Robin Hood for the lungs? A respiratory metaboreflex that ‘steals’ blood flow from locomotor muscles
http://jp.physoc.org/content/537/1/2.full.pdf
Exercise-Induced Metabolic Acidosis: Where do the Protons come from?
Robert A Robergs
The widespread belief that intense exercise causes the production of “lactic acid” that contributes to acidosis is erroneous. In the breakdown of a glucose molecule to 2 pyruvate molecules, three reactions release a total of four protons, and one reaction consumes two protons. The conversion of 2 pyruvate to 2 lactate by lactate dehydrogenase (LDH) also consumes two protons. Thus lactate production retards rather than contributes to acidosis. Proton release also occurs during ATP hydrolysis. In the transition to a higher exercise intensity, the rate of ATP hydrolysis is not matched by the transport of protons, inorganic phosphate and ADP into the mitochondria. Consequently, there is an increasing dependence on ATP supplied by glycolysis. Under these conditions, there is a greater rate of cytosolic proton release from glycolysis and ATP hydrolysis, the cell buffering capacity is eventually exceeded, and acidosis develops. Lactate production increases due to the favorable bioenergetics for the LDH reaction. Lactate production is therefore a consequence rather than a cause of cellular conditions that cause acidosis. Researchers, clinicians, and sports coaches need to recognize the true causes of acidosis so that more valid approaches can be developed to diminish the detrimental effects of acidosis on their subject/patient/client populations.
Intermittent Hypoxia Research in the Former Soviet Union:
Tatiana V. Serebrovskaya Department of Hypoxic States, Bogomoletz Institute of Physiology, Kiev Ukraine
This review aims to summarize the basic research in the field of intermittent hypoxia in the Soviet Union and the Commonwealth of Independent States (CIS) that scientists in other Western countries may not be familiar with, since Soviet scientists were essentially cut off from the global scientific community for about 60 years. In the 1930s the concept of repeated hypoxic training was developed and the following induction methods were utilized: repeated stays at high-mountain camps for several weeks, regular high altitude flights by plane, training in altitude chambers, and training by inhalation of low-oxygen-gas mixtures. To the present day, intermittent hypoxic training (IHT) has been used extensively for altitude preacclimatization; for the treatment of a variety of clinical disorders, including chronic lung diseases, bronchial asthma, hypertension, diabetes mellitus, Parkinson's disease, emotional disorders, and radiation toxicity, in prophylaxis of certain occupational diseases; and in sports. The basic mechanisms underlying the beneficial effects of IHT are mainly in three areas: regulation of respiration, free-radical production, and mitochondrial respiration. It was found that IHT induces increased ventilatory sensitivity to hypoxia, as well as other hypoxia-related physiological changes, such as increased hematopoiesis, alveolar ventilation and lung diffusion capacity, and alterations in the autonomic nervous system. Due to IHT, antioxidant defense mechanisms are stimulated, cellular membranes become more stable, Ca2+ elimination from the cytoplasm is increased, and O2 transport in tissues is improved. IHT induces changes within mitochondria, involving NAD-dependent metabolism, that increase the efficiency of oxygen utilization in ATP production. These effects are mediated partly by NO-dependent reactions. The marked individual variability both in animals and humans in the response to, and tolerance of, hypoxia is described. Studies from the Soviet Union and the CIS significantly contributed to the understanding of intermittent hypoxia and its possible beneficial effects and should stimulate further research in this direction in other countries.
http://www.ncbi.nlm.nih.gov/pubmed/12162864
Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia:
An enduring hypothesis in exercise physiology holds that a limiting cardiorespiratory function determines maximal exercise performance as a result of specific metabolic changes in the exercising skeletal muscle, so-called peripheral fatigue. The origins of this classical hypothesis can be traced to work undertaken by Nobel Laureate A. V. Hill and his colleagues in London between 1923 and 1925. According to their classical model, peripheral fatigue occurs only after the onset of heart fatigue or failure. Thus, correctly interpreted, the Hill hypothesis predicts that it is the heart, not the skeletal muscle, that is at risk of anaerobiosis or ischaemia during maximal exercise. To prevent myocardial damage during maximal exercise, Hill proposed theexistence of a ‘governor’ in either the heart or brain to limit heart work when myocardial ischaemia developed. Cardiorespiratory function during maximal exercise at different altitudes or at different oxygen fractions of inspired air provides a definitive test for the presence of a governor and its function. If skeletal muscle anaerobiosis is the protected variable then, under conditions in which arterial oxygen content is reduced, maximal exercise should terminate with peak cardiovascular function to ensure maximum delivery of oxygen to the active muscle. In contrast, if the function of the heart or some other oxygen-sensitive organ is to be protected, then peak cardiovascular function will be higher during hyperoxia and reduced during hypoxia compared with normoxia. This paper reviews the evidence that peak cardiovascular function is reduced during maximal exercise in both acute and chronic hypoxia with no evidence for any primary alterations in myocardial function. Since peak skeletal muscle electromyographic activity is also reduced during hypoxia, these data support a model in which a central, neural governor constrains the cardiac output by regulating the mass of skeletal muscle that can be activated during maximal exercise in both acute and chronic hypoxia.
http://jeb.biologists.org/cgi/content/abstract/204/18/3225
The anticipatory regulation of performance: the physiological basis for pacing strategies and the development of a perception-based model for exercise performance.
During self-paced exercise, the exercise work rate is regulated by the brain based on the integration of numerous signals from various physiological systems. It has been proposed that the brain regulates the degree of muscle activation and thus exercise intensity specifically to prevent harmful physiological disturbances. It is presently proposed how the rating of perceived exertion (RPE) is generated as a result of the numerous afferent signals during exercise and serves as a mediator of any subsequent alterations in skeletal muscle activation levels and exercise intensity. A conceptual model for how the RPE mediates feedforward, anticipatory regulation of exercise performance is proposed, and this model is applied to previously described research studies of exercise in various conditions, including heat, hypoxia and reduced energy substrate availability. Finally, the application of this model to recent novel studies that altered pacing strategies and performance is described utilising an RPE clamp design, central nervous system drugs and the provision of inaccurate duration or distance feedback to exercising athletes.
http://www.ncbi.nlm.nih.gov/pubmed/19224911
