Severe Exercise and Exercise Training Exert Opposite Effects on Human Neutrophil Apoptosis via Altering the Redox Status

Neutrophil spontaneous apoptosis, a process crucial for immune regulation, is mainly controlled by alterations in reactive oxygen species (ROS) and mitochondria integrity. Exercise has been proposed to be a physiological way to modulate immunity; while acute severe exercise (ASE) usually impedes immunity, chronic moderate exercise (CME) improves it. This study aimed to investigate whether and how ASE and CME oppositely regulate human neutrophil apoptosis. Thirteen sedentary young males underwent an initial ASE and were subsequently divided into exercise and control groups. The exercise group (n = 8) underwent 2 months of CME followed by 2 months of detraining. Additional ASE paradigms were performed at the end of each month. Neutrophils were isolated from blood specimens drawn at rest and immediately after each ASE for assaying neutrophil spontaneous apoptosis (annexin-V binding on the outer surface) along with redox-related parameters and mitochondria-related parameters. Our results showed that i) the initial ASE immediately increased the oxidative stress (cytosolic ROS and glutathione oxidation), and sequentially accelerated the reduction of mitochondrial membrane potential, the surface binding of annexin-V, and the generation of mitochondrial ROS; ii) CME upregulated glutathione level, retarded spontaneous apoptosis and delayed mitochondria deterioration; iii) most effects of CME were unchanged after detraining; and iv) CME blocked ASE effects and this capability remained intact even after detraining. Furthermore, the ASE effects on neutrophil spontaneous apoptosis were mimicked by adding exogenous H2O2, but not by suppressing mitochondrial membrane potential. In conclusion, while ASE induced an oxidative state and resulted in acceleration of human neutrophil apoptosis, CME delayed neutrophil apoptosis by maintaining a reduced state for long periods of time even after detraining

Respostas cardio-respiratórias em pacientes com traumatismo raquimedular Cardiorespiratory responses of patients with spinal cord injuries

O objetivo desta pesquisa foi investigar as variáveis cardio-respiratórias (Pa, FC, VO2, VCO2 e Ve) durante a Estimulação Elétrica Neuromuscular (EENM) do quadríceps em portadores de lesão medular. Participaram da pesquisa dez pacientes (cinco paraplégicos e cinco tetraplégicos). O protocolo do teste consistiu em 10 minutos de repouso, 20 minutos de EENM dos quadriceps e 10 minutos de recuperação. Durante a EENM foram constatados baixos valores de VO2 e VCO2. Os paraplégicos apresentaram rápida cinética dos gases e os tetraplégicos lenta cinética dos gases. Houve o aumento da Pa sistólica e da FC. Ainda, os valores das variáveis cardio-respiratórias foram inversamente relatadas para o nível de lesão, ou seja, quanto maior o nível de lesão, menor os valores. Portanto, a maioria dos pacientes apresentaram algumas limitações nas respostas cardio-respiratórias, indicando realização de exercício exaustivo, mas apresentaram capacidade de realização de exercício induzido artificialmente, possivelmente devido aos benefícios da EENM.<br>The objective of this study was to investigate cardiorespiratory responses (Heart Rate, Blood Pressure, VO2, VCO2 e Ve) to Neuromuscular Electrical Stimulation (NMES) of the quadriceps in patients with spinal cord injury. Ten patients (five paraplegics and five tetraplegics) participated in this study. The protocol of the test consisted of ten minutes of rest, twenty minutes of NMES of the quadriceps and ten minutes of recovery. The findings in this study indicated that, during NMES, the patients demonstrated low levels of VO2 and VCO2 and slow gas kinetics for tetraplegic individuals, and a fast gas kinetics for paraplegic individuals. Moreover, there were increases in blood pressure and heart rate. Cardiorespiratory responses increased with descending spinal cord injury level, meaning that the more severe the lesion, the lower the values. Therefore, most of the patients presented some limitations in cardiorespiratory responses, indicating the performance of exhaustive exercise, but the use of NMES can elicit improvements in exercise tolerance due to its benefits

Voluntary exercise prevents oxidative stress in the brain of phenylketonuria mice

BACKGROUND: High phenylalanine levels in phenylketonuria (PKU) have been associated with brain oxidative stress and amino acid imbalance. Exercise has been shown to improve brain function in hyperphenylalaninemia and neurodegenerative diseases. This study aimed to verify the effects of exercise on coordination and balance, plasma and brain amino acid levels, and brain oxidative stress markers in PKU mice.METHODS: Twenty wild-type (WT) and 20 PAH(enu2) (PKU) C57BL/6 mice were placed in cages with (exercise, Exe) or without (sedentary, Sed) running wheels during 53 days. At day 43, a balance beam test was performed. Plasma and brain were collected for analyses of amino acid levels and the oxidative stress parameters superoxide dismutase (SOD) activity, sulfhydryl and reduced glutathione (GSH) contents, total radical-trapping antioxidant potential (TRAP), and total antioxidant reactivity (TAR).RESULTS: SedPKU showed poor coordination (p &lt; 0.001) and balance (p &lt; 0.001), higher plasma and brain phenylalanine (p &lt; 0.001), and increased brain oxidative stress (p &lt; 0.05) in comparison to SedWT. ExePKU animals ran less than ExeWT (p = 0.018). Although no improvement was seen in motor coordination and balance, exercise in PKU restored SOD, sulfhydryl content, and TRAP levels to controls. TAR levels were increased in ExePKU in comparison to SedPKU (p = 0.012). Exercise decreased plasma and brain glucogenic amino acids in ExePKU, but did not change plasma and brain phenylalanine in both WT and PKU.CONCLUSIONS: Exercise prevents oxidative stress in the brain of PKU mice without modifying phenylalanine levels. Hence, exercise positively affects the brain, demonstrating its value as an intervention to improve brain quality in PKU.</p