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.

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.

Effects of Six Months Training on Physical Capacity and Metaboreflex Activity in Patients with Multiple Sclerosis.

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.

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.

Diving response after a one-week diet and overnight fasting.

BACKGROUND: We hypothesized that overnight fasting after a short dietary period, especially with carbohydrates, could allow performing breath-hold diving with no restraint for diaphragm excursion and blood shift and without any increase of metabolism, and in turn improve the diving response. METHODS: During two separate sessions, 8 divers carried out two trials: (A) a 30-m depth dive, three hours after a normal breakfast and (B) a dive to the same depth, but after following a diet and fasting overnight. Each test consisted of 3 apnea phases: descent, static and ascent whose durations were measured by a standard chronometer. An impedance cardiograph, housed in an underwater torch, provided data on trans-thoracic fluid index (TFI), stroke volume (SV), heart rate (HR) and cardiac output (CO). Mean blood pressure (MBP), arterial O2 saturation (SaO2), blood glucose (Glu) and blood lactate (BLa) were also collected. RESULTS: In condition B, duration of the static phase of the dive was longer than A (37.8 ± 7.4 vs. 27.3 ± 8.4 s respectively, P < 0.05). In static phases, mean ∆ SV value (difference between basal and nadir values) during fasting was lower than breakfast one (-2.6 ± 5.1 vs. 5.7 ± 7.6 ml, P < 0.05). As a consequence, since mean ∆ HR values were equally decreased in both metabolic conditions, mean ∆ CO value during static after fasting was lower than the same phase after breakfast (-0.4 ± 0.5 vs. 0.4 ± 0.5 L · min(-1) respectively, P < 0.05). At emersion, despite the greater duration of dives during fasting, SaO2 was higher than A (92.0 ± 2.7 vs. 89.4 ± 2.9 % respectively, P < 0.05) and BLa was lower in the same comparison (4.2 ± 0.7 vs. 5.3 ± 1.1 mmol∙L(-1), P < 0.05). CONCLUSIONS: An adequate balance between metabolic and splancnic status may improve the diving response during a dive at a depth of 30 m, in safe conditions for the athlete's health.

Ischemic preconditioning reduces hemodynamic response during metaboreflex activation.

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.

Metaboreflex activity in multiple sclerosis patients.

PURPOSE: The muscle metaboreflex activation has been shown essential to reach normal hemodynamic response during exercise. It has been demonstrated that patients with multiple sclerosis (MS) have impaired autonomic functions and cardiovascular regulation during exercise. However, to the best of our knowledge, no previous research to date has studied the metaboreflex in MS patients. The purpose of this study was to investigate the hemodynamic response to metaboreflex activation in patients with MS (n = 43) compared to an age-matched, control group (CTL, n = 21). METHODS: 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 hemodynamics between the PEMI and the CER test was calculated and this procedure allowed for the assessment of the metaboreflex response. Hemodynamics was estimated by impedance cardiography. RESULTS: The MS group showed a normal mean blood pressure (MBP) response as compared to the CTL group (+6.5 ± 6.9 vs. +8 ± 6.8 mmHg, respectively), but this response was achieved with an increase in systemic vascular resistance, that was higher in the MS with respect to the CTL group (+137.6 ± 300.5 vs. -14.3 ± 240 dyne · s(-1) cm(-5), respectively). This was the main consequence of the MS group's incapacity to raise the stroke volume (-0.65 ± 10.6 vs. +6.2 ± 12.8 ml, respectively). CONCLUSION: It was concluded that MS patients have an impaired capacity to increase stroke volume (SV) in response to low level metaboreflex, even if they could sustain the MBP response by vasoconstriction. This was probably a consequence of their chronic physical de-conditioning.

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype.

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.

Physiological responses and energy expenditure during competitive fencing.

Fencing is an Olympic sport in which athletes fight one against one using bladed weapons. Contests consist of three 3-min bouts, with rest intervals of 1 min between them. No studies investigating oxygen uptake and energetic demand during fencing competitions exist, thus energetic expenditure and demand in this sport remain speculative. The aim of this study was to understand the physiological capacities underlying fencing performance. Aerobic energy expenditure and the recruitment of lactic anaerobic metabolism were determined in 15 athletes (2 females and 13 males) during a simulation of fencing by using a portable gas analyzer (MedGraphics VO2000), which was able to provide data on oxygen uptake, carbon dioxide production and heart rate. Blood lactate was assessed by means of a portable lactate analyzer. Average group energetic expenditure during the simulation was (mean ± SD) 10.24 ± 0.65 kcal·min(-1), corresponding to 8.6 ± 0.54 METs. Oxygen uptakeand heart rate were always below the level of anaerobic threshold previously assessed during the preliminary incremental test, while blood lactate reached its maximum value of 6.9 ± 2.1 mmol·L(-1) during the final recovery minute between rounds. Present data suggest that physical demand in fencing is moderate for skilled fencers and that both aerobic energy metabolism and anaerobic lactic energy sources are moderately recruited. This should be considered by coaches when preparing training programs for athletes.