GLOSSARY

Adipokine is an adipose-associated signal, not necessarily from adipocytes alone.

Adipose tissue contains several cell types, so adipokines are not restricted to adipocyte secretion. Molecules can associate with inflammation or insulin sensitivity without proving causation or treatment utility. Human and animal sources may differ. Adipokine ratios are not universal athletic targets; assays, units and energy state must be specified. A research pathway cannot alone justify a supplement or establish that changing one circulating protein will improve performance.

Muscle, liver, bone and adipose tissue produce signals alongside their other functions. Myokine, hepatokine and lipokine group molecules by source or nature, with unequal evidence across members. Blood detection does not prove a unique source. Cellular and animal findings about muscle or bone cannot be converted directly into human hormonal treatment or performance products; human outcomes and measurement methods must be established rather than assuming all organ-derived signals have proven athletic uses.

Leptin mainly conveys adipose information about energy stores and availability and also responds to intake changes. Its relation to fat mass is not perfectly fixed; reduced intake can affect it before major weight change. High leptin does not necessarily mean greater satiety, nor is low leptin always a separate disease. Leptin resistance is a regulatory concept not conclusively diagnosed from hunger or one concentration alone without clinical context.

Sensitivity is response to a given signal and is not identical to hormone concentration or receptor number. Receptor abundance, binding and downstream signaling can each alter response. Maximum responsiveness also differs from a shift in sensitivity. One blood value cannot describe all tissue receptors; assay type and target tissue are needed to interpret resistance or sensitivity rather than treating these as directly interchangeable concentration measurements.

Reduced or increased energy intake can change appetite, storage and expenditure signals; these responses are not simply matters of willpower. A short postmeal change differs from adaptations over weeks of weight change. An energy deficit need not immediately produce large weight loss, and surplus does not become exclusively muscle. In sport, the rate of change, training quality, energy availability and health matter more than pursuing a supposed fat-burning hormone.

Exercise mode, intensity, duration, recruited muscle, training history and prior food influence hormonal responses. Acute changes differ from baseline adaptations after training. Higher concentration does not necessarily mean greater secretion or tissue effect, because clearance, plasma volume and receptors also matter. Performance develops through combined adaptations, so targeting a hormone peak is not sufficient for session design or supplement selection; actual recovery and performance must remain part of evaluation.