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Mechanisms of failed recovery following postural perturbations on a motorized treadmill mimic those associated with an actual forward trip.

OBJECTIVE: To examine the recovery strategies employed during a treadmill acceleration task, to determine if mechanisms that contributed to failed recoveries on a motorized treadmill are the same general biomechanical mechanisms that contributed to falls from a trip, and to determine if failed recovery responses could be modified to allow for successful recoveries on subsequent trials. DESIGN: A motorized treadmill was used to induce postural perturbations in healthy older adults. BACKGROUND: Previously, we induced trips in older adults to identify the mechanisms of failed recovery. However, inducing trips is not a clinically practical test for identifying older adults who are predisposed to falling. METHODS: Safety-harnessed older adults stood on a treadmill that was accelerated from 0 to 0.89 m/s to impose a postural perturbation. Recoveries were classified as successful (n=42) or failed (n=23). Selected biomechanical variables were calculated using motion analysis methods. RESULTS: Initial failed recoveries had slower reaction times, shorter step lengths, and greater trunk flexion angles and velocities. Subjects who failed on the initial attempt modified their recovery strategy to successfully recover. The biomechanics of these recoveries resembled those used by subjects who successfully recovered on their initial attempt. CONCLUSIONS: The biomechanical mechanisms involved with a failed treadmill recovery mimic those responsible for failed recoveries from an induced trip. Subjects who failed on their initial recovery response made modifications allowing successful recoveries on subsequent attempts. RELEVANCE: This protocol may be useful as a testing and rehabilitation tool for fall recovery.

Accidental Falls↗

Glycogen synthesis in muscle fibers during active recovery from intense exercise.

PURPOSE: There is evidence that active recovery impairs glycogen repletion in skeletal muscles of fasted individuals. Our main goal was to examine the impact of active recovery on the glycogen stores of the different muscle fiber types. METHODS: Eight endurance-trained individuals cycled for 2.5 min at 130% [OV0312]O(2peak) followed by a 30-s all-out cycling sprint. After exercise, the participants were subjected to either a passive recovery or an active recovery protocol that consisted of pedalling for 45 min at 40% [OV0312]O(2peak). RESULTS: During active recovery, blood lactate and pH returned more rapidly toward preexercise levels than during passive recovery. In contrast, average muscle glycogen content remained at stable levels during active recovery (209 +/- 32 and 202 +/- 30 mmol.kg-1 at 0 and 45 min of recovery, respectively) but increased significantly in response to passive recovery (from 185 +/- 27 to 283 +/- 42 mmol.kg-1). The pattern of change in periodic acid-Schiff staining intensity across muscle fibers suggests that the impact of active recovery on average muscle glycogen content is different from that observed at the levels of the individual muscle fibers, with active recovery having no effect on glycogen resynthesis in Type II muscle fibers but causing glycogen breakdown in Type I muscle fibers. Although active recovery was also associated with higher plasma catecholamines and lower insulin levels, such an unfavorable hormonal environment had no effect on glycogen resynthesis in Type II muscle fibers. CONCLUSION: Active recovery in comparison to passive recovery does not affect glycogen resynthesis in Type II muscle fibers despite being associated with an unfavorable hormonal environment but results in a marked glycogen mobilization in Type I muscle fibers.

Adult↗

The effect of various recovery modalities on subsequent performance, in consecutive supramaximal exercise.

Different recovery strategies from maximal exercise seem to induce different lactate utilization patterns without significantly affecting performance on one subsequent maximal exercise. It remains unclear however, how varying recovery modalities affects repeated maximal exercise. To study this, we examined in 16 subjects, the influence of passive (P), active leg (L) and active arm (A) twenty minutes recovery periods separating a series of four exhaustive exercises, up to two minutes duration. Significant decreases in performance between the first and fourth exercise were observed in all recovery series but a significant decrease in performance in the second exercise was observed during passive recovery alone (p < 0.01). When the different types of recovery are compared, a more pronounced decrement in performance was found during passive recovery when first and last exercises are compared (p < 0.04). Pedaling duration in each successive exercise was unaffected in A or L but was significantly shorter in P (p < 0.03). Highly significant differences in mean blood lactate kinetics were found for the three recovery patterns used, with more elevated peak and nadir levels in passive recovery, intermediate values in active arm and lowest concentrations in active leg recovery. However, no correlation was found between performance and lactate concentration at the onset of exercise (r = -0.15; p = NS). Mean heart rates were similar throughout the experimental protocol except for a lower cardiac frequency during the last 5 minutes of passive recovery (p < 0.01). Blood hematocrits showed higher hemoconcentrations in repeated exercise during passive recovery (p < 0.01) despite significantly lower total fluid losses in this group. A significant correlation between peak hematocrit and blood lactate was also found (r = 0.67; p < 0.001). We conclude that the type of recovery has a significant effect on blood lactate elimination kinetics, and active recovery is beneficial in the preservation of performance during repeated maximal exercise. Furthermore, plasma shifts across the extra and intravascular spaces are induced by maximal exercise, and appear to closely follow blood lactate kinetics.

Adult↗

Factors influencing the haematological recovery after allogeneic bone marrow transplantation in leukaemia patients treated with methotrexate-containing GVHD prophylaxis: a single-centre experience.

In the present single institution study of 66 leukaemia patients (28 AML, 23 ALL, 15 CML), the factors influencing haematological recovery after allogeneic bone marrow transplantation (alloBMT) were analysed retrospectively in order to identify the optimal conditions required for a rapid haematological recovery after alloBMT. All patients received GVHD prophylaxis with cyclosporine A plus methotrexate. The mean number of days required to achieve > or = 0.5 x 109/l neutrophil count after alloBMT was 17 (median 17, range 9 to 27 days) and 19 patients (28.8%) had rapid neutrophil recovery within 15 days after alloBMT. The haematological recovery was more rapid in the 38 patients without GVHD or with only grade I GVHD. Furthermore, 50% and 40% of patients receiving 10 (n = 18) or 5 (n = 20) micrograms/kg/day G-CSF had rapid neutrophil recovery within 15 days after alloBMT, versus only 7.1% of patients not receiving G-CSF post-transplant (n = 28), p < 0.001. The neutrophil recovery was similar in patients receiving either fresh or cryopreserved allografts and either TBI-containing or busulfan-containing conditioning regimen. A significant correlation was found between neutrophil recovery and either the MNC or CFU-GM content of the allografts, r = 0.33, p < 0.01. The mean number of days required for neutrophil recovery was only 16 days (median 16, range 9 to 24 days) in patients receiving allografts containing > 1 x 10(5) CFU-GM/kg (n = 28) versus 19 days (median 19, range 13 to 27 days) in patients receiving allografts containing < 1 x 10(5) CFU-GM/kg (n = 35). Three patients receiving allografts containing less than 0.5 x 10(5) CFU-GM/kg had primary neutrophil engraftment failure. The mean number of days required to achieve 20 x 109/l platelet count was 21 (median 20, range 11 to 50 days) and 30 patients (46.9%) had platelet recovery within 20 days after alloBMT. The platelet recovery after alloBMT was not significantly affected by the type of leukaemia, conditioning regimen, or G-CSF administration. The mean number of days required for platelet recovery after alloBMT was only 20 days (median 18 days) in patients receiving allografts containing > 1.0 x 10(5) BFU-E/kg (n = 35) versus 23 days (median 20 days) in patients receiving allografts containing < 1.0 x 10(5) BFU-E/kg (n = 24). Seven patients receiving allografts containing less than 0.5 x 10(5) BFU-E/kg had primary platelet engraftment failure. The present study has identified the high number of progenitor cells in the allografts infused and the daily administration of G-CSF post-transplant as the optimal combination for a rapid neutrophil recovery after alloBMT. More significantly, the number of BFU-E in allografts was the most significant factor to determine platelet recovery after alloBMT. The development of GVHD of grade II or more during the first weeks after alloBMT was associated with slower haematological recovery and longer period of fever during neutropenia and hospitalisation.

Acute Disease↗

[ST segment depression during recovery after treadmill exercise test in stable patients with previous myocardial infarction].

BACKGROUND: The significance of exercise-induced ST segment depression is well known while limited data are available on the clinical/prognostic power of ST depression occurring only during recovery. Aim of the study was to clarify the clinical/prognostic value of "recovery only" ST depression in stable patients late from myocardial infarction (AMI) and to determine whether the addition of recovery data to exercise parameters improves the interpretation of exercise test. METHODS: From a population of 766 consecutive patients (mean age: 57.2 +/- 8.6 yrs.; male: 89%) who underwent a Bruce Treadmill test at least 1 year after a Q wave AMI and whose exercise data were prospectively entered in the database of our Institution, 4 different Groups were identified: 1) 99 patients with a negative exercise test; 2) 53 patients with "exercise only" ST depression; 3) 140 patients with "exercise and recovery" ST depression; 4) 31 patients with "recovery only" ST depression. The main clinical and exercise data and a cardiac follow-up (average mean length: 1530 +/- 600 day) were evaluated by one-way analysis of variance, Bonferroni T-test, chi-square, relative risk (RR) with 95% confidence intervals (CI), Kaplan-Meler method and log-rank. RESULTS: Baseline clinical parameters were similar in the 4 Groups except for older age in Group 3 compared to Group 2 (< 0.05) and higher prevalence of anterior AMI in Group 4 compared to others (= 0.004). Patients with exercise and recovery ST depression or with "recovery only" ST depression had significantly less exercise tolerance than patients with negative exercise test or "exercise only" ST depression [exercise duration (< 0.05, Group 1 vs. 3, vs. 4; Group 2 vs. 3), peak rate pressure product (< 0.05), maximal heart rate (< 0.05; Group 1 vs. 2; vs. 3; vs. 4)]. Exercise-induced ST depression was higher and angina was significantly more frequent in patients with exercise and recovery ST depression as well as an high Mark's risk score (< 0.001). Only patients with exercise and recovery ST depression demonstrated significantly higher risk of overall mortality (RR: 1.35, CI: 1.04-1.74), unstable angina (RR: 1.34, CI: 1.09-1.65) or revascularisation procedures (RR: 1.51, CI: 1.25-1.83). Relative risk of patients with "recovery only" ST depression was similar to that of subjects with "exercise only" ST depression. CONCLUSIONS: In stable patients with old Q wave AMI, "recovery only" ST depression is rate, but does represent a true sign of ischemia. It could be associated with indirect indexes of worse ventricular function. The prognostical power of "recovery only" ST depression is mild, although similar to that of "exercise only" ST depression. Moreover the presence of ST depression not only during exercise but also during the recovery phase identifies patients with more severe prognosis. Therefore the inclusion of findings from the recovery phase in the analysis of the exercise test could increase the predictive power of the test itself.

Aged↗

Effects of the muscle pump and body posture on cardiovascular responses during recovery from cycle exercise.

The purpose of the study was to characterize the effects of muscular contractions (the muscle pump) and body posture on cardiovascular responses during recovery from moderate exercise in the upright-sitting or supine positions. Heart rate (HR), stroke volume (SV), and cardiac output (CO) were measured in seven young male subjects at rest and during 10-min of cycle exercise at 60% of peak oxygen uptake (VO2peak). This was followed by either complete rest for 5 min (inactive recovery) or cycling at VO2peak for 5 min (active recovery) in the upright or supine positions. In the upright position, an initial rapid decrease in HR was followed by a gradual decrease in HR, and this response was similar when comparing inactive and active recoveries. Upright SV during inactive recovery decreased gradually to the pre-exercise resting level, whereas upright SV during active recovery remained significantly elevated. In contrast, in the supine position, the HR during active recovery decreased, but remained significantly higher than that during inactive recovery. Changes in supine SV were similar when comparing inactive and active recovery. Thus, maintenance of SV and HR resulted in significantly greater CO during active recovery than during inactive recovery, regardless of body position. HR was greater during supine active-recovery than during supine inactive-recovery, and there was no difference in SV. These data suggest that the muscle pump is less important in facilitating venous return and vagal resumption in the supine position as compared to the upright position.

Adult↗

An empirical conceptualization of the recovery orientation.

OBJECTIVE: The recovery movement is having a growing impact on policy for people with severe mental illness. The empirical literature on the recovery orientation, however, is scant, and no empirical conceptualization of recovery has been published. METHOD: We identified items reflecting recovery themes and measuring aspects of subjective experience, and used principle components and confirmatory factor analyses to develop an empirical conceptualization of the recovery orientation, using data from a large, systematic study of schizophrenia. RESULTS: We identified four domains of the recovery orientation: empowerment, hope and optimism, knowledge and life satisfaction. CONCLUSIONS: We propose here an initial approach to measuring and conceptualizing recovery attitudes. We also suggest that the evidence-based practice (EBP) movement may help to identify interventions that promote the recovery orientation and help to advance recovery attitudes. We suggest that there is a bidirectional relationship between recovery attitudes and the positive clinical outcomes that are the goals of EBPs. Through the use of empirically derived conceptualizations of recovery, EBPs can provide a mechanism for identifying treatments that promote the recovery orientation. The conceptualization proposed here can, thus, serve as a tool to assess changes in recovery attitudes during participation in specific EBPs.

Adult↗

Does adjunctive midazolam reduce recovery agitation after ketamine sedation for pediatric procedures? A randomized, double-blind, placebo-controlled trial.

STUDY OBJECTIVE: Despite widespread use of adjunctive benzodiazepines during ketamine sedation, their efficacy in reducing recovery agitation in children has never been studied. We wished to characterize the nature and severity of recovery agitation after ketamine sedation in children treated in the emergency department and to determine whether the addition of adjunctive midazolam reduces the magnitude of such recovery agitation. METHODS: The study was a randomized, double-blind, clinical trial of adjunctive midazolam versus placebo during ketamine sedation. We enrolled 104 children aged 12 months to 15 years (median age, 6 years) at a combined university medical center and children's hospital. Subjects received either intravenous midazolam (0.05 mg/kg up to 2 mg) or placebo after intravenous administration of a ketamine loading dose (1.5 mg/kg). Treating physicians and nurses independently noted the presence of crying, hallucinations, and nightmares during recovery and graded recovery agitation by using a 100-mm visual analog scale. Preprocedure agitation and external stimulation during recovery were also graded. The time from ketamine injection until each subject met the recovery criteria was recorded. RESULTS: Fifty-three subjects received midazolam, and 51 received placebo. Potentially confounding variables were similar between the groups. Sedation efficacy, adverse effects, and recovery time were also similar between groups. Interobserver agreement between physician and nurse assessments was substantial. Median physician assessment of recovery agitation was 4 mm (interquartile range, 2 to 19) in the midazolam group and 5 mm (interquartile range, 3 to 14) in the placebo group (difference -1; 95% confidence interval -3 to 2; P =.705). Recovery agitation was moderately correlated with preprocedure agitation (rho=0.486) but not with external stimulation during recovery (rho=0.147). CONCLUSION: Recovery agitation is common but generally of very low magnitude after ketamine sedation in children in the ED. We observed a median physician rating of 5 mm on a 100-mm visual analog scale, a score that we believe to be clinically insignificant. The degree of recovery agitation after ketamine sedation is significantly related to the degree of preprocedure agitation. In this study, concurrent midazolam did not diminish such agitation and had no measurably beneficial effect. Use of adjunctive benzodiazepines in pediatric ketamine sedation appears unnecessary.

Adjuvants, Anesthesia↗

Effect of combined active recovery from supramaximal exercise on blood lactate disappearance in trained and untrained man.

The purpose of this study was to determine the effect of different modalities of individualized active recovery on blood lactate disappearance after supramaximal exercise in subjects with different levels of aerobic fitness. Fourteen healthy subjects (7 trained and 7 untrained subjects mean age 20 +/- 1.5 and 19.5 +/- 1.5, respectively) participated in this study. They performed three supramaximal intermittent exercises at 60 % of the time to exhaustion at 120 % of the maximum aerobic power (MAP) with 5-min recovery periods (2 x 5 min). The third exercise was followed by 20 min of recovery. The effects of four types of recovery were compared in trained and untrained subjects: passive recovery (PR), an active recovery at an intensity corresponding to the first anaerobic ventilatory threshold minus 20 % (VT1), an active recovery at an intensity corresponding to the second anaerobic ventilatory threshold minus 20 % (VT2) and a combined active recovery (CR) which consisted of 7 min at VT2 followed by 13 min at VT1. Blood lactate levels were measured at rest and during the recovery periods. Peak blood lactate after supramaximal exercise was observed significantly earlier with VT2 and CR (4th min) than VT1 and PR (7th min) in trained and in untrained subjects. Combined active recovery (CR) showed a significantly faster lactate disappearance than did PR, VT1, or VT2 from the 7th min of recovery in trained subjects (p < 0.05) and at the 20th min in untrained subjects (p < 0.05). CR and VT2 conditions showed earlier peak blood lactate (4th min) than PR or VT1 (7th min). Blood lactate disappearance was faster in trained than untrained subjects during combined active recovery. This result suggests that the level of physical fitness plays an important role mainly in the pattern of blood lactate decrease during combined active recovery.

Adult↗

Functional recovery in the avian ear after hair cell regeneration.

Trauma to the inner ear in birds, due to acoustic overstimulation or ototoxic aminoglycosides, can lead to hair cell loss which is followed by regeneration of new hair cells. These processes are paralleled by hearing loss followed by significant functional recovery. After acoustic trauma, functional recovery is rapid and nearly complete. The early and major part of functional recovery after sound trauma occurs before regenerated hair cells become functional. Even very intense sound trauma causes loss of only a proportion of the hair cell population, mainly so-called short hair cells residing on the abneural mobile part of the avian basilar membrane. Uncoupling of the tectorial membrane from the hair cells during sound overexposure may serve as a protection mechanism. The rapid functional recovery after sound trauma appears not to be associated with regeneration of the lost hair cells, but with repair processes involving the surviving hair cells. Small residual functional deficits after recovery are most likely associated with the missing upper fibrous layer of the tectorial membrane which fails to regenerate after sound trauma. After aminoglycoside trauma, functional recovery is slower and parallels the structural regeneration more closely. Aminoglycosides cause damage to both types of hair cells, starting at the basal (high frequency) part of the basilar papilla. However, functional hearing loss and recovery also occur at lower frequencies, associated with areas of the papilla where hair cells survive. Functional recovery in these low frequency areas is complete, whereas functional recovery in high frequency areas with complete hair cell loss is incomplete, despite regeneration of the hair cells. Permanent residual functional deficits remain. This indicates that in low frequency regions functional recovery after aminoglycosides involves repair of nonlethal injury to hair cells and/or hair cell-neural synapses. In the high frequency regions functional recovery involves regenerated hair cells. The permanent functional deficits after the regeneration process in these areas are most likely associated with functional deficits in the regenerated hair cells or shortcomings in the synaptic reconnections of nerve fibers with the regenerated hair cells. In conclusion, the avian inner ear appears to be much more resistant to trauma than the mammalian ear and possesses a considerable capacity for functional recovery based on repair processes along with its capacity to regenerate hair cells. The functional recovery in areas with regenerated hair cells is considerable but incomplete.

Aminoglycosides↗

Influence of light physical activity on cardiac responses during recovery from exercise in humans.

To examine the influence of light exercise on cardiac responses during recovery from exercise, we measured heart rate (HR), stroke volume (SV), and cardiac output (Qc) in five healthy untrained male subjects in an upright position before, during, and after 10-min steady-state cycle exercise at an exercise intensity of 170 W, corresponding to a mean of 68 (SD 4)% of maximal oxygen uptake. The recovery phase was evaluated separately for three different conditions: 10 min of complete rest (passive recovery), 7 min of pedalling at 20-W exercise intensity followed by 3 min of rest (partially active recovery), and 7 min of pedalling at 40-W exercise intensity followed by 3 min of rest (partially active recovery), on an upright cycle ergometer. The time courses of decreases in HR in the two active recovery phases at different exercise intensities were almost identical to those in the passive recovery phase. However, the subsequent HR reductions during the rest after active recovery at 20 W and at 40 W were mean 7.5 (SD 4.4) and mean 10.0 (SD 3.1) beats x min(-1), respectively, both of which were significantly larger (P < 0.05 and P< 0.005) than the corresponding reduction [1.4 (SD 2.5) beats min(-1)] for passive recovery. The SV values at the two exercise intensities during the active recovery periods were maintained at levels similar to that during 170-W steady-state exercise. In contrast, the SV during passive recovery decreased gradually to a level significantly below the initial baseline level at rest before exercise (P < 0.05). The resultant time courses of CO values during active recovery were significantly higher (each P < 0.05) than that during passive recovery. It was concluded from these findings that light post-exercise physical activity plays an important role in facilitating the venous return from the muscles and in restoring the elevated HR to the pre-exercise resting level.

Adult↗

Inhibition of post-ischemic ventricular recovery by low concentrations of prostacyclin in isolated working rat hearts: dependency on concentration, ischemia duration, calcium and relationship to myocardial energy metabolism.

The objective of this study was to characterize the effect of prostacyclin (PGI2) on ventricular function following total global ischemia in isolated working rat hearts and to investigate the mechanism of its action. Ischemia was initiated for 10, 15, 20 or 25 min with or without treatment with PGI2. Increasing durations of ischemia resulted in a progressive decline in high energy phosphate (HEP) stores, an elevation in tissue lactate, and incomplete recovery of function with reperfusion. Prostacyclin at either 1 or 10 ng/ml had no effect on HEP levels or total adenine nucleotides, and tissue lactate was not significantly affected by PGI2 in hearts made ischemic for 10 to 20 min, but both PGI2 concentrations significantly elevated lactate levels after 25 min ischemia. Reperfusion recovery of left ventricular function was complete following 10 and 15 min ischemia, but incomplete recovery was evident following 20 min ischemia (77% of pre-ischemic function); and although PGI2 had no direct effect on the function of aerobically perfused hearts, recovery of aortic flow with 1 ng/ml PGI2 after 20 min of ischemia was reduced to approximately 20% (P less than 0.01). This depression in recovery was associated with significantly increased lactate levels during reperfusion. At a concentration of 10 ng/ml PGI2 did not depress ventricular recovery or elevate lactate content after 20 min ischemia. When hearts made ischemic for 20 min were analyzed, a significant negative correlation was found between ventricular recovery (aortic flow rate) and lactate concentration; however, no correlation existed between recovery and ATP levels. After 25 min of ischemia, five of eight (62.5%) untreated hearts demonstrated some degree of ventricular recovery, however, only two of ten hearts studied demonstrated any measurable functional recovery with either PGI2 concentration. This effect of PGI2 to reduce or prevent recovery of ventricular function following either 20 or 25 min of ischemia as well as the corresponding elevation in lactate levels was prevented by treatment with the calcium channel blocker verapamil. This study therefore shows that PGI2 at critical low concentrations can depress left ventricular recovery following total ischemia. This effect of PGI2 becomes more pronounced as ischemia duration is prolonged and is associated with elevated tissue lactate levels. The studies with verapamil suggest that PGI2 may be acting via the slow calcium channel to increase lactate levels and depress ventricular recovery following prolonged periods of ischemia.

Adenine Nucleotides↗

Mapping and measuring addiction recovery: Recommended protocols through the PHENX toolkit.

BACKGROUND: Addiction "recovery" has served as a positive conceptual basis for major public health frameworks, communication strategies, and policies. With greater research interest and increasing explication of the recovery construct a multitude of measures have emerged, prompting a need to reach consensus on recommendations to enable better data harmonization and cross-study syntheses. The PhenX (consensus measures for Phenotypes and eXposures) Toolkit (www.phenxtoolkit.org) is a freely accessible catalog of validated protocols designed to promote data comparability across clinical, epidemiological, and genomic research, yet contained no recovery-specific measures. METHOD: In 2024, a Substance Use and Recovery Working Group (SURWG) followed a well-established and detailed PhenX consensus process to identify and recommend protocols suitable for recovery research. Protocols were chosen based on criteria including recovery specificity, brevity, psychometrics, scoring simplicity, and non-proprietary access. The broader scientific community (12 national/regional organizations) provided feedback (respondent N&#x2009;=&#x2009;86) on the SURWG's preliminary recommendation which was incorporated into final decisions. RESULTS: In 2025, the PhenX Toolkit released 15 new recommended protocols across three broad recovery elements: 1. Biopsychological (post-acute withdrawal; craving), 2. Socio-ecological (social relationships;social network characteristics; substance use goal; recovery identity; recovery capital), 3. Treatment and recovery services (Treatment and Recovery Services Use; Satisfaction; and Happiness in Recovery; Mutual-Help). CONCLUSIONS: This PhenX Toolkit SURWG process resulted in a new Substance Use Recovery Specialty Collection of recommended protocols with specific multidimensional applicability. As such, they provide the field with pre-vetted tools that researchers can employ with some confidence to enhance empirical efficiency and return on national research investment.

Humans↗

Postoperative pain and quality of recovery.

PURPOSE OF REVIEW: Quality of recovery is recognized as a valid and important outcomes measurement in clinical care and research. The increasing interest in evaluating quality of recovery reflects the overall increased interest in patient-focused assessments. Assessment of quality of recovery incorporates measuring many dimensions or domains including physiologic endpoints, adverse events and psychosocial status. Unlike 'traditional' outcomes that focus on major morbidity and mortality, quality of recovery assesses 'nontraditional' outcomes focused around patient-oriented endpoints. By adversely influencing the many domains assessed by quality of recovery, postoperative pain may have a general detrimental effect on quality of recovery. RECENT FINDINGS: Studies utilizing validated instruments to assess quality of recovery have revealed that different levels of postoperative pain may differentially affect quality of recovery. In addition, quality of recovery in the immediate postoperative period may predict long-term quality of life. SUMMARY: Higher levels of postoperative pain typically correlate with a decrease in quality of recovery. Different analgesic techniques and regimens may differentially influence quality of recovery, with preliminary evidence suggesting that some regional analgesic techniques may provide superior quality of recovery, quality of life and patient satisfaction. Further studies are needed to elucidate the effects of different analgesic techniques on quality of recovery.

Journal Article↗

Psychosocial, hemostatic, and inflammatory correlates of delayed poststress blood pressure recovery.

OBJECTIVE: Delayed poststress cardiovascular recovery has been associated with cardiovascular disease risk. This study assessed relationships between systolic blood pressure (BP) recovery, psychosocial risk factors, and delayed recovery of inflammatory and hemostatic variables. METHOD: Data were analyzed from 228 middle-aged men and women from the Whitehall Psychobiology study who performed color/word and mirror-tracing tasks. Systolic BP recovery was assessed as the difference between baseline and levels recorded 40 to 45 minutes poststress. Associations were analyzed with socioeconomic markers (grade of employment, education, income), psychosocial factors (social isolation, hostility, mental health, financial strain), and recovery of heart rate, heart rate variability, von Willebrand factor, factor VIII clotting activity, plasma fibrinogen, and plasma viscosity. RESULTS: Systolic BP was on average 6.19 +/- 9.6 mm Hg higher on recovery than baseline. Delayed BP recovery was associated with lower grade of employment, lower education and lower income independently of age, gender, and systolic BP stress reactivity. Delayed BP recovery was related to social isolation and poor mental health independently of age, gender, socioeconomic position, and task reactivity. Delayed systolic BP recovery was also associated with delayed recovery in diastolic BP, heart rate, factor VIII, and plasma viscosity but not delayed heart rate variability recovery, independently of age, gender, body mass, and task reactivity. CONCLUSION: Socioeconomic and psychosocial risk factors for cardiovascular disease are related to delays in poststress recovery. Delayed systolic BP recovery may be a marker for prolonged responses in hemostatic variables that have a direct influence on cardiovascular disease pathogenesis.

Biomarkers↗

Concepts of recovery: competing or complementary?

PURPOSE OF REVIEW: Within the last 5 years, concepts of recovery have taken center stage in psychiatry as the overarching goal of mental health services. In the course of this shift towards recovery, clinicians and consumers (and many others) have struggled to make the concept of recovery both measurable and meaningful. The clinical concept of recovery has focused upon the remission of symptoms and restoration of functioning. A rehabilitation model of recovery has been a more subjective and consumer-oriented concept that focuses on the full lives that are lived within the context of enduring disability. RECENT FINDINGS: A review of the literature addressing the concepts of recovery over the last 2 years demonstrates that authors are rarely explicit about the perspective of recovery from which they are writing. Almost all of the representative papers, however, struggled with how best to define, measure and validate recovery in its broadest terms. Several authors reviewed the history of recovery and offered conceptual discussions of either their first-person experiences or implications for mental health practice. Other authors, regardless of their perspective on recovery, sought to more concretely define criteria for recovery, for the purposes of recovery measure development or more rigorous research of the concept. SUMMARY: As authors struggle to reconcile these often competing concepts of recovery, we suggest that both concepts are useful for different purposes and populations and that the synthesis of the two will offer a broader perspective on life with, after, or despite mental illness.

Journal Article↗

Na+/H+ exchange inhibitors reverse lactate-induced depression in postischaemic ventricular recovery.

1. By use of pharmacological approaches, the present study examined the hypothesis that the deleterious effect of lactate on postischaemic ventricular recovery may be mediated, at least in part, by enhanced activation of the Na+/H+ exchanger at the time of reperfusion. 2. Spontaneously beating isolated hearts of the rat were subjected to 15 min zero-flow global ischaemia followed by 30 min reperfusion. The effects of lactate (10, 20 or 40 mM) were studied by adding it 20 min before ischaemia whereas reperfusion was carried out with lactate-free buffer. 3. Pretreatment with 20 or 40 mM lactate significantly reduced postischaemic recovery of developed force to 17 +/- 3% and 16 +/- 4% of preischaemic values (P < 0.05) compared to a 78 +/- 4% recovery in control hearts. Similarly, recovery in ventricular rate was significantly reduced to 34 +/- 7.6% and 38 +/- 12% with 20 and 40 mM lactate, respectively compared to 97.5 +/- 6.4% recovery in control hearts. At a concentration of 10 mM, lactate was without effect on either force or ventricular rate recovery. 4. Coadministration of either of two Na+/H+ exchange inhibitors, amiloride (174 microM) or 5-N,N-hexamethylene amiloride (HMA, 1 microM) with lactate and inclusion of the two drugs during the first 5 min of reperfusion resulted in reversal of lactate-induced inhibition of force recovery with observed recoveries of 69 +/- 6.7% and 64 +/- 5% with amiloride and HMA, respectively. Similarly, recovery in ventricular rate was significantly enhanced to 92 +/- 10% and 89 +/- 6% with amiloride and HMA, respectively compared to 38 +/- 12% recovery in control hearts. In the presence of amiloride or HMA, force recovery in lactate-treated hearts was significantly increased to 68 +/- 16% and 72 +/- 4.7% of preischaemic values, respectively.6. In spontaneously beating hearts, resting tension changes during both ischaemia and reperfusion were not statistically different between treatment groups. However, in paced hearts pretreated with 40 mM lactate the elevation in resting tension during the first 5 min of reperfusion, was significantly reduced by both amiloride and HMA.7. Changes in functional recoveries produced by either lactate or Na+/H+ exchange inhibitors were unrelated to alterations in high energy phosphate depletion during ischaemia or to repletion of these compounds after 30 min reperfusion either in spontaneously beating or electrically paced hearts.8. The results suggest that stimulated Na'/H+ exchange activation at reflow contributes, at leastpartially, to lactate-induced depression of postischaemic recovery.

Amiloride↗

Skeletal muscle fat and carbohydrate metabolism during recovery from glycogen-depleting exercise in humans.

The primary aim of the present study was to determine whether intramuscular triacylglycerol (IMTG) utilization contributed significantly to the increase in lipid oxidation during recovery from exercise, as determined from the muscle biopsy technique. In addition, we also examined the regulation of pyruvate dehydrogenase (PDHa) and changes in muscle acetyl units during an 18 h recovery period after glycogen-depleting exercise. Eight endurance-trained males completed an exhaustive bout of exercise (approximately 90 min) on a cycle ergometer followed by ingestion of carbohydrate (CHO)-rich meals (64-70 % of energy from carbohydrate) at 1, 4 and 7 h of recovery. Duplicate muscle biopsies were obtained at exhaustion, and 3, 6 and 18 h of recovery. Despite the large intake of CHO during recovery (491 +/- 28 g or 6.8 +/- 0.3 g kg-1), respiratory exchange ratio values of 0.77 to 0.84 indicated a greater reliance on lipid as an oxidative fuel. However, there was no net IMTG utilization during recovery. IMTG content at exhaustion was 23.5 +/- 3.5 mmol (kg dry wt)-1, and remained constant at 24.6 +/- 2.6, 25.7 +/- 2.8 and 28.4 +/- 3.0 mmol (kg dry wt)-1 after 3, 6 and 18 h of recovery. Muscle glycogen increased significantly from 37 +/- 11 mmol (kg dry wt)-1 at exhaustion, to 165 +/- 13, 250 +/- 18, and 424 +/- 22 mmol (kg dry wt)-1 at 3, 6 and 18 h of recovery, respectively. PDHa was reduced at 6 and 18 h when compared to exhaustion, but did not change during the recovery period. Acetyl-CoA, acetylcarnitine and pyruvate contents declined significantly after 3 h of recovery compared to exhaustion, and thereafter remained unchanged. We conclude that IMTG has a negligible role in contributing to the enhanced fat oxidation during recovery from exhaustive exercise. Despite the elevation of glucose and insulin following high-CHO meals during recovery, CHO oxidation and PDH activation were decreased, supporting the hypothesis that glycogen resynthesis is of high metabolic priority. Plasma fatty acids, very low density lipoprotein triacylglycerols, as well as intramuscular acetylcarnitine stores are likely to be important fuel sources for aerobic energy, particularly during the first few hours of recovery.

Adult↗