PubMed · 9266908
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A Simon, G Veress, I Berényi. 1997. Oxygen deficit during exercise testing.. https://doi.org/10.1378/chest.112.2.567-a
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This paper deals with the subject of anaerobic threshold measurements for athletes involved in aerobic or aerobic/anaerobic sports. Traditionally, anaerobic threshold has been determined using invasive tests or using a non-invasive technique using steady-state heart-rate/work rate data. Non-invasive tests have the advantage of not requiring specialised equipment, but the acquisition of steady-state information can be problematic. This paper demonstrates how dynamical data can be used to accurately determine the steady-state heart-rate/work-rate curve (SSHW curve) using neural network dynamic models.
INTRODUCTION: The identification of the HR (or RPE) associated with blood lactate concentrations of 2.5 mmol x L(-1)(aerobic threshold) (AerT) and 4.0 mmol x L(-1)(anaerobic threshold) (AnT) is a common method for defining training intensities. It is often assumed that the HR at AerT and AnT changes with changes in fitness, much as the power output (Watts: W) associated with AerT and AnT is known to change. METHODS: We studied speed skaters (N = 13, 7 male, 6 female) during spring (deconditioned) and fall (conditioned) evaluations, using cycle ergometry (stage duration = 5 min) to determine W, HR, and RPE at AerT, AnT, and at maximal exercise (3000 (female) and 5000 (male) m cycle time trials). RESULTS: In the spring vs. fall evaluations, the power output at AerT was 127+/-12 vs 162+/-9 W (P<0.05), at AnT was 216+/-14 vs. 230+/-13 W (P<0.05), and at maximal exercise was 341+/-15 vs. 364+/-19 W (P<0.05); HR at AerT was 129+/-6 vs. 130+/-7 bpm (P>0.05), at AnT was 162+/-7 vs. 164+/-7 bpm (P>0.05), and at maximal exercise was 196+/-6 vs. 198+/-5 bpm (P>0.05); RPE at AerT was 2.7+/-0.9 vs. 2.6+/-0.8 (P>0.05), at AnT was 5.3+/-1.0 vs. 5.3+/-0.9 (P>0.05). CONCLUSIONS: These data suggest that although power output at AerT, AnT, and maximal exercise changes significantly with conditioning, there is no systematic change in the associated values for HR and/or RPE used as practical markers of training intensity. Accordingly, a single well-conducted evaluation may allow evaluation of appropriate training markers that may be longitudinally stable.
BACKGROUND: Exercise training increases exercise capacity in patients with reduced ventricular function in part through improved skeletal muscle metabolism, but the effect training might have on abnormal ventilatory and gas exchange responses to exercise has not been clearly defined. METHODS: Twenty-five male patients with reduced ventricular function after a myocardial infarction were randomized to either a 2-month high-intensity residential exercise training program or to a control group. Before and after the study period, upright exercise testing was performed with measurements of ventilatory gas exchange, lactate, arterial blood gases, cardiac output, and pulmonary artery and wedge pressures. RESULTS: In the exercise group, peak VO2 and VO2 at the lactate threshold increased 29 and 39%, respectively, whereas no increases were observed among controls. Maximal cardiac output increased only in the exercise group (1.7 L x min(-1), P < 0.05), and no changes in rest or peak exercise pulmonary pressures were observed in either group. At baseline, modest inverse relationships were observed between pulmonary wedge pressure and peak VO2 both at rest (r = -0.56, P < 0.05) and peak exercise (r = -0.43, P < 0.05). Maximal VE/VCO2 was inversely related to maximal cardiac output (r = -0.72, P < 0.001). Training did not have a significant effect on these relationships. Training lowered VE/VO2, heart rate, and blood lactate levels at matched work rates throughout exercise and tended to lower maximal Vd/Vt. The slope of the relationship between VE and VCO2 was reduced after training in the exercise group (0.33 pre vs 0.27 post, P < 0.01), whereas control patients did not differ. CONCLUSIONS: Exercise training among patients with reduced left ventricular function results in a systematic improvement in the ventilatory response to exercise. Training increased maximal cardiac output, tended to lower Vd/Vt, and markedly improved the efficiency of ventilation. Peak VO2 and ventilatory responses to exercise were only modestly related to pulmonary vascular pressures, and training had no effect on the relationships between exercise capacity, ventilatory responses, and pulmonary pressures.