Abstract
The present review aims to examine the effects of high blood lactate levels in healthy adult humans, for instance, after a period of exhaustive exercise, on the functioning of the cerebral cortex. In some of the examined studies, high blood lactate levels were obtained not only through exhaustive exercise but also with an intravenous infusion of lactate while the subject was immobile. This allowed us to exclude the possibility that the observed post-exercise effects were nonspecific (e.g., cortical changes in temperature, acidity, etc.). We observed that, in both experimental conditions, high levels of blood lactate are associated with a worsening of important cognitive domains such as attention or working memory or stress, without gender differences. Moreover, in both experimental conditions, high levels of blood lactate are associated with an improvement of the primary motor area (M1) excitability. Outside the frontal lobe, the use of visual evoked potentials and somatosensory evoked potentials allowed us to observe, in the occipital and parietal lobe respectively, that high levels of blood lactate are associated with an amplitude’s increase and a latency’s reduction of the early components of the evoked responses. In conclusion, significant increases of blood lactate levels could exercise a double-action in the central nervous system (CNS), with a protecting role on primary cortical areas (such as M1, primary visual area, or primary somatosensory cortex), while reducing the efficiency of adjacent regions, such as the supplementary motor area (SMA) or prefrontal cortex. These observations are compatible with the possibility that lactate works in the brain not only as an energy substrate or an angiogenetic factor but also as a true neuromodulator, which can protect from stress. In this review, we will discuss the mechanisms and effects of lactic acid products produced during an anaerobic exercise lactate, focusing on their action at the level of the central nervous system with particular attention to the primary motor, the somatosensory evoked potentials, and the occipital and parietal lobe.
Highlights
AtIntroduction the beginning of the twentieth century, British physiologists W.M
We will discuss the mechanisms and effects of lactic acid products produced during an anaerobic exercise lactate, focusing on its action at the level of the central nervous system with particular attention to the primary motor, the somatosensory evoked potentials, and to the occipital and parietal lobe
As an increase in lactate induced by an infusion in a subject at rest causes no change in excitability either at the spinal level or at the brainstem level, it was concluded that the raise of blood lactate levels induced by an exhaustive exercise is not per se capable of increasing the excitability of subcortical structures
Summary
AtIntroduction the beginning of the twentieth century, British physiologists W.M. Fletcher and F.G. It was thought that the increase in lactate was responsible for demonstrated that, in the absence of oxygen, muscles are capable of continuing their contraction by muscle fatigue [2]; later, this theory was abandoned [3], and it was proposed that lactate producing lactate [1]. Have shown that the nerve tissue receives lactate from the blood but is to produce it at the level of the astrocytes. By contrast, blood lactate levels had little effect on the activity of the high-affinity transporter MCT2 [11]. We will discuss the mechanisms and effects of lactic acid products produced during an anaerobic exercise lactate, focusing on its action at the level of the central nervous system with particular attention to the primary motor, the somatosensory evoked potentials, and to the occipital and parietal lobe
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