Acarbose can be used as a longevity molecule blunt postprandial glucose levels and also seems to confer some longevity benefits by remodeling gut microbiota. It works by slowing down the digestion of carbohydrates in the small intestine, thereby reducing the amount of glucose that enters the bloodstream.
Here is an article we wrote to describe the exact mechanisms of acarbose:
In terms of its effects on muscle mass and strength, it is important to note that acarbose works through a mechanism that is independent of mTOR inhibition. This means that acarbose does not reduce protein synthesis, which is necessary for muscle growth and maintenance. Therefore, it is unlikely that acarbose would have a negative impact on muscle mass or strength.
It is important to differentiate acarbose from metformin in this regard, another commonly used drug for managing blood sugar levels. Metformin works by activating AMPK, which is an enzyme that regulates cellular energy levels. There is evidence that it may also blunt the effects of exercise by reducing mitochondrial adaptations and limiting muscle adaptations.
Here is the study that produced these results:
This could be for a couple of reasons:
- Metformin is anti-inflammatory and reduces reactive oxygen species and oxidative stress (This is true of acarbose, although it is mediated through a different pathway).
In one context, this is a good thing. Reducing chronic inflammation does improve overall health systemically.
We also know though, that exercise is pro-inflammatory and increases oxidative stress transiently. These inflammatory molecules and transient oxidate stresses act as signals that drive muscle repair and growth after a bout of exercise. The thought is that metformin is blunting these signals and simultaneously blunting the adaptations.
Acarbose reduces inflammation and oxidative stress, but it’s mostly conferring those benefits by decreasing the spike in glucose levels by reducing carbohydrate breakdown.
Metformin works through mitochondrial inhibition. Specifically, metformin inhibits complex I of the electron transport chain, which is the first step in generating ATP, the main energy currency of cells. This inhibition leads to a decrease in the production of ATP, which in turn activates a signaling pathway that results in increased glucose uptake by cells and improved insulin sensitivity.
It is thought that metformin could also blunt the effects of exercise with respect to mitochondrial density adaptations to cardiovascular training.
Acarbose does not have the same drawback because it’s simply blocking the breakdown of carbohydrates.
Acarbose is unlikely to have a negative impact on muscle mass or strength, as it works independently of mTOR inhibition. It is also different than metformin in its potential effects on muscle health, as metformin may limit the beneficial effects of exercise on muscle adaptations.