Avena sativa coleoptile segments show an anomalous increase in elongation growth following a short period of oxygen deprivation (tested between 0 and 60 min) lasting 20-30 min (Anaero-biosis-Aerobiosis transition effect = ANA effect). The increase in growth rate is 600% and is commensurate with that observable following an auxin treatment. This hyperelongation growth, in contrast to the auxin-induced growth, begins without a lag phase. The growth “burst” following anaerobiosis is similarly to auxin-induced elongation growth, and is suppressed increasingly by neutral or more alkaline buffers. Hyperelongation growth is suppressed by respiratory inhibitors and uncouplers. A complete inhibition is effected with KCN (0.5 mM) sodium azide (0.5 mM) and CCCP (1 μM); amytal (in the range 0.5 to 1 mM) and sodium arsenate (0.1 to 1 mM) are strong inhibitors. Some of these compounds (KCN, arsenate, amytal) cause a slight increase of the ANA effect in very low concentrations, which is probably due to the K+ or Na+ ions present; on their own, these ions have a strong positive influence on the ANA effect. During anaerobiosis the ATP level sinks around 75% and almost returns to the old value, following the supply of air, within one minute. The cell sap pH drops from 6.3 to 5.9 during anaerobiosis within 20 min. This lowering is mainly due to an increase in lactic acid concentration. Other acids such as citric, malic, and aspartic acids show insignificant changes in concentration. The NADH content increases during anaerobiosis, whereas that of NADPH drops almost as much. The mentioned changes in concentration of lactic acid, NADH and NADPH return to the control value within 20-30 min; thus the differences exist as long as hyperelongation growth is under way. Possible relationships between the mentioned chemical changes and hyperelongation growth are discussed. One of the possible explanations is the following: the lowering of the cytoplasmic pH (normally around pH 7) during anaerobiosis due to the formation of lactic acid causes an activation of H+-ATPases in the plasmalemma and ER, since their optimum activity occurs in a pH of 5.5 to 6.5. This activation causes a greater H+-excretion into the cell wall compartment, and thus hyperelongation growth following supply of air and of ATP.