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

Factors Compromising Cerebral Oxygen Delivery During Exercise

Because sustained static and dynamic exercise requires continuous or frequent repetitive neuronal firing in several motor areas, the brain seems to be more vulnerable to hypoxia during exercise. Furthermore, an elevated CBF does not compensate for a low arterial PO2 during strenuous exercise because pronounced hyperventilation will lower arterial carbon dioxide tension (PCO2) and cause constriction (less vasodilation) of the arterioles in the brain. This seems irrational because the primary function of the cerebral circulation is to ensure homeostasis in the brain by providing oxygen for mitochondrial respiration and removal of waste products from the cerebral metabolism. Cerebral autoregulation, metabolic regulation, and CO2 (hydrogen ion; H+)-mediated vasodilatation are the most important mechanisms to ensure that CBF remains adequate. However, CO2 reactivity seems to dominate, and during exercise associated with hyperventilation-induced reductions of the arterial CO2 tension, CBF may decline despite increased metabolic activity in motor areas of the brain.[24] Both at rest and during exercise, the cerebral perfusion is influenced strongly by PaCO2, and the cerebral CO2 reactivity (percentage change in CBF per millimeters of mercury change in PaCO2) may even increase from approximately 3%-4% at rest to 4%-5% during exercise[13,23,28]. It is not unusual to see reductions of the arterial PCO2 by 6-10 mm Hg during maximal exercise and exercise with hyperthermia, which, in turn, may reduce global CBF by 30% compared with moderate intense exercise at a normal temperature response.[23,28]

Cerebral blood flow is distributed heterogeneously and largely depends on the neuronal activity in the different regions of the brain. Dynamic exercise is associated with activation of several areas of the brain, and when the intensity does not exceed the ventilatory threshold (and arterial PCO2 remains fairly stable), flow to these activated areas will increase linearly with the exercise intensity[13,30]. When the intensity exceeds the ventilatory threshold, both global and regional CBF decline as PaCO2 decreases (Fig. 2). Although neuronal activity and metabolic needs keep increasing in the motor areas, regional CBF will decline as exercise intensity increases toward maximum, and regional CBF (e.g., to the motor cortex) may return to similar levels as at rest. According to equation 1 in "Cerebral Metabolism and Mitochondrial PO2" section, this uncoupling of metabolism and flow will cause a reduction in the mitochondrial PO2 in the activated motor areas.

Middle cerebral artery blood flow velocity during incremental exercise, with (open symbols) and without (solid symbols) "adjustments" for arterial carbon dioxide tension (Rasmussen, P., H.H. Stie, B. Nielsen, et al., unpublished manuscript/observations, 2005). Data are mean ± SE for 7 subjects.

However, exercise causes hemoconcentration (secondary to increased filtering of plasma in the muscle capillaries) and, based on the assumption that the arterial saturation remains unchanged, CaO2 may increase by 5%-10% during exercise. Therefore, with a normal atmospheric (and arterial) PO2, the exercise-induced hemoconcentration causes the oxygen delivery to motor areas of the brain to be slightly higher during maximal exercise compared with that during rest but lower than that during submaximal exercise and lower than would be expected on the basis of the neuronal activity in the activated motor areas.[14] Nonetheless, oxygen supply seems to be sufficient to support the aerobic metabolism in the brain during maximal exercise ( Table ). However, in subjects with severe EIAH, which may lower the arterial PO2 to less than 70 mm Hg and saturation to less than 88%, the cerebral oxygen delivery may be disturbed to an extent where it begins to influence aerobic metabolism in the brain as Pmito may be reduced by approximately 10 mm Hg. Similarly, low atmospheric and arterial PO2 when exercising at a high altitude may reduce the cerebral capillary oxygenation levels and limit mitochondrial PO2 to support the cerebral metabolism. At rest, lactate spillover increases when the cerebral oxygen delivery is reduced by more than approximately 15% and the mitochondrial PO2 decreases by more than 6-7 mm Hg (Fig. 1; see [29]). It is more difficult to use increased lactate spillover as an indicator of inadequate oxygen delivery during strenuous exercise because the brain begins to metabolize lactate during high intensity exercise.[2] Although endogenous lactate production in some brain areas may increase with strenuous exercise, it is likely that such an increase will be hidden by the high arterial lactate levels and the marked increase in the cerebral uptake of carbohydrates (including both blood glucose and lactate) in response to brain activation.[2]

Although exercise with superimposed hypoxia may compromise cerebral autoregulation and the ability to increase and to maintain an adequate cardiac output seems to influence the CBF response to exercise, the influence of changes in CBF arising secondary to changes in mean arterial pressure are of minor importance for maintenance of oxygen delivery to the brain. Thus, compared with the relatively large changes in CBF and arterial oxygen content with changes in arterial CO2 and O2 tension, the influence of arterial blood pressure is much smaller, and because mean arterial pressure increases during exercise, this would support rather than compromise oxygen delivery to the brain.

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