Inadequate Cerebral Oxygen Delivery and Central Fatigue during Strenuous Exercise

Lars Nybo; Peter Rasmussen

Disclosures

Exerc Sport Sci Rev. 2007;35(3):110-118. 

In This Article

Responses During Strenuous Exercise

During submaximal exercise, oxygen delivery to the brain seems to be more than adequate because Pmito increases. There is an unchanged lactate release and global metabolic rate during such exercise. However, Pmito and capillary oxygen saturation during strenuous exercise ( Table ) declines when hyperventilation-induced hypocapnia lowers or blunts an increase in CBF. During the three conditions where PaO2 and arterial oxygen saturation (SaO2) remain fairly unchanged (i.e., maximal exercise and submaximal and maximal exercise with hyperthermia), the drop in Pmito is limited to 5-6 mm Hg; therefore, it is below the level where Pmito begins to restrict the cerebral metabolic function and motor performance. The 5- to 6-mm Hg drop in Pmito is close to the reduction that may be tolerated without impairment in cerebral function, as confirmed by that lack of a change in lactate spillover from the brain during submaximal exercise with hyperthermia and during maximal exercise with or without hyperthermia, and the marked lactate uptake by the brain when the arterial lactate concentration rises. When cerebral oxygen delivery becomes inadequate to support aerobic metabolism during exercise with severe hypoxia, the brain does not take up lactate, although the arterial concentration increases to similar levels as during maximal exercise. The reduction in Pmito during submaximal exercise with progressive hyperthermia is similar to that of maximal exercise, but arterial lactate remains low (~2 mM), and there is no change in lactate balance across the brain. Taken together, these observations indicate that a reduction in cerebral Pmito of 5-6 mm Hg may be tolerated without impaired aerobic energy turnover and, consequently, without changes in anaerobic metabolism of glucose in the brain.

The observation of a 7% increase in the CMRO2 during exercise with hyperthermia, despite an approximately 20% reduction in CBF, provides support of an adequate oxygen delivery to the brain. On the other hand, the cerebral temperature at exhaustion, which is higher by 1.5°C-2°C if we compare with normothermic exercise and increased by approximately 3°C compared with rest, would predict an even greater increase in the CMRO2. Assuming a Q10 of 2, (which is the normal Q10 temperature coefficient for metabolic processes including the cerebral metabolism[24]), CMRO2 should increase by at least 13% compared with that in control exercise. Therefore, it cannot be excluded that low oxygen delivery during submaximal exercise with hyperthermia restricts an even larger increase in the CMRO2, and the blackout or fainting occasionally experienced by hyperthermic athletes may relate to inadequate oxygen delivery to the brain. However, the central fatigue arising with hyperthermia during submaximal exercise is probably largely related to a direct inhibitory effect of high brain temperature on motor outflow.[24] Likewise, factors other than cerebral oxygen delivery seems to be of greater importance for the development of fatigue during maximal exercise. When maximal exercise is performed during hyperthermic conditions, cerebral oxygenation may decline at a faster rate than that during normothermic conditions,[9] and that could be involved with the reduced time to exhaustion; however, it seems more likely that the marked reduction in cardiac output and subsequent impairment of oxygen delivery to the exercising muscles is the factor involved with reduced performance during maximal exercise with hyperthermia.

In contrast, when arterial hypoxia is superimposed either during exposure to high altitude or as consequence of EIAH, the reduction in Pmito is so pronounced that inadequate oxygen delivery to the brain may become a significant factor influencing the development of fatigue. As calculated from the data by Imray et al.[12] during exercise on Chacaltaya at 5260 m above sea level and by Rasmussen et al. (unpublished manuscript/observation, 2006) during simulated altitude (~6000 m), the reductions in cerebral oxygen delivery, cerebral oxygenation, and Pmito are likely to impair both the cerebral metabolism and motor performance. During exercise with severe arterial hypoxia, the brain does not display a net uptake of lactate, despite increases in arterial lactate to similar levels as during maximal exercise with normoxia, indicating that the cerebral oxygen status does not allow for an uptake and metabolism of lactate, and it is likely that endogenous lactate production by the brain becomes so large that the lactate gradient between the blood and the brain disappears. Furthermore, during acute hypoxia, the exercise CMRO2 is lower than that during exercise with normal PaO2 when both compared with the same absolute exercise intensity or matched to exercise, resulting in similar arterial lactate levels, cardiovascular stress, and perceived exertion (Rasmussen, Nybo, Peterson, et al., unpublished manuscript/observation, 2006). In contrast, acclimatized subjects exhibited no difference in CBF, oxidative metabolism, or lactate release when exercise performed on Chacaltaya was compared with rest or submaximal exercise at sea level.[21] The differences between this study[21] and those by Imray et al.[12] and Rasmussen et al. (unpublished manuscript/observation, 2006) may relate to the differences between acute exposure and responses in acclimatized subjects, but it may also relate to the differences in exercise intensities. The workload in the study by Moller et al.[21] was rather low, and it seems that cerebral oxygen delivery in acclimatized subjects may be adequate at rest and low exercise intensities but becomes challenged as maximal workload is approached (Fig. 3).

Changes in cerebral oxygen delivery at different altitudes (, 150 m; , 3,610 m; , 4,750 m; , 5,260 m). (Reprinted from Imray, C.H., S.D. Myers, K.T. Pattinson, A.R. Bradwell, C.W. Chan, S. Harris, P. Collins, and A.D. Wright. Effect of exercise on cerebral perfusion in humans at high altitude. J. Appl. Physiol. 99:699-706, 2005. Copyright © 2005 The American Physiological Society. Used with permission.)

When subjects with EIAH perform maximal exercise, the cerebral oxygen delivery may decrease by approximately 25% because of the combined effect of reduced arterial saturation and lowered CBF, and this may cause reductions in Pmito from 6 and up to 13 mm Hg, depending on the level of arterial hypoxemia and hyperventilation-induced reduction of CBF. In endurance-trained subjects, SaO2 may decrease to below 88% and hyperventilation-induced reductions in PaCO2 by 8-10 mm Hg during maximal exercise,[22] and Pmito is reduced by more than 10 mm Hg and to such an extent that it impairs motor performance. Similarly, Nielsen et al.[22] reported that well-trained rowers experiencing a drop in SaO2 from 98% to 92% during maximal exercise also displayed reduced NIRS-determined COLD from 80 to 65 mm Hg; however, cerebral desaturation was prevented, and performance improved when oxygen supplementation was provided and the arterial oxygen saturation maintained. Although the improvement in performance may relate to enhanced oxygen delivery to the exercising muscles and prevention of muscle fatigue,[1] the reduction in cerebral oxygen saturation and Pmito is of such magnitude that it may affect motor performance during maximal exercise in subjects with EIAH. Therefore, oxygen supplementation may also contribute to improved performance by preventing central fatigue arising secondary to reductions of Pmito.

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