Given that nicotinamide crosses cell membranes via diffusion, these results suggest enhanced biosynthesis of NAD⁺ via incorporation of nicotinamide in response to acute exercise in PBMCs. (10/13)

Interestingly, acute exercise led to a profound increase in gene expression and protein abundance of NAMPT, the core enzyme of NAD⁺ salvage pathway. On a protein level similar effects were visible for NMNAT1, a further NAD⁺ salvage pathway enzyme. (8/13)

In two complementary trials we investigated the impact of acute exercises on gene expression and protein abundance of key NAD⁺ metabolism enzymes as well as NAD⁺ precursors and intracellular NAD⁺ coenzymes. (6/13)

NAD⁺ metabolism is integral to cell metabolism and function. Several studies have suggested that different diseases and ageing are associated with a cellular decline in NAD⁺. Thus, NAD⁺-boosting strategies have become a promising therapeutic avenue. (2/13)

In contrast, far fewer investigations have identified molecular targets of these exerkines such as exerkine receptors. (10/13)

Additionally, we highlight various trials applying monoclonal antibodies as exerkine receptor blockers to investigate exerkine receptor signalling and tissue adaption in humans. (7/13)

Besides a summary of exerkine receptors as molecular targets of exerkines, we also describe the downstream signal transduction and biological tissue adaptions triggered by exerkine receptor signalling. (6/13)

Additionally, exerkines can induce cellular adaption in a direct manner, or in an indirect manner, e.g., via stimulation of immune cells. (4/13)

Exercise is marked by a profound mobilization of biomolecules termed "exerkines", including proteins, metabolites, lipids, and nucleic acids. To unravel cause and consequence of exercise-mediated health effects, we separated "exerkine kinetics" from "exerkine dynamics". (2/13)