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Inorganic phosphate (P(i)) plays a key role in diverse physiological functions. Recent studies have indicated that P(i) affects Akt signaling through the sodium-dependent phosphate cotransporter. Akt signaling, in turn, plays an important role in liver development; however, the effects of high dietary P(i) on the liver have not been investigated. Here, we examined the effects of high dietary phosphate on the liver in developing mice. We found that high dietary P(i) increased liver mass through enhancing Akt-related cap-dependent protein translation, cell cycle progression, and angiogenesis. Thus careful regulation of P(i) consumption may be important in maintaining normal development of the liver.

Multiple physiological functions were monitored in ten men who performed two 30-min periods of 150-W ergometer exercise during 120-min exposures to O2 at 2.0 ATA. There were no convulsions or electroencephalographic manifestations of increased excitability. Sequential measurements of peripheral visual fields, pulmonary mechanical function, mental performance, and cardiovascular function during the resting recovery after each of the two exercise periods were not detectably altered from pre-exercise control values. Pre- and post-exposure measurements of visual acuity, accommodation, pupil diameter, visual cortical activity, and retinal electrical activity also revealed no significant differences. While CNS symptoms were absent, average arterial PCO2 rose by about 5 mm Hg during both exercise periods. This finding was confirmed in six subjects who performed four 6-min periods of continuous exercise at 50, 100, 150, and 200 W while breathing O2 at 2.0 ATA. Average arterial PCO2 rose nearly linearly from 34.3 mm Hg at rest to 44.0 mm Hg at 200 W. Arterial PCO2-related increments in brain blood flow and PO2 may explain part or all of the known detrimental influence of exercise on CNS O2 tolerance.