The enteric nervous system (ENS) is organized into two plexuses—submucosal and myenteric—which regulate smooth muscle contraction, secretion, and blood flow along the gastrointestinal tract under the influence of the rest of the autonomic nervous system (ANS). Interstitial cells of Cajal (ICCs) are mainly located in the submucosa between the two muscle layers and at the intramuscular level. They communicate with neurons of the enteric nerve plexuses and smooth muscle fibers and generate slow waves that contribute to the control of gastrointestinal motility. They are also involved in enteric neurotransmission and exhibit mechanoreceptor activity. A close relationship appears to exist between oxidative stress and gastrointestinal diseases, in which ICCs can play a prominent role. Thus, gastrointestinal motility disorders in patients with neurological diseases may have a common ENS and central nervous system (CNS) nexus. In fact, the deleterious effects of free radicals could affect the fine interactions between ICCs and the ENS, as well as between the ENS and the CNS. In this review, we discuss possible disturbances in enteric neurotransmission and ICC function that may cause anomalous motility in the gut.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons in the spinal cord, cerebral cortex, and medulla oblongata. Most patients present a clinical phenotype of classic ALS—with predominant atrophy, muscle weakness, and fasciculations—and survival of 3 to 5 years following diagnosis. In the present review, we performed a literature search to provide an update on the etiology and pathophysiological mechanisms involved in ALS. There are two types of ALS: the familial form with genetic involvement, and the sporadic form with a multifactorial origin. ALS pathophysiology is characterized by involvement of multiple processes, including oxidative stress, glutamate excitotoxicity, and neuroinflammation. Moreover, it is proposed that conditioning risk factors affect ALS development, such as susceptibility to neurodegeneration in motor neurons, the intensity of performed physical activity, and intestinal dysbiosis with involvement of the enteric nervous system, which supports the existing theories of disease generation. To improve patients’ prognosis and survival, it is necessary to further deepen our understanding of the etiopathogenesis of ALS.

Soria, M, Ansón, M, Lou-Bonafonte, JM, Andrés-Otero, MJ, Puente, JJ, and Escanero, J. Fat oxidation rate as a function of plasma lipid and hormone response in endurance athletes. J Strength Cond Res 34(1): 104–113, 2020—Plasma lipid changes during incremental exercise are not well known. The aim of this study was to investigate the relationship among fat oxidation rate, plasma lipids, and hormone concentrations in well-trained athletes. Twenty-six trained triathletes completed a graded cycle ergometer test to exhaustion increasing by 0.5 W·kg⁻¹ every 10 minutes. Fat oxidation rates were determined using indirect calorimetry. For each individual, maximal fat oxidation (MFO), the intensity at which MFO occurred (Fat_max), and the intensity at which fat oxidation became negligible (Fat_min) were determined. Blood samples for lipids and hormones analysis were collected at the end of each stage of the graded exercise test. All variables studied except insulin showed an increase at the end of incremental protocol with respect to basal levels. Free fatty acid reached significant increase at 60%Vo ₂max and maximal levels at 70%Vo ₂max. Low-density lipoprotein (LDL) and triglycerides (TG) decreased and showed lowest levels at 60%Vo ₂max and reaching significant increases after 80%Vo ₂max. High-density lipoprotein reached significant increase at 60%Vo ₂max. Adrenaline and noradrenaline increased until the end of the incremental exercise, and significant differences were from 50%Vo ₂max. These results suggest that exercise intensities are related to plasma lipids levels. In the zone when lipids oxidation is maximal, plasma LDL and TG variation differs from other lipids. These results may have application for the more adequate exercise intensity prescription to maximize the beneficial effects of exercise.

We evaluated the in vivo effects of melatonin treatment on oxidative damage in the liver in an experimental model of ischemia–reperfusion. A total of 37 male Sprague-Dawley rats were randomly divided into four groups: control, ischemia, ischemia + reperfusion, and ischemia + reperfusion + melatonin. Hepatic ischemia was maintained for 20 min, and the clamp was removed to initiate vascular reperfusion for 30 min. Melatonin (50 mg/kg body weight) was intraperitoneally administered. Fluidity was measured by polarization changes in 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene-p-toluene sulfonate). After 20 min of ischemia, no significant changes were observed in cell and mitochondrial membrane fluidity levels, lipid peroxidation, and protein carbonylation. However, after 30 min of reperfusion, membrane fluidity decreased compared to controls. Increases in lipid and protein oxidation were also seen in hepatic homogenates of animals exposed to reperfusion. Melatonin injected 30 min before ischemia and reperfusion fully prevented membrane rigidity and both lipid and protein oxidation. Livers from ischemia–reperfusion showed histopathological alterations and positive labeling with antibodies to oxidized lipids and proteins. Melatonin reduced the severity of these morphological changes and protected against in vivo ischemia–reperfusion-induced toxicity in the liver. Therefore, melatonin might be a candidate for co-treatment for patients with hepatic vascular occlusion followed by reperfusion.