Regulation of cerebral blood flow and metabolism during exercise

Abstract

What is the topic of this review? The manuscript collectively combines the experimental observations from >100 publications focusing on the regulation of cerebral blood flow and metabolism during exercise from 1945 to the present day. What advances does it highlight? This article highlights the importance of traditional and historical assessments of cerebral blood flow and metabolism during exercise, as well as traditional and new insights into the complex factors involved in the integrative regulation of brain blood flow and metabolism during exercise. The overarching theme is the importance of quantifying cerebral blood flow and metabolism during exercise using techniques that consider multiple volumetric cerebral haemodynamics (i.e. velocity, diameter, shear and flow). Cerebral function in humans is crucially dependent upon continuous oxygen delivery, metabolic nutrients and active regulation of cerebral blood flow (CBF). As a consequence, cerebrovascular function is precisely titrated by multiple physiological mechanisms, characterized by complex integration, synergism and protective redundancy. At rest, adequate CBF is regulated through reflexive responses in the following order of regulatory importance: fluctuating arterial blood gases (in particularly, partial pressure of carbon dioxide), cerebral metabolism, arterial blood pressure, neurogenic activity and cardiac output. Unfortunately, the magnitude that these integrative and synergistic relationships contribute to governing the CBF during exercise remains unclear. Despite some evidence indicating that CBF regulation during exercise is dependent on the changes of blood pressure, neurogenic activity and cardiac output, their role as a primary governor of the CBF response to exercise remains controversial. In contrast, the balance between the partial pressure of carbon dioxide and cerebral metabolism continues to gain empirical support as the primary contributor to the intensity-dependent changes in CBF observed during submaximal, moderate and maximal exercise. The goal of this review is to summarize the fundamental physiology and mechanisms involved in regulation of CBF and metabolism during exercise. The clinical implications of a better understanding of CBF during exercise and new research directions are also outlined.

Dynamic cerebral autoregulation across the cardiac cycle during 8 hr of recovery from acute exercise

“…The latter finding could be derived to the fact that the MICT condition was calculated to occur at roughly 50%-60% VO2max, which was insufficient to reach significance from baseline values, but was sufficient to elicit the expected elevations to CBV (Table 1). Collectively, the physiological changes seen during the three conditions employed in this investigation are in agreement with previous work that have examined physiological measurements during exercise Smith & Ainslie, 2017). Furthermore, individuals are able to maintain exercise up to an intensity of roughly 60%-70% of their VO 2max for prolonged durations as this intensity is typically below the anaerobic threshold (Mateika & Duffin, 1995).…”

“…Koch et al (2005) also observed a decrease in phase following dynamic resistance exercise during the early recovery period (80 s). The change in phase angle across the cardiac cycle in the current study following MICT exercise may be attributed to more compliancy within the dilated vasculature, known to occur during moderate exercise Smith & Ainslie, 2017). Such dilation likely occurred throughout the entirety of the MICT protocol, due to hyperpnea-induced vasodilation, which potential led to more compliant vasculature.…”

“…Maintaining oxygen supply and nutrient delivery to cerebral tissue is therefore of critical importance, both at rest and during exercise, as the brain has limited substrate storage (Willie, Tzeng, Fisher, & Ainslie, ). Cerebral blood flow velocity (CBV) has been shown to increase 10%–20% during moderate intensity exercise (~60%–70% of an individual's maximal oxygen uptake; VO 2max ), as a result of parallel increases of neuronal activity, metabolism, and regional CBV (Marsden et al, ; Ogoh & Ainslie, , ; Smith & Ainslie, ). During more intense exercise, CBV has been shown to either plateau or decrease, with the extent of reduction associated with the degree of hyperventilation‐induced cerebral vasoconstriction (Larsen, Rasmussen, Overgaard, Secher, & Nielsen, ; Ogoh & Ainslie, ; Smith & Ainslie, ; Subudhi et al, ).…”

Cerebral metabolism, oxidation and inflammation in severe passive hyperthermia with and without respiratory alkalosis

“…The cerebral metabolic response to hyperthermia can perhaps be gleaned from exercising data, but again the findings are inconsistent (see review by Smith et al . ). For example, Nybo et al .…”

CO2 supplementation dissociates cerebral oxygenation and middle cerebral artery blood velocity during maximal cycling

“…7 The increase in MCA V mean during low to moderate exercise is attributed, at least in part, to the initial increase in arterial carbon dioxide tension (PaCO 2 ) in response to exercise metabolism. Yet, as exercise intensity progresses, MCA V mean is either plateuing or reduced toward the resting value, dependent on the magnitude of hyperventilation-induced hypocapnia, 3,4,8 that may reduce PaCO 2 to as low as ~29 mmHg. 9 A similar response pattern is described for the NIRS-determined frontal lobe oxygenation (ScO 2 ) with an increase during low intensity exercise and then a gradual decrease when exercise intensity approaches a maximal level and exercise-induced hypocapnia develops.…”