Neuroimmunological and neuroenergetic aspects in exercise-induced fatigue.

Feelings of fatigue not only occur in chronic and acute disease states, but also during prolonged strenuous exercise as a symptom of exhaustion. The underlying mechanisms of fatigue in diseases seem to rely on neuroinflammatory pathways. These pathways are interesting to understand exerciseinduced fatigue regarding immune system to brain signaling and effects of cerebral cytokines. Activation of the immune system incurs a high-energy cost, also in the brain. In consequence immune cells have high energetic priority over other tissues, such as neurons. A neuronal inactivation and corresponding changes in neurotransmission can also be induced by end products of ATP metabolism and elicit feelings of fatigue in diseases and after intensive and prolonged exercise bouts. Since there are no existing models of exercise-induced fatigue that specifically address interactions between neuroimmunologic mechanisms and neuroenergetics, this article is combining scientific evidence across a broad range of disciplines in order to propose an inflammation- and energy-based model for exercise-induced fatigue.

The inflammation paradox: Why are Tsimane protected against Western diseases while Westerners are not?

We here describe two apparent paradoxes concerning high CRP levels and NCD risk. One has emerged from observational studies in the Amazon region showing that the indigenous Tsimane in Bolivia appear protected against non-communicable diseases (NCDs) such as obesity, type 2 diabetes, and cardiovascular diseases despite increased inflammatory markers. These findings stand in contrast to Western societies, where an increasing body of evidence demonstrates that low-grade-inflammation is the driver of NCDs. The second paradox has emerged from two field studies (Eifel studies) conducted in 2013 and 2014 with Westerners who returned to a simulated Palaeolithic lifestyle in a National park for 4 days. We had detected elevated inflammation markers, despite otherwise anti-inflammatory effects of these interventions as indicated by metabolic blood parameters. We here propose three hypotheses for this second inflammatory paradox.

Corrigendum to "Influence of a 10-Day Mimic of Our Ancient Lifestyle on Anthropometrics and Parameters of Metabolism and Inflammation: The "Study of Origin"".

[This corrects the article DOI: 10.1155/2016/6935123.].

The sedentary (r)evolution: Have we lost our metabolic flexibility?

During the course of evolution, up until the agricultural revolution, environmental fluctuations forced the human species to develop a flexible metabolism in order to adapt its energy needs to various climate, seasonal and vegetation conditions. Metabolic flexibility safeguarded human survival independent of food availability. In modern times, humans switched their primal lifestyle towards a constant availability of energy-dense, yet often nutrient-deficient, foods, persistent psycho-emotional stressors and a lack of exercise. As a result, humans progressively gain metabolic disorders, such as the metabolic syndrome, type 2 diabetes, non-alcoholic fatty liver disease, certain types of cancer, cardiovascular disease and Alzheimer´s disease, wherever the sedentary lifestyle spreads in the world. For more than 2.5 million years, our capability to store fat for times of food shortage was an outstanding survival advantage. Nowadays, the same survival strategy in a completely altered surrounding is responsible for a constant accumulation of body fat. In this article, we argue that the metabolic disease epidemic is largely based on a deficit in metabolic flexibility. We hypothesize that the modern energetic inflexibility, typically displayed by symptoms of neuroglycopenia, can be reversed by re-cultivating suppressed metabolic programs, which became obsolete in an affluent environment, particularly the ability to easily switch to ketone body and fat oxidation. In a simplified model, the basic metabolic programs of humans' primal hunter-gatherer lifestyle are opposed to the current sedentary lifestyle. Those metabolic programs, which are chronically neglected in modern surroundings, are identified and conclusions for the prevention of chronic metabolic diseases are drawn.

Prototype for in situ detection of atmospheric NO3 and N2O5 via laser-induced fluorescence.

We describe a prototype designed for in situ detection of the nitrate radical (NO3) by laser-induced fluorescence (LIF) and of N2O5 by thermal dissociation followed by LIF detection of NO3. An inexpensive 36 mW continuous wave multi-mode diode laser at 662 nm is used to excite NO3 in the B2E'(0000) <-- X2A'2(0000) band. Fluorescence is collected from 700 to 750 nm. The prototype has a sensitivity to NO3 of 76 ppt for a 60 s integration with an accuracy of 8%. Although this sensitivity is adequate for studies of N205 in many environments, it is much less sensitive (about 300 times) than expected based on a comparison of previously measured photophysical properties of NO2 and NO3. This implies much stronger nonradiative coupling of electronic states in NO3 than in NO2.