GLOSSARY

Hyperglycemia is glucose above the reference appropriate to timing and state.

Blood glucose reflects food entry, endogenous production and tissue removal under coordinated insulin, glucagon and other neural and hormonal signals. A transient meal response is not the same as persistent impaired glucose tolerance; sampling method and timing matter. Measuring glucose is not directly measuring all energy available to muscle. Glycogen, exercise intensity and other fuels also enter sports interpretation, so one curve cannot by itself rate every meal or establish a diagnosis.

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.

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.