Frontal cerebral cortex blood flow, oxygen delivery and oxygenation during normoxic and hypoxic exercise in athletes

Abstract

Non-technical summary Exercise capacity is limited at high altitude where hypoxia (i.e. decreased amount of inspired oxygen resulting in decreased oxygen in the blood) is present, but it is unknown whether a reduction in the oxygen delivered to the brain constitutes the signal to the brain to prematurely terminate exercise. We show that during hypoxic exercise equivalent to exercise at ∼4000 m above sea-level, the oxygen delivered to the brain during intense exercise is ∼60% less than that delivered to the brain at comparable exercise intensity at sea-level. These results show that reduction in the oxygen delivered to the brain could constitute the signal to limit maximal exercise capacity in hypoxia, and help us understand better why exercise capacity is limited at high altitude. Moreover, a plausible mechanism of exercise limitation in patients who present decreased oxygen in the blood during exercise due to pulmonary and/or cardiac disease is revealed.Abstract During maximal hypoxic exercise, a reduction in cerebral oxygen delivery may constitute a signal to the central nervous system to terminate exercise. We investigated whether the rate of increase in frontal cerebral cortex oxygen delivery is limited in hypoxic compared to normoxic exercise. We assessed frontal cerebral cortex blood flow using near-infrared spectroscopy and the light-absorbing tracer indocyanine green dye, as well as frontal cortex oxygen saturation (S tO 2 %) in 11 trained cyclists during graded incremental exercise to the limit of tolerance (maximal work rate, WR max ) in normoxia and acute hypoxia (inspired O 2 fraction (F IO 2 ), 0.12). In normoxia, frontal cortex blood flow and oxygen delivery increased (P < 0.05) from baseline to sub-maximal exercise, reaching peak values at near-maximal exercise (80% WR max : 287 ± 9 W; 81 ± 23% and 75 ± 22% increase relative to baseline, respectively), both leveling off thereafter up to WR max (382 ± 10 W). Frontal cortex S tO 2 % did not change from baseline (66 ± 3%) throughout graded exercise. During hypoxic exercise, frontal cortex blood flow increased (P = 0.016) from baseline to sub-maximal exercise, peaking at 80% WR max (213 ± 6 W; 60 ± 15% relative increase) before declining towards baseline at WR max (289 ± 5 W). Despite this, frontal cortex oxygen delivery remained unchanged from baseline throughout graded exercise, being at WR max lower than at comparable loads (287 ± 9 W) in normoxia (by 58 ± 12%; P = 0.01). Frontal cortex S tO 2 % fell from baseline (58 ± 2%) on light and moderate exercise in parallel with arterial oxygen saturation, but then remained unchanged to exhaustion (47 ± 1%). Thus, during maximal, but not light to

Modified Beer-Lambert law for blood flow

“…4(B), 4(C)). In practice the situation is helped by differences in magnitude of cerebral versus extra-cerebral flow (e.g., cerebral flow is quite often 10 times larger than extra-cerebral flow) [60]. We note here that the sensitivity to cerebral flow changes (Fig.…”

Exercise Regulation of Cognitive Function and Neuroplasticity in the Healthy and Diseased Brain

“…This increase in blood flow appears to aid in earlier recall for complex spatial objects. 8,9 Further, in elderly subjects, 6 months of aerobic training has been shown to mitigate age-related decline in both verbal and spatial memory, 10 while a low activity, 8-week yoga intervention significantly improved performance on task switching, working memory, and the n-back task. 11 In young males, high-intensity cycling has been associated with better acquisition and retention 7 days later on the visuomotor tracking task.…”

The influence of a mild thermal challenge and severe hypoxia on exercise performance and serum BDNF

“…High altitude also decreases exercise performance (Vogiatzis et al 2011). Amann and Calbet (2008) reported the effects of oxygen availability on fatigue development and exercise performance and concluded that hypoxia exacerbates the development of fatigue via direct effects on muscular performance and central nervous system motor activation via inhibitory feedback from muscles.…”