Physical Demands of Sprinting in Professional Road Cycling.

The aim of this study was to quantify the demands of road competitions ending with sprints in male professional cycling. 17 races finished with top-5 results from 6 male road professional cyclists (age, 27.0±3.8 years; height, 1.76±0.03 m; weight, 71.7±1.1 kg) were analysed. SRM power meters were used to monitor power output, cadence and speed. Data were averaged over the entire race, different durations prior to the sprint (60, 10, 5 and 1 min) and during the actual sprint. Variations in power during the final 10 min of the race were quantified using exposure variation analysis. This observational study was conducted in the field to maximize the ecological validity of the results. Power, cadence and speed were statistically different between various phases of the race (p<0.001), increasing from 316±43 W, 95±4 rpm and 50.5±3.3 km·h(-1) in the last 10 min, to 487±58 W, 102±6 rpm and 55.4±4.7 km·h(-1) in the last min prior to the sprint. Peak power during the sprint was 17.4±1.7 W·kg(-1). Exposure variation analysis revealed a significantly greater number of short-duration high-intensity efforts in the final 5 min of the race, compared with the penultimate 5 min (p=0.010). These findings quantify the power output requirements associated with high-level sprinting in men's professional road cycling and highlight the need for both aerobic and anaerobic fitness.

Examining pacing profiles in elite female road cyclists using exposure variation analysis.

OBJECTIVE: In this study, the amplitude and time distribution of power output in a variety of competitive cycling events through the use of a new mathematical analysis was examined: exposure variation analysis (EVA). DESIGN: Descriptive field study. SETTING: Various professional road cycling events, including; a 5-day-eight-stage tour race, a 1-day World Cup event and the Australian National Individual Time Trial Championships. PARTICIPANTS: 9 elite female cyclists (mean (SD), mass = 57.8 (3.4) kg, height = 167.3 (2.8) cm, Vo(2)peak = 63.2 (5.2) ml kg(-1) min(-1)). INTERVENTIONS: None. MAIN OUTCOME MEASUREMENTS: The variation in power output and the quantification of the total time and acute time spent at various exercise intensities during competitive professional cycling were examined. Predefined levels of exercise intensity that elicited first ventilation threshold, second ventilation threshold and maximal aerobic power were determined from a graded exercise test performed before the events and compared with power output during each event. RESULTS: EVA exposed that power output during the time trial was highly variable (EVA(SD) = 2.81 (0.33)) but more evenly distributed than the circuit/criterium (4.23 (0.31)) and road race events (4.81 (0.96)). CONCLUSION: EVA may be useful for illustrating variations in the amplitude and time distribution of power output during cycling events. The specific race format influenced not only the overall time spent in various power bands, but also the acute time spent at these exercise intensities.

The power profile predicts road cycling MMP.

Laboratory tests of fitness variables have previously been shown to be valid predictors of cycling time-trial performance. However, due to the influence of drafting, tactics and the variability of power output in mass-start road races, comparisons between laboratory tests and competition performance are limited. The purpose of this study was to compare the power produced in the laboratory Power Profile (PP) test and Maximum Mean Power (MMP) analysis of competition data. Ten male cyclists (mean+/-SD: 20.8+/-1.5 y, 67.3+/-5.5 kg, V O (2 max) 72.7+/-5.1 mL x kg (-1) x min (-1)) completed a PP test within 14 days of competing in a series of road races. No differences were found between PP results and MMP analysis of competition data for durations of 60-600 s, total work or estimates of critical power and the fixed amount of work that can be completed above critical power (W'). Self-selected cadence was 15+/-7 rpm higher in the lab. These results indicate that the PP test is an ecologically valid assessment of power producing capacity over cycling specific durations. In combination with MMP analysis, this may be a useful tool for quantifying elements of cycling specific performance in competitive cyclists.

Time course of haemoglobin mass during 21 days live high:train low simulated altitude.

The aim of this study was to determine the time course of changes in haemoglobin mass (Hb(mass)) in well-trained cyclists in response to live high:train low (LHTL). Twelve well-trained male cyclists participated in a 3-week LHTL protocol comprising 3,000 m simulated altitude for ~14 h/day. Prior to LHTL duplicate baseline measurements were made of Hb(mass), maximal oxygen consumption (VO(2max)) and serum erythropoietin (sEPO). Hb(mass) was measured weekly during LHTL and twice in the week thereafter. There was a 3.3% increase in Hb(mass) and no change in VO(2max) after LHTL. The mean Hb(mass) increased at a rate of ~1% per week and this was maintained in the week after cessation of LHTL. The sEPO concentration peaked after two nights of LHTL but there was only a trivial correlation (r = 0.04, P = 0.89) between the increase in sEPO and the increase in Hb(mass). Athletes seeking to gain erythropoietic benefits from moderate altitude need to spend >12 h/day in hypoxia.

Influence of starting strategy on cycling time trial performance in the heat.

The purpose of this study was to determine the influence of starting strategy on time trial performance in the heat. Eleven endurance trained male cyclists (30+/-5 years, 79.5+/-4.6 kg, VO(2max) 58.5+/-5.0 ml x kg x (-1) min(-1)) performed four 20-km time trials in the heat (32.7+/-0.7 degrees C and 55% relative humidity). The first time trial was completed at a self-selected pace (SPTT). During the following time trials, subjects performed the initial 2.5-km at power outputs 10% above (10% ATT), 10% below (10% BTT) or equal (ETT) to that of the average power during the initial 2.5-km of the self-selected trial; the remaining 17.5-km was self-paced. Throughout each time trial, power output, rectal temperature, skin temperature, heat storage, pain intensity and thermal sensation were taken. Despite significantly (P<0.05) greater power outputs for 10% BTT (273+/-45W) compared with the ETT (267+/-48W) and 10% ATT (265+/-41W) during the final 17.5-km, overall 20-km performance time was not significantly different amongst trials. There were no differences in any of the other measured variables between trials. These data show that varying starting power by +/-10% did not affect 20 km time trial performance in the heat.

Core temperature and hydration status during an Ironman triathlon.

BACKGROUND: Numerous laboratory based studies have documented that aggressive hydration strategies (approximately 1-2 litres/h) are required to minimise a rise in core temperature and minimise the deleterious effects of hyperthermia on performance. However, field data on the relations between hydration level, core body temperature, and performance are rare. OBJECTIVE: To measure core temperature (Tcore) in triathletes during a 226 km Ironman triathlon, and to compare Tcore with markers of hydration status after the event. METHOD: Before and immediately after the 2004 Ironman Western Australia event (mean (SD) ambient temperature 23.3 (1.9) degrees C (range 19-26 degrees C) and 60 (14)% relative humidity (44-87%)) body mass, plasma concentrations of sodium ([Na+]), potassium ([K+]), and chloride ([Cl-]), and urine specific gravity were measured in 10 well trained triathletes. Tcore was measured intermittently during the event using an ingestible pill telemetry system, and heart rate was measured throughout. RESULTS: Mean (SD) performance time in the Ironman triathlon was 611 (49) minutes; heart rate was 143 (9) beats/min (83 (6)% of maximum) and Tcore was 38.1 (0.3) degrees C. Body mass significantly declined during the race by 2.3 (1.2) kg (-3.0 (1.5)%; p < 0.05), whereas urine specific gravity significantly increased (1.011 (0.005) to 1.0170 (0.008) g/ml; p < 0.05) and plasma [Na+], [K+], and [Cl-] did not change. Changes in body mass were not related to finishing Tcore (r = -0.16), plasma [Na+] (r = 0.31), or urine specific gravity (r = -0.37). CONCLUSION: In contrast with previous laboratory based studies examining the influence of hypohydration on performance, a body mass loss of up to 3% was found to be tolerated by well trained triathletes during an Ironman competition in warm conditions without any evidence of thermoregulatory failure.

The class III antiarrhythmic effect of sotalol exerts a reverse use-dependent positive inotropic effect in the intact canine heart.

OBJECTIVES: We sought to study the rate related effects of sotalol on myocardial contractility and to test the hypothesis that the class III antiarrhythmic effect of sotalol has a reverse use-dependent positive inotropic effect in the intact heart. BACKGROUND: Antiarrhythmic drugs exert significant negative inotropic effects. Sotalol, a beta-adrenergic blocking agent with class III antiarrhythmic properties, may augment contractility by virtue of its ability to prolong the action potential duration (APD). METHODS: In 10 anesthetized dogs, measurements of left ventricle (LV) peak (+)dP/dt and simultaneous endocardial action potentials were made during baseline conditions and after sequential administration of esmolol and sotalol. In addition, electrical and mechanical restitution curves were constructed at a basic pacing cycle length of 600 ms by introducing a test pulse of altered cycle length ranging from 200 ms to 2,000 ms. RESULTS: In the steady state pacing experiments, sotalol prolonged the APD in a reverse use-dependent manner; such an effect was not seen with esmolol. At cycle lengths exceeding 400 ms, LV (+)dP/dt was significantly higher with sotalol than it was with esmolol. There was a direct relation between APD and LV (+)dP/dt with sotalol (r = 0.46, p < 0.001), but there was no significant relation between APD and LV (+)dP/dt with esmolol (r = 0.27, p = NS). Results in the single beat (restitution) studies were qualitatively similar to the steady state results; APD (at cycle length >400 ms) and LV (+)dP/dt (at cycle length >600 ms) were significantly higher with sotalol than they were with esmolol. CONCLUSIONS: The reverse use-dependent prolongation of APD by sotalol is associated with a positive inotropic effect.

The impact of a simulated grand tour on sleep, mood, and well-being of competitive cyclists.

AIM: Professional cycling is considered one of the most demanding of all endurance sports. The three major professional cycling stages races (i.e. Tour de France, Giro d'Italia and Vuelta a España) require cyclists to compete daily covering between ~150-200 km for three consecutive weeks. Anecdotal evidence indicates that such an event has a significant effect on the sleep, mood, and general well-being of cyclists, particularly during the latter stages of the event. The primary aim of this study was to simulate a grand tour and determine the impact a grand tour has on the sleep, mood, and general well-being of competitive cyclists. METHODS: Twenty-one male cyclists (M±SD, age 22.2±2.7 years) were examined for 39 days across three phases (i.e. baseline, simulated grand tour, and recovery). Sleep was assessed using sleep diaries and wrist activity monitors. Mood and general well-being were assessed using the Brunel Mood Scale (BRUMS) and Visual Analogue Scales (VAS). RESULTS: The amount and quality of sleep as assessed by the wrist activity monitors declined during the simulated grand tour. In contrast, self-reported sleep quality improved throughout the study. Cyclists' mood and general well-being as indicated by vigour, motivation, physical and mental state declined during the simulated tour. CONCLUSION: Future investigations should examine sleep, mood and well-being during an actual grand tour. Such data could prove instrumental toward understanding the sleep and psychological changes that occur during a grand tour.

Increase in defibrillation threshold in non-thoracotomy implantable defibrillators using a biphasic waveform.

We have previously reported a chronic increase in defibrillation threshold in a non-thoracotomy implantable cardioverter-defibrillator (ICD) system using monophasic waveforms. To determine if this phenomenon is related to the lead system or the waveform used, we studied the chronic defibrillation threshold in consecutive patients receiving an ICD capable of delivering biphasic waveforms with the same lead system previously evaluated. Twenty-five patients received an ICD with biphasic shock waveform and have been followed for 4 to 15 months. All have undergone defibrillation threshold measurements using the identical testing protocol with biphasic waveforms at implant and at 2 months. Coronary artery disease was present in 15, idiopathic dilated cardiomyopathy in 9, and valvular heart disease in 1. The presenting arrhythmia was ventricular fibrillation in 11, ventricular tachycardia in 10, and syncope with inducible ventricular tachycardia in 4. The configuration of the shocking electrodes was randomized; the lead-only configuration was used in 14 patients (56%), and a subcutaneous patch was used in the remaining patients. Mean defibrillation threshold using a step-down technique was 9.8 +/- 1.0 J at implant, 13.2 +/- 1.6 J at 2 months, and 12.4 +/- 1.5 J at 6 months (p = 0.01 by analysis of variance). There was no change in clinical status, cardiac size, radiographic lead position, or impedance between implant and 2 months. These findings suggest the increase in defibrillation threshold in this ICD system is not related to the type of waveform used, but rather is a feature of non-thoracotomy as opposed to epicardial electrodes.

Interval-dependent changes in left ventricular contractile state in lone atrial fibrillation and in atrial fibrillation associated with coronary artery disease.

In atrial fibrillation (AF), beat-to-beat changes in left ventricular (LV) systolic performance are caused by variations in filling (preload), aortic pressure (afterload), and ventricular inotropic or contractile state. These factors are known to be influenced by the preceding diastolic or RR interval (RR1), but the independent impact of variations in the pre-preceding RR interval (RR2) on contractile state is not well defined. This aspect was studied in 10 patients with lone AF and 8 with coronary artery disease by measuring LV peak ejection velocity (V[pe] Doppler echocardiography) in 80 to 100 consecutive cardiac cycles. V(pe) was plotted against RR1 for beats with a short RR2 and for beats with a long RR2. Such function-interval plots indicate a direct relation between V(pe) and RR1 (for RR1 = 500 to 1,000 ms). In lone AF, the slope (linear fit) of V(pe) versus RR1 was similar for short and long RR2 (slopes = 46 and 50 s[-1]). V(pe), calculated from best linear fit and a common RR1, was consistently higher when RR2 was short than when it was long. At an RR1 = 750 ms, V(pe) (% of max) was 87 +/- 6% when RR2 was short versus 76 +/- 6% when RR2 was long, p <0.05. Results were similar in patients with coronary artery disease and the observed interval-dependent potentiation of contractile state was preserved in patients with a low ejection fraction. By comparing V(pe) at a common RR1, the effects of time-dependent changes in LV preload and afterload are minimized if not abolished. Thus, differences in V(pe) reflect differences in contractile state caused by variations in RR2. Data confirm interval-dependent alterations in contractile state that are likely an expression of the force-frequency relation. Studies of LV function in AF should incorporate a consideration of cycle length-dependent changes in LV contractile state.

Effect of rhythm regularization on left ventricular contractility in patients with atrial fibrillation.

In 10 patients with atrial fibrillation, echocardiographic measures of left ventricular function-interval relations were used to assess contractility and to test the hypothesis that rhythm regularization produces a higher contractile state than is seen when the rhythm is irregular. Regularization, following direct-current cardioversion, did not augment ventricular contractility above that seen during atrial fibrillation.

The role of coronary revascularization in recipients of an implantable cardioverter-defibrillator.

The impact of adjuvant coronary revascularization was studied in a group of 138 recipients of an implantable cardioverter-defibrillator, all of whom had ischemic heart disease as the cause of their arrhythmias. Patients chosen for revascularization had more severe anatomic, symptomatic, or physiologic evidence of active ischemia. There were no operative deaths among 23 patients who actually underwent coronary artery bypass combined with cardioverter-defibrillator implantation; however, operative mortality by the intention-to-treat principle was 8% (2/25). Total cardiac survival was better for patients who underwent revascularization than for those patients who had "high-risk" characteristics and did not undergo revascularization. Stratified subgroup analysis demonstrated significant survival advantages favoring revascularization in patients with three-vessel or left main coronary artery disease, class III or IV angina, and an ejection fraction greater than 25%. Multivariate analysis revealed that low ejection fraction and left main coronary artery disease were independent predictors of decreased survival.

Transvenous versus transthoracic cardioverter-defibrillator implantation. A comparative analysis of morbidity, mortality, and survival.

The hypothesis that transvenous implantation of a cardioverter-defibrillator is associated with less morbidity than use of a transthoracic approach was investigated in a retrospective series of 146 patients. None of these patients had concomitant heart procedures, and the preoperative characteristics of the two groups were similar. When analyzed by actual technique used (transvenous, 57 patients; transthoracic, 89 patients) and by the intention-to-treat method (transvenous, 65 patients, 8 of whom actually underwent thoracotomy; thoracotomy, 81 patients), transvenous implantation was associated with a lower incidence of postoperative respiratory complications and atrial fibrillation. Total cardiac mortality and freedom from sudden cardiac death in the transvenous and transthoracic groups were comparable at 2 years.

A critical comparison of the hematologic, cardiovascular, and pulmonary response to steroids and nonsteroidal anti-inflammatory drugs in a model of sepsis and adult respiratory distress syndrome.

Improved survival of patients receiving high-dose steroid therapy in sepsis and adult respiratory distress syndrome (ARDS) has been reported, but such therapy and its benefits remain controversial. Recently research has been directed toward manipulation of the arachidonic acid cascade. Improved survival and hemodynamics with administration of nonsteroidal anti-inflammatory drugs (NSAID) have been reported in animal models of sepsis and ARDS. The purpose of this study was to compare the effects of steroids (methylprednisolone) and NSAID (ibuprofen) in a porcine model of septic ARDS induced by a continuous infusion of live Pseudomonas aeruginosa. Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250 ml tidal volume and 0.5 Fio2. Pigs were randomly assigned to one of five groups: groups I and II received respective doses of 12.5 mg/kg ibuprofen and 30 mg/kg methylprednisolone at 20 and 210 minutes after baseline; group III had P. aeruginosa only; groups IV and V received respective doses of ibuprofen and methylprednisolone at 20 and 210 minutes of sepsis. Significant pulmonary edema, increased intrapulmonary shunting, hypoxemia, hemoconcentration, and systemic hypotension occurred with P. aeruginosa infusion. In septic animals treated with ibuprofen normal systemic arterial pressure was maintained, hemoconcentration was decreased, and oxygenation was improved with a significant decrease in shunting and pulmonary edema. Administration of methylprednisolone improved hemoconcentration and cardiac index, but no significant effect on pulmonary edema, intrapulmonary shunting, or oxygenation was observed. The results of this study demonstrated a significant beneficial effect of ibuprofen and we would encourage controlled clinical trials of this drug in the management of sepsis and ARDS. On the other hand, methylprednisolone was found to be relatively ineffective in treatment of circulatory collapse and ARDS associated with sepsis.

Collagen gene expression in rat left ventricle: interactive effect of age and exercise training.

Whether or not exercise training of sufficient intensity and duration to produce left ventricle (LV) hypertrophy also regulates deposition of interstitial collagen and cross-linking at the pretranslational level is unknown. Therefore, the effects of exercise training on gene expression for the two principal fibrillar collagens in LV, types I and III, were assessed in young adult (5 mo), middle-aged (15 mo), and old (26 mo) rats. We also evaluated the potential interaction of changes in mRNA for these procollagens with alterations in LV extracellular matrix characteristics by simultaneously measuring collagen concentration (hydroxyproline) and extent of mature collagen cross-linking (hydroxylysylpyridinoline, HP). Ten weeks of treadmill running resulted in LV hypertrophy and an increased maximal oxygen uptake in all three age groups of trained rats compared with sedentary controls. Percent collagen in rat LV almost doubled (P < 0.0001) from 5 to 26 mo of age, an increase unaffected by exercise training. With aging, a significant decline in expression of mRNAs for both collagen type I (P < 0.005) and type III (P < 0.001) was observed in LV free wall (LVF) but not septum (LVS). Training prevented this decline in LVF mRNAs for the two principal fibrillar collagens in middle-aged rats whereas it attenuated the decline in senescent animals. HP concentration increased significantly with aging in both LVF (P < 0.005) and LVS (P < 0.01). Training modulated this effect, but again only in LVF, so that HP was significantly lower (P < 0.05) in this region of the LV in old trained rats compared with sedentary counterparts. We conclude that exercise training modulates the effects of aging on collagen gene mRNAs and HP cross-linking regionally within the LV.

Impaired interval exercise responses in elite female cyclists at moderate simulated altitude.

The effect of hypoxia on the response to interval exercise was determined in eight elite female cyclists during two interval sessions: a sustained 3 x 10-min endurance set (5-min recovery) and a repeat sprint session comprising three sets of 6 x 15-s sprints (work-to-relief ratios were 1:3, 1:2, and 1:1 for the 1st, 2nd, and 3rd sets, respectively, with 3 min between each set). During exercise, cyclists selected their maximum power output and breathed either atmospheric air (normoxia, 20.93% O(2)) or a hypoxic gas mix (hypoxia, 17.42% O(2)). Power output was lower in hypoxia vs. normoxia throughout the endurance set (244+/-18 vs. 226+/-17, 234+/-18 vs. 221+/-25, and 235+/-18 vs. 221+/-25 W for 1st, 2nd, and 3rd sets, respectively; P< 0.05) but was lower only in the latter stages of the second and third sets of the sprints (452+/-56 vs. 429+/-49 and 403+/-54 vs. 373+/- 43 W, respectively; P<0.05). Hypoxia lowered blood O(2) saturation during the endurance set (92.9+/-2.9 vs. 95.4+/-1.5%; P<0.05) but not during repeat sprints. We conclude that, when elite cyclists select their maximum exercise intensity, both sustained (10 min) and short-term (15 s) power are impaired during hypoxia, which simulated moderate ( approximately 2,100 m) altitude.

Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling.

For 5 days, eight well-trained cyclists consumed a random order of a high-carbohydrate (CHO) diet (9.6 g. kg(-1). day(-1) CHO, 0.7 g. kg(-1). day(-1) fat; HCHO) or an isoenergetic high-fat diet (2.4 g. kg(-1). day(-1) CHO, 4 g. kg(-1). day(-1) fat; Fat-adapt) while undertaking supervised training. On day 6, subjects ingested high CHO and rested before performance testing on day 7 [2 h cycling at 70% maximal O(2) consumption (SS) + 7 kJ/kg time trial (TT)]. With Fat-adapt, 5 days of high-fat diet reduced respiratory exchange ratio (RER) during cycling at 70% maximal O(2) consumption; this was partially restored by 1 day of high CHO [0.90 +/- 0.01 vs. 0.82 +/- 0.01 (P < 0.05) vs. 0.87 +/- 0.01 (P < 0.05), for day 1, day 6, and day 7, respectively]. Corresponding RER values on HCHO trial were [0. 91 +/- 0.01 vs. 0.88 +/- 0.01 (P < 0.05) vs. 0.93 +/- 0.01 (P < 0.05)]. During SS, estimated fat oxidation increased [94 +/- 6 vs. 61 +/- 5 g (P < 0.05)], whereas CHO oxidation decreased [271 +/- 16 vs. 342 +/- 14 g (P < 0.05)] for Fat-adapt compared with HCHO. Tracer-derived estimates of plasma glucose uptake revealed no differences between treatments, suggesting muscle glycogen sparing accounted for reduced CHO oxidation. Direct assessment of muscle glycogen utilization showed a similar order of sparing (260 +/- 26 vs. 360 +/- 43 mmol/kg dry wt; P = 0.06). TT performance was 30.73 +/- 1.12 vs. 34.17 +/- 2.48 min for Fat-adapt and HCHO (P = 0.21). These data show significant metabolic adaptations with a brief period of high-fat intake, which persist even after restoration of CHO availability. However, there was no evidence of a clear benefit of fat adaptation to cycling performance.

Successful laparoscopic repair of paraesophageal hernia.

OBJECTIVE: To evaluate prospectively the safety and efficacy of laparoscopic surgical techniques in the repair of types II and III paraesophageal hernias. DESIGN: Case series. SETTING: Tertiary-care, university-affiliated hospitals. PATIENTS: Twelve consecutive patients undergoing elective laparoscopic repair of type II or type III paraesophageal hernias. Patients were available for follow-up for 1 to 17 months postoperatively. INTERVENTIONS: All patients underwent laparoscopic paraesophageal hernia reduction and repair. Eight patients with gastroesophageal reflux disease underwent concurrent laparoscopic Nissen fundoplication. MAIN OUTCOME MEASURES: Operative times, operative complications, and estimated blood loss were recorded. Postoperative outcome measurements included length of hospital stay, postoperative complications, postoperative gastrointestinal tract symptoms, and patient satisfaction. RESULTS: All patients had successful completion of paraesophageal hernia repair laparoscopically with no recurrences, and with an overall minor morbidity rate of 25%, major morbidity rate of 8%, and no deaths. Eight of 12 patients with concomitant reflux disease underwent successful laparoscopic Nissen fundoplication with complete control of reflux symptoms. The average hospital stay for patients with uncomplicated courses was 2.5 days. Long-term (> 6 weeks) postfundoplication symptoms occurred in 13% of those patients who underwent fundoplication. Eleven (92%) of 12 patients described good to excellent results with complete or near complete control of all preoperative symptoms. CONCLUSIONS: Laparoscopic repair of types II and III paraesophageal hernias can be performed under elective circumstances by experienced laparoscopic surgeons, with acceptable morbidity and comparable short-term efficacy. Addition of a concomitant antireflux procedure should be reserved for those patients with clear preoperative evidence of reflux disease secondary to a mechanically defective lower esophageal sphincter. Patients with a normal lower esophageal antireflux barrier do not need a concomitant antireflux procedure.

Muscle pathology in the neuroleptic malignant syndrome.

In a fatal case of neuroleptic malignant syndrome, a muscle sample taken within 1 h of death showed acute myopathic features with absence of muscle glycogen and neutral lipid. These features suggest that hyperpyrexia in this syndrome may be caused by heat production from uncoupled phosphorylation in muscle and imply that the primary biochemical abnormality responsible for this uncontrolled heat production might be muscular rather than hypothalamic.

Combined use of non-thoracotomy cardioverter defibrillators and endocardial pacemakers.

OBJECTIVE: To study the potential interactions in patients with endocardial permanent pacemakers and non-thoracotomy implantable cardioverter defibrillator (ICD) systems. DESIGN: Case series and cohort study. SETTING: Tertiary referral centre. PATIENTS: Fifteen consecutive patients with both endocardial pacemakers (12 dual chamber and three single chamber) and non-thoracotomy ICD systems. MAIN OUTCOME MEASURES: Detection inhibition of induced ventricular fibrillation; double counting; and pacemaker function after shocks. In the evaluation of detection inhibition, 124 VF inductions were analysed for detection duration compared with induced VF episodes in controls with an ICD but without a pacemaker. RESULTS: Two patients (13%) showed detection inhibition of VF and required pacemaker system change at the time of the ICD implant. With the final lead position, despite frequent pacemaker undersensing of VF, ICD detection of VF was not inhibited during any induction, and neither initial detection nor redetection times for VF were different from controls. Double/triple counting of pacemaker artefact and evoked electrogram was noted in three patients (20%). In two, this was remedied during the implantation procedure, and in the other it was abolished when amiodarone treatment was discontinued. Pacemaker function was affected by ICD discharges in two patients, one who showed postshock atrial undersensing and loss of capture, and another whose pacemaker reverted to VVI mode. CONCLUSIONS: When careful testing is performed at implantation to detect and remedy device interactions, non-thoracotomy ICD treatment and endocardial pacemakers can be used safely in combination.