Franco Melis

CHRONIC ETHANOL CONSUMPTION IN RATS: CORRELATION BETWEEN MEMORY PERFORMANCE AND HIPPOCAMPAL ACETYLCHOLINE RELEASE IN VIVO

The effects of chronic alcohol consumption on memory performance and hippocampal acetylcholine release in vivo were investigated in rats. Rats were allowed to drink 25% (v/v) ethanol solution as the only source of fluid for nine consecutive months, whereas control rats received only tap water. Memory performance was tested by the acquisition of shuttle box active and passive avoidance. Chronic ethanol-consuming rats were not impaired in the acquisition of the active avoidance response task, whereas in the passive avoidance task, latency scores of treated rats were significantly lower than in controls. The basal release of acetylcholine in freely moving rats, assessed by the microdialysis technique, was significantly decreased in ethanol-treated rats. Impairment in memory performance, as assessed in the passive avoidance task, was significantly correlated with hippocampal acetylcholine release in vivo.

Increased hippocampal acetylcholine release during a working memory task.

In this study we examined whether the food-reinforced alternation performance was associated with increased acetylcholine output in the dorsal hippocampus. Rats were trained to acquire the task using a T-maze. The control group consisted of rats introduced into the T-maze to run only on the day of dialysis. Acetylcholine release increased significantly in control rats only in the first 10 min after they were put into the T-maze. In trained rats acetylcholine output increased in the waiting cage as well as during trials in the T-maze. The increase in acetylcholine output in rats that had learned the task was significantly greater than in control rats.

The non-competitive NMDA-receptor antagonist MK-801 prevents the massive release of glutamate and aspartate from rat striatum induced by 1-methyl-4-phenylpyridinium (MPP+)

The concentrations of dopamine (DA) and of the excitatory amino acids (EAAs) glutamate (Glu) and aspartate (Asp) were measured in dialysates from the striatum of awake rats in order to study the link between the release of DA and of EAAs induced by the infusion of 1-methyl-4-phenylpyridinium ion (MPP+). DA and EAAs were detected simultaneously by HPLC-EC. The infusion of MPP+ at the concentration of 1 mM elevated DA levels in the perfusates, but did not affect EAA release. However, MPP+ at 10 mM maximally stimulated Glu and Asp release to 230- and 68-fold of baseline, respectively. In this condition, pretreatment with the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (5 mg/kg, i.p.) prevented the MPP(+)-induced EAA release. In contrast, MK-801 had no effect on DA release induced either by 1 or 10 mM MPP+. These results suggest that MPP(+)-induced DA and EAA release are independently regulated processes. In addition, the finding that MK-801 inhibits MPP(+)-induced EAA release suggests that EAAs may act on NMDA receptors to stimulate their own release through a positive-feedback mechanism.

Physiological responses and energy cost during a simulation of a Muay Thai boxing match

Muay Thai is a martial art that requires complex skills and tactical excellence for success. However, the energy demand during a Muay Thai competition has never been studied. This study was devised to obtain an understanding of the physiological capacities underlying Muay Thai performance. To that end, the aerobic energy expenditure and the recruitment of anaerobic metabolism were assessed in 10 male athletes during a simulation match of Muay Thai. Subjects were studied while wearing a portable gas analyzer, which was able to provide data on oxygen uptake, carbon dioxide production, and heart rate (HR). The excess of CO2 production (CO2 excess) was also measured to obtain an index of anaerobic glycolysis. During the match, group energy expenditure was, on average (mean +/- standard error of the mean), 10.75 +/- 1.58 kcal.min-1, corresponding to 9.39 +/- 1.38 metabolic equivalents. Oxygen uptake and HRs were always above the level of the anaerobic threshold assessed in a preliminary incremental test. CO2 excess showed an abrupt increase in the first round, and reached a value of 636 +/- 66.5 mL.min-1. This parameter then gradually decreased throughout the simulation match. These data suggest that Muay Thai is a physically demanding activity with great involvement of both the aerobic metabolism and anaerobic glycolysis. In particular, it appears that, after an initial burst of anaerobic glycolysis, there was a progressive increase in the aerobic energy supply. Thus, training protocols should include exercises that train both aerobic and anaerobic energetic pathways.

Role of heart rate and stroke volume during muscle metaboreflex-induced cardiac output increase: differences between activation during and after exercise

We hypothesized that the role of stroke volume (SV) in the metaboreflex-induced cardiac output (CO) increase was blunted when the metaboreflex was stimulated by exercise muscle ischemia (EMI) compared with post-exercise muscle ischemia (PEMI), because during EMI heart rate (HR) increases and limits diastolic filling. Twelve healthy volunteers were recruited and their hemodynamic responses to the metaboreflex evoked by EMI, PEMI, and by a control dynamic exercise were assessed. The main finding was that the blood pressure increment was very similar in the EMI and PEMI settings. In both conditions the main mechanism used to raise blood pressure was a CO elevation. However, during the EMI test CO was increased as a result of HR elevation whereas during the PEMI test CO was increased as a result of an increase in SV. These results were explainable on the basis of the different HR behavior between the two settings, which in turn led to different diastolic time and myocardial performance.

Estimating stroke volume from oxygen pulse during exercise.

This investigation aimed at verifying whether it was possible to reliably assess stroke volume (SV) during exercise from oxygen pulse (OP) and from a model of arterio-venous oxygen difference (a-vO(2)D) estimation. The model was tested in 15 amateur male cyclists performing an exercise test on a cycle-ergometer consisting of a linear increase of workload up to exhaustion. Starting from the analysis of previous published data, we constructed a model of a-vO(2)D estimation (a-vO(2)D(est)) which predicted that the a-vO(2)D at rest was 30% of the total arterial O(2) content (CaO(2)) and that it increased linearly during exercise reaching a value of 80% of CaO(2) at the peak workload (W(max)) of cycle exercise. Then, the SV was calculated by applying the following equation, SV = OP/a-vO(2)D(est), where the OP was assessed as the oxygen uptake/heart rate. Data calculated by our model were compared with those obtained by impedance cardiography. The main result was that the limits of agreement between the SV assessed by impedance cardiography and the SV estimated were between 22.4 and -27.9 ml (+18.8 and -24% in terms of per cent difference between the two SV measures). It was concluded that our model for estimating SV during effort may be reasonably applicable, at least in a healthy population.

Hemodynamic during a postexertional asystolia in a healthy athlete : a case study

Hemodynamic events leading to spontaneous postexertional vasovagal syncope are not completely understood because of the lack of beat-to-beat data. We report a case study of a young athlete who undergoes a syncopal episode during the recovery period following a maximal cycle-ergometer test. The episode was monitored by an impedance cardiograph which can gather noninvasively beat-to-beat the flow of heart rate (HR), stroke volume (SV), cardiac output (CO), diastolic filling rate (SV/DT), and myocardial contractility index (PEP/LVET). The most important findings of this report are the dramatic reduction of SV/DT preceding the syncope, the increment of SV together with the reduction of HR preceding and following the syncope, the prompt recovery of CO values after the syncopal episode despite the bradycardia, and the reduction of PEP/LVET after the syncope. This report confirms the importance of active recovery immediately after strenuous exercise and supports the hypothesis that the reduction of SV/DT in the presence of an inotropic stimulation can trigger the vasovagal reaction.

Haemodynamic effect of metaboreflex activation in men after running above and below the velocity of the anaerobic threshold

Previous studies have shown that the muscle metaboreflex, along with its effect on peripheral vasculature, is capable of inducing substantial enhancement in cardiac performance, stroke volume and cardiac output. This study was designed to determine whether the metaboreflex recruited by means of postexercise muscle ischaemia (PEMI) after running at two intensities was capable of eliciting similar enhancement in these cardiovascular parameters. In eight healthy male athletes the metaboreflex was studied with the PEMI method at the start of recovery from running bouts at a velocity of 30% above (PEMI‐AVAT) or below (PEMI‐BVAT) the anaerobic threshold previously assessed. Control exercise recovery tests at the same intensities were also conducted. Haemodynamics were evaluated by means of impedance cardiography. The main results were that: (1) the PEMI‐AVAT test induced an increase in stroke volume, which was not present during the other protocol conditions; (2) the PEMI‐AVAT test also induced a blunted heart rate response compared with the control situation, but this relative bradycardia was fully compensated by the stroke volume increment so that cardiac output was maintained and even increased in comparison with the other protocol sessions; and (3) finally, there was no detectable increase in systemic vascular resistance during PEMI‐AVAT. These results provide evidence that, like what has previously been reported for small muscle mass exercise, metaboreflex activation after running is capable of enhancing cardiac performance and stroke volume. Moreover, this study strengthens the concept that the cardiovascular response to metaboreflex is not merely the consequence of an increase in systemic vascular resistance.

Hemodynamic responses to metaboreflex activation: insights from spinal cord-injured humans

This investigation was conducted to study the hemodynamic consequences of spinal cord injury (SCI) during post-exercise muscle metaboreflex activation in SCI subjects. The hemodynamic response to metaboreflex recruitment was assessed in ten SCI patients and nine healthy controls (CTL) by means of impedance cardiography. The main results were (1) the metaboreflex-induced blood pressure rise was blunted in SCI subjects compared with normals, (2) the CTL group achieved the blood pressure response via cardiac output increase, while the SCI subjects could not use this mechanism, (3) the CTL group was able to enhance stroke volume and ventricular filling rate in response to the metaboreflex, whereas the SCI group could not. It was concluded that in healthy individuals, the hemodynamic response to the metaboreflex is an integrated phenomenon that depends mainly on a flow-mediated mechanism, whereas in SCI individuals the reduced venous return impairs this mechanism.

Haemodynamic responses following intermittent supramaximal exercise in athletes.

We aimed to investigate haemodynamics during active and passive recovery following repeated bouts of supramaximal exercise. Seven male athletes underwent two sessions of supramaximal exercise which consisted of a warm‐up and of five bouts of cycling at the maximum speed possible for 30 s against a resistance equivalent to 150% of the maximum workload achieved in a previous incremental test. Bouts were separated by 1 min of recovery and followed by 10 min of recovery which was either active (pedalling at 40 W) or passive (completely rest seated on the cycle). Haemodynamic variables were evaluated by means of impedance cardiography. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean blood pressure (MBP), thoracic electrical impedance (Z0) as an inverse index of central blood volume, and systemic vascular resistance (SVR) were assessed. The main findings were that active recovery, with respect to passive recovery, induced higher changes from baseline in HR (+29.1 ± 4.5 versus+15.6 ± 2.9 beats min−1 at the 10th minute of recovery, P < 0.05), SV (+19.9 ± 5.6 versus–6.4 ± 3.3 ml, P < 0.01) and CO (+3.8 ± 1.2 versus+0.4 ± 0.2 l min−1, P < 0.01). Furthermore, MBP was similar between the two kinds of recovery despite an increase in Z0 during passive compared to active recovery. These results suggest that the faster haemodynamic recovery towards baseline and the decrease in cardiac preload during passive recovery may be successfully prevented by cardiovascular regulatory mechanisms which include an increase in SVR, thus avoiding a drop in blood pressure.