Uphill versus downhill high-intensity training effectiveness in preserving vascular function and exercise performance in runners who reduce their regular endurance training.

Purpose: The COVID-19 restrictions have limited outdoor physical activities. High-intensity training (HIT) may be a valid indoor alternative. We tested whether an indoor HIT is effective in maintaining vascular function and exercise performance in runners who reduce their usual endurance training, and whether a downhill HIT is as effective as an uphill one for such purposes. Methods: Sixteen runners performed the same 6-week HIT either uphill (UP, eight runners) or downhill (DOWN, eight runners). Eight runners continuing their usual endurance training acted as a control group (CON). The following data were collected before vs after our HIT: vascular conductance during rapid leg vasodilation to assess vasodilation capacity; V̇O2max through running incremental test to exhaustion; 2000 m running time; neuromuscular indexes related to lower-limb muscle strength. Results: Both uphill and downhill HIT failed in maintaining the pre-HIT leg vasodilation capacity compared to CON, which was, however, blunted more after uphill than downhill HIT. V̇O2max and 2000 m time were similar after downhill HIT compared to CON, and augmented after uphill HIT compared to CON and DOWN. Indexes of lower-limb muscle strength were similar before vs after HIT and among groups. Conclusion: Our HIT was ineffective in maintaining the pre-HIT leg vasodilation capacity compared to runners continuing their usual low-intensity endurance training, but did not lead to reductions in V̇O2max, 2000 m time performance, and indexes related to lower-limb muscle strength. Our data show an appealing potential for preserving exercise performance with low cardiorespiratory effort via downhill running.

Energy cost and efficiency of Venetian rowing on a traditional, flat hull boat (Bissa).

The total net metabolic power output (E, kW) required to scull a traditional, flat hull boat--the "Bissa", 9.02 m long and weighting about 500 kg including the crew-was assessed at different constant speeds (nu) ranging from 2.44 to 3.75 m s(-1). E increased with the speed: E = 0.417 x e (0.664v ); r (2) = 0.931. The amount of metabolic energy spent per unit distance (C, J m(-1)) to move the "Bissa", calculated by dividing E by the corresponding nu, was a linear function of nu: C = 0.369 nu -0.063; r (2) = 0.821. The hydrodynamic resistance met by the boat in the water--drag (D, N)--was estimated by analysing the decay of the reciprocal of nu as a function of time measured during several spontaneous deceleration tests carried out in still water and by knowing the total mass of the watercraft plus crew. D increased as a square function of speed: D = 12.76 v (2). This allowed us to calculate the drag efficiency (g(d)), as the ratio of D to C: g(d) increased from 8.9 to 13.7% in the range of the speeds tested. The "Bissa" turned out to be as economical as other flat hull, traditional watercrafts, such as the bigger Venetian gondola, and her g(d) was similar to that of other modern and traditional watercrafts.

Evidence of parasympathetic impairment in some patients with cardiac syndrome X.

OBJECTIVES: Cardiac syndrome X (SX) is a clinical condition characterised by angina, positive exercise stress test and negative coronary angiography; it has often been attributed to sympathetic hyperactivity. Here we tested the hypothesis that a parasympathetic, rather than a sympathetic, dysfunction could be the cause of the autonomic imbalance observed in SX. METHODS: In 20 subjects with diagnosed SX and in 12 age-matched controls, we studied autonomic function by performing spectral analysis of RR interval and finger arterial pressure (SAP), in supine position and during head-up tilting. We also carried out a set of tests of parasympathetic function. RESULTS: The group of SX patients did not differ significantly from control subjects in any of the variables tested. In a subgroup of 13 SX, however, tilting increased the low-frequency power of SAP, but did not induce the expected increase in low-frequency and decrease in high-frequency power of RR. These patients, in supine position, had significantly lower sinus arrhythmia and a higher ratio of low to high frequency of RR, in comparison with control subjects. We interpreted these differences as signs of reduced parasympathetic, but essentially normal sympathetic, activity. The parasympathetic tests confirmed vagal impairment in the same SX subjects. On the other hand, all the tests indicated normal parasympathetic functions in the control subjects and in those SX patients who displayed the expected spectral changes in tilting. CONCLUSIONS: In about two thirds of the patients with SX, the pathophysiological mechanism causing the symptoms could be related to the reduced parasympathetic tone, rather than to an augmented sympathetic activity.

The effect of Bitis gabonica (Gaboon viper) snake venom on external iliac and mesenteric arterial circulation in the dog.

The effects of Gaboon viper (Bitis gabonica) venom on external iliac and mesenteric arterial blood flow and resistance were investigated in eight anaesthetized, close-chest dogs. Venom doses in the range 0.125-0.5 mg/kg produced a profound fall in external iliac and mesenteric arterial resistance, which recovered to control values after 30 min. After a third dose of venom, the mean arterial blood pressure failed to recover and the animals died after a period of severe hypotension. External iliac arterial blood flow rose concomitantly with the fall in external iliac resistance and decreased to a value significantly below control after 30 min. Paradoxically, mesenteric blood flow fell during the period of vasodilation. The results suggest that widespread vasodilation of muscle vascular beds (of which the external iliac circulation is representative) leads to shunting of blood away from the less-dilated mesenteric circulation. Venom-induced peritoneal haemorrhage caused a fall in blood volume and increase in viscosity. These undoubtedly contributed to the severe haemodynamic deterioration of the preparations after the third injection of the venom.

The effect of gaboon viper (Bitis gabonica) venom on cardiac stroke work in the anaesthetized rabbit.

The effect of Bitis gabonica venom administered intravenously in the rabbit at the dose of 0.125 mg/kg (approximately 10% of LD50) has been studied. Venom caused marked changes in cardiovascular parameters principally a precipitous but transient fall in total peripheral resistance and arterial blood pressure. Furthermore in the period occurring between 5 and 30 min after the injection of venom, a transient increase in stroke work was observed as a result of the ejection of an increased stroke volume against a blood pressure which had already returned to normal. Such a transient inotropic effect has also been observed in other small mammals and could be attributed to an adrenergic mechanism.

Preservation of rabbit hearts with different cardioplegic solutions at low temperature.

An organ-preserving solution, including in its composition also organic molecules, prepared at the University of Wisconsin (UW), has been successfully used for preservation of liver, pancreas and kidney, and has recently been tested for long-term storage of isolated hearts. We have compared the effectiveness of the UW solution with that of a standard crystalloid cardioplegic solution (St. Thomas, ST) in the functional and structural preservation of isolated hearts. The hearts taken from 24 rabbits were mounted on a Langendorff preparation. After assessment of the left ventricular function by an intraventricular balloon, 40 ml of either cardioplegic solution were injected to arrest the hearts (12 UW and 12 ST), which were then immersed in the same solution for 4 h at 4 degrees C without perfusion. After this period, the hearts were normothermally reperfused with oxygenated Krebs-Henseleit solution for 30 min, and finally left ventricular function was assessed again. An electron microscopic evaluation was performed as well. Significantly higher recovery of left ventricular developed pressure (p < 0.01) and of negative dP/dt (p < 0.05), was observed after preservation with UW, while no difference on positive dP/dt was found. After reperfusion, left ventricular end-diastolic pressure significantly rose with ST (p < 0.01), but did not change with UW; the difference between ST and UW was significant (p < 0.01). Tissue water content was significantly lower in the hearts preserved with UW (p < 0.05). Electron microscopic examination revealed generally good preservation with no substantial difference between the two solutions.(ABSTRACT TRUNCATED AT 250 WORDS)

Biochemical and morphological changes in isolated rabbit hearts after prolonged hypothermic ischaemia: comparison of two cardioplegic solutions.

This work evaluates the myocardial protective potential of potassium cardioplegia on ischaemically arrested and reperfused hearts by two cardioplegic solutions: the University of Wisconsin solution (UW) and the standard crystalloid solution of St. Thomas' Hospital (ST). Evaluation of myocardial preservation was based on creatine kinase and lactate releases and on high-energy phosphate preservation of isolated rabbit hearts after 4 hours' hypothermic ischaemia. A morphometric ultrastructural evaluation of mitochondria in cardiomyocytes was also performed. The hearts of 24 rabbits were normothermally perfused with oxygenated Krebs-Henseleit solution for 30 min (Langendroff preparation), and the baseline contractile performance and biochemical parameters were evaluated. The hearts were then arrested and stored in the cardioplegic solutions (12 UW and 12 ST) at 4 degrees C for 4 hours. The hearts were then rewarmed and reperfused with oxygenated Krebs-Henseleit solution for further 30 min. At the end of reperfusion, creatine phosphate and high energy phosphates were higher with UW (p < 0.05); creatine kinase release during reperfusion was significantly lower with UW both at 15 min (p < 0.01) and at 30 min (p < 0.05). Lactate release during the first 15 min of reperfusion was about doubled (p < 0.05) with respect to controls in both groups; at 30 min this increase had almost vanished (+8%) with UW but not with ST (+30%). Ultrastructural morphometry did not show any significant difference at the level of mitochondria between the two treatments. The results indicate, for UW, an improved myocardial preservation associated with relative retention of high-energy phosphates and higher recovery of mechanical function, accelerated metabolic recovery and reduced stress of cell membranes.

The heart as a biological clock: phase-locking between heart and efferent vagal activity.

Experiments were performed to evaluate whether the negative inotropic effect of efferent vagal stimulation is more strictly related to the number of stimuli falling with each cardiac cycle (St/c) or to the number of stimuli per second (St/s). Therefore, vagal stimulations were performed in anaesthetized dogs either with constant frequency (CONT), or with trains of 3 stimuli triggered by each atrial activation (SYNCHR). An atrial contractility index was measured while increasing heart rate by artificial heart pacing during CONT and SYNCHR vagal stimulations. The negative inotropic parasympathetic effect was reduced in the former protocol (St/s constant, St/c reduced) and did not change in the latter. It was concluded that the effect of vagal stimulation is more strictly related to St/c rather than to St/s. We suggest that the heart cycle operates as a biological clock with respect to cardiac vagal control.

Adaptations to endurance training in the healthy elderly: arm cranking versus leg cycling.

The effect in healthy elderly subjects of cycle ergometer or arm ergometer training on peak oxygen consumption (VO(2peak)) and ventilatory threshold (VT) was studied. The aim was to determine the benefit of each training modality on specific and cross exercise capacity. The cross-effect was also evaluated as an index of the central nature of the adaptive response to training. Twelve non-smoking healthy males (age: 67 +/- 5 year; body mass: 75 +/- 9 kg) were randomly divided in two age-matched groups of six, performing an arm cranking (ARM) or a cycloergometer (CYC) training (12-week, 30 min, 3 times/week), while a third group of 6 subjects (age: 73 +/- 4 year; body mass: 80 +/- 8 kg) performed no training (control, C). At baseline and following the intervention, subjects carried out an incremental test to exhaustion both on the ergometer on which they trained (specific test) and on the other ergometer (cross test). Respiratory variables were measured breath by breath and heart rate (HR) was recorded. Peak oxygen consumption (VO(2peak)), ventilation (VE(peak)), oxygen pulse (O2P(peak)) and heart rate (HR(peak)) were averaged over the last 10 s of exercise. Following training, while HR(peak) remained unchanged, significantly higher W(peak), VO(2peak), VE(peak) and O2P(peak) were obtained in both training groups, on both ergometers. The amplitude of the increase in W(peak), VO(2peak) and O2P(peak) was significantly higher for specific than for cross tests ( approximately 19% vs. approximately 8 % in CYC; approximately 22% vs. approximately 9% in ARM, P < 0.01) while the increase in same test condition was similar. No change was observed in the C group. The results indicate that aerobic training brought about with different muscle masses, produce similar improvements in maximal and submaximal exercise capacity. Roughly half of such improvements are specific to exercise mode, which suggests peripheral adaptations to training. The other half is non-specific since it influences also the alternative exercise modality, and is probably due to central adaptations.

[Effects of Bitis gabonica venom on heart dynamics and circulatory resistance in the rabbit]. / Effetti del veleno di Bitis gabonica sulla dinamica cardiaca e sulle resistenze circolatorie, nel coniglio.

The effect on the cardiovascular system of intravenous injections of Bitis gabonica venom was studied on 10 urethan anesthetized rabbits, by giving the venom in three successive doses of .125 (I Dose), .250 (II Dose) and .500 (III Dose) mg/kg. In partial agreement with already reported data, the results of our experiments showed a powerful but transient fall of total peripheral resistance, which seemed to be relatively independent of doses. A cardiotoxic action leading to severe reduction of cardiac output was also found, but only at the II Dose; this effect was apparently irreversible, and was not enhanced by the III Dose. Moreover, a prompt bradicardic effect after each administration was found, which may not be attributed to direct effects of the venom on the cardiac pacemaker cells.

Interference of sympathetic innervation with reactive hyperemia in dog's skeletal muscle.

The reactive hyperaemia (RH) after 30 sec arterial occlusion was studied in normal and chromically sympathectomized dog hindlimbs, under general chloralose anaesthesia. RH reached higher peak flow in the sympathectomized limbs, but the percent increase of flow was the same in both hindlimbs. The time course of RH was reduced in normal limbs, thus leading to a 35% decrease of the excess flow. The above results were explained on the basis of an economizing activity of the sympathetic basal tone on available oxygen due to effects on the microvasculature as well as on the cell metabolism. The autonomic tone is also responsible for steeper reduction of blood flow after RH in the normal limbs due to enhanced myogenic reaction.

Haemodynamic effects of withdrawal of efferent cervical vagal stimulation on anesthetized dogs--relative importance of chronotropic and non-chronotropic mechanisms.

The aim of the present work was to study changes in cardiac output (CO) and arterial blood pressure (ABP) following either interruption of artificial efferent vagal stimulations (STOP), or suppression of negative chronotropic effects, during uninterrupted vagal stimulations (PACE). Experiments were performed on 7 anesthetized, open-chest dogs. A computerized data acquisition system was used to record CO (electromagnetic flowmeter), ABP, right atrial pressure and electrocardiogram; 9 parameters were automatically elaborated. The peripheral stumps of both vagus nerves, sectioned at the neck, were stimulated for long control periods (at least 3 min) with brief trains of stimuli triggered by atrial P waves. Records were started during steady-state vagal stimulations, and consisted of paired trials: in the first step the vagal stimulators were turned off (STOP); in the second step the heart was paced at the same rate reached at the end of the preceding step, but vagal stimulation was continued (PACE). Observations lasted two min after each step. Results indicate rapid rise in CO and ABP after STOP, up to 30% and 10%, respectively, in 10 s, followed by slow reduction in CO and further increase in ABP (22% and 15%, respectively, at 120 s). Thus STOP caused rapid and sustained improvements in the cardiac performance. After PACE changes in CO and ABP were smaller and followed a slower time-course. The greater effects of STOP with respect to PACE were attributed to non-chronotropic mechanisms, accounting for about 50% of the overall haemodynamic consequences of vagal withdrawal. Since peak aortic flow velocity and acceleration were increased after STOP, stroke volume was reduced much less than after PACE, despite equal rise in heart rate, and similar shortening in the ejection time. Evidence was presented of enhanced atrial and ventricular contractility after STOP. Experiments performed after beta-blockade in 5 dogs substantially confirmed the results. It is concluded that vagal withdrawal, which is an important aspect in many physiological situations, constitutes a rather powerful strategy for rapid enhancement of the cardiovascular performance, through different mechanisms, in addition to cardioacceleration.

'Non-chronotropic' mechanisms on withdrawal of efferent vagal stimulation in anesthetized dogs.

Withdrawal of the efferent vagal tone to the heart is an important factor of the increase of cardiac output (CO) and arterial blood pressure (ABP) in several conditions, such as exercise, emotion, postural changes. Vagal withdrawal enhances cardiovascular performance both by increasing heart rate (HR) and by other mechanisms, which were globally named 'non-chronotropic mechanisms'. The nature of these non-chronotropic mechanisms was studied in open-chest dogs under morphine-chloralose anesthesia. After cutting the cervical vagi and all the branches of the stellate ganglia except for the ansae subclaviae, the animals were prepared for recording HR, ABP, CO and left ventricular pressure (LVP). The experiments started during control vagal stimulations and consisted either in turning the vagal stimulators off (STOP), or in raising HR by atrial placing without withdrawing vagal stimulation (PACE), or in turning the vagal stimulators off while keeping HR constant by atrial pacing since the control vagal stimulation (STPA). Thus, STOP, PACE and STPA produced withdrawal of all vagal effects, of the chronotropic effects and of the non-chronotropic effects, respectively. Non-chronotropic mechanisms were evaluated both as the effects of STPA and as the difference between the effects of STOP and PACE. Experiments were repeated during stellate ganglion stimulation and during simultaneous atrio-ventricular pacing, to evaluate the role of vagosympathetic interactions and of atrial contractility. CO increased by 25% after STOP, by 20% after PACE and by 5% after STPA in the absence of sympathetic stimulation and by 30% after STOP, by 20% after PACE and by 10% after STPA during sympathetic stimulation. Stellate ganglion stimulation doubled non-chronotropic effects probably by potentiating vagal effects on myocardial contractility: after STPA the maximum LVdP/dt increased by 2% without sympathetic stimulation and by 7% with sympathetic stimulation. In all conditions, the increases in ABP after STOP, PACE and STPA were small and not statistically different between STOP and PACE. Simultaneous atrio-ventricular pacing in the absence of sympathetic stimulation nearly abolished non-chronotropic mechanisms, since CO increased to about the same extent both with STOP and with PACE. It is concluded that non-chronotropic mechanisms on vagal withdrawal consist mainly in the enhancement of atrial contractility and in the release of vagal restraint on the sympathetic effects upon the ventricles.

Role of the autonomic nervous system in the control of heart rate and blood pressure in the defence reaction in conscious dogs.

The present study was performed on conscious, chronically instrumented dogs, which underwent selective blockade of sympathetic adrenergic and vagal outflows. Excitements were performed on these animals in normal states (N), after chronic treatment with guanethidine, for sympathetic blockade (SB), after cold vagal blockade (VB), and after combined sympathetic and vagal blockade (SB + VB). Heart rate and arterial blood pressure were monitored in all the experiments, while a group of dogs was also tested with an electromagnetic flowmeter on the superior mesenteric artery. The role of the sympathetic and parasympathetic controls in the defence reaction was assumed from comparison of experiments performed in the presence or in the absence of each (or both) autonomic component(s). In the SB + VB condition, excitement was followed by sudden hypotension, without changes in heart rate. In VB experiments, a brief and transient hypotension appeared, followed by gradually developed hypertension, while heart rate progressively rose in about 5 s; there was no sudden increase in mesenteric vascular resistance, which contrasted with the very marked reaction in N experiments. Under vagal control alone (SB), the stimulus elicited prompt tachycardia and hypertension, followed by a period of moderately reduced blood pressure. We conclude that, while the defence reaction leads to a sudden fall of arterial blood pressure, in the absence of compensatory mechanisms, both branches of the autonomic nervous system play a protective role against hypotension. In addition, the modulation of the vagal outflow, leading to sudden changes in the heart performance, seems to be responsible for the initiation of the overall haemodynamic adjustments following excitements. The possibility that withdrawal of the parasympathetic outflow to the heart may raise arterial blood pressure was verified in a special experiment in which artificial vagal stimulation in a conscious (vagal blocked) dog, was turned off for brief periods, before and after guanethidine. This led to changes in blood pressure and heart rate very similar to those seen at the onset of the defence reaction, both in N and SB conditions.

Protective effect of selenium in cardiac ischemia and reperfusion.

The purpose of the present investigation was to establish whether pretreatment with selenium enhances the stores of selenium-dependent glutathione peroxidase in the tissues and to verify if and to what extent alterations of mechanical and biochemical cardiac properties induced by ischemia in the myocardium may be thus prevented. Ten rats had sodium selenite (6 micrograms/day) added to their drinking water for 4 weeks, while 10 control rats received no treatment. At the end of 4 weeks, the hearts were perfused by the Langendorff technique with oxygenated Krebs-Henseleit solution at a rate of 10 ml/min for 30 minutes at 37 degrees C. Ischemia was then induced by reducing the perfusion to 1 ml/min for 60 minutes; reperfusion followed at the control rate for a further 30 minutes. Isometrically developed pressure and its maximum first derivative at different ventricular volumes was measured before and after the ischemic period. Lactate and creatine kinase activity were measured in the effluent throughout. Tissue concentrations of adenine nucleotides and creatine phosphate and lutathione peroxidase activity were estimated after reperfusion. The rats treated with selenium showed a wide-spread increase in the activity of Se-dependent glutathione peroxidase in all tissues. There was an improved recovery of ventricular contraction during reperfusion and an increased myocardial content of adenine nucleotides and creatine phosphate. During reperfusion, the loss of creatine kinase into the perfusate was less in the treated animals, and there was a similar trend for the production of lactate.(ABSTRACT TRUNCATED AT 250 WORDS)

Isohemic blood volume expansion in normal and areflexive dogs.

The hemodynamic and renal responses to rapid intravascular volume expansion (VE) were studied in normal and areflexive dogs. "Isohemic" expansion was performed by infusing autologous blood (averaging 453 ml) thoroughly mixed with the circulating blood. In areflexive dogs cardiac output and arterial pressure doubled immediately after VE and fell back to control within 70 min; in normal dogs the circulatory response was less than one-third as great, but arterial pressure failed to return to control within 120 min. In the areflexive dogs, water, electrolyte, and total osmolar urinary output rose three- to fivefold after VE and declined thereafter, roughly following arterial pressure. In normal dogs the urine flow increased 40% immediately and rose further up to 70% in 60 min. No evidence for a natriuretic hormone was seen. It is concluded that mechanical factors are mainly responsible for the increased excretion of water and solutes after VE. Direct nervous reflexes to the kidney seemed to play a quantitatively minor role in the renal response.

Effects of combined stimulation of right and left vagus nerves on heart rate in rabbits.

The negative chronotropic effects of combined stimulations of the right and left vagus nerves were compared with the effects of single nerve stimulations in 10 urethan anesthetized rabbits. The combined stimulations gave smaller effects than single nerve stimulations at double frequency, over a wide range of frequencies: this was more evident for the right vagus compared with right plus left, rather than vice versa. It is concluded that the effects of combined stimulations are partially occluded and that the left vagus has smaller effects than the right vagus, although such difference becomes apparent only with combined stimulations. Possible mechanisms of occlusion are discussed.

Cardiac alpha-1 adrenoceptors are not involved in heart rate control of the anaesthetized dog.

To study the possible role of cardiac postsynaptic alpha-1 adrenoceptors in heart rate control of the anaesthetized open-chest dog we injected a specific alpha-1 agonist (amidephrine) into the right coronary artery or stimulated electrically the right stellate ganglion. Reflex influences were minimized by bilateral cervical vagotomy and de-afferentiation of both stellate ganglia. Activation of alpha-2, beta- and muscarinic receptors was prevented by intravenous administration of yohimbine, propranolol and atropine, respectively. Since alpha-1 receptor stimulation could affect heart rate indirectly via coronary constriction, a continuous intracoronary infusion of adenosine (0.25 mg/kg/h) was given. Amidephrine did not affect heart rate at the lower dose (1-10 microgram). After the highest dose (100 micrograms) the maximum variation in heart rate was an increase of 2.2 +/- 1.1 bpm at 3 min after injection (mean +/- SEM; P less than 0.05). This slight cardioacceleration was simultaneous with an aortic pressure rise of 13.8 +/- 3.4 mm Hg and it was abolished by alpha-1 blockade with prazosin (1 mg/kg i.v.). After propranolol (1 mg/kg +0.5 mg/kg/h) the residual positive chronotropic effect of sympathetic stimulation (12.2 +/- 4.0 bpm) was not significantly altered (13.8 +/- 5.7 bpm) by prazosin administration. Similar results were recorded without adenosine infusion. We conclude that in the anaesthetized dog chronotropic effects directly mediated by alpha-1 adrenoceptors either do not exist or lack physiological significance.