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.

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.

Role of Blood Pressure in Mediating Carotid Artery Dilation in Response to Sympathetic Stimulation in Healthy, Middle-Aged Individuals.

OBJECTIVES: Carotid artery diameter responses to sympathetic stimulation, i.e., carotid artery reactivity (CAR), represent a novel test of vascular health and relates to cardiovascular disease (CVD)/risk. This study aims to understand the relationship between the increase in blood pressure and carotid artery diameter response during the CAR-test in healthy, middle-aged men. METHODS: Sample consisted of 40 normotensive men (aged 31-59 years) with no history of CVD of currently taking medication. Noninvasive ultrasound was used to measure carotid artery diameter during the cold pressor test (CPT), with CAR% being calculated as the relative change from baseline (%). Mean arterial pressure (MAP) was measured with beat-to-beat blood pressure recording. RESULTS: CAR% was 4.4 ± 5.4%, peaking at 92 ± 43 seconds. MAP increased from 88 ± 9 mmHg to 110 ± 15 mmHg, peaked at 112 ± 38 seconds, which was significantly later than the diameter peak (P = 0.04). The correlation between resting MAP and CAR% was weak (r = 0.209 P = 0.197). Tertiles based on resting MAP or MAP-increase revealed no significant differences between groups in subject characteristics including age, body mass index, or CAR% (all P > 0.05). Subgroup analysis of individuals with carotid constriction (n = 6) vs. dilation (n = 34), revealed no significant difference in resting MAP or increase in MAP (P = 0.209 and 0.272, respectively). CONCLUSION: Our data suggest that the characteristic increase in MAP during the CPT does not mediate carotid artery vasomotion.

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.

Occurrence of cardiac output decrease (via stroke volume) is more pronounced in women than in men during prolonged dry static apnea.

Little is known about sex differences in autonomic cardiovascular regulation of the diving response, and the few available studies of these differences were conducted on subjects with limited or no diving experience. We examined the influence of sex on hemodynamics during dry static apnea (SA) in eight male and eight female elite divers matched for their breath hold (BH) ability. Hemodynamics was assessed by means of simultaneous echocardiography and impedance cardiography measurements, and arterial pressure and oxygen saturation ([Formula: see text]) were also collected. In the first quarter (AP25%) and half (AP50%) of apnea duration cardiac output (CO) showed a more rapid and intense decrease in women than in men (-43% vs. -17% during AP25% and -40% vs. -19% during AP50%, respectively, P < 0.05). At the same time points, systemic vascular resistance (SVR) increased more in women than in men (+22% vs. +100% at AP25% and +48% vs. +107% at AP50%, respectively, P < 0.05). [Formula: see text] progressively declined in both groups, but men showed a more pronounced decrease than women at the end of apneas (-13% vs. -5%, respectively, P < 0.05). In men the higher the body surface area values the longer the apnea, while in women the higher the SVR response the longer the apnea. In elite female divers, the magnitude of CO decrease during dry SA was larger than in male divers. The capacities to store oxygen and to reduce O2 consumption play a pivotal role in BH performance, but their extent seems to be different in the sexes. NEW & NOTEWORTHY This is the first study in which the influence of sex on hemodynamics during dry static apnea has been investigated in two groups of elite divers matched for their breath hold ability. We also show the correlation between the performances obtained by divers during a real competition and their anthropometric, respiratory, and cardiovascular characteristics.

Case Study: Physical Capacity and Nutritional Status Before and After a Single-Handed Yacht Race.

During solitary sailing, the sailor is exposed to sleep deprivation and difficulties in consuming regular meals. Sailor weight loss is often reported. In the present case study, we describe changes in the physical capacity and nutritional status of an athlete attempting a single-handed yacht race around the globe. An Italian male ocean racer (Gaetano Mura) asked for our help to reach an optimum level of physical and nutritional preparation. We planned his diet after assessing his anthropometric parameters and body composition, as well as his usual energy intake and nutritional expenditure. The diet consisted of 120 meals stored in sealed plastic bags. Before his departure, GM performed two incremental exercise tests (cycle ergometry and arm crank ergometry) to assess his physical capacity. Cardiac functions were also estimated by Doppler echocardiography. All measures and exercise tests were repeated 10 days after GM finished the race, which lasted 64 days. Anthropometric measures did not change significantly, with the exception of arm fat area and thigh muscle area, which decreased. There were evident increments in maximum oxygen intake and maximum workload during arm cranking after the race. On the contrary, maximum oxygen uptake and maximum workload decreased during cycling. Finally, end-diastolic and stroke volume decreased after the race. It was concluded that nutritional counseling was useful to avoid excessive changes in nutritional status and body composition due to 64 days of solitary navigation. However, a reduction in physical leg capacity and cardiovascular functions secondary to leg disuse were present.

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.

Physical Capacity and Energy Expenditure of Cavers.

Caves are an extreme environment for humans because of the high humidity, mud, darkness, and slippery conditions. Explorations can last many hours or even days, and require extensive climbing and ropework. Very little is known about the physical capacity of cavers and their energy expenditure (EE) during caving. The physical capacity of 17 (7 females) expert cavers (age 43.9 ± 7.3 years) was assessed during an incremental cycle-ergometer test (IET) with gas exchange analysis. Moreover, a wearable metabolic band (Armband Fit Core) was used to estimate their EE during caving. In terms of physical capacity, the IET showed that cavers had a maximum oxygen uptake (VO2max) of 2,248.7 ± 657.8 ml·min-1 (i.e., 32.4 ± 6.4 ml·kg-1·min-1), while anaerobic threshold (AT) occurred on average at 74.5% of VO2max. Results from caving sessions provided an average time spent in cave of 9.4 ± 1.2 h while the average EE was 268.8 ± 54.8 kcal·h-1, which corresponded to about 40% of VO2max measured during IET. A mean distance of 10.6 ± 2.2 km was covered by subjects. Data from the present investigation provide evidence that cavers have a level of aerobic physical capacity only slightly higher than that of sedentary people, thereby suggesting that a high aerobic fitness is not needed by cavers. Moreover, during caving the EE was on average well below the level of AT. However, in absolute terms, the total EE was elevated (i.e., 2,672.3 ± 576 kcal in total) due to the long time spent in caving.

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.

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.