Combined mental task and metaboreflex impair cerebral oxygenation in patients with type 2 diabetes mellitus.

Cardiovascular regulation is altered by type 2 diabetes mellitus (DM2), producing an abnormal response to muscle metaboreflex. During physical exercise, cerebral blood flow is impaired in patients with DM2, and this phenomenon may reduce cerebral oxygenation (COX). We hypothesized that the simultaneous execution of a mental task (MT) and metaboreflex activation would reduce COX in patients with DM2. Thirteen individuals suffering from DM2 (6 women) and 13 normal age-matched controls (CTL, 6 women) participated in this study. They underwent five different tests, each lasting 12 min: postexercise muscle ischemia (PEMI) to activate the metaboreflex, control exercise recovery (CER), PEMI + MT, CER + MT, and MT alone. COX was evaluated using near-infrared spectroscopy with sensors applied to the forehead. Central hemodynamics was assessed using impedance cardiography. We found that when MT was superimposed on the PEMI-induced metaboreflex, patients with DM2 could not increase COX to the same extent reached by the CTL group (101.13% ± 1.08% vs. 104.23% ± 2.51%, P < 0.05). Moreover, patients with DM2 had higher mean blood pressure and systemic vascular resistance as well as lower stroke volume and cardiac output levels compared with the CTL group, throughout our experiments. It was concluded that patients with DM2 had reduced capacity to enhance COX when undertaking an MT during metaboreflex. Results also confirm that patients with DM2 had dysregulated hemodynamics during metaboreflex, with exaggerated blood pressure response and vasoconstriction. This may have implications for these patients' lack of inclination to exercise.

Metaboreflex-mediated hemodynamic abnormalities in individuals with coronary artery disease without overt signs or symptoms of heart failure.

This study was devised to investigate the effect of coronary artery disease (CAD) without overt signs of heart failure on the cardiovascular responses to muscle metaboreflex activation. We hypothesized that any CAD-induced preclinical systolic and/or diastolic dysfunction could impair hemodynamic response to the metaboreflex test. Twelve men diagnosed with CAD without any sign or symptoms of heart failure and 11 age-matched healthy control (CTL) subjects participated in the study. Subjects performed a postexercise muscle ischemia (PEMI) test to activate the metaboreflex. They also performed a control exercise recovery test to compare data from the PEMI test. The main results were that the CAD group reached a similar mean arterial blood pressure response as the CTL group during PEMI. However, the mechanism by which this response was achieved was different between groups. In particular, CAD achieved the target mean arterial blood pressure by increasing systemic vascular resistance (+383.8 ± 256.6 vs. +91.2 ± 293.5 dyn·s-1·cm-5 for the CAD and CTL groups, respectively), the CTL group by increasing cardiac preload (-0.92 ± 8.53 vs. 5.34 ± 4.29 ml in end-diastolic volume for the CAD and CTL groups, respectively), which led to an enhanced stroke volume and cardiac output. Furthermore, the ventricular filling rate response was higher in the CTL group than in the CAD group during PEMI ( P < 0.05 for all comparisons). This study confirms that diastolic function is pivotal for normal hemodynamics during the metaboreflex. Moreover, it provides evidence that early signs of diastolic impairment attributable to CAD can be detected by the metaboreflex test. NEW & NOTEWORTHY Individuals suffering from coronary artery disease without overt signs of heart failure may show early signs of diastolic dysfunction, which can be detected by the metaboreflex test. During the metaboreflex, these subjects show impaired preload and stroke volume responses and exaggerated vasoconstriction compared with controls.

Ischemic preconditioning reduces hemodynamic response during metaboreflex activation.

Ischemic preconditioning (IP) has been shown to improve exercise performance and to delay fatigue. However, the precise mechanisms through which IP operates remain elusive. It has been hypothesized that IP lowers the sensation of fatigue by reducing the discharge of group III and IV nerve endings, which also regulate hemodynamics during the metaboreflex. We hypothesized that IP reduces the blood pressure response during the metaboreflex. Fourteen healthy males (age between 25 and 48 yr) participated in this study. They underwent the following randomly assigned protocol: postexercise muscle ischemia (PEMI) test, during which the metaboreflex was elicited after dynamic handgrip; control exercise recovery session (CER) test; and PEMI after IP (IP-PEMI) test. IP was obtained by occluding forearm circulation for three cycles of 5 min spaced by 5 min of reperfusion. Hemodynamics were evaluated by echocardiography and impedance cardiography. The main results were that after IP the mean arterial pressure response was reduced compared with the PEMI test (means ± SD +3.37 ± 6.41 vs. +9.16 ± 7.09 mmHg, respectively). This was the consequence of an impaired venous return that impaired the stroke volume during the IP-PEMI more than during the PEMI test (-1.43 ± 15.35 vs. +10.28 ± 10.479 ml, respectively). It was concluded that during the metaboreflex, IP affects hemodynamics mainly because it impairs the capacity to augment venous return and to recruit the cardiac preload reserve. It was hypothesized that this is the consequence of an increased nitric oxide production, which reduces the possibility to constrict venous capacity vessels.

Cardio-metabolic responses during horse riding at three different speeds.

PURPOSE: The purpose of the present investigation was to study the metabolic demand and cardiovascular response during a typical horse riding session. METHODS: To this aim, 19 (9 male, 10 female) riders, regularly participating in competitions, were enrolled. They underwent a preliminary, incremental exercise test on a cycle-ergometer to assess their anaerobic threshold (AT) and VO2max. Then, participants underwent a riding training session, which comprised periods of walking, trotting, and cantering for a total of 20 min. Oxygen uptake (VO2), carbon dioxide production (VCO2), and heart rate (HR) were obtained throughout the preliminary and riding test by means of a portable metabolic system. Moreover, excess of CO2 production (CO2excess) and oxygen pulse (OP) were also calculated to obtain an estimate of anaerobic glycolysis and stroke volume. RESULTS: The main result was that all collected parameters remained below the AT level throughout the riding session, with the exception of HR that approached the AT level only during cantering. In detail, during cantering, average VO2, VCO2, HR, CO2excess, and OP values were 1289 ± 331 mL min(-1), 1326 ± 266 mL min(-1), 158 ± 22 bpm, 215 ± 119 mL min(-1), and 7.8 ± 1.6 mL/bpm, respectively. CONCLUSIONS: It was concluded that riding imposes only light to moderate stress on the aerobic and anaerobic energy systems. Moreover, cardiovascular reserve is only moderately recruited in terms of inotropism, while chronotropism can be stimulated more.

Mean Blood Pressure Assessment during Post-Exercise: Result from Two Different Methods of Calculation.

At rest the proportion between systolic and diastolic periods of the cardiac cycle is about 1/3 and 2/3 respectively. Therefore, mean blood pressure (MBP) is usually calculated with a standard formula (SF) as follows: MBP = diastolic blood pressure (DBP) + 1/3 [systolic blood pressure (SBP) - DBP]. However, during exercise this proportion is lost because of tachycardia, which shortens diastole more than systole. We analysed the difference in MBP calculation between the SF and a corrected formula (CF) which takes into account changes in the diastolic and systolic periods caused by exercise-induced tachycardia. Our hypothesis was that the SF potentially induce a systematic error in MBP assessment during recovery after exercise. Ten healthy males underwent two exercise-recovery tests on a cycle-ergometer at mild-moderate and moderate-heavy workloads. Hemodynamics and MBP were monitored for 30 minutes after exercise bouts. The main result was that the SF on average underestimated MBP by -4.1 mmHg with respect to the CF. Moreover, in the period immediately after exercise, when sustained tachycardia occurred, the difference between SF and CF was large (in the order of -20-30 mmHg). Likewise, a systematic error in systemic vascular resistance assessment was present. It was concluded that the SF introduces a substantial error in MBP estimation in the period immediately following effort. This equation should not be used in this situation.

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype.

Patients suffering from obesity and metabolic syndrome (OMS) manifest a dysregulation in hemodynamic response during exercise, with an exaggerated systemic vascular increase. However, it is not clear whether this is the consequence of metabolic syndrome per se or whether it is due to concomitant obesity. The aim of the present investigation was to discover whether OMS and noncomplicated obesity resulted in different hemodynamic responses during the metaboreflex. Twelve metabolically healthy but obese subjects (MHO; 7 women), 13 OMS patients (5 women), and 12 normal age-matched controls (CTL; 6 women) took part in this study. All participants underwent a postexercise muscle ischemia protocol to evaluate the metaboreflex activity. Central hemodynamics were evaluated by impedance cardiography. The main result shows an exaggerated increase in systemic vascular resistance from baseline during the metaboreflex in the OMS patients as compared with the other groups (481.6 ± 180.3, -0.52 ± 177.6, and -60.5 ± 58.6 dynes·s(-1)·cm(-5) for the OMS, the MHO, and the CTL groups, respectively; P < 0.05). Moreover, the MHO subjects and the CTL group showed an increase in cardiac output during the metaboreflex (288.7 ± 325.8 and 703.8 ± 276.2 ml/m increase with respect to baseline), whereas this parameter tended to decrease in the OMS group (-350 ± 236.5 ml/m). However, the blood pressure response, which tended to be higher in the OMS patients, was not statistically different between groups. The results of the present investigation suggest that OMS patients have an exaggerated vasoconstriction in response to metaboreflex activation and that this fact is not due to obesity per se.

Effect of aging on hemodynamic response to metaboreflex activation.

PURPOSE: The aim of the present investigation was to assess the role of aging on the contribution of diastolic function during metaboreflex activation. In particular, it aimed to determine whether age-related impairment in diastolic function would produce a different hemodynamic response in elderly subjects (EG) as compared to young controls (CTL). METHODS: Hemodynamic response to metaboreflex activation obtained by post-exercise muscle ischemia (PEMI) was gathered in 22 EG and 20 healthy CTL. Subjects also performed a control exercise recovery (CER) test to compare data from the PEMI test. RESULTS: The main results showed that the EG group reached higher mean arterial blood pressure (MAP) increment than the CTL group during the PEMI test (+11.2 ± 8.6 vs 6.1 ± 6.4 mmHg in the EG and CTL group, respectively). Moreover, the mechanism by which this response was achieved was different between the two groups. In detail, EG reached the target MAP by increasing systemic vascular resistance (+235.2 ± 315.1 vs -44.4 ± 167.7 dynes s(-1) cm(-5) for the EG and the CTL group, respectively), whereas MAP response in the CTL was the result of an increase in cardiac pre-load (-1.5 ± 11.2 vs 14 ± 13.7 ml in end-diastolic volume for the EG and the CTL group, respectively), which led to a rise in stroke volume and cardiac output. Moreover, early filling peak velocities showed a higher response in the CTL than EG group. CONCLUSIONS: This study demonstrates that diastolic function is important for normal hemodynamic adjustment during the metaboreflex and to avoid excessive vasoconstriction.

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.

Effects of acute vasodilation on the hemodynamic response to muscle metaboreflex.

The aim of the present study was to test the contribution of stroke volume (SV) in hemodynamic response to muscle metaboreflex activation in healthy individuals. We hypothesized that an acute decrease in cardiac afterload and preload due to the administration of a vasodilating agent could reduce postexercise muscle ischemia (PEMI)-induced SV response. Ten healthy males (age 33.6 ± 1.3 yr) were enrolled and randomly assigned to the following study protocol: 1) PEMI session, 2) control exercise recovery (CER) session, 3) PEMI after sublingual administration of 5 mg of isosorbide dinitrate (ISDN), and 4) CER after ISDN. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were a blunted SV response during metaboreflex following acute arterial and venous vasodilation, associated with a reduction in cardiac diastolic time and filling, and a decrement of systemic vascular resistance. These hemodynamic changes restrain blood pressure response during metaboreflex activation. Our results indicate that hemodynamic response to metaboreflex activation is a highly integrated phenomenon encompassing complex interplay between heart rate, cardiac performance, preload, and afterload and that impairment of one or more of these parameters leads to altered hemodynamic response to metaboreflex.

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.

Effect of Combined Mental Task and Metaboreflex Activation on Hemodynamics and Cerebral Oxygenation in Patients With Metabolic Syndrome.

Objective: The hemodynamic response to muscle metaboreflex has been reported to be significantly altered by metabolic syndrome (MS), with exaggerated systemic vascular resistance (SVR) increments and reduced cardiac output (CO) in comparison to healthy controls (CTLs). Moreover, patients with metabolic disorders, such as type 2 diabetes, have proven to have impaired cerebral blood flow in response to exercise. Thus, we hypothesized that contemporary mental task (MT) and metaboreflex would result in reduced cerebral oxygenation (COX) in these patients. Methods: Thirteen MS patients (five women) and 14 normal age-matched CTLs (six women) were enrolled in this study. All the participants underwent five different tests, each lasting 12 min: post-exercise muscle ischemia (PEMI) to activate the metaboreflex, control exercise recovery (CER), PEMI + MT, CER + MT, and MT alone. Cerebral oxygenation was evaluated using near-infrared spectroscopy with sensors applied to the forehead. Hemodynamics were measured using impedance cardiography. Results: The main results show that MS patients had higher SVR and lower CO levels compared to the CTL group during metaboreflex activation. Stroke volume and ventricular filling and emptying rates were also significantly reduced. Moreover, when MT was added to PEMI, COX was significantly increased in the CTL group with respect to the baseline (103.46 ± 3.14%), whereas this capacity was reduced in MS patients (102.37 ± 2.46%). Conclusion: It was concluded that (1) patients with MS showed hemodynamic dysregulation during the metaboreflex, with exaggerated vasoconstriction and that (2) as compared to CTL, MS patients had reduced capacity to enhance COX when an MT superimposed the metaboreflex.

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.

Hemodynamic abnormalities during muscle metaboreflex activation in patients with type 2 diabetes mellitus.

Metaboreflex is a reflex triggered during exercise or postexercise muscle ischemia (PEMI) by metaboreceptor stimulation. Typical features of metaboreflex are increased cardiac output (CO) and blood pressure. Patients suffering from metabolic syndrome display hemodynamic abnormalities, with an exaggerated systemic vascular resistance (SVR) and reduced CO response during PEMI-induced metaboreflex. Whether patients with type 2 diabetes mellitus (DM2) have similar hemodynamic abnormalities is unknown. Here we contrast the hemodynamic response to PEMI in 14 patients suffering from DM2 (age 62.7 ± 8.3 yr) and in 15 age-matched controls (CTLs). All participants underwent a control exercise recovery reference test and a PEMI test to obtain the metaboreflex response. Central hemodynamics were evaluated by unbiased operator-independent impedance cardiography. Although the blood pressure response to PEMI was not significantly different between the groups, we found that the SVR and CO responses were reversed in patients with DM2 as compared with the CTLs (SVR: 392.5 ± 549.6 and -14.8 ± 258.9 dyn·s-1·cm-5; CO: -0.25 ± 0.63 and 0.46 ± 0.50 l/m, respectively, in DM2 and in CTL groups, respectively; P < 0.05 for both). Of note, stroke volume (SV) increased during PEMI in the CTL group only. Failure to increase SV and CO was the consequence of reduced venous return, impaired cardiac performance, and augmented afterload in patients with DM2. We conclude that patients with DM2 have an exaggerated vasoconstriction in response to metaboreflex activation not accompanied by a concomitant increase in heart performance. Therefore, in these patients, blood pressure response to the metaboreflex relies more on SVR increases rather than on increases in SV and CO. NEW & NOTEWORTHY The main new finding of the present investigation is that subjects with type 2 diabetes mellitus have an exaggerated vasoconstriction in response to metaboreflex activation. In these patients, blood pressure response to the metaboreflex relies more on systemic vascular resistance than on cardiac output increments.

Blood Flow Restriction Training Reduces Blood Pressure During Exercise Without Affecting Metaboreflex Activity.

Objective: Blood flow restriction training (BFRT) has been proposed to induce muscle hypertrophy, but its safety remains controversial as it may increase mean arterial pressure (MAP) due to muscle metaboreflex activation. However, BFR training also causes metabolite accumulation that may desensitize type III and IV nerve endings, which trigger muscle metaboreflex. Then, we hypothesized that a period of BFR training would result in blunted hemodynamic activation during muscle metaboreflex. Methods: 17 young healthy males aged 18-25 yrs enrolled in this study. Hemodynamic responses during muscle metaboreflex were assessed by means of postexercise muscle ischemia (PEMI) at baseline (T0) and after 1 month (T1) of dynamic BFRT. BFRT consisted of 3-min rhythmic handgrip exercise applied 3 days/week (30 contractions per minute at 30% of maximum voluntary contraction) in the dominant arm. On the first week, the occlusion was set at 75% of resting systolic blood pressure (always obtained after 3 min of resting) and increased 25% every week, until reaching 150% of resting systolic pressure at week four. Hemodynamic measurements were assessed by means of impedance cardiography. Results: BFRT reduced MAP during handgrip exercise (T1: 96.3 ± 8.3 mmHg vs. T0: 102.0 ± 9.53 mmHg, p = 0.012). However, no significant time effect was detected for MAP during the metaboreflex activation (P > 0.05). Additionally, none of the observed hemodynamic outcomes, including systemic vascular resistance (SVR), showed significant difference between T0 and T1 during the metaboreflex activation (P > 0.05). Conclusion: BFRT reduced blood pressure during handgrip exercise, thereby suggesting a potential hypotensive effect of this modality of training. However, MAP reduction during handgrip seemed not to be provoked by lowered metaboreflex activity.

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.

Hemodynamic Responses during Enduro-Motorcycling Performance.

Much of the information available in the literature on physiological responses during Enduro motorcycling is related to heart rate (HR) and blood lactate (BLa). The aim of this work was to investigate the hemodynamic changes that occur during a 10-min session of Enduro motorcycling. Fifteen skilled riders were enrolled on the study and all participants underwent an Enduro-motorcycling session on a standard track. Hemodynamics were assessed using a miniaturized impedance cardiograph. Results show that HR significantly increased from 96.5 ± 12.8 bpm at rest to 153.1 ± 17.7 bpm during riding, while stroke volume (SV) increased from 53.5 ± 14.1 to 72.2 ± 22.1 ml and cardiac output (CO) from 5.0 ± 1.1 to 10.9 ± 3.0 L·min-1. Moreover, ventricular emptying rate (VER) increased from 192.9 ± 43.0 to 324.1 ± 83.6 ml·s1 and ventricular filling rate (VFR) from 141.1 ± 160.5 to 849 ± 309 ml·s-1. Taken together, these data suggest that Enduro motorcycling induces substantial cardiovascular activation, not only in terms of chronotropism but also in terms of cardiac performance and pre-load, thereby increasing SV and CO. Finally, it is likely that sympathetic-mediated venous constriction occurred. This in turn improved VFR and recruited the Frank-Starling mechanism and inotropic reserve. It was concluded that Enduro motorcycling is a challenging activity for the cardiovascular apparatus.

Hemodynamic response to muscle reflex is abnormal in patients with heart failure with preserved ejection fraction.

The aim of the present investigation was to assess the role of cardiac diastole on the hemodynamic response to metaboreflex activation. We wanted to determine whether patients with diastolic function impairment showed a different hemodynamic response compared with normal subjects during this reflex. Hemodynamics during activation of the metaboreflex obtained by postexercise muscle ischemia (PEMI) was assessed in 10 patients with diagnosed heart failure with preserved ejection fraction (HFpEF) and in 12 age-matched healthy controls (CTL). Subjects also performed a control exercise-recovery test to compare data from the PEMI test. The main results were that patients with HFpEF achieved a similar mean arterial blood pressure (MAP) response as the CTL group during the PEMI test. However, the mechanism by which this response was achieved was markedly different between the two groups. Patients with HFpEF achieved the target MAP via an increase in systemic vascular resistance (+389.5 ± 402.9 vs. +80 ± 201.9 dynes·s-1·cm-5 for HFpEF and CTL groups respectively), whereas MAP response in the CTL group was the result of an increase in cardiac preload (-1.3 ± 5.2 vs. 6.1 ± 10 ml in end-diastolic volume for HFpEF and CTL groups, respectively), which led to a rise in stroke volume and cardiac output. Moreover, early filling peak velocities showed a higher response in the CTL group than in the HFpEF group. This study demonstrates that diastolic function is important for normal hemodynamic adjustment to the metaboreflex. Moreover, it provides evidence that HFpEF causes hemodynamic impairment similar to that observed in systolic heart failure.NEW & NOTEWORTHY This study provides evidence that diastolic function is important for normal hemodynamic responses during the activation of the muscle metaboreflex in humans. Moreover, it demonstrates that diastolic impairment leads to hemodynamic consequences similar to those provoked by systolic heart failure. In both cases the target blood pressure is obtained mainly by means of exaggerated vasoconstriction than by a flow-mediated mechanism.

Improvement in hemodynamic responses to metaboreflex activation after one year of training in spinal cord injured humans.

Spinal cord injured (SCI) individuals show an altered hemodynamic response to metaboreflex activation due to a reduced capacity to vasoconstrict the venous and arterial vessels below the level of the lesion. Exercise training was found to enhance circulating catecholamines and to improve cardiac preload and venous tone in response to exercise in SCI subjects. Therefore, training would result in enhanced diastolic function and capacity to vasoconstrict circulation. The aim of this study was to test the hypothesis that one year of training improves hemodynamic response to metaboreflex activation in these subjects. Nine SCI individuals were enrolled and underwent a metaboreflex activation test at the beginning of the study (T0) and after one year of training (T1). Hemodynamics were assessed by impedance cardiography and echocardiography at both T0 and T1. Results show that there was an increment in cardiac output response due to metaboreflex activity at T1 as compared to T0 (545.4 ± 683.9 mL · min(-1) versus 220.5 ± 745.4 mL · min(-1), P < 0.05). Moreover, ventricular filling rate response was higher at T1 than at T0. Similarly, end-diastolic volume response was increased after training. We concluded that a period of training can successfully improve hemodynamic response to muscle metaboreflex activation in SCI subjects.

Physiological responses and energy expenditure during competitive fencing.

Fencing is an Olympic sport in which athletes fight one against one using bladed weapons. Contests consist of three 3-min bouts, with rest intervals of 1 min between them. No studies investigating oxygen uptake and energetic demand during fencing competitions exist, thus energetic expenditure and demand in this sport remain speculative. The aim of this study was to understand the physiological capacities underlying fencing performance. Aerobic energy expenditure and the recruitment of lactic anaerobic metabolism were determined in 15 athletes (2 females and 13 males) during a simulation of fencing by using a portable gas analyzer (MedGraphics VO2000), which was able to provide data on oxygen uptake, carbon dioxide production and heart rate. Blood lactate was assessed by means of a portable lactate analyzer. Average group energetic expenditure during the simulation was (mean ± SD) 10.24 ± 0.65 kcal·min(-1), corresponding to 8.6 ± 0.54 METs. Oxygen uptakeand heart rate were always below the level of anaerobic threshold previously assessed during the preliminary incremental test, while blood lactate reached its maximum value of 6.9 ± 2.1 mmol·L(-1) during the final recovery minute between rounds. Present data suggest that physical demand in fencing is moderate for skilled fencers and that both aerobic energy metabolism and anaerobic lactic energy sources are moderately recruited. This should be considered by coaches when preparing training programs for athletes.

Effect of beetroot juice supplementation on aerobic response during swimming.

The beneficial effects of beetroot juice supplementation (BJS) have been tested during cycling, walking, and running. The purpose of the present study was to investigate whether BJS can also improve performance in swimmers. Fourteen moderately trained male master swimmers were recruited and underwent two incremental swimming tests randomly assigned in a pool during which workload, oxygen uptake (VO2), carbon dioxide production (VCO2), pulmonary ventilation (VE), and aerobic energy cost (AEC) of swimming were measured. One was a control swimming test (CSW) and the other a swimming test after six days of BJS (0.5 l/day organic beetroot juice containing about 5.5 mmol of NO3⁻). Results show that workload at anaerobic threshold was significantly increased by BJS as compared to the CSW test (6.3 ± 1 and 6.7 ± 1.1 kg during the CSW and the BJS test respectively). Moreover, AEC was significantly reduced during the BJS test (1.9 ± 0.5 during the SW test vs. 1.7 ± 0.3 kcal·kg⁻¹1·h⁻¹ during the BJS test). The other variables lacked a statistically significant effect with BJS. The present investigation provides evidence that BJS positively affects performance of swimmers as it reduces the AEC and increases the workload at anaerobic threshold.