["The Journal of Physiology, EarlyView. ", "\nAbstract figure legend This study examined a two‐component cascade model linking upstream dynamic cerebral autoregulation (dCA) with downstream microvascular function (MF) to explain how blood pressure oscillations influence cortical oxygenation. Transfer function analysis in the frequency domain was applied to quantify H1(f) (MAP→CBFV; dCA), H2(f) (CBFV→O2Hb; MF), and H0(f) (MAP→O2Hb; empirical total response). The proposed cascade model (Hc(f) = H1(f) x H2(f)) showed strong agreement with empirical transfer function in gain, phase and coherence across all frequency ranges at supine rest. Forced oscillations at 0.05 Hz induced by sit–stand manoeuvres further strengthened this agreement. These findings support the cascade model as a mechanistic framework linking arterial pressure fluctuations to cortical oxygenation and demonstrate its physiological relevance.\n\n\n\n\n\n\n\n\n\nAbstract\nCerebral blood flow is stabilized through dynamic adjustments across both macro‐ and microvascular compartments. While dynamic cerebral autoregulation (dCA) quantifies upstream pressure–flow coupling, downstream microvascular responses are less well characterized and may represent a distinct but functionally linked process. This study tested whether a two‐component cascade model, treating dCA and an empirically derived index of microvascular function (MF) as sequential stages can represent the integrated regulation of cortical oxygenation. Data from 41 healthy adults (20–45 years) were analysed. Beat‐to‐beat mean arterial pressure (MAP), middle cerebral artery flow velocity (CBFV) and cortical oxyhaemoglobin (O2Hb) were recorded during supine spontaneous oscillations and forced oscillations at 0.05 Hz using repeated sit–stand manoeuvres. Transfer function analysis quantified frequency‐domain gain, phase and coherence for MAP→CBFV (dCA), CBFV→O2Hb (MF) and MAP→O2Hb (total pathway). The cascade model was computed as the product of dCA and MF transfer functions. The cascade model derived indices showed strong correlations with total pathway gain, phase and coherence measures during both spontaneous and forced oscillations, with improved linear coupling under forced oscillations. These results support the applicability of a two‐component cascade model for integrated cerebrovascular regulation and suggest that serial interactions between macrovascular and microvascular regulatory mechanisms jointly shape the frequency‐dependent propagation of arterial pressure to brain‐tissue oxygenation dynamics.\n\n\n\n\n\n\n\n\n\nKey points\n\nCerebral blood flow is stabilized by coordinated regulation across large arteries and microvessels, but their dynamic interaction has not been experimentally modelled.\nWe examined whether a two‐component cascade model linking upstream dynamic cerebral autoregulation and downstream microvascular function can explain how blood pressure oscillations influence cortical oxygenation.\nIn 41 healthy adults, we recorded beat‐to‐beat blood pressure, middle cerebral artery blood flow velocity and near‐infrared spectroscopy‐derived oxygenation during rest and sit–stand manoeuvres, and analysed them using transfer function analysis.\nGains, phases and coherences derived from the cascade model closely matched those from the direct blood pressure–O2Hb relationship, particularly under forced oscillations during sit–stand, demonstrating the model's physiological relevance.\nThe cascade model provides a mechanistic framework to separate and quantify large‐ and small‐vessel contributions to cerebral blood flow regulation, with potential application in future studies of ageing and cerebrovascular disease.\n\n\n"]