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To determine the effect of two forms of warm-up on postexercise bronchoconstriction in athletes with exercise-induced asthma, 12 moderately trained persons with asthma (age = 26.5 +/- 2.2 yr; height = 169.2 +/- 2.6 cm; weight = 64.3 +/- 2.6kg; VO2max = 52.7 +/- 1.3 ml.kg-1.min-1) were tested under three experimental conditions; continuous warm-up (CW), interval warm-up (IW), and control (C). CW consisted of 15 min of treadmill running at a velocity corresponding to 60% VO2max followed by an exercise challenge test (ET = 6 min at 90% VO2max). IW involved 8 x 30-s runs (1.5 min rest between bouts of exercise), at an intensity equivalent to 100% VO2max, followed by an ET. C consisted of only the ET. FEV1, FVC, and MMEFR were measured prior to the experimental conditions, repeated before the ET, and every 2 min during a 25-min passive recovery period, using a Breon spirometer. Postexercise changes in pulmonary function were recorded as the largest decrese in FEV1, FVC, and MMEFR during the recovery period, and expressed as a percentage of baseline values. Significant differences were detected in %FEV1 (34. 6,16.7,29.7: P = 0.009), %FVC (30.0,10.7,21.0: P = 0.03), and %MMEFR (50.0,30.2,43.4: P = 0.05), in comparing C, CW, and IW, respectively. Scheffe's test detected significance (P0.05) between C and CW for all three dependent variables; no statistical significance between C and IW or IW and CW occurred. These data indicate that a continuous warm-up of 15 min at 60% VO2max can significantly decrease postexercise bronchoconstriction in moderately trained athletes.

In 10 nonasthmatic subjects and 11 patients with asthma, we measured pulmonary resistance (RL), functional residual capacity (FRC), and specific conductance (sGaw) before, during, and after submaximal treadmill exercise. Nonasthmatic subjects did not change RL, FRC, or sGaw from base-line resting values during or after exercise. In patients with asthma, RL decreased significantly during exercise, both when exercise was begun from the control resting state and from conditions of elevated RL after a preceding period of exercise. When asthmatic patients inhaled a standardized dose of aerosolized histamine, the increase in RL during exercise was significantly less than the increase in RL when they breathed histamine at rest. When patients hyperventilated at rest with tidal volumes, breathing frequencies, and end-tidal CO2 tensions similar to those during exercise conditions, bronchodilatation also occurred, and the increase in RL following inhaled histamine during isocapnic hyperventilation was also less than at rest. Since bronchodilatation and inhibition of histamine-induced bronchoconstriction occur during both exercise and isocapnic hyperventilation, we suggest that the mechanism of bronchodilatation during exercise may not necessarily be related to metabolic factors associated with exercise.

A general procedure for aligning crystals on the Buerger precession camera is described. For cases where the arcs on the goniometer head are tilted unfavourably when the precession condition is approximately met, the usual setting corrections may readily be resolved into components along the arcs. This is effected by adopting a consistent right-handed system and measuring the angular displacement of the head from a reference position. This principle may also be applied to achieve transfer of a crystal from a Weissenberg to a precession camera in the desired orientation.

In order to determine the effects of an inhaled bronchodilator on the acute effects of ozone exposure on competitive cyclists, three subjects exercised on a stationary cycle ergometer for one hour in 0.34 +/- 0.02 ppm ozone, 29.8 +/- 0.3 degrees C. and 36.5 +/- 0.5% relative humidity under three experimental conditions. The initial test involved no pre-medication and served as a control. Using a double blind protocol the subjects were either given a placebo or salbutamol (200 micrograms via aerosol) prior to the second and third exposures. Pre- and post-exercise pulmonary function tests demonstrated a reduction in forced vital capacity (FVC) and forced expiratory volume in one second (FEV1), however, the magnitude of this reduction was not changed by the administration of salbutamol. These data suggest that pre-treatment with salbutamol is ineffective in reducing or eliminating pulmonary discomfort or respiratory dysfunction.

We measured pressures in 2 lung regions in 5 seated subjects with 2 esophageal balloons placed 7.2 +/- 0.6 cm (mean +/- SE) apart in the mid-thorax in order to obtain the esophageal pressure gradient (EPG). Pressure differences between the lower thoracic balloon and a balloon placed in the stomach were obtained to measure transdiaphragmatic pressure (pdi). Inspiratory maneuvers were made from functional residual capacity (FRC) at either low inspiratory flow rates (slow VI) (mean slow VI: 0.22 +/- 0.05 L/sec) or at rapid flow rates (fast VI) (2.15 +/- 0.15 L/s). At FRC the mean EPG was 0.19 +/- 0.04 cm H2O/cm. The mean EPG was consistently lower at 500 cc above FRC during fast VI (0.14 +/- 0.03 cm H2O/cm) than during slow VI (0.28 +/- 0.05 cm H2O/cm) (P less than 0.001, paired 't' test). Fast VI results in amplification of pressure in the lower as compared to the upper region wih reduction in EPG. Diaphragmatic contraction appears to influence alterations in EPG during fast VI.

Salbutamol and treadmill performance in non-atopic athletes. Med. Sci. Sports Exerc., Vol. 15, No. 6, pp. 520-522, 1983. Nineteen aerobic, non-atopic, athletes (10 females, 9 males) were studied in a double-blind fashion to determine the effect of a therapeutic dosage of salbutamol on pulmonary function, oxygen consumption (VO2max), heart rate (HR), and anaerobic threshold (AT). A placebo and salbutamol (in aerosol form) were administered in a dosage of two puffs four times per day. Forced vital capacity (FVC), FEV1.0, and mid-maximal expiratory flow were assessed prior to a maximal treadmill run, and at 5, 10, and 15 min of recovery. Resting and maximal HR, VO2max, AT, and VE were determined prior to and immediately after the 1-wk experimental period. Pre-test results showed no evidence of airway obstruction in any athlete. There was no significant change in any pulmonary function variable as a result of salbutamol administration. Maximal oxygen consumption showed a slight, nonsignificant (P greater than 0.05) decrease in both the salbutamol and placebo groups. There was also a similar nonsignificant decrease in pulmonary function in both groups. Resting and maximal HR and AT were unchanged. These results indicate that therapeutic administration of a selective beta-2 agonist does not affect pulmonary function or performance-related variables in non-atopic elite athletes.

Salbutamol and treadmill performance in non-atopic athletes. Med. Sci. Sports Exerc., Vol. 15, No. 6, pp. 520-522, 1983. Nineteen aerobic, non-atopic, athletes (10 females, 9 males) were studied in a double-blind fashion to determine the effect of a therapeutic dosage of salbutamol on pulmonary function, oxygen consumption (VO2max), heart rate (HR), and anaerobic threshold (AT). A placebo and salbutamol (in aerosol form) were administered in a dosage of two puffs four times per day. Forced vital capacity (FVC), FEV1.0, and mid-maximal expiratory flow were assessed prior to a maximal treadmill run, and at 5, 10, and 15 min of recovery. Resting and maximal HR, VO2max, AT, and VE were determined prior to and immediately after the 1-wk experimental period. Pre-test results showed no evidence of airway obstruction in any athlete. There was no significant change in any pulmonary function variable as a result of salbutamol administration. Maximal oxygen consumption showed a slight, nonsignificant (P greater than 0.05) decrease in both the salbutamol and placebo groups. There was also a similar nonsignificant decrease in pulmonary function in both groups. Resting and maximal HR and AT were unchanged. These results indicate that therapeutic administration of a selective beta-2 agonist does not affect pulmonary function or performance-related variables in non-atopic elite athletes.

In the well‐known problem of the eastward deflection of a falling object much physical insight is gained by viewing the motion from an inertial frame.

The apparent discrepancy in the final horizontal velocity viz. 0 and 2ωh=ωgT2 is removed by noting that in my description, the final velocity (relative to the space fixed axes) is V=gT downwards, which possess the small component V sin θ=Vθ=ωgT2 for θ small, as the required transverse velocity component in the rotated axes.