We examined the effects of hypoxia on exercise-induced diaphragmatic fatigue. Eleven subjects with a mean maximal O2 uptake of 52.4 +/- 0.7 ml.kg-1.min-1 completed one normoxic (arterial O2 saturation 96-94%) and one hypoxic (inspiratory O2 fraction = 0.15; arterial O2 saturation 83-77%) exercise test at 85% maximal O2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (BPNS) was used to determine the pressure generation of the diaphragm pre- and postexercise at 1, 10, and 20 Hz. There was increased flow limitation during hypoxic vs. normoxic exercise. There was a decrease in hypoxic exercise time (normoxic 24.9 +/- 0.7 min vs. hypoxic 15.8 +/- 0.8 min; P < 0.05). After exercise the BPNS transdiaphragmatic pressure (Pdi) was significantly reduced at 1 and 10 Hz after both exercise tests. The BPNS Pdi was recovered to control values by 60 min postnormoxic exercise but was still reduced 90 min posthypoxic exercise. The mean percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Experiencing the same amount of diaphragm fatigue in a shorter time period in hypoxic exercise may have been due to 1) the increased expiratory flow limitation and diaphragmatic muscle work, 2) decreased O2 transport to the diaphragm, and/or 3) increased levels of circulating metabolites.
The double product (DP) is the product of the heart rate (HR) and systolic blood pressure (SBP). The double product break point (DPBP) is a physiologic threshold that occurs at similar exercise intensities to that of the ventilatory threshold (VT). The influence of aerobic exercise training on the DPBP has not yet been examined. The purpose of this study was to examine whether aerobic exercise training (ET) increases the exercise intensity at which the DPBP occurs, and whether it increases in a similar fashion to the VT. Seven males and 11 females, all sedentary (mean ± SD: age = 29.9 ± 10.5 yr) underwent supervised cardiopulmonary exercise testing using a cycle ergometer ramp protocol at baseline and after eight weeks of vigorous ET on a cycle ergometer. The VT was determined by gas analysis and the V-slope method. Experienced observers using standardized instructions visually determined the DPBP. Following ET, VO 2peak , maximal workload, and body composition variables all showed significant positive changes. The VO 2 at which the DPBP and VT occurred increased significantly from baseline to follow-up (p <.001). At baseline and at follow-up, the DPBP and VT did not differ. The DPBP and VT were significantly correlated to each other at both time points. Results suggest that the DPBP responds to ET in a similar fashion to that of the VT, and may be an easier and more useful marker of the VT for exercise training purposes.
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