Seven subjects underwent a standard localized exercise of calf muscles in order to investigate whether the metabolic exercise‐induced steady‐state, as revealed by the evaluation of inorganic phosphate/phosphocreatine ratio, depends on the conditioning of the muscle just prior to the exercise. The experimental protocols consisted of two separate experiments using first [31P]nuclear magnetic resonance spectroscopy and second (on 3 subjects) infrared oxyphotometry to respectively follow variation of energy metabolism and tissular deoxygenation. The exercise consisted of 240 successive plantar flexions (0.5 Hz frequency) against a high load equivalent to SO% of the maximal voluntary contraction. This exercise was accomplished before cold exercise and after warm exercise, a warming‐up period bringing to approximately 50% ofVo2max. The results showed that: (1) steady‐state level of phosphate/phosphocreatine and intracellular acidosis was significantly lowered by warming‐up; (2) cold and warm exercise steady‐state of calculated adenosine diphosphate values were not significantly different; (3) cold exercise rapidly induced a high tissular deoxygenation that is not observed during warm exercise; and (4) time‐constant of phosphocreatine resynthesis is lowered after warm exercise but the initial slope of time‐evolution is not modified. Parallel experiments also showed that phosphate/phosphocreatine steady‐state was not modified in comparison with warm exercise when the same power of exercise was reached by stepwise incrementation of the charge. From these results we postulate that a better tissue oxygenation due to a global or localized warming‐up allows to reach the same mechanical performance with a lower decrease of PCr content, owing to a faster adjustment of oxidative metabolism during the transitional period. However the aerobic pathway flux during the steady‐state is probably the same before and after the warming‐up despite different values of phosphate/phosphocreatine. As a consequence it can be assumed that this ratio is not a good indicator of the rate of muscle oxidative metabolism during the steady‐st