Proceedings of The Physiological Society

University College Cork (2004) J Physiol 560P, C15

Communications

SHORT LATENCY OF HUMAN CARDIOVASCULAR CHANGES DURING AEROBIC TRAINING

Delaney,Timothy ; Bell,Christopher ;

1. Physiology, Trinity College Dublin, Dublin, Ireland.


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% VO2max 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 VO2max 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.

Where applicable, experiments conform with Society ethical requirements