The use of perioperative cardiopulmonary exercise testing (CPET) to evaluate the risk of adverse perioperative events and inform the perioperative management of patients undergoing surgery has increased over the last decade. CPET provides an objective assessment of exercise capacity preoperatively and identifies the causes of exercise limitation. This information may be used to assist clinicians and patients in decisions about the most appropriate surgical and non-surgical management during the perioperative period. Information gained from CPET can be used to estimate the likelihood of perioperative morbidity and mortality, to inform the processes of multidisciplinary collaborative decision making and consent, to triage patients for perioperative care (ward vs critical care), to direct preoperative interventions and optimization, to identify new comorbidities, to evaluate the effects of neoadjuvant cancer therapies, to guide prehabilitation and rehabilitation, and to guide intraoperative anaesthetic practice. With the rapid uptake of CPET, standardization is key to ensure valid, reproducible results that can inform clinical decision making. Recently, an international Perioperative Exercise Testing and Training Society has been established (POETTS www.poetts.co.uk) promoting the highest standards of care for patients undergoing exercise testing, training, or both in the perioperative setting. These clinical cardiopulmonary exercise testing guidelines have been developed by consensus by the Perioperative Exercise Testing and Training Society after systematic literature review. The guidelines have been endorsed by the Association of Respiratory Technology and Physiology (ARTP).

It is unclear whether hypoxia alters the kinetics of O2 uptake (VO2) during heavy exercise [above the lactic acidosis threshold (LAT)] and how these alterations might be linked to the rise in blood lactate. Eight healthy volunteers performed transitions from unloaded cycling to the same absolute heavy work rate for 8 min while breathing one of three inspired O2 concentrations: 21% (room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing 12% O2 slowed the time constant but did not affect the amplitude of the primary rise in VO2 (period of first 2-3 min of exercise) and had no significant effect on either the time constant or the amplitude of the slow VO2 component (beginning 2-3 min into exercise). Baseline heart rate was elevated in proportion to the severity of the hypoxia, but the amplitude and kinetics of increase during exercise and in recovery were unaffected by level of inspired O2. We conclude that the predominant effect of hypoxia during heavy exercise is on the early energetics as a slowed time constant for VO2 and an additional anaerobic contribution. However, the sum total of the processes representing the slow component of VO2 is unaffected.

Using a motorized treadmill the study investigated the effects of the ingestion of 3 g of caffeinated coffee on: the time taken to run 1500 m; the selected speed with which athletes completed a 1-min 'finishing burst' at the end of a high-intensity run; and respiratory factors, perceived exertion and blood lactate levels during a high intensity 1500-m run. In all testing protocols decaffeinated coffee (3 g) was used as a placebo and a double-blind experimental design was used throughout. The participants in the study were middle distance athletes of club, county and national standard. The results showed that ingestion of caffeinated coffee: decreases the time taken to run 1500 m (P < 0.005); increases the speed of the 'finishing burst' (P < 0.005); and increases Vo2 during the high-intensity 1500-m run (P < 0.025). The study concluded that under these laboratory conditions, the ingestion of caffeinated coffee could enhance the performance of sustained high-intensity exercise. Keywords: Caffeine, ergogenic acid, Vo2, blood lactate Caffeine has long been considered as a substance capable of enhancing performance or physiological functions1 and as a result of its reported ergogenic effects, the International Olympic Committee (IOC) have banned the use of high levels of caffeine. However, since caffeine is commonly found in many foods that are taken as part of the 'normal' diet, when testing for the drug the banned level is set above 15 ig ml-1 urine which is reported to represent the ingestion of 500-600 mg of caffeine (five to six cups of coffee) in a 1-2 h period2. Therefore in practical terms this dosage is only likely to be exceeded through the use of tablets, injections, suppositories or the deliberate ingestion of large amounts3. medulla increasing the secretion of catecholamines; the release of calcium ions from the sarcoplasmic reticulum; and the oxidation of free fatty acids which would produce a glycogen-sparing effect during prolonged exercise.Research into the effects of caffeine has tended to concentrate upon endurance activities such as marathon running or prolonged cyclingI7, with other investigations studying its effects upon maximal strength and power8 9. However, relatively little research has looked at the effects of caffeine upon high-intensity prolonged exercise, where the relative importance of the different physiological parameters required to produce a high level of performance and the physiological causes of fatigue can differ from those of endurance and short-term high-intensity exercise.The aim of this investigation was therefore to study the effect(s) of low doses of caffeine (approximately equivalent to the amount found in two strong cups of coffee) on a number of factors during prolonged high-intensity exercise. The study utilized doses of caffeine that would realistically be ingested by a sports performer before exercise as part of their 'normal' dietary habits without contravening the doping control regulations. Materials and methods

Adult preterm birth survivors, especially those who developed BPD, continue to experience respiratory symptoms and exhibit clinically important levels of pulmonary impairment.

Objective-To determine the aerobic work capacity of patients with the chronic fatigue syndrome and compare it with that of two control groups, and to assess the patients' perception of their level of activity before and during illness.Design-A symptom limited' exercise treadmill test with on line gas analysis and blood sampling was used. Subjects were assessed by one investigator, who was blind to the group which they were in.

In patients suffering from primary pulmonary hypertension (PPH), a raised pulmonary vascular resistance may limit the ability to increase pulmonary blood flow as work rate increases. We hypothesised that oxygen uptake (VO2) may not rise appropriately with increasing work rate during incremental cardiopulmonary exercise tests. Nine PPH patients and nine normal subjects performed symptom-limited maximal continuous incremental cycle ergometry exercise. Mean peak VO2 [1.00 (SD 0.22) compared to 2.58 (SD 0.64) l x min(-1)] and mean VO2 at lactic acidosis threshold [LAT, 0.73 (SD 0.17) compared to 1.46 (SD 0.21 x 1) ml x min(-1)] were much lower in patients than in normal subjects (both P<0.01, two-way ANOVA with Tukey test). The mean rate of change of VO2 with increasing work rate above the LAT [5.9 (SD 2.1) compared to 9.4 (SD 1.3) ml x min(-1) x W(-1), p<0.01)] was also much lower in patients than in normal subjects [apparent delta efficiency 60.3 (SD 38.8)% in patients compared to 31.0 (SD 4.9)% in normal subjects]. The patients displayed lower mean values of end-tidal partial pressure of carbon dioxide than the normal subjects at peak exercise [29.7 (SD 6.8) compared to 42.4 (SD 5.8) mm Hg, P<0.01] and mean oxyhaemoglobin saturation [89.1 (SD 4.1) compared to 93.6 (SD 1.8)%, P<0.05]. Mean ventilatory equivalents for CO2 [49.3 (SD 11.4) compared to 35.0 (SD 7.3), P<0.05] and O2 [44.2 (SD 10.7) compared to 29.9 (SD 5.1), P<0.05] were greater in patients than normal subjects. The sub-normal slopes for the VO2-work-rate relationship above the LAT indicated severe impairment of the circulatory response to exercise in patients with PPH. The ventilatory abnormalities in PPH suggested that the lung had become an inefficient gas exchange organ because of impaired perfusion of the ventilated lung.

We have examined the use of a 6-min corridor walk test in the assessment of functional capacity in 16 patients with chronic cardiac failure. VO2 was determined concurrently by a portable 'Oxylog'. Three tests were performed sequentially, and although there was a significant increase in distance walked and highest VO2 achieved between the first and second tests, good reproducibility was attained between the second and third tests. Both walk test variables correlated well with previously determined peak achieved VO2, and NYHA classes were separated adequately. Corridor walk testing, with or without measurement of VO2 should be a useful adjunct to maximal exercise testing in interventional studies.

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