From adrenaline to a fat cell signal
Intense exercise prompts the adrenal medulla to release catecholamines, chiefly adrenaline (epinephrine), into the bloodstream. When adrenaline reaches a fat cell and binds beta-adrenergic receptors, it activates a G-protein that stimulates adenylyl cyclase, raising the level of the second messenger cyclic AMP (cAMP) inside the cell.
Rising cAMP activates protein kinase A (PKA), which is the relay that translates the external hormone signal into action on the cell's stored fat.
How stored triglyceride is broken down
PKA phosphorylates and activates the lipolytic machinery, including hormone-sensitive lipase (HSL), and helps mobilize adipose triglyceride lipase (ATGL). Working in sequence, these enzymes cleave stored triglycerides into free fatty acids and glycerol, which can then leave the cell and be used as fuel elsewhere.
Whether those released fatty acids are actually burned, rather than re-stored, depends on overall energy demand and balance across the body. The cascade describes mobilization, not guaranteed fat loss. This is general educational information about physiology, not medical advice.