Influence of post-warm-up recovery time on swim performance in international swimmers

ObjectivesSwimmers must enter a marshalling call-room 20 min prior to racing, which results in some swimmers completing their warm-up 45 min pre-race. Since a recovery period longer than 15–20 min may prove problematic, this study examined 200 m freestyle performance after a 20 and 45 min post-warm-up recovery period.DesignEight international swimmers completed this randomised and counter-balanced study.MethodsAfter a standardised warm-up, swimmers rested for either 20 (20 min) or 45 min (45 min) prior to completing a 200 m freestyle time-trial (TT). Core temperature (T_core), blood lactate (BL), heart rate and rate of perceived exertion (RPE) were recorded at baseline, post-warm-up, pre-TT, immediately post-TT and at 3 min post-TT.ResultsT_core was similar after the warm-up under both conditions, however, at pre-TT T_core was greater under 20 min (mean ± SD; 20 min 37.8 ± 0.2 vs. 45 min 37.5 ± 0.2 °C; P = 0.002). BL was similar between conditions at all-time points before the TT (P > 0.05). Swimmers demonstrated a 1.5 ± 1.1% improvement in performance under 20 min (20 min 125.74 ± 3.64 vs. 45 min 127.60 ± 3.55 s; P = 0.01). T_core was similar between conditions at immediately post-TT and 3 min post-TT (P > 0.05), however, BL was higher at these time points under 20 min (P < 0.05). Heart rate and RPE were similar between conditions at all-time points (P > 0.05).Conclusions200 m freestyle performance is faster 20 min post-warm-up when compared to 45 min probably due to better T_core maintenance. This has implications for swim race preparation as warm-up procedures should be completed close to entering the pre-race call room, in order to maintain elevated core temperature.     

The influence of passive heat maintenance on lower body power output and repeated sprint performance in professional rugby league players

Objectives: The pre-competition warm-up mediates many temperature related physiological changes which generally lead to an improvement in performance. However, after ceasing exercise body temperature declines rapidly, which reduces some of the benefits of the initial warm-up. We examined the effects of a passive heat maintenance strategy on post-warm-up core temperature (T_core) and performance in professional rugby league players. Design: Twenty professional rugby league players completed this randomised and counter-balanced study. Methods: After a standardised warm-up, players completed a countermovement jump (CMJ) before resting for 15 min wearing normal training attire (control) or wearing a passive heat maintenance jacket (PHM), players then completed another CMJ and a repeated sprint protocol (RSA). T_core was measured at baseline, post-warm-up, pre-RSA and post-RSA. CMJ were analysed for peak power output (PPO), and RSA for fastest, mean and total sprint time. Results: Post-warm-up T_core (mean ± SD; control 37.70 ± 0.28; PHM 37.70 ± 0.27 °C; p = 0.741) and PPO (control 5220 ± 353 vs. PHM 5213 ± 331 W; p = 0.686) were similar between conditions. At pre-RSA, PHM was associated with greater T_core (control 37.14 ± 0.31 vs. PHM 37.51 ± 0.30 °C; p < 0.001) and PPO (control 4868 ± 345 vs. PHM 5056 ± 344 W; p < 0.001) when compared to control. The decline in PPO from post-warm-up to pre-RSA was related to the drop in T_core (r = 0.71; p < 0.001). During the RSA, fastest, mean and total sprint time were all improved under PHM compared to control (p < 0.05). Conclusions: Passive heat maintenance is an effective method of attenuating the post-warm-up decline in T_core and improves PPO and repeated sprint ability in professional rugby league players.     

Dose response study of lidocaine 1% for spinal anaesthesia for lower limb and perineal surgery

Purpose

To compare the sensory and motor block produced by three different volumes of intrathecal lidocaine 1% and thereby determine the appropriate volume to administer for surgery of the lower limbs and perineum.

Methods

Forty-eight patients scheduled for perineal or lower limb surgery were randomly assigned to receive 4, 6 or 8 ml lidocaine 1% intrathecally. The onset, spread, duration and regression of analgesia and motor block and side effects were evaluated (by a blinded observer whenever possible).

Results

The maximum cephalad spread in the 6 ml (T₈ ± 3) and 8 ml (T₄ ± 1.7) groups were higher than the 4 ml group (T₁₂ ± 2.2,P < 0.01). In the 4 ml group, six patients (33%) did not achieve analgesia to T₁₂ and four (22%) did not have complete motor blockade. Patients given 8 ml had longer duration of block (duration at T₁₂: 104 ± 23vs 60 ± 24, 67 ± 14 min,P < 0.01; 8 mlvs 4, 6 ml) and slower recovery times (sensory recovery: 188 ± 27vs 142 ± 27, 157 ± 28 min,P < 0.01; 8 mlvs 4, 6 ml). Two patients (18%) from the 8 ml group and one (5%) from the 6 ml group had transient hypotension.

Conclusion

Four millilitres intrathecal lidocaine 1% is adequate for perineal surgery but for lower limb procedures, 6 ml is more appropriate as it consistently provides sensory analgesia above L₁ dermatome and complete motor block. Eight ml gives an unnecessarily high block with higher incidence of hypotension.     

Evaluation of adverse effects of vaccines: the case-control approach

When the hypothesis of a link between vaccination and a possible adverse outcome arises, further investigation is required to confirm or refute the suspicion. Given the rarity of most serious adverse effects, a case-control approach will often be chosen. This paper discusses aspects of the design, analysis and interpretation of case-control studies to evaluate vaccine adverse effects. Potential biases (and how to minimise such biases) in the selection of cases and assessment of vaccine exposure and the potential for confounding are discussed. Finally the increasing use of electronic databases in the evaluation of vaccine adverse effects is considered.     

Hydroxyl radical production and lipid peroxidation paralles selective post-ischemic vulnerability in gerbil brain

The salicylate trapping method was used to investigate the changes in hydroxyl radical (·OH) levels in the selectively vulnerable hippocampus compared to the cerebral cortex of gerbils subjected to a 10 min period of near complete forebrain ischemia. Salicylate-derived 2,5-dihydroxybenzoic acid (2,5-DHBA) was measured in sham-operated animals and at 1, 5, and 15 min of reperfusion. A basal level of 2,5-DHBA was also seen in non-ischemic gerbil brain, both in the hippocampus and cortex. The hippocampal basal level was 160% higher than in the cortex (P < .01). Treatment with the cytochrome P450 inhibitor SKF-525A (50 mg/kg s.c. 30 min before measurement) did not affect this basal level in either hippocampus or cortex, which argues against a contribution of metabolic salicylate hydroxylation as its source. In contrast, pretreatment with the arachidonic acid cyclo-oxygenase inhibitor ibuprofen (20 mg/kg s.c.) decreased (?68.8%) the level of salicylate hydroxylation in the hippocampus, but not the cortex. In animals subjected to 10 min of forebrain ischemia, a selective increase in 2,5-DHBA was observed in the hippocampus at 1 min of reprerfusion which subsided by 5 min. No increase in salicylate hydroxylation was apparent in the cortex within the same time frame. The increase in ·OH in the hippocampus at 1 min of reperfusion was accompanied by a significant decrease (?15%; P < .03) in the hippocampal levels of vitamin E. No loss of vitamin E was observed in the cortex at the same time. It is hypothesized that the selective ischemic vulnerability of the hippocampus is mechanistically related to a selective post-ischemic burst in ·OH in that region. Moreover, this may be based upon an intrinsically higher level of oxidative stress in that region as a by-product of greater arachidonic acid turnover. © 1993 Wiley-Liss, Inc.     

Anticipating pressure necrosis in intestinal obstruction

When intestinal obstruction is caused by an adhesive band, unsuspected pressure necrosis of the intestinal wall may be hidden by the band. Isolation of the lesion by proximal and distal noncrushing bowel clamps before the adhesive band is divided effectively prevents gross contamination and fecal peritonitis with their prohibitive mortality.     

Electronic reporting of infections associated with hemodialysis

Monitoring infections and antibiotic resistance patterns in dialysis populations is an important component of efforts to improve patient safety and quality of health care. The objective of this report is to update findings from the Dialysis Surveillance Network and describe the soon-to-be-available National Healthcare Safety Network. METHODS: Volunteer dialysis centers in the DSN submitted reports of hospitalizations, outpatient intravenous antimicrobial starts, and positive blood cultures. From these reports, an online system calculated rates of important adverse events. For this report, we summarize adverse-event data submitted to the DSN from September 1999 through March 2005. RESULTS: There were 53,804 events in the 321,519 patient-months during the period of analysis. The rate of hospitalization was 13 per 100 patient-months; the rate of outpatient IV vancomycin starts was 3 per 100 patient-months. The rate of vascular access infection was 3.1 per 100 patient-months and varied from 0.6 for fistulas to 10. 1.for temporary catheters. Of the 8,359 blood isolates reported, 77% (6,427) were primary bacteremias (5,275 were catheter-associated, 1,152 were fistula- or graft-associated), 19% (1,587) were secondary bacteremias, and 4% (345) were contaminants. CONCLUSIONS: Infection-related adverse events remain lowest among patients with vascular access in the form of fistulas and grafts. In the future, adverse events in dialysis will be monitored in the NHSN. The new, Web-based, NHSN surveillance system allows centers to monitor their rates and compare with other outpatient dialysis centers. In 2006, CDC plans to open enrollment for outpatient dialysis centers not already in the DSN.     

A LIPOGENIC TOXIN RELEASED THROUGH THE INTERACTION OF A NEW CYTOPATHIC AGENT (LIPOVIRUS) AND CULTURED HUMAN CELLS

The release of a toxic product from cultured human cells infected by a new cytopathic agent (the lipovirus) was described. This toxin was dissociable from the infectious particles. It induced sudanophilia of human and mouse cells, an increase in the total fatty acid content, and a change in the major constituent fatty acids. Similar toxin was not demonstrated in cultures infected by the vaccinia herpes simplex, adeno 3, polyoma, polio 1 and 2, Coxsackie B1, parainfluenza A, and Rous sarcoma viruses. Preliminary characterization indicated that this toxin was resistant to tryptic digestion and could not be dialyzed or neutralized by human gamma globulin. It was inactivated at 58°C for 30 minutes, but stable at 37°, 4°, and –60°C. The significance of these findings is discussed.