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Heart rate recovery and treadmill exercise score as predictors of mortality in patients referred for exercise ECG.

CONTEXT: Both attenuated heart rate recovery following exercise and the Duke treadmill exercise score have been demonstrated to be independent predictors of mortality, but their prognostic value relative to each other has not been studied. OBJECTIVE: To assess the associations among abnormal heart rate recovery, treadmill exercise score, and death in patients referred specifically for exercise electrocardiography. DESIGN AND SETTING: Prospective cohort study conducted in an academic medical center between September 1990 and December 1997, with a median follow-up of 5.2 years. PATIENTS: A total of 9454 consecutive patients (mean [SD] age, 53 [11] years; 78% male) who underwent symptom-limited exercise electrocardiographic testing. Exclusion criteria included age younger than 30 years, history of heart failure or valvular disease, pacemaker implantation, and uninterpretable electrocardiograms. MAIN OUTCOME MEASURES: All-cause mortality, as predicted by abnormal heart rate recovery, defined as failure of heart rate to decrease by more than 12/min during the first minute after peak exercise, and by treadmill exercise score, defined as (exercise time) - (5 x maximum ST-segment deviation) - (4 x treadmill angina index). RESULTS: Three hundred twelve deaths occurred in the cohort. Abnormal heart rate recovery and intermediate- or high-risk treadmill exercise score were present in 20% (n = 1852) and 21% (n = 1996) of patients, respectively. In univariate analyses, death was predicted by both abnormal heart rate recovery (8% vs 2% in patients with normal heart rate recovery; hazard ratio [HR], 4.16; 95% confidence interval [CI], 3.33-5.19; chi(2) = 158; P<.001) and intermediate- or high-risk treadmill exercise score (8% vs 2% in patients with low-risk scores; HR, 4.28; 95% CI, 3.43-5.35; chi(2) = 164; P<.001). After adjusting for age, sex, standard cardiovascular risk factors, medication use, and other potential confounders, abnormal heart rate recovery remained predictive of death (among the 8549 patients not taking beta-blockers, adjusted HR, 2.13; 95% CI, 1.63-2.78; P<.001), as did intermediate- or high-risk treadmill exercise score (adjusted HR, 1. 49; 95% CI, 1.15-1.92; P =.002). There was no interaction between these 2 predictors. CONCLUSIONS: In this cohort of patients referred specifically for exercise electrocardiography, both abnormal heart rate recovery and treadmill exercise score were independent predictors of mortality. Heart rate recovery appears to provide additional prognostic information to the established treadmill exercise score and should be considered for routine incorporation into exercise test interpretation. JAMA. 2000;284:1392-1398.

Adult↗

In vitro factor VIII recovery during the delivery of ultrapure factor VIII concentrate by continuous infusion.

Factor VIII (FVIII) replacement by continuous infusion has been advocated as a cost-effective method for maintaining stable plasma levels of FVIII in the hemophilia A patients during surgery or life-threatening hemorrhage. Continuous delivery of monoclonal or recombinant FVIII concentrates to our pediatric patients using a traditional delivery system (dilution in normal saline of 2-10 U/ml infused at a rate of 20 ml/hr) has frequently yielded higher than expected factor usage to achieve desired levels and unexpected variability in plasma levels under presumed steady-state conditions. To determine if diminished in vitro FVIII recovery was responsible for these observations, a study of four ultrapure concentrates during 8 hr of in vitro continuous delivery was performed using four delivery systems. When reconstituted concentrate was added to normal saline in polyvinylchloride bags at a concentration of 10 U/ml (method IA), monoclonal products showed a stable recovery of 84-109% of time 0 levels. Recombinant product recovery dropped to 57-76% of time 0 levels before reapproximating the time 0 level at 2 hr. The addition of 10 mg/ml human albumin to the bags (method IB) did not improve recoveries. When reconstituted concentrate was delivered undiluted (method IIA), the early drop in recombinant recovery was eliminated; stable recovery of 78-117% of time 0 level was achieved with all products. In using method IA, a large discrepancy was seen between the actual time 0 recoveries and those expected based on vial assays, most striking for recombinant products (49-57% of expected. Method IIA allowed 75-90% recovery; addition of 20 mg/ml albumin of reconstituted but undiluted concentrate (method IIB) maximized recovery at 85-98% of expected.

Albumins↗

Relationship between ventilation and arterial potassium concentration during incremental exercise and recovery.

The purpose of this study was to compare the relationship of ventilation (VE) with pH, arterial concentrations of potassium [( K+]a), bicarbonate [( HCO3-]a), lactate [( la]a), and acid-base parameters which would affect hyperpnoea during exercise and recovery. To assess this relationship, ten healthy male subjects exercised with intensity increasing as a ramp function of 20 W.min-1 until voluntary exhaustion and they were then allowed a 5-min recovery period. Breath-by-breath gas exchange data, [HCO3-]a, pH, [la]a, [K+]a and blood gases were determined during both exercise and recovery. Using a linear regression method, the VE/[K+]a relationship was analysed during both exercise and recovery. Several interesting results were obtained: a significant relationship between [K+]a and VE was observed during recovery as well as during exercise; the VE at any given values of [K+]a was significantly higher during recovery than during exercise and out of those factors affecting exercise hyperpnoea, only [K+]a had a similar time-course to VE during recovery. Changes in [K+]a during recovery were shown to occur significantly faster than VE with an [K+]a time constant of 70.0 s, SD 16.2 as opposed to 105.5 s, SD 10.0 for VE (P less than 0.01). These results provided further evidence that [K+]a might play an important role as a substance which can stimulate exercise hyperpnoea as has been suggested by other workers. The present study also showed that during recovery [K+]a contributed significantly to the control of VE.

Adult↗

Blood lactate responses in older swimmers during active and passive recovery following maximal sprint swimming.

The purpose of this study was to determine the effect of age on three blood lactate parameters following maximal sprint swimming. The parameters examined were maximal blood lactate concentration, time to reach maximal blood lactate concentration, and half recovery time to baseline lactate concentration. These parameters were examined in 16 male competitive masters swimmers (n = 4 for each age group: 25-35, 36-45, 46-55, and 56 plus years) during both passive and active recovery following a maximal 100 m freestyle sprint. Passive recovery consisted of 60 min sitting in a comfortable chair and active recovery consisted of a 20-min swim at a self-selected pace. Capillary blood samples were obtained every 2 min up to 10 min of recovery then at regular intervals to the end of the recovery period. Curves of blood lactate concentration against time were drawn and the three parameters determined for each condition for each subject. There were no significant differences between age groups in any of the lactate parameters examined. A significant difference (P less than 0.05) was noted in each of the parameters between active and passive recovery over all age groups. As expected, active recovery produced lower maximal blood lactate concentrations, lower time to maximal blood lactate values, and lower half recovery times. These data suggest that intensive swimming training may prevent or delay the decline with age in the physiological factors affecting blood lactate values following a maximal sprint swim. Older sprint swimmers appeared to be capable of producing and removing lactic acid at the same rate as younger swimmers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The recovery of alpha-adrenoceptor function and binding sites after phenoxybenzamine. An index of receptor turnover?

The recovery of peripheral alpha-adrenoceptor function and binding sites was studied in male New Zealand white rabbits after treatment with the irreversible adrenoceptor antagonist phenoxybenzamine. Phenoxybenzamine (5 mg/kg) was administered intravenously and the animals studied 30 min to 12 days later. Pressor dose response curves to intravenous phenylephrine, noradrenaline and guanabenz were constructed in vivo in conscious animals. The contractile response of abdominal aorta and renal artery to phenylephrine and noradrenaline was examined in vitro and the recovery of specific prazosin and clonidine binding to spleen membranes investigated in radioligand binding studies. The half life (t 1/2) for recovery of maximum pressor response in vivo ranged from 0.9 +/- 0.2 days for phenylephrine to 1.4 +/- 0.1 days for guanabenz. The t 1/2 for recovery of ED50 was not significantly different to t 1/2 for recovery of maximum pressor response and ranged from 0.8 +/- 0.2 days for noradrenaline to 1.3 +/- 0.3 days for phenylephrine. Half life for recovery of maximum response and EC50 in the isolated tissues was similar to that obtained in vivo for recovery of pressor responses and ranged from 0.4 +/- 0.1 days for the EC50 of noradrenaline in the renal artery to 1.2 +/- 0.6 days for maximum response to phenylephrine in the abdominal aorta. The rate of recovery of specific clonidine binding did not differ significantly from the rate of recovery of pressor responses to the alpha 2-selective agonist guanabenz. t 1/2 for maximum number of specific clonidine binding sites, Bmax was 1.6 +/- 0.9 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Recovery of brain and plasma cholinesterase activities in ducklings exposed to organophosphorus pesticides.

Brain and plasma cholinesterase (ChE) activities were determined for mallard ducklings (Anas platyrhynchos) exposed to dicrotophos and fenthion. Recovery rates of brain ChE did not differ between ducklings administered a single oral dose vs. a 2-week dietary dose of these organophosphates. Exposure to the organophosphates, followed by recovery of brain ChE, did not significantly affect the degree of brain ChE inhibition or the recovery of ChE activity at a subsequent exposure. Recovery of brain ChE activity followed the general model Y = a + b(logX) with rapid recovery to about 50% of normal, followed by a slower rate of recovery until normal ChE activity levels were attained. Fenthion and dicrotophos-inhibited brain ChE were only slightly reactivated in vitro by pyridine-2-aldoxime methiodide, which suggested that spontaneous reactivation was not a primary method of recovery of ChE activity. Recovery of brain ChE activity can be modeled for interpretation of sublethal inhibition of brain ChE activities in wild birds following environmental applications of organophosphates. Plasma ChE activity is inferior to brain ChE activity for environmental monitoring, because of its rapid recovery and large degree of variation among individuals.

Animals↗

Extinction and spontaneous recovery of ataxic tolerance to ethanol in rats.

RATIONALE AND OBJECTIVES: Two experiments with rats using an ethanol ataxia method investigated extinction and spontaneous recovery of tolerance. Tolerance extinction has been shown with a variety of drugs and methods, but until now it has not been shown with ethanol ataxia. Extinction was investigated here because of its connection with cue exposure treatments, and also to allow an assessment of spontaneous recovery. Spontaneous recovery is the return of conditioned responses, such as those potentially contributing to tolerance, when time passes after extinction. In terms of response topography it resembles instances of relapse in humans. Its demonstration constitutes one technique for illustrating that the effects of extinction are often temporary. There are no published reports showing a recovery of tolerance to any drug due to the passage of time after extinction. A demonstration of spontaneous recovery contributes to an understanding of the effects and time course of tolerance extinction. It also raises the possibility that spontaneous recovery involving drug tolerance has mechanisms similar those involved in instances of spontaneous recovery studied more extensively with non-drug methods. METHODS: In one experiment, ataxic tolerance was conditioned to a strobelight conditioned stimulus (CS) by exposing rats to the strobelight while experiencing the effects of an ethanol injection. Tolerance was extinguished in 17 or 24 once-daily trials by presenting the strobelight without ethanol (with saline). The effect of those numbers of trials was assessed on the day after extinction in the presence of the strobelight when ethanol was again injected. The effect was compared to the effect of the strobelight and ethanol in naive rats and in rats that had received only tolerance conditioning. In a second experiment, ataxic tolerance was conditioned and then extinguished over 17 trials, just as in the other experiment. Different groups were then tested 1, 12, 18, and 24 days after extinction in the presence of the strobelight when ethanol was again injected. RESULTS: Ataxic tolerance was fully extinguished after either 17 or 24 trials, as shown by comparisons with the naive and conditioning-only controls. Tolerance was greater (it recovered) when the strobelight CS was reintroduced 24, 18, and even 12 days after extinction, compared with testing 1 day after extinction. CONCLUSIONS: Conditioned ataxic tolerance can be extinguished, just as other conditioned tolerances can. More important, the return of tolerance over time after extinction represents spontaneous recovery of ethanol tolerance, and indicates that as in other conditioning preparations, extinction does not result in unlearning of the original conditioning association. The identification of spontaneous recovery of tolerance isolates a robust source of the potential for drug use relapse: the mere passage of time after extinction.

Animals↗

Parathyroid hormone concentrations during and after two periods of high intensity exercise with and without an intervening recovery period.

The purpose of this study was to examine the effect of a recovery period between two periods of exercise on bone metabolism and related hormones. Concentrations of serum parathyroid hormone ([PTH]), plasma ionized calcium ([Ca(2+)]) and total calcium were measured. A group of 12 healthy men aged 20-27 years participated in this study. They took part in two exercise protocols (P(1) and P(2)) on two separate weeks. The exercise in P(1) comprised two successive periods of 21 min each at 70% and 85% of maximal oxygen uptake; P(2) comprised two periods of exercise at the same intensities but separated by 40 min of recovery. Venous blood samples were collected 1 day before the sessions (control), before each protocol, during (7th and 21st min), at the end (42nd min in P(1) and 82nd min in P(2)) and after 24 h of recovery. The [PTH] was significantly elevated during the two protocols ( P<0.01), remained raised in P(1) after 24 h of recovery ( P<0.05) and was significantly lower ( P<0.01) at the end of P(2) when compared to P(1). The [Ca(2+)] decreased significantly during and at the end of the two protocols ( P<0.01) and had returned to control values after 24 h of recovery. Plasma lactate concentration increased during the two protocols ( P<0.01) and returned to control values after recovery. These results indicate firstly that [Ca(2+)] decreases during continuous exercise as [PTH] increases and remains raised after 24 h of recovery, secondly that a recovery period between two periods of exercise attenuates the variations in [Ca(2+)] and [PTH], and thirdly that recovery may have anabolic effects on bone. However, the small physiological changes observed prevent us from forming any firm conclusion about this.

Adult↗

The use of the [1,2-13C]acetate recovery factor in metabolic research.

To provide guidelines on the correct application of the acetate recovery factor in metabolic research, we investigated the influence of exercise intensity and infusion protocol on [1,2-(13)C]acetate label recovery during exercise. Eight cyclists were studied during [1,2-(13)C]acetate infusion for 1 h at rest followed by three 30-min stages of cycling exercise at a workload of 40, 55 and 75% maximal workload ( W(max)), respectively (protocol 1). Four cyclists were subsequently studied following [1,2-(13)C]acetate infusion in three separate trials while cycling at the same workloads but in the absence of any pre-exercise infusion period (protocol 2). Finally, we observed the cyclists during [1,2-(13)C]acetate infusion at a 40% W(max) workload after 4 h of pre-exercise infusion (protocol 3). Acetate recovery increased from 13.7 (0.4)%, after 1 h of rest, to a plateau value of 75.1 (2), 91.2 (0.7) and 101 (2)% during exercise at 40, 55 and 75% W(max) workloads, respectively. In protocol 2, without prior infusion time, fractional label recovery was substantially lower at each separate workload. In contrast, when applying an extensive pre-exercise infusion period of 4 h, acetate recovery rates were substantially increased compared to the values observed in protocols 1 and 2 during exercise at a 40% W(max) workload. In conclusion, in contrast to resting conditions, acetate recovery reaches a plateau value during exercise. Though this plateau value is repeatedly used to correct for label recovery in various exercise studies, our data clearly show that acetate label recovery during exercise not only depends on the exercise intensity but also on the applied infusion protocol. Therefore, theoretical acetate recovery factors taken from previous literature are not generally applicable.

Acetates↗

Long recovery times improve the detection of cellular resistance in vitro.

In vitro cytotoxicity testing is used increasingly during the development of clinical treatment protocols. These tests are influenced by many variables, not all of which have been assessed systematically yet. We analyzed the influence of the recovery time between the end of treatments and measurements on the detection of cellular resistance. The development of resistance to cisplatin and radiation was chosen as a model since the schedule of these treatments is the objective of several ongoing clinical trials. C6 rat glioma, T98G, 86HG-39, A172 human glioma and TE671 human rhabdomyo-sarcoma cells were pretreated with radiation or cisplatin. The cellular resistance was then compared in pretreated and wild-type cells using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) test. In all cell lines, apparent drug concentrations killing 50% of the cells were dependent on the recovery time. In A172 cells this concentration was 10.3+/-02.1 microM after 48 h but decreased to 3.56+/-0.44 microM after 120 h recovery time (P < 0.001). After recovery times of more than 168 h, 53% of all pretreated cell lines were resistant to cisplatin or radiation, 25% were unchanged and 22% were more sensitive. However, only half the resistant cells could be identified when the MTT test was done with only 48 h recovery time. The sensitivity of detection increased from 0.46 to 0.83 when the recovery time of the test system was extended from 48 h to 168 h. The specificity was not dependent on the recovery time. Experiments showing resistance after short recovery times are reliable, but lack of resistance can only be shown in experiments with long recovery times. Cisplatin treatment can result in resistance to radiation in glioma cells.

Animals↗

Some recovery processes in mutual-help groups for persons with mental illness; II: qualitative analysis of participant interviews.

Previous research suggests that consumer operated services facilitate recovery from serious mental illness. In part I of this series, we analyzed the content of the GROW program, one example of a consumer operated service, and identified several processes that Growers believe assists in recovery. In this paper, we review the qualitative interviews of 57 Growers to determine what actual participants in GROW acknowledge are important processes for recovery. We also used the interviews to identify the elements of recovery according to these Growers. Growers identified self-reliance, industriousness, and self-esteem as key ingredients of recovery. Recovery was distinguished into a process-an ongoing life experience-versus an outcome, a feeling of being cured or having overcome the disorder. The most prominent element of GROW that facilitated recovery was the support of peers. Gaining a sense of personal value was also fostered by GROW and believed to be important for recovery. The paper ends with a discussion of the implications of these findings for the ongoing development of consumer operated services and their impact on recovery.

Adaptation, Psychological↗

Sinus node recovery times following the spontaneous termination of supraventricular tachycardia and following atrial overdrive pacing: a comparison.

We compared the pauses that followed the spontaneous termination of supraventricular tachyarrhythmias with the pauses that followed the cessation of atrial overdrive pacing in 21 patients. In 10 patients with abnormal sinus node function and in 11 patients with normal sinus node function we recorded the spontaneous termination of supraventricular tachyarrhythmia in the clinical electrophysiology laboratory; a strong correlation (r = 0.94) was found between the maximal spontaneous sinus node recovery time and the maximal paced sinus node recovery time. A weaker correlation was found between the paced and spontaneous sinus node recovery times (r = 0.57) when the spontaneous termination of supraventricular tachyarrhythmia was recorded during ambulatory electrocardiographic recording in seven patients. Spontaneous sinus node recovery times were significantly shorter than maximal paced sinus node recovery times (p less than 0.001). However, no significant difference was detected between the paced and spontaneous sinus node recovery times when atrial pacing was performed at the rate of the tachycardia. We conclude that spontaneous and postpacing sinus node recovery times are closely correlated. The paced sinus node recovery time is, however, frequently more prolonged than spontaneous sinus node recovery time because of probable atriosinus entrance block during rapid supraventricular tachycardia.

Adult↗

Accelerated recovery of antigen-presenting cell activity by the administration of interleukin 1 alpha in 5-fluorouracil-treated mice.

In this study, we investigated the effect of human recombinant interleukin-1 alpha (IL-1 alpha) on antigen-presenting cell (APC) activity of spleen cells in mice treated with 5-fluorouracil (5-FU). APC activity was determined by the antigen-specific proliferation of T cell clone D10.G4.1 cells. When mice were injected with 5-FU, APC activity of spleen cells was suppressed. The administration of IL-1 alpha accelerated the recovery from this suppression. The most accelerated recovery was observed when these mice were administered with IL-1 alpha both before and after the 5-FU treatment. The recovery was also accelerated when the mice were injected with IL-1 alpha after the 5-FU treatment, but not when injected before the 5-FU treatment. The injection of 5-FU also decreased the cell numbers of whole spleen cells, B cells, and non-T non-B cells (Ig- and Thy-1- cells). The administration of IL-1 alpha accelerated the recovery of the decreased cell numbers. Both B cells and non-T non-B cells possessed APC activity, but most APC activity of unseparated spleen cells was carried by non-T non-B cells. B cells possessed only 1/20 of the APC activity of non-T non-B cells. The injection of 5-FU decreased APC activity of both B cells and non-T non-B cells, but the administration of IL-1 alpha accelerated its recovery. Thus, the accelerated recovery of APC activity by IL-1 alpha was suggested to be due to the recovery in the numbers of APC activity-bearing cell subpopulations and also due to the recovery of the APC activity of each subpopulation. Possible mechanisms for the recovery were discussed.

Animals↗

ATP precursor depletion and postischemic myocardial recovery.

Although cardioplegia reduces myocardial metabolism during ischemia, adenosine triphosphate (ATP) depletion occurs, which may contribute to poor functional recovery after reperfusion. Augmenting myocardial adenosine during ischemia is successful in improving ATP repletion and myocardial recovery following ischemia. If adenosine is an important determinant of ischemic tolerance, then depletion or elimination of myocardial adenosine should lead to poor functional and metabolic recovery after ischemia. To test this hypothesis, isolated, perfused rabbit hearts were subjected to 120 min of 34 degrees C ischemia. Hearts received St. Thomas cardioplegia alone or cardioplegia containing 200 microM adenosine, or cardioplegia containing 15, 5, 2.5, or 0.025 micrograms/ml adenosine deaminase (ADA), which catalyzes the breakdown of adenosine to inosine, making adenosine unavailable as an ATP precursor. Functional recovery was determined and myocardial nucleotide levels were measured before, during, and after ischemia. Following ischemia and reperfusion, control hearts recovered to 51 +/- 3% of preischemic developed pressure (DP). There was significantly better recovery in adenosine-augmented hearts (68 +/- 7%), while ADA hearts had significantly worse recovery. Hearts treated with 0.025 microgram/ml ADA recovered to only 29 +/- 5% of DP and higher dose ADA hearts failed to demonstrate any recovery of systolic function. Furthermore, adenosine enhanced metabolic recovery, whereas ADA resulted in greatly depleted ATP and precursor reserves. Postischemic developed pressure closely paralleled the availability of myocardial adenosine, consistent with the hypothesis that myocardial adenosine levels at end ischemia and early reperfusion are important determinants of functional recovery after global ischemia.

Adenosine↗

Recovery from anorexia nervosa: a Durkheimian interpretation.

Attempts to explain "eating disorders" in contemporary western society have concentrated on aetiology at the expense of resolution. Most "recovered" anorectics, however, question medical definitions of "anorexia nervosa" and clinical criteria for recovery. This article refers to a study of 32 people at different stages of the recovery process, to reconceptualize the problem in sociological terms. Durkheim's account of asceticism offers a fresh interpretive framework in which anorexia and recovery are understood as the negative and positive phases respectively of a ritual of self-transformation. In western culture, where appropriate myths and rituals of re-incorporation are not readily available following a period of symbolic fasting, it is not surprising that recovery from anorexia is not automatic. Participants in this study referred to anorexia as a spiritual quest and for them recovery involved a re-discovery (or creation) of a threefold connection: inner, with others and with "nature". These connections are, for them, the defining features of spirituality. The negative phase of the ritualistic quest (anorexia) involves a confrontation with the inevitability of death as a condition of the positive phase (recovery) in which people actively choose life. This new theoretical approach provides a non-medicalized understanding of anorexia and simultaneously enables a re-interpretation of the fasting of medieval women saints. Recent scholarship in this area is re-evaluated to demonstrate that the continuity between asceticism and anorexia lies in the use of food as a metaphorical attempt to confront the universal problem of one's own mortality. In certain historical situations, asceticism served a socially valuable symbolic purpose. In contemporary society, however, this meaning is no longer available. Instead, it is recovery which constitutes the active and metaphorical "rebellion" against forces of social control. Finally, the work of Van Gennep is used to explore some of the specific ritual processes through which people effect the self-transformation from suffering to recovery, providing further insights into how recovery takes place from a wide range of other sufferings as well.

Anorexia Nervosa↗

Assessing autonomic function by analysis of heart rate recovery from exercise in healthy subjects.

Although delayed recovery of heart rate (HR) after exercise indicates poor prognosis, the relative role of parasympathetic reactivation versus sympathetic withdrawal in controlling exercise HR recovery remains controversial. Quantifying HR recovery is difficult because the rate of recovery varies with exercise level. This study develops a model of HR recovery applicable to multiple exercise levels simultaneously. Using the Levenberg-Marquardt method for nonlinear models, HR curves for 11 healthy volunteers recovering from 4 different levels of exercise were fit to equations incorporating 1 first-order time constant for parasympathetic reactivation and 1 for sympathetic withdrawal. Results provided time constants for parasympathetic reactivation of 44 +/- 37 seconds and for sympathetic withdrawal of 65 +/- 56 seconds. The model fit the HR recovery curves very closely, explaining 99.7 +/- 0.1% of the variance in the data. In conclusion, this study presents a unique method for quantitatively testing theories on the relative roles of sympathetic withdrawal and parasympathetic reactivation during recovery from exercise. It provides indexes of dynamic sympathetic and parasympathetic functions, with the parasympathetic system having a faster response time. It supports theories of coordinated interaction of parasympathetic reactivation and sympathetic withdrawal during exercise recovery and does not support using simple measures of exercise HR recovery as indexes of vagal function alone.

Adult↗

The voltage dependence of recovery from use-dependent block by QX-222 separates mechanisms for drug egress in the cardiac sodium channel.

In neuronal sodium channels of squid giant axons, recovery from QX-222 block is slowed by hyperpolarization. However, in ventricular cells, hyperpolarization speeds recovery. Previously, we showed that isoform-specific residues in the external side of the cardiac sodium channel isoform (D1P-loop C373 and D4S6 T1752) influence use-dependent block (UDB) by lidocaine. To determine whether these isoformspecific residues contribute to the contrasting voltage-dependent recovery observed in ventricular myocytes, we measured recovery rates from UDB by QX-222 at holding potentials of 120, 140, 160 and 180 mV for wild-type cardiac channel (WT), the mutants C373Y (CY) and T1752V (TV), and C373Y/T1752V (CY/TV). Unlike neuronal channels, cardiac sodium channels recovered from QX block faster at hyperpolarized potentials. All mutations slowed QX-222 recovery, with the greatest rate reduction observed for the double mutant, indicating that the isoform-specific residues define external drug paths. The recovery rates varied linearly with voltage over the range tested, and we used the slopes of rate versus voltage plots to quantify voltage dependence. The TV mutation caused reduction in recovery rates without changing the slope, indicating that the mutation closed a voltage-independent egress path. The CY mutation, however, flattened the slope and reduced the voltage dependence of recovery. In addition, the reduction in rate caused by CY/TV is less than the sum of those for CY and TV, suggesting that the impacts of these two residues are interrelated. Therefore, we propose that the isoform-specific residues C373 and T1752 change recovery from UDB by distinct mechanisms but determine a common drug egress path.

Cell Line↗

Effects of organic and inorganic additives on flotation recovery of washed cells of Saccharomyces cerevisiae resuspended in water.

Separation of microbial cells by flotation recovery is usually carried out in industrial reactors or wastewater treatment systems, which contain a complex mixture of microbial nutrients and excretion products. In the present study, the separation of yeast cells by flotation recovery was carried out using a simple flotation recovery systems containing washed yeast cells resuspended in water in order to elucidate the effects of additives (defined amounts of organic and inorganic acids, ethanol, surfactants and sodium chloride) on the cellular interactions at interfaces (cell/aqueous phase and cell/air bubble). When sodium chloride, organic acids (notably propionic, succinic and acetic acids) and organic surfactants (sodium dodecyl sulphate (SDS), cetyltrimethylammonium bromide (CTAB) and Nonidet P40) were added to the flotation recovery system, significant increases in the cell recovery of yeast hydrophobic cells (Saccharomyces cerevisiae, strain FLT-01) were observed. The association of ethanol to acetic acid solution (a minor by-product of alcoholic fermentation) in the flotation recovery system, containing washed cells of strain FLT-01 resuspended in water, leading to an increased flotation recovery at pH 5.5. Thus, the association among products of the cellular metabolism (e.g., ethanol and acetic acid) can improve yeast cell recovery by flotation recovery.

Acetic Acid↗