Among modern neuroimaging techniques, functional magnetic resonance imaging (fMRI) is unique in that it can measure brain activity at a high spatial resolution and investigate a broad range of brain activities. Additionally, the Blood Oxygen Level Dependent (BOLD) signals strongly correlate with local field potentials (LFPs) and represent the activity of neurons, as evidenced by concurrent electrophysiology and fMRI studies. However, it is important to understand that fMRI does not directly measure neuronal activity or oxygen metabolism. Instead, it focuses on hemodynamic changes triggered by alterations in neural activity, that appear as variations in the BOLD signal. A pivotal element of the BOLD response involves a sudden increase in cerebral blood flow exceeding that required for oxidative metabolism. In essence, the BOLD signal results from a hemodynamic response shaped by a complex interplay among neurovascular coupling processes. This intricate cascade involves changes in oxygen metabolism, cerebral blood flow (CBF), and cerebral blood volume (CBV). The neurovascular unit encompasses four principal components: neurons, endothelial cells, pericytes, and astrocytes. This tightly regulated system establishes neurovascular coupling, entailing alterations in blood flow and nutrient delivery due to neuronal activity. Cerebral blood flow denotes the volume of blood flowing through arteries, arterioles, and capillaries within a specific tissue volume over time. Cerebral blood volume, on the other hand, refers to the amount of blood present in cerebral vessels at a given moment. Although separate, cerebral blood flow and cerebral blood volume are interconnected within the vasculature that governs blood flow. The cerebral metabolic rate of oxygen (CMRO2 ) signifies the quantity of oxygen utilized by the brain for its metabolic functions and reflects oxygen metabolism. Researchers typically employ indirect techniques, such as BOLD-fMRI, due to their high spatial resolution and noninvasive, non-ionizing nature, to estimate oxygen metabolism and thus neuronal activity. However, alterations in oxygen metabolism might not consistently lead to equivalent changes in CBF from the baseline level. Agreement in the literature regarding the extent of this partial mismatch has yet to be reached. Elevated baseline CBF can reduce the anticipated BOLD change resulting from increased neuronal metabolism due to saturated hemodynamics. Consequently, in the absence of additional data, fMRI signals offer qualitative rather than quantitative insights into neuronal metabolism. Under such circumstances, manipulating breathing conditions that influence CBF emerges as a valuable strategy to procure supplementary data, particularly in calibrated BOLD-fMRI studies.