A 12-Week Vigorous Exercise Protocol in a Healthy Group of Persons over 65: Study of Physical Function by means of the Senior Fitness Test.

The aim of this study was to assess the effects of vigorous exercise on functional abilities by means of a Senior Fitness Test (SFT) in a group of elderly adults. Twenty healthy and inactive people performed vigorous exercise (VE: 12 men and 8 women, aged 69.6 ± 3.9 years). At the beginning of the study (T0) and after 3 months (T1), each subject's functional ability was tested for muscular strength, agility, cardiovascular fitness, flexibility, and balance. The VE was designed with continuous and interval exercise involving large muscle activities. Functional exercises were performed between 60% and 84% of heart rate reserve (HRR) for a duration of 65 minutes. Five out of the 6 SFTs performed were found significantly improved: Chair Stand (T0 12.4 ± 2.4, T1 13.5 ± 2.6, p < 0.01), Arm Curl (T0 14.2 ± 3.6, T1 16.6 ± 3.6, p < 0.01), 2 min step (T0 98.2 ± 15.7, T1 108.9 ± 16.2, p < 0.01), Chair Sit-and-Reach (T0 -9.9 ± 7.7 cm, T1 1.7 ± 6.3 cm, p < 0.01), and Back Scratch (T0 -15.8 ± 10.9 cm, T1 -8.4 ± 13.1 cm, p < 0.01). Our results suggest that a high intensity protocol and functional exercises can improve functional mobility and muscle endurance in those over 65 years of age. SFTs are an effective method for assessing improvements in the functional capacity of elderly adults.

Nervous Facilitation in Cardiodynamic Response of Exercising Athletes to Superimposed Mental Tasks: Implications in Depressive Disorder.

INTRODUCTION: Motor commands to perform exercise tasks may also induce activation of cardiovascular centres to supply the energy needs of the contracting muscles. Mental stressors per se may also influence cardiovascular homeostasis. We investigated the cardiovascular response of trained runners simultaneously engaged in mental and physical tasks to establish if aerobically trained subjects could develop, differently from untrained ones, nervous facilitation in the brain cardiovascular centre. Methods : Cardiovascular responses of 8 male middle-distance runners (MDR), simultaneously engaged in mental (colour-word interference test) and physical (cycle ergometer exercise) tasks, were compared with those of 8 untrained subjects. Heart rate, cardiac (CI) and stroke indexes were assessed by impedance cardiography while arterial blood pressures were assessed with a brachial sphygmomanometer. Results : Only in MDR simultaneous engagement in mental and physical tasks induced a significant CI increase which was higher (p<0.05) than that obtained on summing CI values from each task separately performed. Conclusion : Aerobic training, when performed together with a mental effort, induced a CI oversupply which allowed a redundant oxygen delivery to satisfy a sudden fuel demand from exercising muscles by utilizing aerobic sources of ATP, thus shifting the anaerobic threshold towards a higher work load. From data of this study it may also be indirectly stated that, in patients with major depressive disorder, the promotion of regular low-intensity exercise together with mental engagement could ameliorate the perceived physical quality of life, thus reducing their heart risk associated with physical stress.

Body composition changes affect energy cost of running during 12 months of specific diet and training in amateur athletes.

Considering the relation between body weight composition and energy cost of running, we tested the hypothesis that by modifying body composition by means of a combined protocol of specific diet and training, the energy cost of motion (Cr) may be reduced. Forty-five healthy and normal-weight subjects were divided into 3 groups that performed a different treatment: the first group attended a dietary protocol (D), the second group participated in a running program (R), and the third group followed both the dietary and running protocols (R&D). Each subject underwent 3 anthropometric and exercise evaluation tests during 1 year (at entry (T0), month 6 (T6), and month 12 (T12)) to assess body composition and Cr adjustments. The mean fat mass (FM) values were reduced in R&D from 12.0 ± 4.0 to 10.4 ± 3.0 kg (p < 0.05 T0 vs. T12) and in the D group from 14.2 ± 5.8 to 11.6 ± 4.7 kg (p < 0.05 T0 vs. T12). Conversely, the mean fat free mass values increased in R&D (from 56.3 ± 8.8 to 58.3 ± 9.8 kg, p < 0.05 T0 vs. T12) and in the D group (from 50.6 ± 13.2 to 52.9 ± 13.6 kg, p < 0.05 T0 vs. T12). The mean Cr values of the 2 groups were significantly modified throughout the 1-year protocol (1.48 ± 0.16 and 1.40 ± 0.15 kcal·kg(-b)·km(-1) in the R&D group at T0 and T12, respectively; 1.83 ± 0.17 and 1.76 ± 0.23 kcal·kg(-b)·km(-1) in D group at T0 to T12, respectively). The R&D and D groups that underwent the diet protocol had a positive change in body composition during the year (FM/fat free mass ratio decline), which determined a Cr reduction.

Heart Rate Unreliability during Interval Training Recovery in Middle Distance Runners.

Heart rate (HR) was tested as a reliable index for recovery management during interval training (IT), considering its relationship with the several factors involved in respiratory, metabolic and cardiovascular homeostasis. Thirteen runners underwent two different IT sessions: at 80% and 120% of the second ventilatory threshold (VT2). Throughout both sessions HR, oxygen uptake (VO2), carbon dioxide production (VCO2) and pulmonary ventilation (VE), were measured by means of a portable gas analyzer. Carbon dioxide production excess (CO2excess), respiratory exchange ratio (RER), oxygen pulse (OP) and oxygen debt (O2debt) were also estimated. A significant increase in HR values (144 versus 150 beats·min(-1) between the first recovery and the last, p < 0.001) was observed at 80% of the VT2 speed. At the over-threshold intensity, HR rose from 159 to 168 beats·min(-1) from the first recovery to the last (p < 0.001). OP showed a declining trend from the first to the last recovery at 80% at the VT2 speed (18.3 versus 16.4 mL·beats(-1), p < 0.05) and between the first and the last recovery in tests performed at 120% of the VT2 speed (17.8 versus 16.3 mL·beats(-1), p < 0.05). No change occurred in CO2excess, VO2, RER, VE and O2debt. On the basis of our research, the use of fixed HR as a reliable index of the established recovery is inaccurate and unfit for training. The phenomenon of cardiac drift to set the restart timing after the repetitions, i.e. by progressively increasing HR values, should be taken into account by coaches. Key pointsDuring an IT session, if recovery time after repetitions is fixed, HR supplies a different indication compared to all the respiratory parameters: HR indicates an incomplete recovery while the other parameters do not.The use of fixed HR values as a reliable index of the established recovery during IT is inaccurate and it may be the cause of under-training.To set the restart timing after repetitions the phenomenon of cardiac drift should be taken into account by coaches.HR drift during recoveries did not appear linked to the CO2excess.

Cardiovascular adjustments in breath-hold diving: comparison between divers and non-divers in simulated dynamic apnoea.

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.

Role of heart rate and stroke volume during muscle metaboreflex-induced cardiac output increase: differences between activation during and after exercise.

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.

Hemodynamic responses to metaboreflex activation: insights from spinal cord-injured humans.

This investigation was conducted to study the hemodynamic consequences of spinal cord injury (SCI) during post-exercise muscle metaboreflex activation in SCI subjects. The hemodynamic response to metaboreflex recruitment was assessed in ten SCI patients and nine healthy controls (CTL) by means of impedance cardiography. The main results were (1) the metaboreflex-induced blood pressure rise was blunted in SCI subjects compared with normals, (2) the CTL group achieved the blood pressure response via cardiac output increase, while the SCI subjects could not use this mechanism, (3) the CTL group was able to enhance stroke volume and ventricular filling rate in response to the metaboreflex, whereas the SCI group could not. It was concluded that in healthy individuals, the hemodynamic response to the metaboreflex is an integrated phenomenon that depends mainly on a flow-mediated mechanism, whereas in SCI individuals the reduced venous return impairs this mechanism.

Physiological responses and energy cost during a simulation of a Muay Thai boxing match.

Muay Thai is a martial art that requires complex skills and tactical excellence for success. However, the energy demand during a Muay Thai competition has never been studied. This study was devised to obtain an understanding of the physiological capacities underlying Muay Thai performance. To that end, the aerobic energy expenditure and the recruitment of anaerobic metabolism were assessed in 10 male athletes during a simulation match of Muay Thai. Subjects were studied while wearing a portable gas analyzer, which was able to provide data on oxygen uptake, carbon dioxide production, and heart rate (HR). The excess of CO2 production (CO2 excess) was also measured to obtain an index of anaerobic glycolysis. During the match, group energy expenditure was, on average (mean +/- standard error of the mean), 10.75 +/- 1.58 kcal.min-1, corresponding to 9.39 +/- 1.38 metabolic equivalents. Oxygen uptake and HRs were always above the level of the anaerobic threshold assessed in a preliminary incremental test. CO2 excess showed an abrupt increase in the first round, and reached a value of 636 +/- 66.5 mL.min-1. This parameter then gradually decreased throughout the simulation match. These data suggest that Muay Thai is a physically demanding activity with great involvement of both the aerobic metabolism and anaerobic glycolysis. In particular, it appears that, after an initial burst of anaerobic glycolysis, there was a progressive increase in the aerobic energy supply. Thus, training protocols should include exercises that train both aerobic and anaerobic energetic pathways.

Haemodynamic effect of metaboreflex activation in men after running above and below the velocity of the anaerobic threshold.

Previous studies have shown that the muscle metaboreflex, along with its effect on peripheral vasculature, is capable of inducing substantial enhancement in cardiac performance, stroke volume and cardiac output. This study was designed to determine whether the metaboreflex recruited by means of postexercise muscle ischaemia (PEMI) after running at two intensities was capable of eliciting similar enhancement in these cardiovascular parameters. In eight healthy male athletes the metaboreflex was studied with the PEMI method at the start of recovery from running bouts at a velocity of 30% above (PEMI-AV(AT)) or below (PEMI-BV(AT)) the anaerobic threshold previously assessed. Control exercise recovery tests at the same intensities were also conducted. Haemodynamics were evaluated by means of impedance cardiography. The main results were that: (1) the PEMI-AV(AT) test induced an increase in stroke volume, which was not present during the other protocol conditions; (2) the PEMI-AV(AT) test also induced a blunted heart rate response compared with the control situation, but this relative bradycardia was fully compensated by the stroke volume increment so that cardiac output was maintained and even increased in comparison with the other protocol sessions; and (3) finally, there was no detectable increase in systemic vascular resistance during PEMI-AV(AT). These results provide evidence that, like what has previously been reported for small muscle mass exercise, metaboreflex activation after running is capable of enhancing cardiac performance and stroke volume. Moreover, this study strengthens the concept that the cardiovascular response to metaboreflex is not merely the consequence of an increase in systemic vascular resistance.

Estimating stroke volume from oxygen pulse during exercise.

This investigation aimed at verifying whether it was possible to reliably assess stroke volume (SV) during exercise from oxygen pulse (OP) and from a model of arterio-venous oxygen difference (a-vO(2)D) estimation. The model was tested in 15 amateur male cyclists performing an exercise test on a cycle-ergometer consisting of a linear increase of workload up to exhaustion. Starting from the analysis of previous published data, we constructed a model of a-vO(2)D estimation (a-vO(2)D(est)) which predicted that the a-vO(2)D at rest was 30% of the total arterial O(2) content (CaO(2)) and that it increased linearly during exercise reaching a value of 80% of CaO(2) at the peak workload (W(max)) of cycle exercise. Then, the SV was calculated by applying the following equation, SV = OP/a-vO(2)D(est), where the OP was assessed as the oxygen uptake/heart rate. Data calculated by our model were compared with those obtained by impedance cardiography. The main result was that the limits of agreement between the SV assessed by impedance cardiography and the SV estimated were between 22.4 and -27.9 ml (+18.8 and -24% in terms of per cent difference between the two SV measures). It was concluded that our model for estimating SV during effort may be reasonably applicable, at least in a healthy population.

Delayed preconditioning-mimetic actions of exercise or nitroglycerin do not affect haemodynamics and exercise performance in trained or sedentary individuals.

Nitroglycerin induces the so-called second window of protection (SWOP), which alleviates myocardial damage and stunning after ischaemia/reperfusion. To determine whether myocardial performance during exercise is improved in the second window of protection, we studied the haemodynamic responses of 12 trained and 11 sedentary individuals during a sequence of maximal tests on a cycle ergometer. A baseline test (basal test) was followed by a second effort performed during the second window of protection (exercise-SWOP test). Haemodynamics was also evaluated after pharmacologically induced SWOP 48 h after transdermal administration of 10 mg of nitroglycerin (pharmacologically induced SWOP test). The exercise-SWOP and pharmacologically induced SWOP tests were separated by a 1-week washout period. Endothelial-dependent vasodilatation after nitroglycerin pre-treatment was also assessed in five sedentary individuals to determine whether nitrate donors could affect vascular function. We found that nitroglycerin pre-treatment did not induce any improvement in haemodynamics in either trained or sedentary individuals, since maximum values of workload, heart rate, stroke volume, cardiac output, myocardial contractility, and double product were similar between the exercise-SWOP and pharmacologically induced SWOP tests in both groups. Furthermore, nitroglycerin pre-treatment did not alter flow-mediated dilation during pharmacologically induced SWOP. Although nitroglycerin pre-treatment alleviates post-ischaemic myocardial stunning, our results suggest that it does not affect the myocardial performance of healthy individuals during exercise performed in the second window of protection, independently of the training status of the individuals. Moreover, nitroglycerin pre-treatment does not ameliorate endothelial function.

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

The muscle metaboreflex is enhanced in chronic heart failure (CHF) patients, and this fact has been associated with the early fatigue shown by these patients in response to exercise. In animal studies of CHF, it was found that the limited capacity to enhance ventricular performance is responsible for a functional shift from a cardiac output to a systemic vascular resistance (SVR) increase in the mechanism by which the cardiovascular system raises blood pressure in response to the metaboreflex. However, the existence of this functional shift is still unknown in humans. The present study was undertaken to test the hypothesis that a similar hemodynamic response was also present in humans with CHF. The hemodynamic response to metaboreflex activation obtained through postexercise ischemia was assessed in nine patients with CHF and nine healthy controls (CTL) by means of impedance cardiography. The main results were that 1) the blood pressure rise due to the metaboreflex was similar in the two groups; 2) the CTL group achieved the blood pressure response via cardiac output increase, and the CHF group, via SVR increase; and 3) stroke volume was enhanced in the CTL group and decreased in the CHF group. This study demonstrates that in CHF patients, metaboreflex recruitment causes a functional shift from flow increase to peripheral vasoconstriction in the mechanism through which blood pressure is increased. The incapacity to enhance cardiac performance and stroke volume is probably the primary cause of this cardiovascular alteration.

Exercise capacity and cardiovascular changes in patients with beta-thalassaemia major.

Despite the introduction of deferoxamine, 50% of thalassaemia major patients die before the age of 35 years predominantly from iron induced heart failure. Indeed, the assessment of myocardial performance may be of particular interest since it can reveal an early myocardial dysfunction. By using impedance cardiography and mass spectrometry, we studied the cardiac function and the oxygen extraction ratio (O(2)ER) of 14 thalassaemic patients and 15 control healthy subjects during an incremental cycle-ergometer test. The achieved mechanical power output and the relative O(2) uptake did not reach any significant difference between groups. At the highest workload, O(2)ER reached significantly higher values in thalassaemic patients versus control subjects while the relationship between cardiac index (CI) and O(2)ER (CI/O(2)ER) decreased showing a lower contribution of cardiovascular system to maintain O(2) uptake. Results of this study imply that CI/O(2)ER allows an early diagnosis of the iron induced myocardial dysfunction, whereas it is not clinically patent yet. To our knowledge, this is the first study revealing an O(2)ER pivotal role as compensatory mechanism to maintain a normal working capacity in subjects suffering from thalassaemia major.

Effect of differences in post-exercise lactate accumulation in athletes' haemodynamics.

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.

Modulation of cardiac contractility by muscle metaboreflex following efforts of different intensities in humans.

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.

Detection of lactate threshold by including haemodynamic and oxygen extraction data.

To date, few attempts have been made to correlate cardiovascular variables to lactate threshold (L(T)). This study was designed to determine the relationship between the accumulation of blood lactate and several haemodynamic variables during exercise. Eight male volunteer cyclists performed an incremental test on an electromagnetically braked cycle-ergometer consisting of a 50 W linear increase in workload every 3 min up to exhaustion. Blood lactate was measured with a portable analyser during each exercise step. Oxygen consumption (VO(2)) and pulmonary ventilation were measured by means of a mass spectrometer while heart rate, stroke volume and cardiac output (CO) were assessed by impedance cardiography. The arterio-venous oxygen difference (A-V O(2) Diff) was obtained by dividing VO(2) by CO. By applying the D(max) mathematical method, L(T) and thresholds of ventilatory and haemodynamic parameters were calculated. The Bland and Altman statistics used to assess agreement between two methods of measurement were applied in order to evaluate the agreement between L(T) and thresholds derived from ventilatory and haemodynamic data. The main result was that most of the haemodynamic variables did not provide thresholds which could be used interchangeably with L(T). Only the threshold of A-V O(2) Diff showed mean values that were no different compared to L(T) together with limits of agreement that were not very wide between thresholds (below +/-25%). Hence of the haemodynamic parameters, A-V O(2) Diff appears to be the one most closely coupled with lactate accumulation and consequently it is also the most suitable for non-invasive calculation of the L(T).

Haemodynamic responses following intermittent supramaximal exercise in athletes.

We aimed to investigate haemodynamics during active and passive recovery following repeated bouts of supramaximal exercise. Seven male athletes underwent two sessions of supramaximal exercise which consisted of a warm-up and of five bouts of cycling at the maximum speed possible for 30 s against a resistance equivalent to 150% of the maximum workload achieved in a previous incremental test. Bouts were separated by 1 min of recovery and followed by 10 min of recovery which was either active (pedalling at 40 W) or passive (completely rest seated on the cycle). Haemodynamic variables were evaluated by means of impedance cardiography. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean blood pressure (MBP), thoracic electrical impedance (Z0) as an inverse index of central blood volume, and systemic vascular resistance (SVR) were assessed. The main findings were that active recovery, with respect to passive recovery, induced higher changes from baseline in HR (+29.1 +/- 4.5 versus +15.6 +/- 2.9 beats min(-1) at the 10th minute of recovery, P < 0.05), SV (+19.9 +/- 5.6 versus -6.4 +/- 3.3 ml, P < 0.01) and CO (+3.8 +/- 1.2 versus +0.4 +/- 0.2 l min(-1), P < 0.01). Furthermore, MBP was similar between the two kinds of recovery despite an increase in Z0 during passive compared to active recovery. These results suggest that the faster haemodynamic recovery towards baseline and the decrease in cardiac preload during passive recovery may be successfully prevented by cardiovascular regulatory mechanisms which include an increase in SVR, thus avoiding a drop in blood pressure.

Exercise-induced and nitroglycerin-induced myocardial preconditioning improves hemodynamics in patients with angina.

In humans, regional myocardial dysfunction during ischemia may be improved by ischemic and pharmacological preconditioning. We assessed the possibility that exercise- and nitroglycerin-induced myocardial preconditioning may improve global cardiac performance during subsequent efforts in patients with angina. Ten patients suffering from chronic stable angina and ten healthy volunteers were studied. Through impedance cardiography we assessed hemodynamics during a maximal exercise test, which was used as a baseline (Bas test) and considered as a preconditioning exercise. The Bas test was followed by a sequence of maximal efforts performed during the first (FWOP; 30 min after the Bas test) and second (SWOP; 48 h after the Bas test) windows of protection conferred by ischemic preconditioning. Hemodynamics was further evaluated during maximal exercise performed 48 h later with pharmacologically induced SWOP (PI-SWOP) obtained by transdermal administration of 10 mg of nitroglycerin. In the angina patients, FWOP, SWOP, and PI-SWOP delayed the time to ischemia and allowed them to achieve higher workloads compared with the Bas test. Furthermore, heart rate and cardiac output at peak exercise were enhanced during all the preconditioning phases with respect to the Bas test. However, only SWOP and PI-SWOP increased myocardial contractility and stroke volume. No changes in hemodynamics were detectable in the control subjects. This study demonstrates that in patients with stable angina, although hemodynamics during exercise can be positively improved during both FWOP and SWOP, differences exist between these two phases. Furthermore, the mimicking of exercise-induced SWOP by PI-SWOP with transdermal nitroglycerin may represent an important clinical aspect.

Hemodynamics during active and passive recovery from a single bout of supramaximal exercise.

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.