The diving response is the sequence of cardiovascular, respiratory and metabolic adjustments produced by apnoea and further strengthened by cooling of the facial area and/or hypoxia. This study aimed at comparing the cardiovascular response to diving of trained divers with that of a control group. In this order, 14 trained divers were compared with 14 non-divers. By means of impedance cardiography and continuous monitoring of arterial pressure, hemodynamic data were collected during three different experimental sessions. Each session included a cycle-ergometer exercise against a workload of 0.5 W kg(-1) of body mass, pedalling in a steady-state condition. During exercise, each subject randomly accomplished 40 s of breath-hold exercise with face immersion (test A) or in air (test B). A control exercise test with normal breathing (test C) was also performed. Divers showed a faster onset of bradycardic response (ANOVA, P < 0.01) and a faster adjustment in systemic vascular resistance (P < 0.001 for divers vs. controls) than did non-divers. Moreover, cardiac output decreased only in divers during the first phase of test A (P < 0.01 for divers vs. controls). The most striking findings were that divers showed a more rapid cardiovascular adjustment with respect to controls, in particular in heart rate and systemic vascular resistance; moreover, with continued apnoea, a delayed increase in myocardial performance and stroke volume occurred and obscured the cardiovascular effects of the diving response.
To verify the relationship between exercise intensity and post-exercise haemodynamics, we studied haemodynamic and lactate responses during 10 min following 3 bicycle tests. Two tests were performed for 3 min at 70% and 130% of the workload corresponding to anaerobic threshold (70% W(at) and 130% W(at) tests), and 1 was performed until exhaustion at 150% of the maximum workload achieved during a previous incremental test (150% W(max) test). During the recovery period after the 150% W(max) test we observed the highest increases in blood lactate with respect to the baseline: at the 9th minute of recovery lactate concentration increased by +9.3 +/- 2.7, +6.4 +/- 3.1, and +1.1 +/- 0.9 mmol x L(-1) in the 150% W(max) (p > 0.05 with respect to the other protocol sessions), 130% W(at), and 70% W(at) tests, respectively. We also observed greater reductions in cardiac pre-load and systemic vascular resistance in the 150% W(max) test than in the 130% W(at) and 70% W(at) tests. However, the cardiac output response successfully faced the increased vasodilatation occurring during 150% W(max) test so that changes in mean blood pressure were similar in the 3 test conditions. This study shows that exercises that yielded different lactate concentrations also led to greater vasodilatation. Nevertheless, mechanisms controlling the cardiovascular apparatus successfully prevented a drop in blood pressure in spite of the cardiovascular stress.
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