A. Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients.

The aim of this work was to study the differences in cardiovascular response during two modes of recovery [active (AR): pedalling at 40 W; and passive (PR): complete rest seated] from a single bout of supramaximal exercise. Eight male amateur soccer players underwent two supramaximal cycle-ergometer tests, each consisting of pedalling against a resistance equivalent to 150% of the maximum workload achieved in a previous incremental test, followed by randomly assigned AR or PR. Cardiodynamic variables were obtained using an impedance cardiograph. Subjects were also connected to a sphygmomanometer, for systolic and diastolic blood pressure, and to a metabolimeter for oxygen uptake (VO(2)) assessments. We measured: heart rate (HR), stroke volume (SV), cardiac output (CO), the inverse of myocardial contractility calculated as pre-ejection period/left ventricular ejection time ratio (PEP/LVET), mean blood pressure (MBP), thoracic electrical impedance ( Z(0)) as an index of central blood volume, and arterio-venous oxygen difference (A-V O(2) Diff.). PR caused a lower CO compared to AR [mean (SE): 7 (0.7) vs. 10.4 (0.6) l.min(-1 )at the 5th min of recovery] due to lower HR [106.2 (3.6) vs. 121.8 (4.5) bpm at the 5th min of recovery], SV [67.1 (5) vs. 86.1 (4.8) ml at the 5th min of recovery], and PEP/VET values [0.44 (0.007) vs. 0.39 (0.015) at the 5th min of recovery]. No differences were found in MBP and Z(0) between PR and AR [95.1 (1.9) vs. 92.3 (2.7) mmHg and 26.2 (1.1) vs. 26.6 (1) Omega respectively at the 5th min of recovery], while A-V O(2) Diff. values were higher during AR than during PR [108.8 (4.3) vs. 75.2 (5.4) ml.l(-1) at the 5th min of recovery]. Thus, although after a single bout of supramaximal exercise SV and CO are lower during PR than during AR, these differences are not due to an impairment of cardiovascular function, but are fully explained by the lesser muscular engagement that leads to a reduction in stimuli deriving from mechanoreceptors and central commands, thus causing a faster return of myocardial contractility and HR to resting values.

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.

We hypothesized that the role of stroke volume (SV) in the metaboreflex-induced cardiac output (CO) increase was blunted when the metaboreflex was stimulated by exercise muscle ischemia (EMI) compared with post-exercise muscle ischemia (PEMI), because during EMI heart rate (HR) increases and limits diastolic filling. Twelve healthy volunteers were recruited and their hemodynamic responses to the metaboreflex evoked by EMI, PEMI, and by a control dynamic exercise were assessed. The main finding was that the blood pressure increment was very similar in the EMI and PEMI settings. In both conditions the main mechanism used to raise blood pressure was a CO elevation. However, during the EMI test CO was increased as a result of HR elevation whereas during the PEMI test CO was increased as a result of an increase in SV. These results were explainable on the basis of the different HR behavior between the two settings, which in turn led to different diastolic time and myocardial performance.