification. During fasting, NEFA transcapillary flux (NEFAtf) across adypocites is strongly negative (outward flow) and becomes close to zero at 180-240min after the ingestion of 40g of fat before becoming strongly negative again. Following a mixed meal (carbohydrates, fat and protein), NEFAtf becomes positive after 60min and stays strongly positive until at least 300min. So, in abscence of insulin, fat can inhibit HSL but to a shorter and lesser degree than with insulin, and there is lack of reesterification. Besides, insulin’s action on NEFA reesterification seems to be dose-dependent and it’s not only related to glucose uptake, but to stimulation of ASP.
Insulin stimulation by different foods
This is probably one of the most controversial topics regarding insulin. Some studies have shown that certain protein-rich foods can stimulate insulin release equally or further than some carbohydrates. In this regard, leucine seems to have a powerful dose-dependent insulinogenic potential. There is also evidence that although reducing postprandial glycemia, the addition of fat to a carbohydrate meal increases postprandial insulin levels and doesn’t affect the insulin response to a protein only meal.
Before low carb advocates start to slit their wrists, these results have to be taken with caution. Most studies show the results after only one meal and in healthy people who follow a “normal” diet (that being rich in carbohydrates). Replacement of carbohydrate with protein reduces the postprandial insulin response, as seen during a low carb ketogenic diet (LCKD). Moreover, LCKD have shown to reduce fasting insulin levels, which follow a linear correlation with insulin release after a glucose load and probably after an insulinogenic stimuli. On the other hand, the glycemic load of a diet has a direct correlation with insulinemia.
We need insulin for a proper physiological function, but the amount needed isn’t that great. Trying to achieve more muscle mass by increasing carbohydrates and plasma insulin levels could not only be detrimental for body composition but also for longevity and health.