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·cm 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. 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.

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.

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 (ϩ383.8 Ϯ 256.6 vs. ϩ91.2 Ϯ 293.5 dyn•s Ϫ1 •cm Ϫ5 for the CAD and CTL groups, respectively), the CTL group by increasing cardiac preload (Ϫ0.92 Ϯ 8.53 vs. 5.34 Ϯ 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 Ͻ 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.

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.

No abstract