A decrease in cerebral oxygenation is induced by prolonged exercise
[39][42] or exercise under mild or severe hypoxia
[43][44], while impaired cognitive performance is not evident in healthy young participants, suggesting a dissociation between an alteration in CBF and subsequent change in oxygen delivery to the brain and cerebral metabolism or cognitive performance. Indeed, albeit with a reduction in CBF during heavy exercise, the elevation of brain neural activity and metabolism might be accompanied by compensatory increases in the uptake of lactate, glucose, and oxygen support for the brain (arterial-jugular venous difference)
[30]. Given that augmented brain neural activity and metabolism are independent of increases in CBF
[45], extensive activation of motor and sensory systems due to the higher-order function of the prefrontal cortex may affect cognitive performance rather than cerebral perfusion in response to exercise.
Regarding metabolism, although the brain relies mainly on glucose at rest, during high-intensity exercise, the brain becomes dependent on lactate delivery
[46][47] and repeated HIIE, which attenuates the increase in systemic blood lactate, resulting in impaired maintenance of HIIE-enhanced cognitive performance (i.e., EF)
[48]. In particular, HIIE may facilitate neuronal activation and excitation levels to the extent that summation is facilitated to improve cognitive performance
[10][49][50]. Neuronal activation is associated with an increase in energy requirements due to the transport of neurotransmitters and ions
[51], and neurons preferentially utilize lactate as a fuel in vivo
[52]. Sustained elevation of arterial/systemic lactate in response to intense exercise promotes the supply of lactate as an energy substrate to meet acute neuronal energy requirements
[53][54][55]. In addition, intravenous infusion of 100 mM L-lactate into rats promoted cognitive recovery by preserving cerebral ATP generation following traumatic brain injury
[56]. Furthermore, Skriver et al. found a correlation between systemic lactate concentration and the acquisition and retention of motor skills
[57]. In addition, lactate supports synaptic activity
[58], long-term potentiation and memory formation
[59], and neuronal plasticity
[60]. These findings suggest that brain function as expressed by cognitive performance depends on the provision of lactate. Indeed, researchers manipulated blood lactate during exercise at a given intensity by repeated HIIE and evaluated whether such manipulation of peripheral lactate metabolism affects brain lactate uptake (i.e., the arterial–jugular venous difference in lactate (a-v diff
lactate)) and EF
[61]. Researchers found that brain lactate uptake is associated with the arterial lactate concentration, and inadequate lactate provision to the brain might attenuate exercise (i.e., HIIE)-enhanced EF
[61], irrespective of increased BDNF and catecholamine, both of which are supposed to relate to cognitive performance
[50][62][63]. Given the reliance on lactate as a fuel for the brain, variations in blood lactate could affect cognitive performance during and after exercise and account for the significance of exercise (i.e., muscle contraction) for brain function.
On the other hand, a recent study demonstrated that chronic lactate administration to mice promotes hippocampal neurogenesis but does not affect cognitive performance
[64]. In addition, Sudo et al. found that recovery of prefrontal oxygenation affected cognitive performance after exhaustive exercise, irrespective of the blood lactate concentration
[65]. Further studies are warranted to understand the role of lactate in brain function in acute and chronic exercise.