ABSTRACr Walking tests, frequently used to document effects of treatment on exercise capacity, have never been standardised. We studied the effects of encouragement on walking test performance in a randomised study that controlled for the nature of the underlying disease, time of day, and order effects. We randomised 43 patients with chronic airflow limitation or chronic heart failure or both to receive or not receive encouragement as they performed serial two and six minute walks every fortnight for 10 weeks. Simple encouragement improved performance (p < 0*02 for the six minute walk), and the magnitude of the effect was similar to that reported for patients in studies purporting to show beneficial effects of therapeutic manoeuvres. Age and test repetition also affected performance. These results demonstrate the need for careful standardisation of the performance of walking tests, and suggest caution in interpreting studies in which standardisation is not a major feature of the study design. Accepted 21 May 1984 ment was given "as necessary." In subsequent experiments using walking tests as measures of exercise capacity encouragement was not held constant. We were concerned that the influence of encouragement might be sufficiently great to rival treatment effects, and therefore we investigated the impact of encouragement on two and six minute walking tests performance in patients with chronic lung and chronic heart disease. Methods PATIENTSWe recruited two groups of subjects who experienced fatigue or dyspnoea while performing activities of daily living. The first, with respiratory conditions, attended a regional referral centre for patients with pulmonary problems and had a best recorded forced expired volume in one second (FEVy) less than 70% of the predicted value. The second group, patients with heart failure, who had been referred by local cardiologists, had impaired left ventricular function demonstrated by angiography, radionuclide scanning, or echocardiography. Exclusion criteria for both groups were as follows:(1) limitation of exercise performance as a result of factors other than fatigue or exertional dyspnoea, 818

The contribution of muscle strength to symptom intensity and work capacity was examined in normal individuals and patients with cardiorespiratory disorders. Respiratory muscle strengths (maximal inspiratory and expiratory pressures) and peripheral muscle strengths (leg extension, leg flexion, seated bench press, and seated row) were measured in 4,617 subjects referred for clinical exercise testing. Subjects then rated the intensity of leg effort, discomfort with breathing (dyspnea), and chest pain (Borg scale) during an incremental exercise task (100 kpm/min each minute) to capacity on a cycle ergometer. Subjects were classified into groups on the basis of pulmonary function, drug therapy for cardiac disorders, and the presence of chest pain during exercise with electrocardiographic changes indicative of myocardial ischemia. Respiratory and peripheral muscle strengths, normalized for differences in age, sex, and height, were significantly reduced in patients with cardiorespiratory disorders compared with normal individuals. Muscle strength was a significant contributor to symptom intensity and work capacity in both health and disease; a two-fold increase in muscle strength was associated with a 25 to 30% decrease in the intensity of both leg effort and dyspnea and a 1.4- to 1.6-fold increase in work capacity. These results emphasize the need for an integrative approach in the assessment and therapeutic management of exercise intolerance, which considers the contribution of muscle weakness to excessive symptoms and reduced work capacity, in addition to the contribution of ventilatory, gas exchange, and circulatory impairments.

Structural Impact is concerned with the behaviour of structures and components subjected to large dynamic, impact and explosive loads which produce inelastic deformations. It is of interest for safety calculations, hazard assessments and energy absorbing systems throughout industry. The first five chapters introduce the rigid plastic methods of analysis for the static behaviour and the dynamic response of beams, plates and shells. The influence of transverse shear, rotatory inertia, finite displacements and dynamic material properties are introduced and studied in some detail. Dynamic progressive buckling, which develops in several energy absorbing systems, and the phenomenon of dynamic plastic buckling are introduced. Scaling laws are discussed which are important for relating the response of small-scale experimental tests to the dynamic behaviour of full-scale prototypes. This text is invaluable to undergraduates, graduates and professionals learning about the behaviour of structures subjected to large impact, dynamic and blast loadings producing an inelastic response.

The time course for the activation of glycogen phosphorylase (Phos) and pyruvate dehydrogenase (PDH) and their allosteric regulators was determined in human skeletal muscle during repeated bouts of maximal exercise. Six subjects completed three 30-s bouts of maximal isokinetic cycling separated by 4-min recovery periods. Muscle biopsies were taken at rest and at 6, 15, and 30 s of exercise during bouts 1 and 3. Phos was rapidly activated within the first 6 s of bout 1 from 12% at rest to 47% at 6 s. The activation of PDH increased from 14% at rest to 48% at 6 s and 95% at 15 s of bout 1. Phos reverted back to basal values at the end of the first bout, whereas PDH remained fully activated. In contrast, in the third bout, PDH was 42% at rest and was activated more rapidly and was nearly completely activated by 6 s, whereas Phos remained at basal levels (range 14-20%). Lactate accumulation was marked in the first bout and increased progressively from 2.7 to 76.1 mmol/kg dry wt with no further increase in bout 3. Glycogen utilization was also marked in the first bout and was negligible in bout 3. The rapid activation of Phos and slower activation of PDH in bout 1 was probably due to Ca(2+) release from the sarcoplasmic reticulum. Lactate accumulation appeared to be due to an imbalance of the relative activities of Phos and PDH. The increase in H(+) concentration may have served to reduce pyruvate production by inhibiting Phos transformation and may have simultaneously activated PDH in the third bout such that there was a better matching between pyruvate production and oxidation and minimal lactate accumulation. As each bout progressed and with successive bouts, there was a decreasing ability to stimulate substrate phosphorylation through phosphocreatine hydrolysis and glycolysis and a shift toward greater reliance on oxidative phosphorylation.

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The relation between end-tidal carbon dioxide tension (PETCO2) measured by infrared analysis and arterial carbon dioxide tension (PaCO2) during exercise was systematically examined in five healthy adults at two power outputs (25 and 50% VO2max) and at three frequencies of breathing (15, 30, and 45 breaths/min). PETCO2-PaCO2 varied between -2.5 and +9.1 Torr, was inversely related to the frequency of breathing (r = 0.475), and directly related to tidal volume (VT; r = 0.791) and CO2 output (r = 0.627). An equation was obtained by multiple regression analysis, to predict PaCO2 from PETCO2: PaCO2 = 5.5 +0.90 PETCO2 -0.0021 VT (r = 0.915). The equation was applied to measurements of PETCO2 obtained in two previous studies in 10 subjects in which PaCO2 had been measured, and was found to predict PaCO2 to within 1.04 Torr (+/- SD) for PaCO2 between 25 and 58 Torr (n = 56; r = 0.962). The effect of the response characteristics of the CO2 analyzer on the measurement of PETCO2 was also systematically examined by comparison with a fast-responding respiratory mass spectrometer.

Dyspnea, leg effort (Borg 0 to 10 scale), ventilation, and heart rate (VEmax/VEcap; HRmax/HRcap expressed as a percentage of capacity) were measured at maximal exercise (cycle ergometer) in 97 patients with chronic airflow limitation (CAL) (FEV, 46.6 +/- 14.23% of predicted) and compared with 320 matched control subjects. Patients with CAL achieved a maximum power output of 86 +/- 39.5 W (60 +/- 23.2% of predicted) compared with 140 +/- 37.5 W (98 +/- 14.5% of predicted) in controls (p less than 0.0001), VEmax/VEcap was 72 +/- 19.3% compared with 53 +/- 18.6% (p less than 0.0001), and HRmax/HRcap was 76 +/- 13.5% compared with 82 +/- 13% (p less than 0.001). These findings were expected. The median intensity of dyspnea was 6 (severe to very severe) and leg effort was 7 (very severe) in both groups, and these findings were unexpected. The patients with CAL were handicapped by an increase in both dyspnea and peripheral muscular effort relative to the actual power output. The rating of dyspnea exceeded leg effort in 25 (26%) of CAL versus 69 (22%) control subjects: the rating of leg effort exceeded dyspnea in 42 (43%) CAL and 117 (36%) control subjects; both were rated equally in 30 (31%) CAL and 134 (42%) control subjects, respectively (NS). VEmax/VEcap and HRmax/HRcap were not significantly different in those limited by dyspnea, leg fatigue, or a combination of both. All values are expressed +/- SD.

Background Patients with chronic airflow obstruction are often limited by muscle fatigue and weakness. As exercise rehabilitation programmes have produced modest improvements at best a study was designed to determine whether specific muscle training techniques are helpful. Methods Thirty four patients with chronic airflow limitation (forced expiratory volume in one second (FEVI)