Accumulation of metabolic end products within skeletal muscle stimulates sensory nerves, thus evoking a pressor response termed "metaboreflex." The aim of this study was to evaluate changes in hemodynamics occurring during metaboreflex activation obtained by postexercise muscle ischemia (PEMI) after two different exercise intensities. In twelve healthy subjects, the metaboreflex was studied with the PEMI method at the start of recovery from one leg-dynamic knee extension performed at intensities of 30% (PEMI 30%) and 70% (PEMI 70%) of the maximum workload achieved in a preliminary test. Control exercise recovery tests at the same intensities were also conducted. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were that 1) during metaboreflex, exercise conducted against the higher workload caused a more pronounced blood pressure increase than the strain conducted against the lower workload; and 2) during PEMI 70%, this blood pressure response was mainly achieved through enhancement of myocardial contractility that increased stroke volume and, in turn, cardiac output, whereas during PEMI 30%, the blood pressure response was reached predominantly by means of vasoconstriction. Thus a substantial enhancement of myocardial contractility was reached only in the PEMI 70% test. These results suggest that hemodynamic regulation during metaboreflex engagement caused by PEMI in humans is dependent on the intensity of the previous effort. Moreover, the cardiovascular response during metaboreflex is not merely achieved by vasoconstriction alone, but it appears that there is a complex interplay between peripheral vasoconstriction and heart contractility recruitment.
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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