Aminophylline increases the contractile force of fatiguing muscles. The effects of aminophylline upon maximal exercise performance are not defined. 6 healthy men performed incremental bicycle ergometry before and after receiving intravenous aminophylline (6 mg/kg). Maximal oxygen uptake, maximum work rate, and maximum minute ventilation were unchanged following aminophylline. Heart rate measured at rest and at 50-watt increments of work rate was significantly increased following aminophylline (p < 0.03). The heart rate response to incremental exercise (Δ HR/ΔVO2) was unchanged by aminophylline. We conclude that aminophylline does not increase maximal exercise performance of healthy men.
We compared determinations of anaerobic threshold (AT) made from measurements of arterial lactate concentration with AT determined from ventilatory response measurements of subjects with chronic airflow obstruction (CAO). Six untrained subjects with CAO performed incremental maximal cycle ergometer tests. Ventilation (VE); O2 uptake (VO2), CO2 output (Vco2); end-tidal CO2 fraction (FETCO2); and end-tidal O2 fraction (FETO2) were measured breath by breath. Arterial lactate concentration was sampled at rest and every 30 s during exercise from an indwelling arterial catheter. For three subjects with more severe airflow obstruction, plots of VE/Vo2 and FETO2 failed to detect AT. In contrast, a systematic increase of the respiratory gas exchange ratio across the lung (R) accompanied increasing arterial lactate concentrations in all 6 subjects. We conclude that progressive increases of VE/VO2 and FETO2 cannot be relied upon for the measurement of AT in patients with severe CAO. Progressive increases of R unaccompanied by decreasing FETCO2 detect AT in CAO
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