evaluation-blood-lactate-plasma-insulin-during-high-intensity

Evaluation of Blood Lactate and Plasma Insulin During High-intensity Exercise by Antecubital Vein Catheterization

The measurement of metabolic and endocrinal markers during physical activity is of relevance to understanding the physiological implications of different ...

University of physical Education

Oxidant antioxidants and adaptive responses to exercise.

Regular exercise has systemic beneficial effects, including the promotion of brain function. The adaptive response to regular exercise involves the up-regulation of the enzymatic antioxidant system and modulation of oxidative damage. Reactive oxygen species (ROS) are important regulators of cell signaling. Exercise, via intensity-dependent modulation of metabolism and/or directly activated ROS generating enzymes, regulates the cellular redox state of the brain. ROS are also involved in the self-renewal and differentiation of neuronal stem cells and the exercise-mediated neurogenesis could be partly associated with ROS production. Exercise has strong effects on the immune system and readily alters the production of cytokines. Certain cytokines, especially IL-6, IL-1, TNF-α, IL-18 and IFN gamma, are actively involved in the modulation of synaptic plasticity and neurogenesis. Cytokines can also contribute to ROS production. ROS-mediated alteration of lipids, protein, and DNA could directly affect brain function, while exercise modulates the accumulation of oxidative damage. Oxidative alteration of macromolecules can activate signaling processes, membrane remodeling, and gene transcription. The well known neuroprotective effects of exercise are partly due to redox-associated adaptation.

Physical exercise, reactive oxygen species and neuroprotection.

The existence of free radicals in living cells was first reported in 1954 and this important finding helped launch the field of free radical biology. However, the discovery that muscular exercise is associated with increased biomarkers of oxidative stress did not occur until 1978. Following the initial report that exercise promotes oxidative stress in humans, many studies have confirmed that prolonged or short-duration high intensity exercise results in increased radical production in active skeletal muscles resulting in the formation of oxidized lipids and proteins in the working muscles. Since these early descriptive studies, the investigation of radicals and redox biology related to exercise and skeletal muscle has grown as a discipline and the importance of this research in the biomedical sciences is widely recognized. This review will briefly summarize the history of research in exercise-induced oxidative stress and will discuss the major paradigm shifts that the field has undergone and continues to experience. We conclude with a discussion of future directions in the hope of stimulating additional research in this important field.

Exercise-induced oxidative stress: past, present and future.

There is an increasing volume of data connecting capacity to respond to exercise training with quality of life and aging. In this study, we used a rat model in which animals were selectively bred for low and high gain in running distance to test t whether genetic segregation for trainability is associated with brain function and signaling processes in the hippocampus. Rats selected for low response (LRT) and high response training (HRT) were randomly divided into control or exercise group that trained five times a week for 30 min per day for three months at 70% VO2max. All four groups had similar running distance before training. With training, HRT rats showed significantly greater increases in VO2max and running distance than LRT rats (p < 0.05). On the reverse Morris Maze test HRT-trained rats outperformed HRT control ones. Significant difference was noted between LRT and HRT groups in redox milieu as assessed by levels of reactive oxygen species (ROS), carbonylation of proteins, nNOS and S-nitroso-cysteine. Moreover the silent information regulator 1 (SIRT1), brain-derived neurotrophic factor (BDNF), ratio of phospho and total cAMP-response element binding protein (CREB), and apoptotic index, also showed significant differences between LRT and HRT groups. These findings suggest that aerobic training responses are not localized to skeletal muscle, but differently involve signaling processes in the brain of LRT and HRT rats.

The rate of training response to aerobic exercise affects brain function of rats.

Obesity-induced inflammatory changes in white adipose tissue (WAT), which caused dysregulated expression of inflammation-related adipokines involving tumor necrosis factor- and monocyte chemoattractant protein-1, contribute to the development of insulin resistance. Moreover, current literature reports state that WAT generates reactive oxygen species (ROS), and the enhanced production of ROS in obese WAT has been closely associated with the dysregulated expression of adipokines in WAT. Therefore, the reduction in excess WAT and oxidative stress that results from obesity is thought to be one of the important strategies in preventing and improving lifestyle-related diseases. Exercise training (TR) not only brings about a decrease in WAT mass but also attenuates obesity-induced dysregulated expression of the adipokines in WAT. Furthermore, some reports indicate that TR affects the generation of oxidative stress in WAT. This review outlines the impact of TR on the expression of inflammation-related adipokines and oxidative stress in WAT.

Exercise Training Attenuates the Dysregulated Expression of Adipokines and Oxidative Stress in White Adipose Tissue.

Silent mating type information regulation 2 homologue 1 (SIRT1) activity and content increased significantly in overload-induced hypertrophy. SIRT1-mediated signalling through Akt, the endothelial nitric oxide synthase mediated pathway, regulates anabolic process in the hypertrophy of skeletal muscle. The regulation of catabolic signalling via forkhead box O 1 and protein ubiquitination is SIRT1 dependent. Overload-induced changes in microRNA levels regulate SIRT1 and insulin-like growth factor 1 signalling.

SIRT1 may play a crucial role in overload-induced hypertrophy of skeletal muscle.

It is debated whether exercise-induced ROS production is obligatory to cause adaptive response. It is also claimed that antioxidant treatment could eliminate the adaptive response, which appears to be systemic and reportedly reduces the incidence of a wide range of diseases. Here we suggest that if the antioxidant treatment occurs before the physiological function-ROS dose-response curve reaches peak level, the antioxidants can attenuate function. On the other hand, if the antioxidant treatment takes place after the summit of the bell-shaped dose response curve, antioxidant treatment would have beneficial effects on function. We suggest that the effects of antioxidant treatment are dependent on the intensity of exercise, since the adaptive response, which is multi pathway dependent, is strongly influenced by exercise intensity. It is further suggested that levels of ROS concentration are associated with peak physiological function and can be extended by physical fitness level and this could be the basis for exercise pre-conditioning. Physical inactivity, aging or pathological disorders increase the sensitivity to oxidative stress by altering the bell-shaped dose response curve.

Exercise, oxidants, and antioxidants change the shape of the bell-shaped hormesis curve.

Nicotinamide (NAM) could enhance the availability of NAD and be beneficial to cell function. However, NAM can inhibit the activities of SIRT1 and PARP. The effect of NAM supplementation on the aging process is not well known. In the present study exogenous NAM (1-0.5% in drinking water) was supplemented for 5 weeks and in the last 4 weeks moderate treadmill running was given to 5 mo and 28 mo old rats. The content of SIRT1 was not effected by NAM treatment alone. However, the activity of SIRT1, judged from the acetylated p53/p53 ratio, increased in both NAM treated age groups, suggesting beneficial effects of exogenous NAM. This was confirmed by the finding of increased PGC-1α and pCREB/CREB ratio in the gastrocnemius muscle of old but not young NAM treated animals. Our data suggest NAM administration can attenuate the aging process in skeletal muscle of rats, but NAM administration together with exercise training might be too great challenge to cope with in the old animals, since it leads to decreased levels of SIRT1.

Exogenous nicotinamide supplementation and moderate physical exercise can attenuate the aging process in skeletal muscle of rats.

Active recovery has been used as a method to accelerate the recovery during intense exercise. It also has been shown to improve performance in subsequent exercises, but little is known about its acute effects on the hormonal and metabolic profile. The aim of this research was to study the effects of active recovery on plasma catecholamines and plasma insulin during a high-intensity interval exercise.

Effects of active recovery during interval training on plasma catecholamines and insulin.

This study aims to elucidate how respiratory rate (RR) patterns may affect respiratory gas exchange variables and performance during incremental intensity- exercise. 10 healthy young men (mean ± SD, age: 20.7 ± 0.5 years, height: 174.3 ± 5.7 cm, and body mass: 72.6 ± 10.4 kg) performed three incremental tests on a cycle ergometer at three different RR (60, 45 and 30 breaths per min) in each trial. During the tests, tidal volume (TV), minute ventilation (VE), fractional content of oxygen (FeO), fractional content of carbon dioxide (FeCO), oxygen uptake (VO), expiratory carbon dioxide (VCO), equivalent of oxygen (EqO), VE/VCO, and respiratory exchange ratio (RER) were determinate breath-by-breath. Additionally, exercise time (as a performance marker) was measured. Statistical analyses for the results were carried out to determine significant differences between the three trials. VCO, VO, and exercise time did not show statistical differences in the three trials. Therefore, we concluded that RR affects some respiratory gas exchange variables but does not influence the VO2max and endurance performance.

Article	Year
Oxidant antioxidants and adaptive responses to exercise. Oxidative medicine and cellular longevity\| PubMed ID: 25878763	2015
Physical exercise, reactive oxygen species and neuroprotection. Free radical biology & medicine\| PubMed ID: 26828019	2016
Exercise-induced oxidative stress: past, present and future. The Journal of physiology\| PubMed ID: 26893258	2016
The rate of training response to aerobic exercise affects brain function of rats. Neurochemistry international\| PubMed ID: 27262284	2016
Exercise Training Attenuates the Dysregulated Expression of Adipokines and Oxidative Stress in White Adipose Tissue. Oxidative medicine and cellular longevity\| PubMed ID: 28168013	2017
SIRT1 may play a crucial role in overload-induced hypertrophy of skeletal muscle. The Journal of physiology\| PubMed ID: 28251652	2017
Exercise, oxidants, and antioxidants change the shape of the bell-shaped hormesis curve. Redox biology\| PubMed ID: 28285189	2017
Exogenous nicotinamide supplementation and moderate physical exercise can attenuate the aging process in skeletal muscle of rats. Biogerontology\| PubMed ID: 28477081	2017
Effects of active recovery during interval training on plasma catecholamines and insulin. The Journal of sports medicine and physical fitness\| PubMed ID: 28488828	2017
How Different Respiratory Rate Patterns affect Cardiorespiratory Variables and Performance. International journal of exercise science\| PubMed ID: 28515830	2017

Zsolt Radak

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