GLOSSARY

Exercise-Induced Glucagon Response is glucagon response coordinating fuel availability during activity.

Glucagon is mainly secreted by alpha cells and supports glucose availability, prominently through the liver. Its response is not simply the inverse of insulin: amino acids and meal type matter, and both can rise after protein. Direct skeletal-muscle effects should not be assumed equivalent to hepatic effects. Their ratio is context-dependent rather than a food-quality score, and changes need secretion, clearance and tissue actions considered together.

Insulin is secreted by pancreatic beta cells and coordinates nutrient use and storage rather than simply being a fat-making hormone. Important effects include muscle and adipose glucose uptake, suppression of hepatic glucose production and regulation of lipolysis. Not every cell needs insulin for glucose entry. Postmeal concentrations vary with meal composition, tissue sensitivity and clearance, so one insulin excursion cannot determine overall dietary quality or an athlete's nutritional needs.

Endogenous glucose production includes glycogen breakdown and new synthesis rather than gluconeogenesis alone. Cellular production and release into blood differ because local use occurs. Contributions change with fasting and activity. Tracers and pool definitions matter; a stable blood glucose can coexist with high turnover. It does not mean fuel is unnecessary or glucose use has stopped, nor does one circulating concentration isolate hepatic versus renal contributions to supply.

For practical use, record meal and training timing, sleep and hunger alongside actual intake and performance trends. When a marker changes, first examine measurement conditions and plausible explanations; food decisions should support adequate supply, tolerance and recovery rather than ending the assessment at one molecular signal or assuming a concentration change automatically establishes a useful intervention.