The brain at work

Abstract

Our understanding of the cerebral blood flow (CBF) response to exercise has evolved dramatically over some 20 years in parallel with the advent of new methods to measure brain perfusion in humans. Previously, the Kety–Schmidt method was the only method available for evaluation of CBF in humans. The outflow from the brain through the internal jugular vein was taken to represent CBF and no change was found during exercise, probably because the spinal veins become more important when humans are upright as is the case for most exercise studies (Ide & Secher, 2000). As a consequence, it was often considered that exercise was the exception for which cerebral ‘activation’ (and maybe thinking?) was not required. Yet, with the introduction of methods that evaluate brain tissue flow (133Xenon-clearance) or inflow to the brain through the common or, ideally the internal carotic artery, an ∼20% increase in CBF during mild- to moderate-intensity dynamic exercise was observed. The CBF then levels out or maybe decreases when exercise becomes intense, with the decrease in the arterial carbon dioxide tension accompanying the exponential increase in ventilation. Thus CBF, and indeed cerebral oxygenation responses during incremental exercise, were hypothesised to follow an inverted U-shaped curve. The vast majority of human studies have applied a transcranial Doppler (TCD) approach to evaluate changes in CBF during exercise. Although this approach has the advantage that it can be used during high-intensity dynamic exercise of a large muscle mass, when using the TCD technique one must assume that the diameter of the isonated artery does not change. This assumption has become universally accepted although TCD was introduced by R. Aaslid (1984) to detect vasospasm after neurosurgical procedures. In support of the supposition that the diameter of the isonated artery at the base of the brain (often the middle cerebral artery (MCA)) remains constant during exercise, an inverted U-shape response to incremental exercise is detected with the TCD, and the magnitude of the increase in mean flow velocity is similar to that determined by other estimates of CBF (∼20%). In contrast, the diameter of the MCA increases in response to hypoxia (Wilson et al. 2011) and constricts in response to the administration of the α1-adrenergic receptor agonist phenylephrine (Ogoh et al. 2011), indicating that there is a need for new ambulatory methods for the evaluation of CBF. In a recent issue of The Journal of Physiology, Vogiatzis et al. (2011) introduced a new method using near-infrared spectroscopy to detect CBF (in the frontal lobe) during progressive exercise after bolus injection of idocyanine green, with and without hypoxia, in trained cyclists. It is comforting that the inverted U-shape CBF response to incremental exercise is confirmed by this initiative, and that the validity of the method is supported by an increase in CBF during hypoxia. Yet, as mentioned by the authors, the determined CBF is unreasonably low (23 ml min−1 100 g−1) compared to a normal value of ∼50 ml min−1 100 g−1 and the increase with CBF during exercise is twice as large as normally found. Near-infrared light has to pass through the skin and the scalp to reach the frontal lobe and the authors consider that the low skin (and scalp) blood flow could influence the result. Accordingly, it would be of value if this method for determination of CBF were repeated during exercise after skin blood flow is eliminated, e.g. by cooling the skin or after the administration of phenylephrine (Ogoh et al. 2011). The TCD technique has been invaluable for the development in understanding the brain at work both under normoxic and hypoxic conditions; however, it is problematic that the TCD evaluation of CBF is expressed as a velocity. Such a limitation may be surmounted by using near-infrared spectroscopy to determine CBF during exercise (Vogiatzis et al. 2011), although the extent of the influence of skin blood flow must be established. Similarly, flow in basal cerebral arteries may be evaluated by duplex ultrasound (Wilson et al. 2011) as it is established for peripheral arteries. Accordingly, we now have two additional methods available to take the evaluation of CBF during hypoxic exercise to new heights and the study by Vogiatzis et al. (2011) provides support to the notion that exercise in hypoxia is limited by cerebral oxygen supply and brain oxygenation.