Detraining is the partial or complete loss of training-induced adaptations, in response to an insufficient training stimulus. Detraining characteristics may be different depending on the duration of training cessation or insufficient training. Short term detraining (less than 4 weeks of insufficient training stimulus) is analysed in part I of this review, whereas part II will deal with long term detraining (more than 4 weeks of insufficient training stimulus). Short term cardiorespiratory detraining is characterised in highly trained athletes by a rapid decline in maximal oxygen uptake (VO2max) and blood volume. Exercise heart rate increases insufficiently to counterbalance the decreased stroke volume, and maximal cardiac output is thus reduced. Ventilatory efficiency and endurance performance are also impaired. These changes are more moderate in recently trained individuals. From a metabolic viewpoint, short term inactivity implies an increased reliance on carbohydrate metabolism during exercise, as shown by a higher exercise respiratory exchange ratio, and lowered lipase activity, GLUT-4 content, glycogen level and lactate threshold. At the muscle level, capillary density and oxidative enzyme activities are reduced. Training-induced changes in fibre cross-sectional area are reversed, but strength performance declines are limited. Hormonal changes include a reduced insulin sensitivity, a possible increase in testosterone and growth hormone levels in strength athletes, and a reversal of short term training-induced adaptations in fluid-electrolyte regulating hormones.