The metabolic syndrome (MS) has been associated with poor performances in multiple cognitive domains, as processing speed, visuo-spatial abilities, and executive functioning. Exercise is a critical factor for MS people’s vulnerability to cognitive dysfunction, because this may be beneficial to reduce cognitive impairment, but limited physical activity and impaired cerebral blood flow in response to exercise have been reported by individuals suffering from MS. Using an attentional interference test, the Bivalent Shape Task (BST), and metaboreflex, we analyzed cognitive performance and cerebral oxygenation (COX) in 13 MS people (five women), and 14 normal age-matched control (CTL, six women). Five different sessions were administered to all participants, each lasting 12 min: control exercise recovery (CER), post-exercise muscle ischemia (PEMI) to activate the metaboreflex, CER + BST, PEMI + BST, and BST alone. During each session, cognitive performance was assessed by means of response times and response accuracy with which participants make the decision and COX was evaluated by near infrared spectroscopy with sensors applied in the forehead. Compared to CTL, MS group performed significantly worse in all sessions ( F = 4.18; p = 0.05; ES = 0.13): their poorest performance was observed in the BST alone session. Moreover, when BST was added to PEMI, individuals of the CTL group significantly increased their COX compared to baseline (103.46 ± 3.14%), whereas this capacity was impaired in MS people (102.37 ± 2.46%). It was concluded that: (1) MS affects cognitive performance; (2) people with MS were able to enhance COX during exercise, but they impair their COX when an attentional interference task was added.
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.
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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