Chronic exercise lowers resting blood pressure, reduces pressor responses to laboratory stress tests and increases microvascular dilator capacity. While these changes are most pronounced after prolonged training, 5-6 weeks of moderate aerobic training is sufficient to induce significant effects (O’Sullivan & Bell, 2001; OSullivan, 2003). We have now studied the latency of onset of these cardiovascular changes during a shorter training period. With institutional ethics approval, 15 sedentary non-obese male subjects (age 21.9 ± 0.4 years, mean ± SEM) were recruited into two groups. Eight subjects undertook moderate aerobic training (cycle ergometry, 30 min at 60% VO_2max 3-4 times/week) for 4 weeks. The remaining 7 subjects acted as controls. Before training commenced and at weekly intervals during the training period, all subjects attended the laboratory where beat-to-beat blood pressure and heart rate were measured at rest and during isometric handgrip to fatigue at 30% maximal power, and forearm reactive hyperaemia was measured by venous occlusion plethysmography following 3 min arterial occlusion. The total 4-week training period increased VO_2max by 10% from 47 ± 1 to 52 ± 1 [ml.kg^-1].min^-1 and increased circulating endothelial cells from 42 ± 5 to 49 ± 4 cells.ml^-1 (P<0.05 each, paired Students t test). These changes are similar in magnitude to those that we have reported previously after 5 weeks training. Resting blood pressure remained at pre-training values over the first week of training but after 2 weeks had fallen from 90 ± 2 to 76 ± 2 mmHg and remained at this level over the ensuing weeks (P<0.001, repeated measures ANOVA). Both systolic and diastolic pressures fell to similar extents. Resting heart rate was not reduced. Prior to training, isometric handgrip caused a rise in heart rate of 29 ± 1 bpm. This fell to 17 ± 3 bpm (P<0.01) at week 3 and remained reduced. Pressor responses to handgrip did not vary significantly during the training period but peak rate-pressure product during exercise was reduced after 3 or more weeks training (pre- 154 ± 12, 3 weeks 125 ± 9 bpm.mmHg^-2, P< 0.05). Prior to training, peak forearm conductance during reactive hyperaemia was 0.12 ± 0.01 [ml.100 ml^-1].min^-1.mmHg^-1. After 2 weeks training the reponse was increased (P<0.001) to 0.23 ± 0.01 [ml.100 ml^-1].min^-1 mmHg^-1 and stabilised at this value. No changes in any measured parameter were seen in the control group. In summary, our results indicate that a number of circulatory effects of intermittent, moderate exercise programmes reach near-maximal levels within 2-3 weeks. We are currently investigating how long these changes persist after cessation of training.