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

Muscle ischemic preconditioning (IP) has been found to improve exercise performance in laboratory tests. This investigation aims at verifying whether performance is improved by IP during self-paced exercise (SPE) in the field. 11 well-trained male runners performed 3 randomly assigned 5 000 m self-paced running tests on an outdoor track. One was the reference (RT) test, while the others were performed following muscle IP (IPT) and a control sham test (ST). Average speeds were measured during each test. Mean values in oxygen uptake (VO2), aerobic energy cost (AEC) during race and post-race blood lactate (BLa) were gathered. Data showed that none of the studied variables were affected by IPT or ST with respect to the RT test. Average speeds were 4.63±0.31, 4.62±0.31 and 4.60±0.25 m·s(-1) for the RT, the ST and the IPT tests, respectively. Moreover, there was no difference among tests in speed reached during each lap. VO2 was 3.5±0.69, 3.74±0.85 and 3.62±1.19 l·min(-1). AEC was 1.04±0.15, 1.08±0.1 and 1.09±0.15 kcal·kg(-1)·km(-1). Finally, post-race BLa levels reached 12.85±3.54, 11.88±4.74 and 12.82±3.6 mmol·l(-1). These findings indicate that performance during SPE is not ameliorated by ischemic preconditioning, thereby indicating that IP is not suitable as an ergogenic aid.

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.

Patients with multiple sclerosis (MS) have an increased systemic vascular resistance (SVR) response during the metaboreflex. It has been hypothesized that this is the consequence of a sedentary lifestyle secondary to MS. The purpose of this study was to discover whether a 6-month training program could reverse this hemodynamic dysregulation. Patients were randomly assigned to one of the following two groups: the intervention group (MSIT, n = 11), who followed an adapted training program; and the control group (MSCTL, n = 10), who continued with their sedentary lifestyle. Cardiovascular response during the metaboreflex was evaluated using the post-exercise muscle ischemia (PEMI) method and during a control exercise recovery (CER) test. The difference in hemodynamic variables such as stroke volume (SV), cardiac output (CO), and SVR between the PEMI and the CER tests was calculated to assess the metaboreflex response. Moreover, physical capacity was measured during a cardiopulmonary test till exhaustion. All tests were repeated after 3 and 6 months (T3 and T6, respectively) from the beginning of the study. The main result was that the MSIT group substantially improved parameters related to physical capacity (+5.31 ± 5.12 ml·min−1/kg in maximal oxygen uptake at T6) in comparison with the MSCTL group (−0.97 ± 4.89 ml·min−1/kg at T6; group effect: p = 0.0004). However, none of the hemodynamic variables changed in response to the metaboreflex activation. It was concluded that a 6-month period of adapted physical training was unable to reverse the hemodynamic dys-regulation in response to metaboreflex activation in these patients.

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.