PubMed · 15586721
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Raymond E Spier. 2004. Words are tools.. https://doi.org/10.1007/s11948-004-0040-6
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The energy expenditure required by the respiratory muscles during exercise is a function of their work rate, cost of breathing, and efficiency. During exercise, ventilatory requirements increase further exacerbating the potential imbalance between inspiratory muscle load and capacity. High level of exercise intensity in conjunction with contracting respiratory muscles is the reason for respiratory muscle fatigue in healthy subjects. Available evidence would suggest that fatigue of the diaphragm and other respiratory muscles is an important mechanism involved in redistribution of blood flow. Reflex mechanisms of sympathoexcitation are triggered in fatigued diaphragm during heavy exercise when cardiac output is not sufficient to adequately meet the high metabolic requirements of both respiratory and limb musculature. It is very likely that local changes in locomotor muscle blood flow may occur during exhaustive endurance exercise and that changes may have important effect on O2 transport to the working locomotor muscles and, therefore, on their fatigability. In a condition when the respiratory muscles receive their share of blood flow at the expense of limb locomotor muscles, minimizing mechanical work of breathing and therefore its metabolic cost allows a greater amount of cardiac output to be available to be delivered to working limb muscles. Malfunction in any of the multiple components responsible for circulatory flow and O2 delivery will limit the blood supply therefore inhibiting the supply of O2 and the energy substrate to the contracting muscles. Studies are needed to overcome these limitations.
BACKGROUND: Existing large-scale metabolic models of sequenced organisms commonly include enzymatic functions which can not be attributed to any gene in that organism. Existing computational strategies for identifying such missing genes rely primarily on sequence homology to known enzyme-encoding genes. RESULTS: We present a novel method for identifying genes encoding for a specific metabolic function based on a local structure of metabolic network and multiple types of functional association evidence, including clustering of genes on the chromosome, similarity of phylogenetic profiles, gene expression, protein fusion events and others. Using E. coli and S. cerevisiae metabolic networks, we illustrate predictive ability of each individual type of association evidence and show that significantly better predictions can be obtained based on the combination of all data. In this way our method is able to predict 60% of enzyme-encoding genes of E. coli metabolism within the top 10 (out of 3551) candidates for their enzymatic function, and as a top candidate within 43% of the cases. CONCLUSION: We illustrate that a combination of genome context and other functional association evidence is effective in predicting genes encoding metabolic enzymes. Our approach does not rely on direct sequence homology to known enzyme-encoding genes, and can be used in conjunction with traditional homology-based metabolic reconstruction methods. The method can also be used to target orphan metabolic activities.
Oxygen is essential for the survival of obligatorily aerobic eukaryotic microorganisms, such as the multicellular fungus Trichoderma reesei. However, the molecular basis for the inability of such cells to survive for extended periods under anoxic conditions is not fully understood. Using cDNA microarray analysis, we show that changes in oxygen availability have a drastic effect on gene expression in T. reesei. The expression levels of 392 (19.6%) out of 2000 genes examined changed significantly in response to hypoxia, transient anoxia, and reoxygenation. In addition to modulating many genes with no previously assigned function, cells respond to hypoxia by readjusting the balance of expression between genes required for energy production and consumption, and altering the expression of genes involved in protective mechanisms and signaling pathways. Moreover, we show that transient anoxia strongly represses genes for enzymes that are critical for glycolysis, and are essential for energy production under anaerobic conditions. Our study thus reveals crucial differences between the facultative anaerobe Saccharomyces cerevisiae and T. reesei with regard to the oxygen-dependent transcriptional control of the glycolytic pathway, which can account for the differential survival of the two species in the absence of oxygen.