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

Low PO

Reductions in the arterial oxygen content (CaO2) lowers maximal work rate and impairs exercise endurance during whole-body exercise. Because changes in CaO2 influences oxygen delivery to all tissues, including the skeletal muscles and the brain, it may be difficult to determine whether performance deteriorates as direct effect of the low PO2 in some of the most active brain regions or whether central motor output becomes reduced secondary to feedback from the muscles and from the increased cardiorespiratory stress that accompanies exercise with a low atmospheric oxygen tension. At moderate hypoxia, the reduced work rate during maximal whole-body exercise is influenced by feedback from the working muscles. Reduced oxygen delivery to exercising muscles accelerates the accumulation of muscle metabolites, and these fatigue-related and sensory fiber-stimulating substances may activate group 3 and 4 muscle afferents and contribute to inhibitory feedback to the CNS during fatiguing exercise. In contrast, during severe hypoxia, afferent feedback seems to be of minor importance because epidural anesthesia (blocking or reducing feedback from group 3 and 4 muscle afferents) has no effect on performance or perceived exertion during maximal exercise, when the inspired oxygen fraction was lowered to approximately 10%.[17]

Further support for a direct effect of reduced cerebral oxygen delivery on motor performance is provided by the study presented in Figure 1. In that study, cerebral oxygen delivery was varied by providing low, normal, or high PO2 in the inspired air either with normal, high, or reduced arterial CO2 tension, and motor performance was evaluated as maximal handgrip strength. When oxygen delivery was reduced by more than 15% below control levels, as a separate effect of either hyperventilation-induced reduction in CBF or inhalation of air with a low PO2, the maximal handgrip strength decreased concurrently with an increase in lactate spillover from the brain, which indicated that cerebral oxygen levels became inadequate to support optimal aerobic metabolism (Fig. 1 and "Cerebral Metabolism and Mitochondrial PO2" section). Although low arterial PO2 or hyperventilation-induced alkalosis may have influenced the ability of the muscles to produce a maximal force, the energy used in the skeletal muscles during a brief maximal contraction is delivered mainly by anaerobic metabolism (net adenosine triphosphate (ATP) and creatine phosphate degradation). It is likely, therefore, that the impaired motor performance observed in the study by Rasmussen et al.[29] relates to central fatigue arising subsequently from inadequate oxygen delivery to the brain.

Cerebral lactate release (top) and maximal voluntary handgrip force (bottom) as a function of cerebral oxygen delivery (percent control). Alterations in central blood flow (CBF) (induced by CO2 breathing, hyperventilation, or normal ventilation) were combined with different levels of CaO2 and PaO2 (10%, 21%, or 100% oxygen in the inspired air) to vary the cerebral oxygen delivery from approximately 60% to approximately 140% of control (supine rest; see 29 for details). Data are mean ± SE for 12 subjects.

Central fatigue may not always appear during a single brief maximal voluntary contraction (MVC), and it may be necessary to use a protocol with repeated or sustained maximal contractions. Both for hypoglycemia- and hyperthermia-induced central fatigue (see [24] for review), well-motivated subjects are capable to establish a maximal neural drive to the muscle for a brief period, despite pronounced fatigue, whereas the ability to sustain a high firing rate of the alpha motor neurons for more than a few seconds becomes markedly impaired. Accordingly, MVC of a small and rested muscle group may be unaffected by exposure to moderate altitude,[6] whereas others have reported[4,7] on the effect of extreme simulated altitude: "in some subjects, the responses to stimuli interpolated during repeated MVC provided evidence of central fatigue at altitude." If a period of rest is allowed between or before brief maximal efforts, there may be enough time for replenishment of brain glycogen and restoration of high-energy phosphate compounds in the relevant brain areas. In contrast, low mitochondrial oxygen tension during sustained motor activation may not allow for adequate maintenance of neuronal and astrocytic homeostasis, and eventually, this will impair the ability to maintain a high level of neuronal firing.

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