Executive Functions and Mood States in Athletes Performing Exercise Under Hypoxia.

Hypoxia can impair cognitive performance, whereas exercise can enhance it. The effects of hypoxia on cognitive performance during exercise appear to be moderated by exercise duration and intensity and by severity and duration of hypoxia and cognitive task. In normal individuals, exercise under hypoxia can evoke adverse post-exercise mood states, such as tension and fatigue. However, little is known about the effects of hypoxia during exercise in trained athletes. The purpose of this study was to investigate how hypoxia affected executive functions and mood states, assessed, respectively, during and post-exercise and to explore the role of motivation moderators, such as inhibition and activation systems (BIS-BAS). Two different sessions of exercise in normoxia and hypoxia (FiO2 13%), each lasting 18 min, were randomly assigned in a counterbalanced order and administered to seventeen male athletes. During exercise bouts, participants performed a mental task (BST) aimed to produce cognitive interference and suppression. Reaction times and accuracy of responses were recorded. After 5 min, all participants completed two questionnaires assessing mood states (ITAMS) and incidence of symptoms potentially related to hypoxia (AMS-C). The results show that hypoxia impairs cognitive performance in terms of slower reaction times, but a high BAS attenuates this effect. Participants with high BAS show an equivalent cognitive performance under hypoxia and normoxia conditions. No effects were found on mood states. Further research is required to investigate the role of BAS, cognitive abilities, and mood states in prolonged hypoxic conditions.

Acute Exercise with Moderate Hypoxia Reduces Arterial Oxygen Saturation and Cerebral Oxygenation without Affecting Hemodynamics in Physically Active Males.

Hemodynamic changes during exercise in acute hypoxia (AH) have not been completely elucidated. The present study aimed to investigate hemodynamics during an acute bout of mild, dynamic exercise during moderate normobaric AH. Twenty-two physically active, healthy males (average age; range 23-40 years) completed a cardiopulmonary test on a cycle ergometer to determine their maximum workload (Wmax). On separate days, participants performed two randomly assigned exercise tests (three minutes pedaling at 30% of Wmax): (1) during normoxia (NORMO), and (2) during normobaric AH at 13.5% inspired oxygen (HYPO). Hemodynamics were assessed with impedance cardiography, and peripheral arterial oxygen saturation (SatO2) and cerebral oxygenation (Cox) were measured by near-infrared spectroscopy. Hemodynamic responses (heart rate, stroke volume, cardiac output, mean arterial blood pressure, ventricular emptying rate, and ventricular filling rate) were not any different between NORMO and HYPO. However, the HYPO test significantly reduced both SatO2 (96.6 ± 3.3 vs. 83.0 ± 4.5%) and Cox (71.0 ± 6.6 vs. 62.8 ± 7.4 A.U.) when compared to the NORMO test. We conclude that an acute bout of mild exercise during acute moderate normobaric hypoxia does not induce significant changes in hemodynamics, although it can cause significant reductions in SatO2 and Cox.

Systolic and diastolic function during cycling at the respiratory threshold between elderly and young healthy individuals.

The hemodynamic consequences of aging have been extensively investigated during maximal incremental exercise. However, less is known about the effects of aging on hemodynamics during submaximal steady-state exercise. The aim of the present investigation was to compare the hemodynamics of healthy elderly and young subjects during an exercise bout conducted at the gas threshold (GET) intensity. Two groups of healthy, physically active subjects were studied: the elderly group-EG (n = 11; > 60 years old) and the young group-YG (n = 13; < 35 years old). Both groups performed a 5-min rectangular exercise test at the GET intensity. Hemodynamics were measured using echocardiography. The main finding was that stroke volume responses were higher in the YG than the EG (72.5 ± 16.7 vs. 52.4 ± 8.4 ml, respectively). The increased stroke volume capacity in the YG was the consequence of a greater capacity to increase cardiac preload and contractility and, to a lesser extent, to reduce systemic vascular resistance. Importantly, the atrial contribution to ventricular diastolic filling was substantially higher in the YG when compared to the EG.

Body composition changes during the lockdown-restart transition due to the SARS-CoV-2 pandemic in a group of professional football players.

BACKGROUND: At the beginning of March 2020, because of the ongoing pandemic, all sport events were suspended in Italy. The Italian Serie A league abruptly interrupted all competitions and teams could not train in a group anymore. These containment measures were gradually eased in May. The aim of this study was to ascertain the impact of the lockdown-restart transition on the body composition of a group of Italian footballers of a Serie A team during the pandemic. METHODS: The body composition of 18 male football players (age 27.6±4.5 years) from an Italian Serie A team was studied by bioelectrical impedance (BIA). Measures were conducted after lockdown, when they restarted to train in group with the ball (T0), and after the first regular match (T1). RESULTS: Results show that there were no changes in body mass, body mass index, fat mass, fat-free mass, and total body water between T0 and T1. Differently, intracellular water, extracellular water, and phase angle were changed. CONCLUSIONS: We concluded that the lockdown did not have any impact in athletes' body composition as they kept training at home. Moreover, the BIA method was able to detect subtle signals of shift in body water compartments (intra cellular and extra cellular water) likely due to the different kind of training conducted during and after the lockdown.

Systolic and Diastolic Functions After a Brief Acute Bout of Mild Exercise in Normobaric Hypoxia.

Acute hypoxia (AH) is a challenge to the homeostasis of the cardiovascular system, especially during exercise. Research in this area is scarce. We aimed to ascertain whether echocardiographic, Doppler, and tissue Doppler measures were able to detect changes in systolic and diastolic functions during the recovery after mild exercise in AH. Twelve healthy males (age 33.5 ± 4.8 years) completed a cardiopulmonary test on an electromagnetically braked cycle-ergometer to determine their maximum workload (Wmax). On separate days, participants performed randomly assigned two exercise sessions consisting in 3 min pedalling at 30% of Wmax: (1) one test was conducted in normoxia (NORMO) and (2) one in normobaric hypoxia with FiO2 set to 13.5% (HYPO). Hemodynamics were assessed with an echocardiographic system. The main result was that the HYPO session increased parameters related to myocardial contractility such as pre-ejection period and systolic myocardial velocity with respect to the NORMO test. Moreover, the HYPO test enhanced early transmitral filling peak velocities. No effects were detected for left ventricular volumes, as end-diastolic, end-systolic, and stroke volume were similar between the NORMO and the HYPO test. Results of the present investigation support the hypothesis that a brief, mild exercise bout in acute normobaric hypoxia does not impair systolic or diastolic functions. Rather, it appears that stroke volume is well preserved and that systolic and early diastolic functions are enhanced by exercise in hypoxia.

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.

Case study: physical capacity and nutritional status before and after climbing two peaks with different altitude (4897-6812 m).

Vinson and Ama Dablam are summits of different altitudes (4897 and 6812 m respectively). There are no published studies comparing physiological adaptations occurring after climbing both peaks yet. This case study compares changes in certain physiological parameters and body composition of a mountaineer who ascended both peaks. The athlete was a mountaineer who already climbed the 7 Summits©. Baseline body composition, physical capacity, and cerebral oxygenation during effort were measured before and after his departure. Body composition was estimated by electrical bio-impedance, while physical capacity was measured with an incremental exercise test (treadmill) conducted in normoxia and in hypoxia corresponding to about 4000 m. Hypoxia was obtained with a hypoxic gas generator. During tests, cerebral oxygenation was estimated with near infrared spectroscopy. The ascent of mount Vinson and Ama Dablam took 4 and 15 days respectively. The ascent of mount Vinson resulted in a 2.0 kg drop in body mass and a reduction in body fat (from 15.5% to 12.1%). The ascent of Ama Dablam reduced body mass by 3.7 kg, with an increase in body fat from 11.9% to 14.7%. Physical capacity was almost unchanged after both expeditions, although there was a reduction in maximum heart rate in relation to workload after Ama Dablam. Finally, after Ama Dablam there was an increase in cerebral oxygenation during effort both in normoxia and hypoxia. It was concluded that the longer duration and the higher altitude during the Ama Dablam expedition resulted in more evident physiological changes.

A brief bout of exercise in hypoxia reduces ventricular filling rate and stroke volume response during muscle metaboreflex activation.

PURPOSE: The hemodynamic consequences of exercise in hypoxia have not been completely investigated. The present investigation aimed at studying the hemodynamic effects of contemporary normobaric hypoxia and metaboreflex activation. METHODS: Eleven physically active, healthy males (age 32.7 ± 7.2 years) completed a cardiopulmonary test on an electromagnetically braked cycle-ergometer to determine their maximum workload (Wmax). On separate days, participants performed two randomly assigned exercise sessions (3 minutes pedalling at 30% of Wmax): (1) one in normoxia (NORMO), and (2) one in normobaric hypoxia with FiO2 set to 13.5% (HYPO). After each session, the following protocol was randomly assigned: either (1) post-exercise muscle ischemia (PEMI) to study the metaboreflex, or (2) a control exercise recovery session, i.e., without metaboreflex activation. Hemodynamics were assessed with impedance cardiography. RESULTS: The main result was that the HYPO session impaired the ventricular filling rate (measured as stroke volume/diastolic time) response during PEMI versus control condition in comparison to the NORMO test (31.33 ± 68.03 vs. 81.52 ± 49.23 ml·s-1,respectively, p = 0.003). This caused a reduction in the stroke volume response (1.45 ± 9.49 vs. 10.68 ± 8.21 ml, p = 0.020). As a consequence, cardiac output response was impaired during the HYPO test. CONCLUSIONS: The present investigation suggests that a brief exercise bout in hypoxia is capable of impairing cardiac filling rate as well as stroke volume during the metaboreflex. These results are in good accordance with recent findings showing that among hemodynamic modulators, ventricular filling is the most sensible variable to hypoxic stimuli.

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.

Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning.

Metabolic syndrome, diabetes, and ischemic heart disease are among the leading causes of death and disability in Western countries. Diabetic cardiomyopathy is responsible for the most severe signs and symptoms. An important strategy for reducing the incidence of cardiovascular disease is regular exercise. Remote ischemic conditioning has some similarity with exercise and can be induced by short periods of ischemia and reperfusion of a limb, and it can be performed in people who cannot exercise. There is abundant evidence that exercise is beneficial in diabetes and ischemic heart disease, but there is a need to elucidate the specific cardiovascular effects of emerging and unconventional forms of exercise in people with diabetes. In addition, remote ischemic conditioning may be considered among the options to induce beneficial effects in these patients. The characteristics and interactions of diabetes and ischemic heart disease, and the known effects of exercise and remote ischemic conditioning in the presence of metabolic syndrome and diabetes, are analyzed in this brief review.

Effects of exercise in normobaric hypoxia on hemodynamics during muscle metaboreflex activation in normoxia.

PURPOSE: Little is known about the cardiovascular effects of the transition from exercise in hypoxia (EH) to normoxia. This investigation aimed to assess hemodynamics during the metaboreflex elicited in normoxia after EH. METHODS: Ten trained athletes (four females and six males, age 35.6 ± 8.4 years) completed a cardiopulmonary test to determine the workload at anaerobic threshold (AT). On separate days, participants performed three randomly assigned exercise sessions (10 min pedalling at 80% of AT): (1) one in normoxia (EN); (2) one in normobaric hypoxia with FiO2 15.5% (EH15.5%); and (3) one in normobaric hypoxia with FiO2 13.5% (EH13.5%). After each session, the following protocol was randomly assigned: either (1) post-exercise muscle ischemia after cycling for 3 min, to study the metaboreflex, or (2) a control exercise recovery (CER) session, without any metaboreflex stimulation. RESULTS: The main result were that both EH15.5% and EH13.5% impaired (p < 0.05) the ventricular filling rate response during the metaboreflex (- 18 ± 32 and - 20 ± 27 ml s-1), when compared to EN (+ 29 ± 32 ml s-1), thereby causing a reduction in stroke volume response (- 9.1 ± 3.2, - 10.6 ± 8.7, and + 5 ± 5.7 ml for EH15.5%, EH13.5% and EN test, respectively, p < 0.05). Moreover, systemic vascular resistance was increased after the EH15.5% and the EH13.5% in comparison with the EN test. CONCLUSIONS: These data demonstrate that moderate exercise in hypoxia impairs the capacity to enhance venous return during the metaboreflex stimulated in normoxia. Overall, there is a functional shift from a flow to vasoconstriction-mediated mechanism for maintaining the target blood pressure during the metaboreflex.

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.

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.

Consequences of Type 1 and 2 Diabetes Mellitus on the Cardiovascular Regulation During Exercise: A Brief Review.

INTRODUCTION: One challenging problem in patients suffering from Diabetes Mellitus (DM) is the elevate incidence of cardiovascular events. Exercise has been proved useful in reducing cardiovascular risks in these patients. However, both type 1 and 2 DM significantly affect the cardiovascular response during exercise. Therefore, on one side exercise is considered to be a valid therapeutic tool for DM, whereas on the other side during exercise these patients may experience troubles in the cardiovascular regulation. BACKGROUND: Several impairments at central and at peripheral level have been reported during exercise in both types of DM. For example, sympathetic dysfunctions have been demonstrated in type 1 and 2 DM. Furthermore, impairments in hemodynamics have been often reported. The purpose of the present paper is to briefly review the latest data on the role played by type 1 and 2 DM in the cardiovascular regulation during dynamic exercise. CONCLUSION: Hemodynamic dysfunctions may develop in both type 1 and 2 DM during exercise. However, these cardiovascular dys-regulations are different between the two kinds of diabetes.

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.

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.

Diving response after a one-week diet and overnight fasting.

BACKGROUND: We hypothesized that overnight fasting after a short dietary period, especially with carbohydrates, could allow performing breath-hold diving with no restraint for diaphragm excursion and blood shift and without any increase of metabolism, and in turn improve the diving response. METHODS: During two separate sessions, 8 divers carried out two trials: (A) a 30-m depth dive, three hours after a normal breakfast and (B) a dive to the same depth, but after following a diet and fasting overnight. Each test consisted of 3 apnea phases: descent, static and ascent whose durations were measured by a standard chronometer. An impedance cardiograph, housed in an underwater torch, provided data on trans-thoracic fluid index (TFI), stroke volume (SV), heart rate (HR) and cardiac output (CO). Mean blood pressure (MBP), arterial O2 saturation (SaO2), blood glucose (Glu) and blood lactate (BLa) were also collected. RESULTS: In condition B, duration of the static phase of the dive was longer than A (37.8 ± 7.4 vs. 27.3 ± 8.4 s respectively, P < 0.05). In static phases, mean ∆ SV value (difference between basal and nadir values) during fasting was lower than breakfast one (-2.6 ± 5.1 vs. 5.7 ± 7.6 ml, P < 0.05). As a consequence, since mean ∆ HR values were equally decreased in both metabolic conditions, mean ∆ CO value during static after fasting was lower than the same phase after breakfast (-0.4 ± 0.5 vs. 0.4 ± 0.5 L · min(-1) respectively, P < 0.05). At emersion, despite the greater duration of dives during fasting, SaO2 was higher than A (92.0 ± 2.7 vs. 89.4 ± 2.9 % respectively, P < 0.05) and BLa was lower in the same comparison (4.2 ± 0.7 vs. 5.3 ± 1.1 mmol∙L(-1), P < 0.05). CONCLUSIONS: An adequate balance between metabolic and splancnic status may improve the diving response during a dive at a depth of 30 m, in safe conditions for the athlete's health.

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.