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Relationship between different recovery curves representing rate-dependent AV nodal function in rabbit heart.

INTRODUCTION: The rate-dependent changes in atrioventricular (AV) nodal conduction time show different characteristics depending upon whether the conduction times are plotted against the atrial interval (AA-recovery curve) or His-atrial interval (HA-recovery curve). This study characterizes these differences in the context of controlled changes of nodal functional properties, determines their functional significance, and tests the hypothesis that they are related solely to the nodal conduction time of the last beat (last conduction time) before the premature beat. METHODS AND RESULTS: Premature nodal conduction times obtained in isolated rabbit heart preparations under various steady-state and transient conditions were plotted as a function of the corresponding HA and AA intervals, as well as the AA interval corrected for the last conduction time. Under all conditions, the corrected AA-recovery curve was indistinguishable in shape from the HA-recovery curve, and as such reflected similar underlying nodal functional properties. Moreover, a selective increase in the last conduction time, induced in the absence of time-dependent effects associated with the functional property of fatigue, shifted the AA-recovery but not the HA-recovery curve upward with respect to the control curve. CONCLUSION: The last conduction time accounts entirely for differences between AA-recovery and HA-recovery curves that otherwise reflect the same underlying nodal functional state. Thus, a consistent assessment of rate-dependent changes in nodal function can be achieved with either measure of recovery time.

Animals↗

Effects of electrolyte and glycerol supplementation on recovery from endurance exercise.

Incomplete recovery from endurance exercise after an overnight rest period is reflected by persisting weight loss and an elevated plasma aldosterone concentration, even in successful competitors. To determine whether supplementation with high doses of electrolytes, with or without glycerol, enhances recovery, the following were measured in 6 Arabian horses before and after completion of a 60 km treadmill exercise test simulating an endurance ride and after 12, 24, 48, and 72 h of recovery: bodyweight; plasma osmolality; plasma concentrations of protein, electrolytes, aldosterone and cortisol; and urine and faecal electrolyte concentrations. Before and during the exercise test, horses were supplemented with a total of 2.4 ml/kg bwt of water (W); 0.2 g/kg bwt KCl and 0.4 g/kg bwt NaCl in 2.4 ml/kg bwt of water (E); or 0.2 g/kg bwt KCl and 0.4 g/kg bwt NaCl in 2.4 ml/kg bwt (3 g/kg bwt) of glycerol (GE). Although weight loss after completion of the simulated ride was greater (P < 0.01) for W (3.2%) than for E and GE (1.0 and 0.9%, respectively), horses supplemented with E or GE experienced further weight loss by 24 h after the simulated ride (2.2 and 2.1% for E and GE, respectively) while bodyweight with W remained unchanged (3.0%) from the finish value. After 48 h of recovery, bodyweight was not different from the starting values with E and GE but remained decreased (P < 0.01) with W throughout the recovery period (2.2% persisting weight loss after 72 h of recovery). Plasma osmolality and plasma Na+ and Cl- concentrations increased (P < 0.01) and plasma protein concentration decreased (P < 0.01) after the exercise test with E and GE but were unchanged with W. Plasma osmolality and protein and electrolyte concentrations returned to pre-exercise values within 12 h of recovery with the exception of a persistent increase in plasma Na+ concentration with GE. The greatest plasma aldosterone concentration was measured after 12 h of recovery with W (1357 pmol/l) and was greater (P < 0.02) than that with E and GE (24 and 304 pmol/l, respectively). Urine production during the simulated ride increased (P < 0.01) with GE and resulted in loss of approximately 20% and essentially 100% of supplemented Na+ and K+, respectively. In contrast, electrolyte losses in faeces were unaffected by electrolyte or glycerol supplementation. In conclusion, supplementation with high doses of electrolytes as hypertonic oral pastes attenuated weight loss during a simulated endurance ride (by enhancing voluntary water intake); however, it did not prevent development of significant weight loss during the initial 24 h of recovery. Glycerol administration resulted in no benefits, and actually increased urine electrolyte losses, in comparison to supplementation with electrolytes alone.

Animal Feed↗

Ovarian hormone status and skeletal muscle inflammation during recovery from disuse in rats.

Resumption of normal muscle loading after a period of disuse initiates cellular processes related to mass accretion. The renewed loading also induces a significant amount of muscle damage and subsequent inflammation. Ovarian hormone depletion delays atrophied myofibre mass recovery. Ovarian hormones are also global regulators of immune system function. The purpose of this study was to determine whether ovarian hormone depletion-induced deficits in myofibre regrowth after disuse atrophy are related to the induction of muscle damage and the associated inflammatory response. We hypothesized that soleus muscle immune cell infiltration and inflammatory gene expression would be both accentuated and prolonged in ovarian hormone-depleted rats during the first week of recovery from disuse atrophy. Intact and ovariectomized (OVX) female rats were subjected to hindlimb suspension for 10 days and then returned to normal ambulation for a recovery period, the rats were killed and the soleus muscle removed for analysis. Although reloading increased both circulating creatine kinase and myofibre membrane disruption, there was no effect of ovarian hormones on these processes during recovery. Muscle neutrophil concentration was increased above baseline regardless of hormone status at days 1 and 3 of recovery; however, this increase was 43% greater at day 3 in the OVX group. Muscle ED1+ and ED2+ macrophage concentrations were increased during recovery in both groups. However, macropage concentrations remained elevated at day 7 of recovery in the OVX group, whereas they returned to control levels in the intact group. Cyclo-oxygenase-2, interleukin-6 and interleukin-1beta muscle mRNA expression increased similarly during recovery, regardless of ovarian hormone status. These results demonstrate that the initial myofibre damage and inflammatory gene expression induced during muscle recovery from disuse atrophy are independent of ovarian hormone status.

Animals↗

The rate of recovery of vision after early monocular deprivation in kittens.

1. Fifteen kittens were monocularly deprived of vision by suturing the lids of the right eye together for various periods of time at different ages. A simple behavioural technique was used to assess the immediate effects of the period of monocular deprivation on the visual acuity of the deprived eye as well as the time course of any subsequent recovery.2. The extent of the recovery of vision was measured under conditions where the animal was either forced to use its deprived eye by performing a reverse suture or where the animal had both eyes open after the initial period of monocular occlusion.3. The initial effects of monocular deprivation were graded in severity according to the age at which the deprivation was imposed, ranging from apparent blindness in animals deprived at 6 weeks of age to only a small loss of acuity in kittens deprived at 12 weeks of age.4. The effects of deprivation imposed from birth were particularly severe, leading to a temporary blindness. Nevertheless after a period of time that became progressively longer with increasing deprivation, all animals showed some recovery of pattern vision over the course of the next 2 or 3 months. The extent of this recovery became progressively less as the period of deprivation was prolonged. There was even some recovery of vision (an acuity of 2.5 cycles/deg) in animals that were deprived throughout the duration of the ;critical period' to 4 months of age.5. Direct comparison of the rate of behavioural recovery between animals that were reverse sutured with that of litter-mates that received binocular input after monocular occlusion to either 45 or 60 days of age proved to be remarkably similar, although the acuity that was eventually attained by the reverse sutured animals was always slightly higher.6. The recoveries observed after reverse suturing were reasonably well correlated with changes observed in the ocular dominance of visual cortical cells under similar circumstances.7. Although the recovery in these animals can be accounted for by the simple notion of a competitive interaction between the two eyes, the recovery observed in animals that had both eyes open after the initial period of deprivation cannot be so readily explained. Evidently there must be an additional non-competitive mechanism of recovery.

Age Factors↗

The effect of lactate on intracellular pH and force recovery of fatigued sartorius muscles of the frog, Rana pipiens.

1. The effects of pHo (extracellular pH) and lactic acid on pHi (intracellular pH) and tetanic force were examined in frog sartorius muscle. Ion-selective microelectrodes were used to measure pHi. Tetanic force was elicited by field stimulation. Experiments were performed in HEPES-buffered solution equilibrated with 100% O2. 2. Mean pHi values (+/- S.E.M.) of unfatigued frog sartorius muscles were 7.14 +/- 0.02 and 7.05 +/- 0.09 at pHo 7.2 and 6.4, respectively. 3. A stimulation at a rate of one 100 ms tetanic contraction per second for 3 min reduced pHi to 6.21 +/- 0.09 and 6.20 +/- 0.04 at pHo 7.2 and 6.4, respectively. Meanwhile at pHo 7.2, the tetanic force (defined as the maximum force developed during a tetanus) decreased by 82.9 +/- 2.6%, the maximum rate of relaxation decreased by 92.9 +/- 0.9%, and the rate constant of the relaxation decreased by 88.5 +/- 1.6%. At pHo 6.4, the decrease in tetanic force, maximum rate of relaxation and rate constant were 90.6 +/- 1.8%, 93.8 +/- 0.5 and 87.5 +/- 2.7%, respectively. 4. The maximum rates of recovery of pHi following fatigue were 0.068 +/- 0.05 and 0.025 +/- 0.05 pH units min-1 at pHo 7.2 and 6.4, respectively. Recovery of normal tetanic force and relaxation rate was also slower at acidic pHo than at neutral pHo. 5. In the presence of 40 mmol l-1 L-lactic acid at pHo 7.2, the maximum rate of pHi recovery following fatigue was only 0.027 +/- 0.03 pH units min-1 at pHo 7.2. The presence of lactic acid also reduced the recovery of the relaxation phase, but not the recovery of tetanic force. 6. It is suggested that pHi recovery is not a limiting factor for tetanic force recovery and that the extracellular H+ inhibits tetanic force recovery by acting at a site located on the outer surface of the sarcolemma. The recovery of the relaxation phase is believed to be pHi dependent.

Animals↗

Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man.

1. The recovery of power output and muscle metabolites was examined following maximal sprint cycling exercise. Fourteen male subjects performed two 30 s cycle ergometer sprints separated by 1.5, 3 and 6 min of recovery, on three separate occasions. On a fourth occasion eight of the subjects performed only one 30 s sprint and muscle biopsies were obtained during recovery. 2. At the end of the 30 s sprint phosphocreatine (PCr) and ATP contents were 19.7 +/- 1.2 and 70.5 +/- 6.5% of the resting values (rest), respectively, while muscle lactate was 119.0 +/- 4.6 mmol (kg dry wt)-1 and muscle pH was 6.72 +/- 0.06. During recovery, PCr increased rapidly to 65.0 +/- 2.8% of rest after 1.5 min, but reached only 85.5 +/- 3.5% of rest after 6 min of recovery. At the same time ATP and muscle pH remained low (19.5 +/- 0.9 mmol (kg dry wt)-1 and 6.79 +/- 0.02, respectively). Modelling of the individual PCr resynthesis using a power function curve gave an average half-time for PCr resynthesis of 56.6 +/- 7.3 s. 3. Recovery of peak power output (PPO), peak pedal speed (maxSp) and mean power during the initial 6 s (MPO6) of sprint 2 did not reach the control values after 6 min of rest, and occurred in parallel with the resynthesis of PCr, despite the low muscle pH. High correlations (r = 0.71-0.86; P < 0.05) were found between the percentage resynthesis of PCr and the percentage restoration of PPO, maxSp and MPO6 after 1.5 and 3 min of recovery. No relationship was observed between muscle pH recovery and power output restoration during sprint 2 (P > 0.05). 4. These data suggest that PCr resynthesis after 30 s of maximal sprint exercise is slower than previously observed after dynamic exercise of longer duration, and PCr resynthesis is important for the recovery of power during repeated bouts of sprint exercise.

Adenosine Triphosphate↗

Whole body and leg acetate kinetics at rest, during exercise and recovery in humans.

We have used a constant [1,2-(13)C]acetate infusion (0.12 micromol x min(-1) x kg( 1)) for 2 h at rest, followed by 2 h of one-legged knee-extensor exercise at 65% of leg maximal workload, and 3 h of recovery in six post-absorptive volunteers to quantify whole-body and leg acetate kinetics and determine whether the whole-body acetate correction factor can be used to correct leg substrate oxidation. The acetate whole-body rate of appearance (R(a)) was not significantly different at rest, during exercise or during recovery (365-415 micromol x min(-1)). The leg net acetate uptake was similar at rest and during recovery (approximately 10 micromol x min(-1)), but increased approximately 5-fold with exercise. At rest the leg acetate uptake (approximately 15 micromol x min(-1)) and release (approximately 5 micromol x min(-1)) accounted for 4 and 1.5 % of whole-body acetate disposal (R(d)) and R(a), respectively. When the leg acetate kinetics were extrapolated to the total body skeletal muscle mass, then skeletal muscle accounted for approximately 16 and approximately 6% of acetate R(d) and R(a). With exercise, leg acetate uptake increased approximately 6-fold, whereas leg acetate release increased 9-fold compared with rest. Whole-body acetate carbon recovery increased with time of infusion at rest and during recovery from 21% after 1.5 h of infusion to 45% in recovery after 7 h of infusion. Leg and whole-body acetate carbon recovery were similar under resting conditions, both before and after exercise. During exercise whole-body acetate carbon recovery was approximately 75%, however, acetate carbon recovery of the active leg was substantially higher (approximately 100%). It is concluded that inactive skeletal muscle plays a minor role in acetate turnover. However, active skeletal muscle enhances several-fold acetate uptake and subsequent oxidation, as well as release and its contribution to whole-body acetate turnover. Furthermore, under resting conditions the whole-body acetate correction factor can be used to correct for leg, skeletal muscle, substrate oxidation, but not during exercise.

Acetates↗

Adaptation and recovery from adaptation in single fiber responses of the cat auditory nerve.

This study examined the time course of adaptation and recovery from adaptation of single auditory-nerve fiber responses. The conditions studied were: (1) adaptation response using low level, 800 Hz or characteristic frequency (CF) stimuli; and (2) onset recovery and whole tone response recovery of a probe tone following a masker of equal frequency with variable silent intervals between the masker offset and probe onset. Single unit responses to 290 ms long, 800 Hz or CF tones presented at 10-30 dB SL were recorded from the auditory nerve of the cat. Adaptation properties were determined and fit to the equation: A(tp) = Yre(-tp/tau Rr) + Yse(-tp/tau Rs) + Ass. Recovery from adaptation was determined by recording the response of a probe tone following a 100-ms masker tone equal in frequency to the probe, and with amplitudes ranging from 20- to 30-dB relative to the probe amplitude. Both the onset recovery and the whole tone recovery were determined for the single unit responses. The onset data were analyzed and fit to either the equation: A (delta xt,tp) = Ass - Yre(-tp/tau Rr) - Yse(- delta t/tau Rs) or A (delta t,tp) = Ass - Yre(- delta t/tau R). The whole tone response showed two distinctive time patterns that could be fit to either an adaptation equation or to the two-time-constant recovery equation, depending on the relative amplitude of the masker and the length of the silent interval between masker offset and probe onset. The results of this study indicate that single fiber time constants are comparable to those measured in previous studies using the auditory-nerve neurophonic (ANN). Likewise, the pattern of recovery of the whole tone response for single fiber responses is comparable to the ANN. Possible sites and mechanisms for adaptation and recovery from adaptation taking into account recent data from electrical stimulation studies and receptor channel morphology and kinetics are discussed.

Animals↗

Influence of pre-exercise acidosis and alkalosis on the kinetics of acid-base recovery following intense exercise.

The purpose of this study was to measure the recovery kinetics of pH and lactate for the conditions of pre-exercise acidosis, alkalosis, and placebo states. Twelve trained male cyclists completed 3 exercise trials (110% workload at VO2max), ingesting either 0.3 g/kg of NH4Cl (ACD), 0.2 g/kg of Na+HCO3- and 0.2 g/kg of sodium citrate (ALK), or a placebo (calcium carbonate) (PLAC). Blood samples (heated dorsal hand vein) were drawn before, during, and after exercise. Exercise-induced acidosis was more severe in the ACD and PLAC trials (7.15 +/- 0.06, 7.21 +/- 0.07, 7.16 +/- 0.06, P < 0.05, for ACD, ALK, PLAC, respectively). Recovery kinetics for blood pH and lactate, as assessed by the monoexponential slope constant, were not different between trials (0.057 +/- 0.01, 0.050 +/- 0.01, 0.080 +/- 0.02, for ACD, ALK, PLAC, respectively). Complete recovery of blood pH from metabolic acidosis can take longer than 45 min. Such a recovery profile is nonlinear, with 50% recovery occurring in approximately 12 min. Complete recovery of blood lactate can take longer than 60 min, with 50% recovery occurring in approximately 30 min. Induced alkalosis decreases metabolic acidosis and improves pH recovery compared to acidodic and placebo conditions. Although blood pH and lactate are highly correlated during recovery from acidosis, they recover at significantly different rates.

Acid-Base Equilibrium↗

Temperature-sensitive recovery of a mutant of Escherichia coli K-12 irradiated with ultraviolet light.

URT-43 is a mutant of Escherichia coli K-12 which gives a much larger number of survivors when ultraviolet (UV)-irradiated bacteria are incubated on agar medium at 30 C than when they are incubated on the medium at 41 C, although in both cases the number of survivors is fewer than that given by its wild-type ancestor. The UV sensitivity of this mutant was found to be markedly influenced by the presence of a high concentration of NaCl or sucrose in the plating medium. Thus, when irradiated bacteria were plated on agar medium containing 2% NaCl or 0.5 m sucrose at 30 C, they exhibited a resistance similar to that of their wild-type ancestor. At 30 C, there was also an extensive recovery in liquid M9 medium supplemented with all of the nutrients required for growth and NaCl or sucrose. At 41 C, however, the recovery was greatly inhibited. Direct chemical analysis of thymine dimers has revealed that no significant amount of the dimer was released from deoxyribonucleic acid during the period of extensive recovery. It was concluded, therefore, that the temperature-sensitive recovery of URT-43 does not accompany excision of the bulk of pyrimidine dimers. To learn the gene function involved in the recovery, double mutants carrying an additional mutation either in a uvr or a rec gene have been investigated for their UV sensitivities and recovery in liquid medium. It was found that recA(-) and recB(-) derivatives retain the ability of undergoing an efficient recovery at a low temperature, whereas uvrB(-) and uvrC(-) derivatives have completely lost this ability. For these reasons, it was concluded that the mechanism responsible for the recovery of URT-43 involves the function controlled by the uvr genes. The results of photoreactivation suggested that most of the entities dealt with during recovery were pyrimidine dimers.

Agar↗

Comparative study of selective media for recovery of Yersinia enterocolitica.

To determine the relative efficacy of pectin agar, cellobiose-arginine-lysine (CAL) agar, Y medium, cefsulodin-irgasan-novobiocin (CIN) agar, MacConkey (MAC) agar, and salmonella-shigella (SS) agar for the recovery of Yersinia enterocolitica, 35 strains of this organism representing the serotypes most commonly associated with human disease in Canada and the United States were inoculated on test media in pure cultures and mixed in fecal specimens. Randomly picked stool specimens were also cultured on these media to determine their selectivity. The ability of test media to support the growth of Y. enterocolitica strains varied markedly. Several strains failed to grow on Y medium, and a few failed to grow on SS agar. There were no significant differences in cultural characteristics and the recovery rates of Canadian and American strains. The combined recovery of the pure cultures of Y. enterocolitica on test media as compared with blood agar was MAC, 75%; SS, 48%; pectin, 70%; CAL, 62%; Y, 15%; and CIN, 85%. The selectivity of the test media expressed as the percent difference of the fecal colony counts obtained on blood agar and the selective media was MAC, 7%; SS, 50%; pectin, 4%; CAL, 65%; Y, >/=99.9%; and CIN, 95%. When stool suspensions containing 10(2) colony-forming units of the test strains were plated, CIN medium yielded 100% recovery of all 35 strains from all fecal samples. The combined recovery rate for other media was CAL, 63%; Y, 14%; and SS, 11%. With 10(1) colony-forming units, CIN yielded a 100% recovery of the test strains, whereas CAL, Y, and SS agar showed a 0% recovery. None of the test organisms was recovered on either MAC or pectin agar at either dilution. The inhibitory effect of Y medium for Y. enterocolitica could be overcome to some extent by reducing the sodium oxalate and sodium desoxycholate content of the medium. One such modified Y medium offered optimum selectivity and ensured greater recovery of Y. enterocolitica when compared with the Y medium. We found CIN agar by far the most effective medium for the recovery of Y. enterocolitica. This medium was highly selective and almost completely inhibited the fecal flora, while at the same time supporting luxuriant growth of Y. enterocolitica. On CIN agar, Y. enterocolitica colonies were distinctive in appearance and measured 1.5 to 4 mm in diameter within 20 to 40 h of incubation.

Culture Media↗

In vitro comparison of NALC-NaOH, tween 80, and C18-carboxypropylbetaine for processing of specimens for recovery of mycobacteria.

A recent article (C. G. Thornton et al., J. Clin. Microbiol. 36:1996-2003, 1998) reported a new specimen-processing method for improved recovery of mycobacteria. This method used C18-carboxypropylbetaine (CB-18) and increased both smear and culture sensitivity. The companion article (C. G. Thornton et al., J. Clin. Microbiol. 36:2004-2013, 1998) described initial improvements to this method. Additional significant parameters of the CB-18 processing method are identified herein. First, eliminating the incubation step was shown to further improve culture sensitivity. Subsequently, recovery of several mycobacterial isolates by the CB-18 method was compared to a contemporary processing method that combines NALC and NaOH (NALC-NaOH) and a Tween 80-based method. Recovery of the tuberculous isolates following NALC-NaOH processing averaged 20% and ranged from 1.6 to 45%, whereas recovery of the nontuberculous isolates averaged 11% and ranged from 0.1 to 55%. Recovery of the tuberculous and nontuberculous isolates by the Tween 80-based method ranged from 22 to 92% and 27 to 93%, respectively, with averages of 58 and 65%, respectively. Recovery of the tuberculous and nontuberculous mycobacteria following CB-18 processing averaged 86 and 73%, respectively, with ranges from 61 to over 100% and from 43 to over 100%, respectively. Other parameters of the CB-18 method were also examined, including recovery versus CB-18 concentration and the relationship between CB-18 concentration and the tuberculocidal effect. The tuberculocidal effect was time dependent but independent of concentration, whereas recovery was directly proportional to concentration. Increasing the CB-18 concentration to 4 mM provided quantitative recovery on solid medium; however, higher concentrations of CB-18 were not compatible with liquid culture. Examination of the relationship between increasing CB-18 and lecithin concentrations suggested that lecithin could not overcome the deleterious effects of CB-18 in liquid culture at these higher concentrations.

Acetylcysteine↗

Photostress recovery in chronic open angle glaucoma.

Photostress recovery time was measured in 30 eyes from 15 patients with chronic open angle glaucoma, and 30 eyes from 15 individuals of a similar age group with no ophthalmological disorder. The average recovery time in patients with glaucoma was 70.47 (SD 35.39) seconds. The average recovery time in the control population was 41.97 (SD 17.34) seconds. This difference was statistically significant (p less than 0.001). There was a small positive correlation between age and recovery time in the control population, whereas there was no correlation between age and recovery time in the glaucoma group. There was no correlation between visual acuity and recovery time for either group. There was also no correlation between intraocular pressure and recovery time for the glaucoma group. It was not possible to control for pupillary dilatation in this study. However, it has been previously demonstrated that pharmacological meiosis will not delay photostress recovery time in normal subjects. This is the first report of photostress recovery testing in patients with chronic open angle glaucoma. The results are discussed in terms of the pathophysiology of glaucoma and previous photostress studies in patients with macular disease.

Adult↗

Effect of different intensities of active recovery on sprint swimming performance.

Active recovery reduces blood lactate concentration faster than passive recovery and, when the proper intensity is applied, a positive effect on performance is expected. The purpose of the study was to investigate the effect of different intensities of active recovery on performance during repeated sprint swimming. Nine male well-trained swimmers performed 8 repetitions of 25 m sprints (8 x 25 m) interspersed with 45 s intervals, followed by a 50 m sprint test 6 min later. During the 45 s and 6 min interval periods, swimmers either rested passively (PAS) or swam at an intensity corresponding to 50% (ACT50) and 60% (ACT60) of their individual 100 m velocity. Blood lactate was higher during PAS compared with ACT50 and ACT60 trials (p < 0.05), whereas plasma ammonia and glycerol concentration were not different between trials (p > 0.05). Mean performance time for the 8 x 25 m sprints was better in the PAS compared with the ACT50 and ACT60 trials (PAS: 13.10 +/- 0.07 vs. ACT50: 13.43 +/- 0.10 and ACT60: 13.47 +/- 0.10s, p < 0.05). The first 25 m sprint was not different across trials (p > 0.05), but performance decreased after sprint 2 during active recovery trials (ACT50 and ACT60) compared with the passive recovery (PAS) trial (p < 0.05). Performance time for the 50 m sprint performed 6 min after the 8 x 25 m sprints was no different between trials (p > 0.05). These results indicate that active recovery at intensities corresponding to 50% and 60% of the 100 m velocity during repeated swimming sprints decreases performance. Active recovery reduces blood lactate concentration, but does not affect performance on a 50 m sprint when 6 min recovery is provided. Passive recovery is advised during short-interval repeated sprint training in well-trained swimmers.

Adolescent↗

Recovery from maximal effort exercise: lactate disappearance and subsequent performance.

The effects of differing recovery patterns following maximal exercise on blood lactate disappearance and subsequent performance were examined. Nine subjects completed four randomly assigned experimental sessions. Each session consisted of a 5-min maximal effort performance test conducted on a Monark bicycle ergometer (T1) followed by 20 min of recovery and a second 5-min maximal effort performance test (T2). Blood lactate levels were measured during min 5, 10, 15, and 20 of recovery. Recovery patterns consisted of passive recovery (PR), active recovery below anaerobic threshold (AR less than AT), active recovery above anaerobic threshold (AR greater than AT), and active recovery above anaerobic threshold while breathing 100% oxygen (AR greater than AT + O2). Blood lactate levels prior to T2 were significantly different across treatments (P less than 0.05). Comparison among treatments and between T1 and T2 revealed no significant differences in work output. It was concluded that while lactate disappearance following severe exercise can be affected by varying the recovery pattern, elevated levels of blood lactate exert no demonstrable effect on maximal effort performance of 5-min duration.

Adult↗

Effects of mode of exercise recovery on thermoregulatory and cardiovascular responses.

To identify the effects of exercise recovery mode on cutaneous vascular conductance (CVC) and sweat rate, eight healthy adults performed two 15-min bouts of upright cycle ergometry at 60% of maximal heart rate followed by either inactive or active (loadless pedaling) recovery. An index of CVC was calculated from the ratio of laser-Doppler flux to mean arterial pressure. CVC was then expressed as a percentage of maximum (%max) as determined from local heating. At 3 min postexercise, CVC was greater during active recovery (chest: 40 +/- 3, forearm: 48 +/- 3%max) compared with during inactive recovery (chest: 21 +/- 2, forearm: 25 +/- 4%max); all P < 0.05. Moreover, at the same time point sweat rate was greater during active recovery (chest: 0.47 +/- 0.10, forearm: 0.46 +/- 0.10 mg x cm(-2) x min(-1)) compared with during inactive recovery (chest: 0.28 +/- 0.10, forearm: 0.14 +/- 0.20 mg x cm(-2) x min(-1)); all P < 0.05. Mean arterial blood pressure, esophageal temperature, and skin temperature were not different between recovery modes. These data suggest that skin blood flow and sweat rate during recovery from exercise may be modulated by nonthermoregulatory mechanisms and that sustained elevations in skin blood flow and sweat rate during mild active recovery may be important for postexertional heat dissipation.

Adult↗

Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women.

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (Tsk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode (P < 0.05). No differences in either Tes or Tsk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.

Adult↗

Dobutamine echocardiography in myocardial hibernation. Optimal dose and accuracy in predicting recovery of ventricular function after coronary angioplasty.

BACKGROUND: Myocardial hibernation is a condition of chronic left ventricular dysfunction associated with severe coronary artery disease whereby significant recovery of function occurs after revascularization. Identification of hibernating myocardium has important prognostic and therapeutic implications. The presence of contractile reserve as assessed by dobutamine echocardiography may be promising in the detection of hibernation. We designed a prospective study to evaluate the accuracy and optimal dose of dobutamine echocardiography for predicting recovery of ventricular function after angioplasty in patients with stable coronary artery disease and ventricular dysfunction. METHODS AND RESULTS: Twenty patients with stable coronary artery disease and segmental ventricular dysfunction scheduled for coronary angioplasty underwent dobutamine echocardiography before revascularization using incremental doses of 2.5, 5, 7.5, 10, 20, 30, and 40 micrograms/kg per minute every 3 minutes. Digital images of all eight stages were displayed simultaneously (two quad screens side by side) and interpreted using a 16-segment ventricular model and a 6-grade scoring system. Serial resting echocardiograms before, early (< 1 week), and late (> or = 6 weeks) after angioplasty were digitized and randomized in a quad-screen format for the assessment of recovery of function. Wall motion score index in the revascularized regions decreased from 2.86 +/- 0.76 before angioplasty to 2.12 +/- 1.03 late after angioplasty (P < .05). Of 320 ventricular segments, 148 had abnormal wall motion at baseline and 114 were revascularized. Recovery of function (> or = 2 grades) occurred in 25% of revascularized segments early and in 33% late after angioplasty. Of the 34 abnormal segments not revascularized, recovery of function occurred in only 1. During dobutamine echocardiography, abnormal segments exhibited one of four responses: biphasic (improvement at low dose and worsening at high dose) in 28% of segments, sustained improvement (persistent improvement till peak dose) in 18%, worsening in 15%, and no change in 39%. A biphasic response had the highest predictive value (72%) for recovery of function followed by worsening only (35%), while the lowest was seen with a "no-change" or sustained improvement response (13% and 15%). Combining biphasic and worsening responses resulted in a sensitivity of 74% and specificity of 73% for assessment of recovery of individual segments and 90% and 60%, respectively, for functional recovery of individual patients (n = 10). In segments with a biphasic response, the low dose at which improvement in wall motion was most prevalent (84%) was 7.5 micrograms/kg per minute and increased to 94% when the 5 and 7.5 micrograms/kg per minute doses were displayed. The reworsening phase of the biphasic response was usually seen with doses > or = 20 micrograms/kg per minute but was also observed as early as the 7.5 micrograms/kg per minute dose. CONCLUSIONS: The wall motion response during dobutamine echocardiography is useful in the prediction of recovery of ventricular function after revascularization in patients with stable coronary artery disease and ventricular dysfunction. The administration of low as well as high doses of dobutamine is needed for optimal evaluation.

Adult↗