Brief episodes of nonlethal ischemia, commonly known as "ischemic preconditioning" (IP), are protective against cell injury induced by infarction. Moreover, muscle IP has been found capable of improving exercise performance. The aim of the study was the comparison of standard exercise performances carried out in normal conditions with those carried out following IP, achieved by brief muscle ischemia at rest (RIP) and after exercise (EIP). Seventeen physically active, healthy male subjects performed three incremental, randomly assigned maximal exercise tests on a cycle ergometer up to exhaustion. One was the reference (REF) test, whereas the others were performed after the RIP and EIP sessions. Total exercise time (TET), total work (TW), and maximal power output (W(max)), oxygen uptake (VO(2max)), and pulmonary ventilation (VE(max)) were assessed. Furthermore, impedance cardiography was used to measure maximal heart rate (HR(max)), stroke volume (SV(max)), and cardiac output (CO(max)). A subgroup of volunteers (n = 10) performed all-out tests to assess their anaerobic capacity. We found that both RIP and EIP protocols increased in a similar fashion TET, TW, W(max), VE(max), and HR(max) with respect to the REF test. In particular, W(max) increased by ∼ 4% in both preconditioning procedures. However, preconditioning sessions failed to increase traditionally measured variables such as VO(2max), SV(max,) CO(max), and anaerobic capacity(.) It was concluded that muscle IP improves performance without any difference between RIP and EIP procedures. The mechanism of this effect could be related to changes in fatigue perception.
These results suggest that the blood pressure response during metaboreflex activation after mild rhythmic exercise is strongly dependent on the capacity to increase cardiac output rather than due to increased vascular resistance.
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.
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