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PubMed2005

Excitation-induced cell damage and beta2-adrenoceptor agonist stimulated force recovery in rat skeletal muscle.

Intensive exercise leads to a loss of force, which may be long lasting and associated with muscle cell damage. To simulate this impairment and to develop means of compensating the loss of force, extensor digitorum longus muscles from 4-wk-old rats were fatigued using intermittent 40-Hz stimulation (10 s on, 30 s off). After stimulation, force recovery, cell membrane leakage, and membrane potential were followed for 240 min. The 30-60 min of stimulation reduced tetanic force to approximately 10% of the prefatigue level, followed by a spontaneous recovery to approximately 20% in 120-240 min. Loss of force was associated with a decrease in K+ content, gain of Na+ and Ca2+ content, leakage of the intracellular enzyme lactic acid dehydrogenase (10-fold increase), and depolarization (13 mV). Stimulation of the Na+-K+ pump with either the beta2-adrenoceptor agonist salbutamol, epinephrine, rat calcitonin gene-related peptide (rCGRP), or dibutyryl cAMP improved force recovery by 40-90%. The beta-blocker propranolol abolished the effect of epinephrine on force recovery but not that of CGRP. Both spontaneous and salbutamol-induced force recovery were prevented by ouabain. The salbutamol-induced force recovery was associated with repolarization of the membrane potential (12 mV) to the level measured in unfatigued muscles. In conclusion, in muscles exposed to fatiguing stimulation leading to a considerable loss of force, cell leakage, and depolarization, stimulation of the Na+-K+ pump induces repolarization and improves force recovery, possibly due to the electrogenic action of the Na+-K+ pump. This mechanism may be important for the restoration of muscle function after intense exercise.

Adrenergic beta-2 Receptor Agonists↗

PubMed2006

Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery.

We examined the effect of two levels of exercise-induced hypotension on esophageal (Tes) and active and nonactive muscle temperatures during and following exercise. Seven males performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their peak oxygen consumption during bilateral knee extensions (VO2sp). This was followed on separate days by 15-min of isolated bilateral knee extensions at moderate (60% VO2sp) (MEI) and high (80% VO2sp) (HEI) exercise intensities, followed by 90 min of recovery. Muscle temperature was measured with an intramuscular probe inserted in the left vastus medialis (Tvm) and triceps brachii (Ttb) muscles under ultrasound guidance. The deepest sensor (tip) was located approximately 10 mm from the femur and deep femoral artery and from the superior ulnar collateral artery and humerus for the Tvm and Ttb, respectively. Additional sensors were located 15 and 30 mm from the tip with an additional sensor located at 45 mm for the Tvm measurements only. Following exercise, mean arterial pressure (MAP) remained significantly below preexercise rest for the initial 60 min of recovery after MEI and for the duration of the postexercise recovery period after HEI (P< or =0.05). After HEI, significantly greater elevations from preexercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP compared with MEI (P< or =0.05). By the end of 90-min postexercise recovery, MAP, Tes, and all muscle temperatures remained significantly greater after HEI than MEI. Furthermore, a significantly shallower muscle temperature profile across Tvm, relative to preexercise rest, was observed at the end of exercise for both HEI and MEI (P< or=0.05), and for 30 min of recovery for MEI and throughout 90 min of recovery for HEI. No significant differences in muscle temperature profile were observed for Ttb. Thus we conclude that the increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude and recovery time of the postexercise esophageal and active muscle temperatures.

Adult↗

PubMed1984

Blood lactate disappearance at various intensities of recovery exercise.

Numerous studies have reported that following intense exercise the rate of blood lactate (La) disappearance is greater during continuous aerobic work than during passive recovery. Recent work indicates that a combination of high- and low-intensity work may be optimal in reducing blood La. We tested this hypothesis by measuring the changes in blood La levels following maximal exercise during four different recovery patterns. Immediately following 50 S of maximal work, subjects (n = 7) performed one of the following recovery treatments for 40 min: 1) passive recovery (PR); 2) cycling at 35% maximal O2 uptake (VO2 max) (35% R); 3) cycling at 65% VO2 max (65% R); 4) cycling at 65% for 7 min followed by cycling at 35% for 33 min (CR). The treatment order was counterbalanced with each subject performing all treatments. Serial blood samples were obtained throughout recovery treatments and analyzed for La. The rate of blood La disappearance was significantly greater (P less than 0.05) in both the 35% R and CR when compared with either the 65% R or PR. No significant difference (P greater than 0.05) existed in the rate of blood La disappearance between the 35% R and CR. These data do not support the hypothesis that exercise recovery at a combination of intensities is superior to a recovery involving continuous submaximal exercise in lowering blood La following maximal work.

Adult↗

PubMed1986

Pulmonary blood flow affects recovery from constriction in dog lung periphery.

The influence of blood flow through the pulmonary circulation on the time course of recovery of the lung periphery from challenge with three bronchoconstrictive agents was studied in dogs. The rate of perfusion of the left lower lobe was varied between 0 and 300 ml/min. A fiber-optic bronchoscope (OD = 5.5 mm) was wedged in a small airway in the same lobe, and resistance to airflow through the collateral system was continuously monitored. The lung was challenged with histamine aerosol for 1 min, or with intravenous boluses of histamine, acetylcholine, or methacholine. The time constant (tau) of recovery from each of the challenges was measured under the various pulmonary blood flow conditions. The mean tau of the recoveries from histamine was inversely related to the rate of blood flow. However, pulmonary blood flow had no effect on recovery from challenge with acetylcholine or methacholine, two agents metabolized by cholinesterase in lung tissue. From this study we conclude that recovery of the lung periphery from histamine is perfusion dependent, whereas recovery from acetylcholine or methacholine is perfusion independent. This suggests that the rate of blood flow through the pulmonary circulation could play an important role in recovery of the peripheral airways from certain mediators of bronchoconstriction.

Acetylcholine↗

PubMed1990

Running during recovery from hindlimb suspension induces transient muscle injury.

The objectives were to study morphological adaptations of soleus muscle to decreased loading induced by hindlimb suspension and the effect of run training during the subsequent recovery period. Adult female Wistar rats were kept for 28 days with hindlimbs suspended. For the next 28 days, rats were assigned to a cage-sedentary or daily running group. Compared with control soleus muscles, 28 days of hindlimb suspension reduced the mass and fiber cross-sectional area to 58 and 53% of control values, respectively, and decreased type I fibers from 92 +/- 2 to 81 +/- 2%. During recovery, clusters of damaged fibers were observed in the soleus muscle, and this observation was more pronounced in trained animals. Type IIc fibers appeared transiently during recovery, and their presence was exacerbated with training, as IIc fibers increased to approximately 20% of the total by day 14 of recovery and were no longer evident at day 28. Although muscle wet mass does not differ as a result of mode of recovery at day 14, training transiently decreased the overall fiber area compared with sedentary recovery at this point. By day 28 of recovery the morphological characteristics of soleus muscle in the trained group did not differ from control muscle, whereas in the sedentary group muscle mass and overall fiber cross-sectional area were approximately 14% less than control values.

Animals↗

PubMed1990

Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease.

This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow "lactacid" component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.

Adult↗

PubMed1997

Excess postexercise oxygen consumption and recovery rate in trained and untrained subjects.

The purpose of this study was to determine whether aerobic fitness level would influence measurements of excess postexercise oxygen consumption (EPOC) and initial rate of recovery. Twelve trained [Tr; peak oxygen consumption (VO2 peak) = 53.3 +/- 6.4 ml . kg-1 . min-1] and ten untrained (UT; VO2 peak = 37.4 +/- 3.2 ml . kg-1 . min-1) subjects completed two 30-min cycle ergometer tests on separate days in the morning, after a 12-h fast and an abstinence from vigorous activity of 24 h. Baseline metabolic rate was established during the last 10 min of a 30-min seated preexercise rest period. Exercise workloads were manipulated so that they elicited the same relative, 70% VO2 peak (W70%), or the same absolute, 1.5 l/min oxygen uptake (VO2) (W1.5), intensity for all subjects, respectively. Recovery VO2, heart rate (HR), and respiratory exchange ratio (RER) were monitored in a seated position until baseline VO2 was reestablished. Under both exercise conditions, Tr had shorter EPOC duration (W70% = 40 +/- 15 min, W1.5 = 21 +/- 9 min) than UT (W70% = 50 +/- 14 min; W1.5 = 39 +/- 14 min), but EPOC magnitude (Tr: W70% = 3.2 +/- 1.0 liters O2, W1.5 = 1.5 +/- 0.6 liters O2; UT: W70% = 3.5 +/- 0.9 liters O2, W1.5 = 2.4 +/- 0.6 liters O2) was not different between groups. The similarity of Tr and UT EPOC accumulation in the W70% trial is attributed to the parallel decline in absolute VO2 during most of the initial recovery period. Tr subjects had faster relative decline during the fast-recovery phase, however, when a correction for their higher exercise VO2 was taken. Postexercise VO2 was lower for Tr group for nearly all of the W1.5 trial and particularly during the fast phase. Recovery HR kinetics were remarkably similar for both groups in W70%, but recovery was faster for Tr during W1.5. RER values were at or below baseline throughout much of the recovery period in both groups, with UT experiencing larger changes than Tr in both trials. These findings indicate that Tr individuals have faster regulation of postexercise metabolism when exercising at either the same relative or same absolute work rate.

Adult↗

PubMed1999

Skeletal muscle phosphocreatine recovery in exercise-trained humans is dependent on O2 availability.

In skeletal muscle, phosphocreatine (PCr) recovery from submaximal exercise has become a reliable and accepted measure of muscle oxidative capacity. During exercise, O2 availability plays a role in determining maximal oxidative metabolism, but the relationship between O2 availability and oxidative metabolism measured by 31P-magnetic resonance spectroscopy (MRS) during recovery from exercise has never been studied. We used 31P-MRS to study exercising human gastrocnemius muscle under conditions of varied fractions of inspired O2 (FIO2) to test the hypothesis that varied O2 availability modulates PCr recovery from submaximal exercise. Six male subjects performed three bouts of 5-min steady-state submaximal plantar flexion exercise followed by 5 min of recovery in a 1.5-T magnet while breathing three different FIO2 concentrations (0.10, 0. 21, and 1.00). Under each FIO2 treatment, the PCr recovery time constants were significantly different, being longer in hypoxia [33. 5 +/- 4.1 s (SE)] and shorter in hyperoxia (20.0 +/- 1.8 s) than in normoxia (25.0 +/- 2.7 s) (P </= 0.05). End-exercise pH was not significantly different among the three treatments (7.08 +/- 0.01 for 0.10, 7.04 +/- 0.01 for 0.21, and 7.04 +/- 0.02 for 1.00). These results demonstrate that PCr recovery is significantly altered by FIO2 and suggest that, after submaximal exercise, PCr recovery, under normoxic conditions, is limited by O2 availability.

Adult↗

PubMed1999

Muscle pump and central command during recovery from exercise in humans.

We sought to determine the relative contributions of cessation of skeletal muscle pumping and withdrawal of central command to the rapid decrease in arterial pressure during recovery from exercise. Twelve healthy volunteers underwent three exercise sessions, each consisting of a warm-up, 3 min of cycling at 60% of maximal heart rate, and 5 min of one of the following recovery modes: seated (inactive), loadless pedaling (active), and passive cycling. Mean arterial pressure (MAP), cardiac output, thoracic impedance, and heart rate were measured. When measured 15 s after exercise, MAP decreased less (P < 0.05) during the active (-3 +/- 1 mmHg) and passive (-6 +/- 1 mmHg) recovery modes than during inactive (-18 +/- 2 mmHg) recovery. These differences in MAP persisted for the first 4 min of recovery from exercise. Significant maintenance of central blood volume (thoracic impedance), stroke volume, and cardiac output paralleled the maintenance of MAP during active and passive conditions during 5 min of recovery. These data indicate that engaging the skeletal muscle pump by loadless or passive pedaling helps maintain MAP during recovery from submaximal exercise. The lack of differences between loadless and passive pedaling suggests that cessation of central command is not as important.

Adult↗

PubMed2003

Recovery of microvascular PO2 during the exercise off-transient in muscles of different fiber type.

The speed with which muscle energetic status recovers after exercise is dependent on oxidative capacity and vascular O(2) pressures. Because vascular control differs between muscles composed of fast- vs. slow-twitch fibers, we explored the possibility that microvascular O(2) pressure (Pmv(O(2)); proportional to the O(2) delivery-to-O(2) uptake ratio) would differ during recovery in fast-twitch peroneal (Per: 86% type II) compared with slow-twitch soleus (Sol: 84% type I). Specifically, we hypothesized that, in Per, Pmv(O(2)) would be reduced immediately after contractions and would recover more slowly during the off-transient from contractions compared with Sol. The Per and Sol muscles of six female Sprague-Dawley rats (weight = approximately 220 g) were studied after the cessation of electrical stimulation (120 s; 1 Hz) to compare the recovery profiles of Pmv(O(2)). As hypothesized, Pmv(O(2)) was lower throughout recovery in Per compared with Sol (end contraction: 13.4 +/- 2.2 vs. 20.2 +/- 0.9 Torr; end recovery: 24.0 +/- 2.4 vs. 27.4 +/- 1.2 Torr, Per vs. Sol; P <or= 0.05). In addition, the mean response time for recovery was significantly faster for Sol compared with Per (45.1 +/- 5.3 vs. 66.3 +/- 8.1 s, Sol vs. Per; P < 0.05). Despite these findings, Pmv(O(2)) rose progressively in both muscles and at no time fell below end-exercise values. These data indicate that, during the recovery from contractions (which is prolonged in Per), capillary O(2) driving pressure (i.e., Pmv(O(2))) is reduced in fast-compared with slow-twitch muscle. In conclusion, the results of the present investigation may partially explain the slowed recovery kinetics (phosphocreatine and O(2) uptake) found previously in 1) fast- vs. slow-twitch muscle and 2) various patient populations, such as those with congestive heart failure and diabetes mellitus.

Animals↗

PubMed1982

Recovery of binocular function in kitten visual cortex.

1. This paper describes the results of an experiment designed to examine the ability of cells in the kitten's visual cortex to regain functional binocular connections following exposure to a brief period of visual deprivation. 2. Normal 4-wk-old kittens were exposed to a total of 12 h of optically induced strabismus over a period of 2 days, and single-unit recordings made the following day indicated that the proportion of striate cortex cells with binocular receptive fields had decreased sharply as a result of this episode of strabismic vision. 3. When these kittens were revived and allowed to experience a recovery period of normal binocular vision lasting either 3 or 7 wk, cortical binocularity returned to a normal level. 4. Statistical analysis revealed that the difference in the level of binocularity observed before and after the period of binocular recovery was highly significant, and comparison of the results from kittens allowed only a 3-wk recovery period with those from kittens allowed a 7-wk period indicated that a similar level of recovery was obtained in each group. 5. Histological reconstruction of electrode penetrations indicated that the recovery of binocular receptive fields occurred uniformly across all cortical laminae. 6. These data are discussed in terms of the results from previous recovery experiments, the relationship between cortical binocularity and the ability to maintain binocular fixation, and the possibility that subliminal cortical input plays a role in the recovery of functional binocular cells.

Animals↗

PubMed2002

Effect of strength and speed of torque development on balance recovery with the ankle strategy.

In the event of an unexpected disturbance to balance, the ability to recover a stable upright stance should depend not only on the magnitude of torque that can be generated by contraction of muscles spanning the lower extremity joints but also on how quickly these torques can be developed. In the present study, we used a combination of experimental and mathematical models of balance recovery by sway (feet in place responses) to test this hypothesis. Twenty-three young subjects participated in experiments in which they were supported in an inclined standing position by a horizontal tether and instructed to recover balance by contracting only their ankle muscles. The maximum lean angle where they could recover balance without release of the tether (static recovery limit) averaged 14.9 +/- 1.4 degrees (mean +/- SD). The maximum initial lean angle where they could recover balance after the tether was unexpectedly released and the ankles were initially relaxed (dynamic recovery limit) averaged 5.9 +/- 1.1 degrees, or 60 +/- 11% smaller than the static recovery limit. Peak ankle torque did not differ significantly between the two conditions (and averaged 116 +/- 32 Nm), indicating the strong effect on recovery ability of latencies in the onset and subsequent rates of torque generation (which averaged 99 +/- 13 ms and 372 +/- 267 N. m/s, respectively). Additional experiments indicated that dynamic recovery limits increased 11 +/- 14% with increases in the baseline ankle torques prior to release (from an average value of 31 +/- 18 to 54 +/- 24 N. m). These trends are in agreement with predictions from a computer simulation based on an inverted pendulum model, which illustrate the specific combinations of baseline ankle torque, rate of torque generation, and peak ankle torque that are required to attain target recovery limits.

Adolescent↗

PubMedDate not supplied

Noradrenergic pharmacotherapy, intracerebral infusion and adrenal transplantation promote functional recovery after cortical damage.

The research described in this review briefly summarizes evidence that short term pharmacological enhancement of noradrenergic (NA) synaptic activity, combined with symptom relevant experience (SRE), promotes functional recovery of some symptoms of cortical damage in rat, cat and human beings even when treatment is initiated from days to weeks after injury. A summary is provided of the numerous drugs tested in rodent cortical injury models which have been proven useful for predicting beneficial or harmful effects on behavioral outcome in human stroke. The pattern of drug effects indicates a central role for NA in functional recovery. Additionally, studies of the effects of direct intraventricular infusion of monoamine neurotransmitters are reviewed and further support the hypothesized role of NA in recovery from some symptoms of cortical injury. The site of NA/SRE interaction to promote recovery from hemiplegia apparently involves the cerebellar hemisphere contralateral to the cortical injury. Microinfusions of NA into the contra- but not ipsilateral cerebellar hemisphere dramatically enhance recovery. Furthermore, like its systemic action, microinfusion of the alpha 1-NA receptor antagonist, phenoxybenzamine, reinstates hemiplegia. A "permanent" symptom of motor cortex injury in the cat is the complete loss of tactile placing contralateral to the injury which does not spontaneously recover for as long as seven years after ablation. This postural reflex is temporarily restored for 8-12 hours following amphetamine administration. However, this permanently lost reflex can be enduringly restored by transplanting catecholamine secreting adrenal tissue into the wound cavity. The experiment is reviewed in detail and involves chromaffin cell autografts into the frontal cortex ablation wound cavity producing a restoration of tactile placing for the 7-10 month duration of the study. This enduring restoration of tactile placing is considered a result of the release of catecholamines into the CNS from the grafted chromaffin cells found, by histochemical methods, surviving 7-10 months after transplant. Lastly, we attribute these delayed treatment effects to an attenuation of a diaschisis, or remote functional depression, in morphologically intact areas anatomically connected to the area of injury. The widespread reduction of glycolytic and oxidative metabolism, produced by focal cortical injury, is normalized by the same treatment which alleviates symptoms and is worsened by drugs which exacerbate deficits. These data support the hypothesis that providing SRE during a period of enhanced NA synaptic activity produces an enduring functional recovery after cortical injury by attenuating remote functional depression. This treatment for enhancing recovery is especially attractive since it is effective even when begun weeks after cortical damage.

Adrenal Glands↗

PubMed2006

Hypoglycaemia-insulin test: discordant growth hormone and cortisol response in paediatric patients regarding recovery from hypoglycaemia with or without oral glucose solution.

BACKGROUND: Hypoglycaemia-insulin test (HIT) is the 'gold standard' for the diagnosis of adrenal-pituitary-hypothalamic axis disorders. Controversy exists on the convenience of recovery from an insulin-induced hypoglycaemia since this test is not risk-free. OBJECTIVE: To ascertain whether recovery from insulin-induced hypoglycaemia with an oral glucose solution produces a different response of growth hormone (GH) and cortisol at different times of the study compared with spontaneous recovery from hypoglycaemia. PATIENTS AND METHODS: Prospective study of 100 children and adolescents with growth delay who underwent an HIT. Patients were consecutively assigned to two groups of 50. In one group recovery from hypoglycaemia occurred spontaneously and in the other recovery was achieved with an oral glucose solution (20 g of glucose) when glycaemia was under 30 mg/dl. The two groups did not differ in age, sex, pubertal status, weight, height and IGF-I levels. RESULTS: The response of GH at 30, 60, 90 and 120 min and cortisol at 10, 60, 90 and 120 min was lower and statistically significant in patients with recovery from hypoglycaemia with oral glucose solution. GH deficiency was diagnosed more frequently in patients recovered with glucose solutions (94%) compared to those with spontaneous recovery (68%). CONCLUSIONS: Oral glucose solution administration when glycaemia was under 30 mg/dl in HIT produced a lower GH and cortisol response to insulin stimulus and a greater frequency of GH deficit diagnosis.

Adolescent↗

PubMed2000

ST-Segment recovery adds to the assessment of TIMI 2 and 3 flow in predicting infarct wall motion after thrombolytic therapy.

BACKGROUND: Early resolution of ST-segment elevation (ST-segment recovery) is associated with an improved outcome after infarction. Whether this relation is present in patients with Thrombolysis In Myocardial Infarction (TIMI) grade 2 or 3 flow (ie, patent) infarct-related arteries is not known. METHODS AND RESULTS: To examine the associations between time to achieve stable 50% ST-segment recovery assessed by continuous ECG monitoring, infarct artery flow, and infarct zone wall motion (at 48 hours), we studied 134 patients who underwent angiography at 99 (interquartile range 92 to 110) minutes after commencing streptokinase, initiated within 12 hours of onset of symptoms of myocardial infarction. Patients with TIMI 2 or 3 flow who failed to achieve early stable ST-segment recovery (50% ST-segment recovery sustained for > or 4 hours with <100 microV change in the peak lead) by 60 or 90 minutes had a higher fraction of chords in the infarct zone >2 SD below normal wall motion (TIMI 2: 55.5% vs 15.3%, P=0.006; and 56.5% vs 26.8%, P=0.01, respectively; and TIMI 3: 48.8% vs 28.3%, P=0.07; and 51.8% vs 29.9%, P=0.03, respectively). Time to stable ST-segment recovery was a multivariate predictor of infarct zone wall motion (P=0.04) independent of TIMI flow grade and the time from symptom onset to streptokinase therapy. CONCLUSIONS: In patients with TIMI 2 or 3 flow in infarct-related artery, early stable ST-segment recovery is associated with improved infarct zone wall motion at 48 hours. ST-segment recovery may provide additional information about the degree of myocyte reperfusion achieved in patients with a patent epicardial infarct-related artery after thrombolytic therapy.

Aged↗

PubMed1988

Postsystolic shortening of acutely ischemic canine myocardium predicts early and late recovery of function after coronary artery reperfusion.

Postsystolic shortening and thickening of ischemic and postischemic myocardium are well-recognized phenomena, but their significance is controversial. To discover whether postsystolic shortening and thickening might represent an active process and to establish their place as possible predictors of functional recovery during and after recovery from ischemia, we examined correlations in severely ischemic dyskinetic myocardial segments in 14 open-chest anesthetized dogs (90 minutes' ischemia, n = 9; 180 minutes' ischemia, n = 5) between the magnitudes of postsystolic shortening and thickening during ischemia and either the magnitudes of systolic shortening and thickening in the same segments before coronary occlusion or the magnitudes of shortening and thickening at 30-60 minutes and at 2-3 weeks after reperfusion. We found positive correlations between preocclusion shortening and postsystolic shortening (r = 0.44, n = 33 myocardial segments; p less than 0.02) and between preocclusion thickening and postsystolic thickening (r = 0.73, n = 13 segments; p less than 0.01), both measured at 5 minutes after onset of ischemia. Strong correlations were found also between postsystolic shortening and thickening measured immediately before reperfusion and systolic shortening and thickening measured after recovery at 2-3 weeks (r = 0.73, n = 28; p less than 0.001 for shortening; r = 0.79, n = 12; p less than 0.01 for thickening). Significant but less-exact correlations were found between postsystolic shortening and thickening measured immediately before reperfusion and early recovery of shortening and thickening at 30-60 minutes after reperfusion (during the "stunned myocardium" period). Postsystolic shortening and thickening persisted early after reperfusion in dogs that had had 90 minutes of ischemia, and this predicted further significant return of function at 2-3 weeks. However, dogs that had had 180 minutes of ischemia did not have postsystolic shortening or thickening during early recovery and showed no further return of function at 2-3 weeks. The magnitudes of postsystolic shortening and thickening immediately before reperfusion were better predictors of late return of function than the histological appearance of the ischemic segments at 2-3 weeks or the magnitude of their blood flow during ischemia (15 +/- 3 micron microspheres). From correlations made immediately before reperfusion with those at functional recovery after reperfusion, we conclude that postsystolic shortening and thickening of dyskinetic myocardial segments are markers of their potential for recovery.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Continuous 12-lead ST-segment recovery analysis in the TAMI 7 study. Performance of a noninvasive method for real-time detection of failed myocardial reperfusion.

BACKGROUND: If a practical, reliable, noninvasive marker of failed reperfusion was available in real time, the benefits of further therapy in this patient subgroup could be tested. We developed a method of 12-lead ST-segment recovery analysis using continuously updated reference points to provide such a marker. METHODS AND RESULTS: In this study, our method was prospectively tested in 144 patients given thrombolytic therapy early in myocardial infarction. All patients had 12-lead continuous ST-segment monitoring and acute angiography, each analyzed in an independent, blinded core laboratory. ST-segment recovery and re-elevation were analyzed up to the moment of angiography, at which time patency was predicted. Predictions were correlated to angiographic infarct artery flow, with TIMI flow 0 to 1 as occluded and TIMI flow 2 to 3 as patent. Infarct artery occlusion was seen on first injection in 27% of patients. The positive predictive value of incomplete ST recovery or ST re-elevation by our method was 71%, negative predictive value 87%, with 90% specificity and 64% sensitivity for coronary occlusion. ST recovery analysis predicted patency in 94% of patients with TIMI 3 flow versus 81% of patients with TIMI 2 flow and predicted occlusion in 57% of patients with collateralized occlusion versus 72% of patients with non-collateralized occlusion. In a regression model including other noninvasive clinical descriptors, ST recovery alone contained the vast majority of predictive information about patency. CONCLUSIONS: In a blinded, prospective, angiographically correlated study design, 12-lead continuous ST-segment recovery analysis shows promise as a practical noninvasive marker of failed reperfusion that may contribute substantially to currently available bedside assessment. Our data also suggest that patients with TIMI 2 flow or with collateralized occlusions may represent a physiological spectrum definable with ST-segment recovery analysis.

Adolescent↗

PubMed1995

Prolonged kinetics of recovery of oxygen consumption after maximal graded exercise in patients with chronic heart failure. Analysis with gas exchange measurements and NMR spectroscopy.

BACKGROUND: Patients with chronic heart failure (CHF) often complain of prolonged dyspnea after exercise. The determinants of oxygen consumption after exercise in these patients are unknown. We hypothesized that the kinetics of oxygen consumption recovery after graded exercise was prolonged in parallel with the recovery of muscle energy stores, was not affected by the exercise level, and could be used to assess the circulatory response to exercise. METHODS AND RESULTS: Seventy-two patients with CHF in Weber's class A (n = 28), B (n = 21), and C/D (n = 23) and 13 healthy subjects performed maximal upright bicycle exercise with breath-by-breath respiratory gas analysis. Kinetics of recovery of ventilation (VE), oxygen consumption (VO2), and CO2 production (VCO2) after exercise were characterized by T1/2, the time to reach 50% of the peak value. T1/2 VO2 (seconds) increased with the severity of CHF (97 +/- 17 for CHF A [P < .05 versus CHF B, P < .05 versus CHF C/D], 119 +/- 22 for CHF B [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF C/D], 155 +/- 55 for CHF C/D [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF B] compared with 77 +/- 17 for control subjects). T1/2 VCO2 and T1/2 VE also increased similarly with the worsening of CHF. T1/2 VO2 was correlated negatively with peak VO2 (r = .65) and was reproducible (r = .96). To study the relation between T1/2 VO2 and the duration of exercise, 10 healthy subjects and 22 patients underwent a second graded test at 75% and/or 50% of peak workload. T1/2 VO2 was minimally shortened, at only 50% of peak workload (P = .02). Finally, 19 patients underwent 31P nuclear magnetic resonance spectroscopy of the anterior compartment of the leg during exercise; the half-time of recovery of the ratio of inorganic phosphate to creatine phosphate (T1/2 Pi/PCr), reflecting the level of involvement of oxidative metabolism in the restoration of energetic metabolites after exercise, was linearly correlated with the half-time of VO2 recovery (r = .70, P < .01). CONCLUSIONS: Postexercise T1/2 VO2 increases when CHF worsens, perhaps in part a result of slower kinetics of recovery of muscle energy stores. The time course of oxygen consumption recovery may represent a simple new criterion for measuring the impairment of the circulatory response to exercise in CHF, even submaximal exercise.

Adult↗