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.

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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.

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 (W max). On separate days, participants performed two randomly assigned exercise sessions (3 minutes pedalling at 30% of W max): (1) one in normoxia (NORMO), and (2) one in normobaric hypoxia with FiO 2 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.

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.