Home About us Contact
|
Home About us Contact | ||
|
|
||
Beats Min (beat + min)
Selected AbstractsEffects of aerobic fitness on hypohydration-induced physiological strain and exercise impairmentACTA PHYSIOLOGICA, Issue 2 2010T. L. Merry Abstract Aim:, Hypohydration exacerbates cardiovascular and thermal strain and can impair exercise capacity in temperate and warm conditions. Yet, athletes often dehydrate in exercise, are hypervolaemic and have less cardiovascular sensitivity to acute hypervolaemia. We tested the hypothesis that trained individuals have less cardiovascular, thermoregulatory and performance affect of hypohydration during exercise. Methods:, After familiarization, six trained [O2 peak = 64 (SD 8) mL kg,1 min,1] and six untrained [O2 peak = 45 (4) mL kg,1 min,1] males cycled 40 min at 70%O2 peak while euhydrated or hypohydrated by 1.5,2.0% body mass (crossover design), before a 40-min work trial with euhydration or ad libitum drinking (in Hypohydration trial), in temperate conditions (24.3,°C, RH 50%, va = 4.5 m s,1). Baseline hydration was by complete or partial rehydration from exercise+heat stress the previous evening. Results:, During constant workload, heart rate and its drift were increased in Hypohydration compared with Euhydration for Untrained [drift: 33 (11) vs. 24 beats min,1 h,1 (10), 95% CI 5,11] but not Trained [14 (3) vs. 13 beats min,1 h,1 (3), CI ,2 to 3; P = 0.01 vs. Untrained]. Similarly, rectal temperature drift was faster in Hypohydration for Untrained only [by 0.57,°C h,1 (0.25); P = 0.03 vs. Trained], concomitant with their reduced sweat rate (P = 0.05) and its relation to plasma osmolality (P = 0.03). Performance power tended to be reduced for Untrained (,13%, CI ,35 to 2) and Trained (,7%, CI: ,16 to 1), without an effect of fitness (P = 0.38). Conclusion:, Mild hypohydration exacerbated cardiovascular and thermoregulatory strain and tended to impair endurance performance, but aerobic fitness attenuated the physiological effects. [source] Cerebral oxygenation decreases during exercise in humans with beta-adrenergic blockadeACTA PHYSIOLOGICA, Issue 3 2009T. Seifert Abstract Aim:, Beta-blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. Methods:, Acting as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non-selective beta-blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near-infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences. Results:, Arterial lactate and cardiac output increased to 15.3 ± 4.2 mm and 20.8 ± 1.5 L min,1 respectively (mean ± SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 ± 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 ± 6 vs. 69 ± 8 beats min,1) and at exercise exhaustion, cardiac output (16.6 ± 3.6 L min,1) and arterial lactate (9.4 ± 3.7 mm) were attenuated with a reduction in exercise capacity from 239 ± 42 to 209 ± 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 ± 10 mmHg; P < 0.05). Conclusion:, Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity. [source] Chronic inhibition of standing behaviour alters baroreceptor reflex function in ratsACTA PHYSIOLOGICA, Issue 3 2009H. Waki Abstract Aim:, To investigate whether daily orthostatic stress during development is an important factor affecting arterial baroreceptor reflex function, we examined the effect of chronic inhibition of upright standing behaviour on the baroreceptor reflex function in rats. Methods:, Upright standing behaviour was chronically inhibited during the developmental period between 3 and 8 weeks of age in Sprague,Dawley rats and heart rate (HR) and aortic nerve activity in response to increased and decreased mean arterial pressure (MAP) was measured after the treatment period. Results:, The baroreceptor cardiac gain in the rats grown without standing behaviour was significantly lower than the control rats grown in a normal commercial cage (1.0 ± 0.1 beats min,1 mmHg,1 vs. 1.6 ± 0.2 beatsmin,1 mmHg,1, P < 0.05). The range of HR change in the MAP,HR functional curve was also lowered by chronic inhibition of orthostatic behaviour (56.2 ± 5.9 beats min,1) compared with that of the control rats (76.8 ± 6.9 beats min,1, P < 0.05). However the aortic afferent function remained normal after the treatment period, indicating that the attenuated baroreceptor reflex function may be due to other mechanisms involving functional alterations in the cardiovascular centres, efferents and/or peripheral organs. Body weight and adrenal weight were not affected by the inhibition of orthostatic behaviour, suggesting that the animals were not exposed to specific stress by this treatment. Conclusion:, These results indicate that active haemodynamic changes induced by orthostatic behaviour are an important factor for setting the basal level of reflex function during development. Moreover, our experimental model may be useful for studying mechanisms of attenuated baroreceptor reflex observed after exposure to a chronic inactive condition. [source] Cardiac natriuretic peptides and continuously monitored atrial pressures during chronic rapid pacing in pigsACTA PHYSIOLOGICA, Issue 2 2000Changes in atrial natriuretic peptide (ANP), N-terminal proatrial natriuretic peptide and brain natriuretic peptide (BNP) were evaluated in relation to continuously monitored atrial pressures in a pacing model of heart failure. Pigs were subjected to rapid atrial pacing (225 beats min,1) for 3 weeks with adjustments of pacing frequencies if the pigs showed overt signs of cardiac decompensation. Atrial pressures were monitored by a telemetry system with the animals unsedated and freely moving. Left atrial pressure responded stronger and more rapidly to the initiation of pacing and to alterations in the rate of pacing than right atrial pressure. Plasma natriuretic peptide levels were measured by radioimmunoassay and all increased during pacing with BNP exhibiting the largest relative increase (2.9-fold increase relative to sham pigs). Multiple regression analysis with dummy variables was used to evaluate the relative changes in natriuretic peptides and atrial pressures and the strongest correlation was found between BNP and left atrial pressure with R,2=0.81. Termination of pacing resulted in rapid normalization of ANP values in spite of persistent elevations in atrial pressures. This may reflect an increased metabolism or an attenuated secretory response of ANP to atrial stretch with established heart failure. In conclusion, 3 weeks of rapid pacing induced significant increases in atrial pressures and natriuretic peptide levels. All the natriuretic peptides correlated with atrial pressures with BNP appearing as a more sensitive marker of cardiac filling pressures than ANP and N-terminal proatrial natriuretic peptide. [source] Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activityEXPERIMENTAL PHYSIOLOGY, Issue 9 2010Jasenka Zubcevic GABAergic neurones are interspersed throughout the nucleus tractus solitarii (NTS), and their tonic activity is crucial to the maintenance of cardiorespiratory homeostasis. However, the mechanisms that regulate the magnitiude of GABAergic inhibition in the NTS remain unknown. We hypothesized that the level of GABAergic inhibition is proportionally regulated by the level of excitatory synaptic input to the NTS from baroreceptors. Using the in situ working heart,brainstem preparation in normotensive and spontaneously hypertensive rats, we blocked GABAA receptor-mediated neurotransmission in the NTS with gabazine (a specific GABAA receptor antagonist) at two levels of perfusion pressure (low PP, 60,70 mmHg; and high PP, 105,125 mmHg) while monitoring the immediate changes in cardiorespiratory variables. In normotensive rats, gabazine produced an immediate bradycardia consistent with disinhibition of NTS circuit neurones that regulate heart rate (HR) which was proportional to the level of arterial pressure (,HR at low PP, ,57 ± 9 beats min,1; at high PP, ,177 ± 9 beats min,1; P < 0.001), suggesting that GABAergic circuitry in the NTS modulating heart rate was arterial pressure dependent. In contrast, there was no significant difference in the magnitude of gabazine-induced bradycardia in spontaneously hypertensive rats at low or high PP (,HR at low PP, ,45 ± 10 beats min,1; at high PP, ,58 ± 7 beats min,1). With regard to thoracic sympathetic nerve activity (tSNA), at high PP there was a significant reduction in tSNA during the inspiratory (I) phase of the respiratory cycle, but only in the normotensive rat (,,tSNA =,18.7 ± 10%). At low PP, gabazine caused an elevation of the postinspiration phase of tSNA in both normotensive (,,tSNA = 23.7 ± 2.9%) and hypertensive rats (,,tSNA = 44.2 ± 14%). At low PP, gabazine produced no change in tSNA during the mid-expiration phase in either rat strain, but at high PP we observed a significant reduction in the mid-expiration phase tSNA, but only in the spontaneously hypertensive rat (,,tSNA =,25.2 ± 8%). Gabazine at both low and high PP produced a reduction in the late expiration phase of tSNA in the hypertensive rat (low PP, ,,tSNA =,29.4 ± 4.4%; high PP, ,tSNA =,22.8 ± 3%), whereas in the normotensive rat this was only significant at high PP (,,tSNA =,42.5 ± 6.1%). Therefore, in the spontaneously hypertensive rat, contrary to the GABAA receptor-mediated control of HR, it appears that GABAA receptor-mediated control of tSNA in the NTS is arterial pressure dependent. This study provides new insight into the origin of GABAergic inhibition in NTS circuitry affecting heart rate and sympathetic activity. [source] Dynamic characteristics of heart rate control by the autonomic nervous system in ratsEXPERIMENTAL PHYSIOLOGY, Issue 9 2010Masaki Mizuno We estimated the transfer function of autonomic heart rate (HR) control by using random binary sympathetic or vagal nerve stimulation in anaesthetized rats. The transfer function from sympathetic stimulation to HR response approximated a second-order, low-pass filter with a lag time (gain, 4.29 ± 1.55 beats min,1 Hz,1; natural frequency, 0.07 ± 0.03 Hz; damping coefficient, 1.96 ± 0.64; and lag time, 0.73 ± 0.12 s). The transfer function from vagal stimulation to HR response approximated a first-order, low-pass filter with a lag time (gain, 8.84 ± 4.51 beats min,1 Hz,1; corner frequency, 0.12 ± 0.06 Hz; and lag time, 0.12 ± 0.08 s). These results suggest that the dynamic characteristics of HR control by the autonomic nervous system in rats are similar to those of larger mammals. [source] Cardiac and coronary function in the Langendorff-perfused mouse heart modelEXPERIMENTAL PHYSIOLOGY, Issue 1 2009Melissa E. Reichelt The Langendorff mouse heart model is widely employed in studies of myocardial function and responses to injury (e.g. ischaemia). Nonetheless, marked variability exists in its preparation and functional properties. We examined the impact of early growth (8, 16, 20 and 24 weeks), sex, perfusion fluid [Ca2+] and pacing rate on contractile function and responses to 20 min ischaemia followed by 45 min reperfusion. We also assessed the impact of strain, and tested the utility of the model in studying coronary function. Under normoxic conditions, hearts from 8-week-old male C57BL/6 mice (2 mm free perfusate [Ca2+], 420 beats min,1) exhibited 145 ± 2 mmHg left ventricular developed pressure (LVDP). Force development declined by ,15% (126 ± 5 mmHg) with a reduction in free [Ca2+] to 1.35 mm, and by 25% (108 ± 3 mmHg) with increased pacing to 600 beats min,1. While elevated heart rate failed to modify ischaemic outcome, the lower [Ca2+] significantly improved contractile recovery (by >30%). We detected minimal sex-dependent differences in normoxic function between 8 and 24 weeks, although age modified contractile function in males (increased LVDP at 24 versus 8 weeks) but not females. Both male and female hearts exhibited age-related reductions in ischaemic tolerance, with a significant decline in recovery evident at 16 weeks in males and later, at 20,24 weeks, in females (versus recoveries in hearts at 8 weeks). Strain also modified tolerance to ischaemia, with similar responses in hearts from C57BL/6, 129/sv, Quackenbush Swiss and FVBN mice, but substantially greater tolerance in BALB/c hearts. In terms of vascular function, baseline coronary flow (20,25 ml min,1 g,1) was 50,60% of maximally dilated flows, and coronary reactive and functional hyperaemic responses were pronounced (up to 4-fold elevations in flow in hearts lacking ventricular balloons). These data indicate that attention to age (and sex) of mice will reduce variability in contractile function and ischaemic responses. Even small differences in perfusion fluid [Ca2+] also significantly modify tolerance to ischaemia (whereas modest shifts in heart rate do not impact). Ischaemic responses are additionally strain dependent, with BALB/c hearts displaying greatest intrinsic tolerance. Finally, the model is applicable to the study of vascular reactivity, providing large responses and excellent reproducibility. [source] Effects of acute vagal nerve stimulation on the early passive electrical changes induced by myocardial ischaemia in dogs: heart rate-mediated attenuationEXPERIMENTAL PHYSIOLOGY, Issue 8 2008Carlos L. Del Rio Parasympathetic activity during acute coronary artery occlusion (CAO) can protect against ischaemia-induced malignant arrhythmias; nonetheless, the mechanism mediating this protection remains unclear. During CAO, myocardial electrotonic uncoupling is associated with autonomically mediated immediate (i.e. type 1A) arrhythmias and can modulate pro-arrhythmic dispersion of repolarization. Therefore, the effects of acutely enhanced or decreased cardiac parasympathetic activity on early electrotonic coupling during CAO, as measured by myocardial electrical impedance (MEI), were investigated. Anaesthetized dogs were instrumented for MEI measurements, and left circumflex coronary arterial occlusions were performed in intact (CTRL) and vagotomized (VAG) animals. The CAO was followed by either vagotomy (CTRL) or vagal nerve stimulation (VNS, 10 Hz, 10 V) in the VAG dogs. Vagal nerve stimulation was studied in two additional sets of animals. In one set heart rate (HR) was maintained by pacing (220 beats min,1), while in the other set bilateral stellectomy preceded CAO. The MEI increased after CAO in all animals. A larger MEI increase was observed in vagotomized animals (+85 ± 9 ,, from 611 ± 24 ,, n= 16) when compared with intact control dogs (+43 ± 5 ,, from 620 ± 20 ,, n= 7). Acute vagotomy during ischaemia abruptly increased HR (from 155 ± 11 to 193 ± 15 beats min,1) and MEI (+12 ± 1.1 ,, from 663 ± 18 ,). In contrast, VNS during ischaemia (n= 11) abruptly reduced HR (from 206 ± 6 to 73 ± 9 beats min,1) and MEI (,16 ± 2 ,, from 700 ± 44 ,). These effects of VNS were eliminated by pacing but not by bilateral stellectomy. Vagal nerve stimulation during CAO also attenuated ECG-derived indices of ischaemia (e.g. ST segment, 0.22 ± 0.03 versus 0.15 ± 0.03 mV) and of rate-corrected repolarization dispersion [terminal portion of T wave (TPEc), 84.5 ± 4.2 versus 65.8 ± 5.9 ms; QTc, 340 ± 8 versus 254 ± 16 ms]. Vagal nerve stimulation during myocardial ischaemia exerts negative chronotropic effects, limiting early ischaemic electrotonic uncoupling and dispersion of repolarization, possibly via a decreased myocardial metabolic demand. [source] Sympathoexcitatory response to peripheral chemoreflex activation is enhanced in juvenile rats exposed to chronic intermittent hypoxiaEXPERIMENTAL PHYSIOLOGY, Issue 6 2006Valdir A. Braga In the present study, we tested the hypothesis that chronic intermittent hypoxia (CIH) produces changes in the autonomic and respiratory responses to acute peripheral chemoreflex activation. To attain this goal, 3-week-old rats were exposed to 10 days of CIH (6% O2 for 40 s at 9 min intervals; 8 h day,1). They were then used to obtain a working heart,brainstem preparation and, using this unanaesthetized experimental preparation, the chemoreflex was activated with potassium cyanide (0.05%, injected via the perfusion system), and the thoracic sympathetic nerve activity (tSNA), heart rate and phrenic nerve discharge (PND) were recorded. Rats subjected to CIH (n= 12), when compared with control animals (n= 12), presented the following significant changes in response to chemoreflex activation: (a) an increase in tSNA (78 ± 4 versus 48 ± 3%); (b) a long-lasting increase in the frequency of the PND at 20 (0.52 ± 0.03 versus 0.36 ± 0.03 Hz) and 30 s (0.40 ± 0.02 versus 0.31 ± 0.02 Hz) after the stimulus; and (c) a greater bradycardic response (,218 ± 20 versus,163 ± 16 beats min,1). These results indicate that the autonomic and respiratory responses to chemoreflex activation in juvenile rats previously submitted to CIH are greatly increased. [source] Exercise Heat Stress does not Reduce Central Activation to non-exercised Human Skeletal MuscleEXPERIMENTAL PHYSIOLOGY, Issue 6 2003Julian Saboisky In this study we measured the central activation ratio (CAR) of the leg extensors and the elbow flexor muscles before and after exhaustive exercise in the heat to determine whether exercise-induced hyperthermia affects the CNS drive to exercised (leg extensors) and/or non-exercised (forearm flexors) muscle groups. Thirteen subjects exercised at fixed intensities representative of a percentage of peak power output (PPO) for 10 min periods (50%, 40%, 60%, 50%) and then at 75% PPO until exhaustion in ambient conditions of 39.3 ± 0.8 °C and 60.0 ± 0.8% relative humidity. Before and immediately following exercise subjects performed a series of maximal voluntary contractions (MVCs) with the leg extensors (exercised muscles) and forearm flexors (non-exercised muscles). The degree of voluntary activation during the sustained MVCs was assessed by superimposing electrical stimulation to the femoral nerve and the biceps brachii. Exercise to exhaustion increased the rectal temperature from 37.2 ± 0.2 to 38.8 ± 0.2 °C (P < 0.0001). The mean heart rate at the end of exercise to exhaustion was 192 ± 3 beats min,1. Leg extensor voluntary force was significantly reduced from 595 ± 143 to 509 ± 105 N following exercise-induced hyperthermia but forearm flexor force was similar before and after exercise. The CAR of the leg extensors decreased from 94.2 ± 1.3% before exercise to 91.7 ± 1.5% (P < 0.02) following exercise-induced hyperthermia. However, the CAR for the forearm flexors remained at similar levels before and after exercise. The data suggest that the central nervous system selectively reduces central activation to specific skeletal muscles as a consequence of exercise-induced hyperthermia. [source] Effects of Direct Sympathetic and Vagus Nerve Stimulation on the Physiology of the Whole Heart , A Novel Model of Isolated Langendorff Perfused Rabbit Heart with Intact Dual Autonomic InnervationEXPERIMENTAL PHYSIOLOGY, Issue 3 2001G. André Ng A novel isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation is described. This preparation allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. These hearts (n= 10) had baseline heart rates of 146 ± 2 beats min,1 which could be increased to 240 ±11 beats min,1 by sympathetic stimulation (15 Hz) and decreased to 74 ± 11 beats min,1 by stimulation of the vagus nerve (right vagus, 7 Hz). This model has the advantage of isolated preparations, with the absence of influence from circulating hormones and haemodynamic reflexes, and also that of in vivo preparations where direct nerve stimulation is possible without the need to use pharmacological agents. Data are presented characterising the preparation with respect to the effects of autonomic nerve stimulation on intrinsic heart rate and atrioventricular conduction at different stimulation frequencies. We show that stimulation of the right and left vagus nerve have differential effects on heart rate and atrioventricular conduction. [source] Cholinergic and adrenergic influences on the heart of the African lungfish Protopterus annectensJOURNAL OF FISH BIOLOGY, Issue 4 2010E. Sandblom Cardiac cholinergic and adrenergic tones were determined in minimally instrumented African lungfish Protopterus annectens. Mean ±S.E. routine heart rate (fH) was 31·6 ± 1·4 beats min,1, cholinergic tone was 34·6 ± 5·2% and adrenergic tone was 9·4 ± 2·3%, while the intrinsic fH after blockade of both adrenergic and cholinergic control systems was 39·1 ± 1·3 beats min,1. It is demonstrated that routine cholinergic tone has probably been underestimated in previous studies on lungfishes, suggesting that withdrawal of vagal tone may provide an important mechanism to increase fH in this group of fishes during, for example, air breathing. [source] Blunting of rapid onset vasodilatation and blood flow restriction in arterioles of exercising skeletal muscle with ageing in male miceTHE JOURNAL OF PHYSIOLOGY, Issue 12 2010Dwayne N. Jackson Exercise capacity and skeletal muscle blood flow are diminished with ageing but little is known of underlying changes in microvascular haemodynamics. Further, it is not clear how the sympathetic nervous system affects the microcirculation of skeletal muscle with ageing or whether sex differences prevail in the regulation of arteriolar diameter in response to muscle contractions. In the gluteus maximus muscle of C57BL/6 mice, we tested the hypothesis that ageing would impair ,rapid onset vasodilatation' (ROV) in distributing arterioles (second-order, 2A) of old (20-month) males (OM) and females (OF) relative to young (3-month) males (YM) and females (YF). Neither resting (,17 ,m) nor maximum (,30 ,m) 2A diameters differed between groups. In response to single tetanic contractions at 100 Hz (duration, 100,1000 ms), ROV responses were blunted by half in OM relative to OF, YM or YF. With no effect in YM, blockade of ,-adrenoreceptors with phentolamine (1 ,m) restored ROV in OM. Topical noradrenaline (1 nm) blunted ROV in YM and YF to levels seen in OM and further suppressed ROV in OM (P < 0.05). To evaluate arteriolar blood flow, red blood cell velocity was measured in 2A of OM and YM; respective heart rates (353 ± 22 vs. 378 ± 15 beats min,1) and carotid arterial blood pressures (76 ± 3 vs. 76 ± 1 mmHg) were not different. Blood flows at rest (0.6 ± 0.1 vs. 1.6 ± 0.2 nl s,1) and during maximum dilatation (2.0 ± 0.8 vs. 5.4 ± 0.8 nl s,1) with sodium nitroprusside (10 ,m) were attenuated >60% (P < 0.05) in OM. Blood flow at peak ROV was blunted by 75,80% in OM vs. YM (P < 0.05). In response to 30 s of rhythmic contractions at 2, 4 and 8 Hz, progressive dilatations did not differ with age or sex. Nevertheless, resting and peak blood flows in YM were 2- to 3-fold greater (P < 0.05) than OM. We suggest that ageing blunts ROV and restricts blood flow to skeletal muscle of OM through subtle activation of ,-adrenoreceptors in microvascular resistance networks. [source] Prolonged strenuous exercise alters the cardiovascular response to dobutamine stimulation in male athletesTHE JOURNAL OF PHYSIOLOGY, Issue 1 2005Robert C. Welsh Prolonged strenuous exercise has been associated with transient impairment in left ventricular (LV) systolic and diastolic function that has been termed ,cardiac fatigue'. It has been postulated that cardiac ,-adrenoreceptor desensitization may play a central role; however, data are limited. Accordingly, we assessed the cardiovascular response to progressive dobutamine stimulation after prolonged strenuous exercise (2 km swim, 90 km bike, 21 km run). Nine experienced male athletes were studied: PRE (2,3 days before), POST (after) and REC (1,2 days later). The cardiovascular response to progressive continuous dobutamine stimulation (0, 5, 20, and 40 ,g kg,1 min,1) was assessed, including heart rate (HR), systolic blood pressure (SBP), LV cavity areas (two-dimensional echocardiography) and contractility (end-systolic elastance, SBP/end-systolic cavity area (ESCA)). POST there was limited evidence of myocardial necrosis (measured by troponin I), while catecholamines were elevated. HR was higher POST (mean ±s.d.; PRE, 58 ± 9; POST, 79 ± 9; REC, 57 ± 7 beats min,1; P < 0.05), while SBP was lower (PRE, 127 ± 15; POST, 116 ± 9; REC, 121 ± 12 mmHg; P < 0.05). A blunted HR, SBP and LV contractility (SBP/ESCA; PRE 29 ± 6 versus POST 20 ± 6 mmHg cm,2; P < 0.05) response to dobutamine was demonstrated POST, with values returning towards baseline in REC. Following prolonged strenuous exercise, the chronotropic and inotropic response to dobutamine stimulation is blunted. This study supports the hypothesis that beta-receptor downregulation and/or desensitization may play a major role in prolonged-strenuous-exercise-mediated cardiac fatigue. [source] Absence of arterial baroreflex modulation of skin sympathetic activity and sweat rate during whole-body heating in humansTHE JOURNAL OF PHYSIOLOGY, Issue 2 2001Thad E. Wilson 1Prior findings suggest that baroreflexes are capable of modulating skin blood flow, but the effects of baroreceptor loading/unloading on sweating are less clear. Therefore, this project tested the hypothesis that pharmacologically induced alterations in arterial blood pressure in heated humans would lead to baroreflex-mediated changes in both skin sympathetic nerve activity (SSNA) and sweat rate. 2In seven subjects mean arterial blood pressure was lowered (,8 mmHg) and then raised (,13 mmHg) by bolus injections of sodium nitroprusside and phenylephrine, respectively. Moreover, in a separate protocol, arterial blood pressure was reduced via steady-state administration of sodium nitroprusside. In both normothermia and heat-stress conditions the following responses were monitored: sublingual and mean skin temperatures, heart rate, beat-by-beat blood pressure, skin blood flow (laser-Doppler flowmetry), local sweat rate and SSNA (microneurography from peroneal nerve). 3Whole-body heating increased skin and sublingual temperatures, heart rate, cutaneous blood flow, sweat rate and SSNA, but did not change arterial blood pressure. Heart rate was significantly elevated (from 74 ± 3 to 92 ± 4 beats min,1; P < 0.001) during bolus sodium nitroprusside-induced reductions in blood pressure, and significantly reduced (from 92 ± 4 to 68 ± 4 beats min,1; P < 0.001) during bolus phenylephrine-induced elevations in blood pressure, thereby demonstrating normal baroreflex function in these subjects. 4Neither SSNA nor sweat rate was altered by rapid (bolus infusion) or sustained (steady-state infusion) changes in blood pressure regardless of the thermal condition. 5These data suggest that SSNA and sweat rate are not modulated by arterial baroreflexes in normothermic or moderately heated individuals. [source] Evaluation of head-only and head-to-tail electrical stunning of farmed eels (Anguilla anguilla, L.) for the development of a humane slaughter methodAQUACULTURE RESEARCH, Issue 5 2002E Lambooij Abstract The overall objective was to evaluate the suitability of electronarcosis as a stunning method for farmed eels. In the first experiment the minimum electrical current needed to induce a general epileptiform insult by head-only stunning was assessed. The individual eels (n = 40) with a live weight of 700,800 g were fixed in a specially designed re-strainer. The EEG (electroencephalogram) and ECG (electrocardiogram) recordings, observation of behaviour and responses to pain stimuli were used to assess unconsciousness, insensibility and cardiac function. The applied current of 150, 200 or 250 V, 50 Hz, AC was delivered via scissor-model stunning tongs for approximately 1 s. A general epileptiform insult was observed in 31 eels for which a successful EEG recording was obtained, using 255 ± 4 V, 545 ± 32 mA, for 1.2 ± 0.2 s. The general epileptiform insult as measured on the EEG was characterized by a tonic/clonic phase and an exhaustion phase. The behaviour showed one phase: tonic cramps alternated by clonic ones. The heart rate was 22 ± 8 beats min,1 (n = 23) prior to stunning. After stunning the ECG revealed fibrillation. In the second experiment the behaviour of seven individual eels able to move freely in water was observed after head-only stunning (250 V). Two phases were distinguished. Limited tonic and clonic cramps combined with backward swimming were followed by heavy clonic cramps combined with unco-ordinated movements such as jumping out of the water. A distinct exhaustion phase was not observed in all animals. In the third experiment a head-to-tail electrical method was examined in 15 eels for rendering the eels unconscious and insensitive prior to slaughter. They were stunned by applying 253 V for 3 s followed by 50 V for 5 min. In the fourth experiment nine eels were head-only stunned with 260 V for 1 s immediately followed by 50 V for 5 min applied from head to tail. Results obtained in these two experiments were similar. After stunning no brain activity and no responses to pain stimuli on the EEG were observed and the ECG showed ventricular extra systolae. It was observed that it might take 60 ± 25 min or longer for a complete recovery. It can be concluded that for effective electrical stunning of eels with a weight of 700,800 g an average current of 545 ± 32 mA (at approximate 250 V, 50 Hz AC) is needed. In this case, within a confidence level of 95% at least 91% of the eels are effectively stunned (n = 31). Therefore, it is recommended to increase the minimum current for an effective stun in practice to 600 mA. Further research is needed to determine the conditions to induce permanent unconsciousness and insensibility of the eels to protect the animals at slaughter. [source] Normovolemia defined according to cardiac stroke volume in healthy supine humansCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2010Morten Bundgaard-Nielsen Summary Background:, Both hypovolemia and a fluid overload are detrimental for outcome in surgical patients but the effort to establish normovolemia is hampered by the lack of an operational clinical definition. Manipulating the central blood volume on a tilt table demonstrates that the flat part of the Frank-Starling curve is reached when subjects are supine and that finding may be applicable for a clinical definition of normovolemia. However, it is unknown whether stroke volume (SV) responds to an increase in preload induced by fluid administration. Methods:, In 20 healthy subjects (23 ± 2 years, mean ± SD), SV was measured by esophageal Doppler before and after fluid administration to evaluate whether SV increases in healthy, non-fasting, supine subjects. Two hundred millilitres of a synthetic colloid (hydroxyethyl starch, HES 130/0·4) was provided and repeated if a ,10% increment in SV was obtained. Results:, None of the subjects increased SV ,10% following fluid administration but there was a minor increase in mean arterial pressure (92 ± 15 to 93 ± 12 mmHg, P = 0·01), while heart rate (HR) (66 ± 12 beats min,1; P = 0·32), cardiac output (4·8 ± 1·1 l min,1; P = 0·25) and the length of the systole corrected to a HR of 60 beats/min (corrected flow time; 344 ± 24 ms; P = 0·31) did not change. Conclusion:, Supporting the proposed definition of normovolemia, non-fasting, supine, healthy subjects are provided with a preload to the heart that does not limit SV suggesting that the upper flat part of the Frank-Starling relationship is reached. [source] Intensity of Nordic Walking in young females with different peak O2 consumptionCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2009Toivo Jürimäe Summary The purpose of this cross - sectional study was to determine the physiological reaction to the different intensity Nordic Walking exercise in young females with different aerobic capacity values. Twenty-eight 19,24-year-old female university students participated in the study. Their peak O2 consumption (VO2 peak kg,1) and individual ventilatory threshold (IVT) were measured using a continuous incremental protocol until volitional exhaustion on treadmill. The subjects were analysed as a whole group (n = 28) and were also divided into three groups based on the measured VO2 peak kg,1 (Difference between groups is 1 SD) as follows: 1. >46 ml min,1 kg,1 (n = 8), 2. 41,46 ml min,1 kg,1 (n = 12) and 3. <41 ml min,1 kg,1 (n = 8). The second test consisted of four times 1 km Nordic Walking with increasing speed on the 200 m indoor track, performed as a continuous study (Step 1 , slow walking, Step 2 , usual speed walking, Step 3 , faster speed walking and Step 4 , maximal speed walking). During the walking test expired gas was sampled breath-by-breath and heart rate (HR) was recorded continuously. Ratings of perceived exertion (RPE) were asked using the Borg RPE scale separately for every 1 km of the walking test. No significant differences emerged between groups in HR of IVT (172·4 ± 10·3,176·4 ± 4·9 beats min,1) or maximal HR (190·1 ± 7·3,191·6 ± 7·8 beats min,1) during the treadmill test. During maximal speed walking the speed (7·4 ± 0·4,7·5 ± 0·6 km h,1) and O2 consumption (30·4 ± 3·9,34·0 ± 4·5 ml min,1 kg,1) were relatively similar between groups (P > 0·05). However, during maximal speed walking, the O2 consumption in the second and third groups was similar with the IVT (94·9 ± 17·5% and 99·4 ± 15·5%, respectively) but in the first group it was only 75·5 ± 8·0% from IVT. Mean HR during the maximal speed walking was in the first group 151·6 ± 12·5 beats min,1, in the second (169·7 ± 10·3 beats min,1) and the third (173·1 ± 15·8 beats min,1) groups it was comparable with the calculated IVT level. The Borg RPE was very low in every group (11·9 ± 2·0,14·4 ± 2·3) and the relationship with VO2and HR was not significant during maximal speed Nordic Walking. In summary, the present study indicated that walking is an acceptable exercise for young females independent of their initial VO2 peak level. However, females with low initial VO2 peak can be recommended to exercise with the subjective ,faster speed walking'. In contrast, females with high initial VO2 peak should exercise with maximal speed. [source] | |||||||||||||