Testing procedures for the assessment of anaerobic energy metabolism during muscular work have not yet gained the relevance of tests assessing maximal aerobic power. The diagnosis of aerobic power allows one, through the choice of an adequate testing protocol, to design a test that mainly measures the power of aerobic metabolism by means of indicators like VO 2max and lactate. With regard to tests for the assessment of anaerobic power and capacity, however, alactic, lactic, and oxidative components of energy expenditure as a whole cannot be differentiated by means of simple parameters (e.g., lactate and time until exhaustion). By means of computer simulations of energy metabolism for supramaximal loads with durations until exhaustion of about 10 s and 60 s as well as the isolated variation of the concentration of muscle phosphocreatine, the maximal rate of lactate production, and the maximal aerobic power (VO 2max ), the influence of the single components on energy metabolism as a whole is presented in a semi-quantitative way. Subsequent testing procedures for the measurement of alactic and lactic power as well as alactic and lactic capacity are presented. Finally critical-power method and method for the determination of maximal accumulated O 2 deficit are described in greater detail, because both methods are widely discussed in contemporary international literature.
Noninvasive cardiac output (CO) measured by arterial pulse analysis was compared with that measured by inert gas rebreathing in six healthy male volunteers. Pulse contour analysis was applied to the pressure wave output of a Finapres, which noninvasively measures continuous arterial pressure in a finger. Data were collected before, during, and after a 10-day 6 degrees head-down tilt experiment. Intravenous saline loading and lower body negative pressure stimuli varied CO over 2.8-9.6 l/min, as measured by the rebreathing technique. Because pulse contour provides only relative changes in CO, to obtain absolute values it must be calibrated against another measurement. Pulse contour data were calibrated every measurement day against the mean of two to four control rebreathing CO measurements before the lower body negative pressure or intravenous saline loading stimuli. Using one averaged calibration factor per subject for a total of 27 days, we compared the results of both methods. The linear regression between pulse contour (Pc CO) and rebreathing CO (Rebr CO) was Pc CO = 0.15 + 0.98(Rebr CO) (r = 0.96). The standard deviation of the difference of the two methods was 0.5 l/min (n = 205), excluding data used for calibration. By monitoring pulse contour CO before and during rebreathing, the rebreathing maneuver itself was shown to produce a substantial increase in CO that was mainly related to an increase in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Pulmonary diffusing capacities (DL) of NO and CO were determined simultaneously from rebreathing equilibration kinetics in anesthetized paralyzed supine dogs (mean body wt 20 kg) after denitrogenation (replacement of N2 by Ar). During rebreathing the dogs were ventilated in closed circuit with a gas mixture containing 0.06% NO, 0.06% 13C18O, and 1% He in Ar for 15 s, with tidal volume of 0.5 liter and frequency of 60/min. The partial pressures of NO, 13C18O, 16O18O, N2, Ar, CO2, and He in the trachea were continuously analyzed by mass spectrometry. Measurements were performed at various O2 levels characterized by the mean end-expired PO2 during rebreathing (PE'O2). In control conditions ("normoxia," PE'O2 = 67 +/- 8 Torr) the following mean +/- SD values were obtained (in ml.min-1.Torr-1): DLNO = 52.4 +/- 11.0 and DLCO = 15.4 +/- 2.9. In hypoxia (PE'O2 = 24 +/- 7 Torr) DLNO increased by 11 +/- 8% and DLCO by 19 +/- 10%, and in hyperoxia (PE'O2 = 390 +/- 26 Torr) DLNO decreased to 87 +/- 3% and DLCO to 56 +/- 8% with respect to values in normoxia. DLNO/DLCO of 3.24 +/- 0.06 (hypoxia), 3.38 +/- 0.31 (normoxia), and 5.54 +/- 1.04 (hyperoxia) were significantly higher than the NO/CO Krogh diffusion constant ratio (1.92) predicted for simple diffusion through aqueous layers. With increasing O2 uptake elicited by 2,4-dinitrophenol, DLNO and DLCO increased and DLNO/DLCO remained close to unchanged. The results suggest that the combined effects of diffusion and chemical reaction with hemoglobin limit alveolar-capillary transport of CO. If it is assumed that reaction kinetics of NO with hemoglobin (known to be extremely fast) are not rate limiting for NO uptake, the contribution of the slow chemical reaction with hemoglobin to the total CO uptake resistance (= 1/DLCO) was estimated to be 38% in hypoxia, 41% in normoxia, and 64% in hyperoxia. The various factors expected to restrict the validity of this analysis are discussed, in particular the effects of functional inhomogeneity.
BackgroundThe purpose of this study was the comparison of the calculated (MLSSC) and experimental power (MLSSE) in maximal lactate steady-state (MLSS) during cycling.Methods13 male subjects (24.2 ± 4.76 years, 72.9 ± 6.9 kg, 178.5 ± 5.9 cm, trueV˙normalO2max: 60.4 ± 8.6 ml min−1 kg−1, trueV˙normalLamax: 0.9 ± 0.19 mmol l-1 s-1) performed a ramp-test for determining the trueV˙normalO2max and a 15 s sprint-test for measuring the maximal glycolytic rate (trueV˙normalLamax). All tests were performed on a Lode-Cycle-Ergometer. trueV˙normalO2max and trueV˙normalLamax were used to calculate MLSSC. For the determination of MLSSE several 30 min constant load tests were performed. MLSSE was defined as the highest workload that can be maintained without an increase of blood-lactate-concentration (BLC) of more than 0.05 mmol l−1 min−1 during the last 20 min. Power in following constant-load test was set higher or lower depending on BLC.ResultsMLSSE and MLSSC were measured respectively at 217 ± 51 W and 229 ± 47 W, while mean difference was −12 ± 20 W. Orthogonal regression was calculated with r = 0.92 (p < 0.001).ConclusionsThe difference of 12 W can be explained by the biological variability of trueV˙normalO2max and trueV˙normalLamax. The knowledge of both parameters, as well as their individual influence on MLSS, could be important for establishing training recommendations, which could lead to either an improvement in trueV˙normalO2max or trueV˙normalLamax by performing high intensity or low intensity exercise training, respectively. Furthermore the validity of trueV˙normalLamax -test should be focused in further studies.
Complex performance diagnostics in sports medicine should contain maximal aerobic and maximal anaerobic performance. The requirements on appropriate stress protocols are high. To validate a test protocol quality criteria like objectivity and reliability are necessary. Therefore, the present study was performed in intention to analyze the reliability of maximal lactate production rate (V.Lamax) by using a sprint test, maximum oxygen consumption (V.O2max) by using a ramp test and, based on these data, resulting power in calculated maximum lactate-steady-state (PMLSS) especially for amateur cyclists. All subjects (n = 23, age 26 ± 4 years) were leisure cyclists. At three different days they completed first a sprint test to approximate V.Lamax. After 60 min of recreation time a ramp test to assess V.O2max was performed. The results of V.Lamax-test and V.O2max-test and the body weight were used to calculate PMLSS for all subjects. The intra class correlation (ICC) for V.Lamax and V.O2max was 0.904 and 0.987, respectively, coefficient of variation (CV) was 6.3% and 2.1%, respectively. Between the measurements the reliable change index of 0.11 mmol·l -1s -1 for V.Lamax and 3.3 mlkg -1min -1 for V.O2max achieved significance. The mean of the calculated PMLSS was 237 ± 72 W with an RCI of 9 W and reached with ICC = 0.985 a very high reliability. Both metabolic performance tests and the calculated PMLSS are reliable for leisure cyclists.
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