Determination of the "anaerobic threshold".
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Biomedical subjects
Publications and source records attributed to R L Hughson.
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The variability in the estimation of the mean response time (MRT) of O2 uptake (VO2) kinetics from single ramp work rate exercise tests was examined in six repetitions by five fit subjects. Work rate increased at 50 W/min from a base line of 25 W to a work rate of 120% ventilatory threshold. Breath-by-breath data were analyzed by linear regression from 2 min after the onset of the ramp to the 120% work rate. Individual subjects showed approximately twofold differences in estimates of MRT; the coefficient of variation from individuals ranged from 18.5 to 29.3%. The MRT obtained as the mean from the individual repetitions did not differ from the MRT obtained from pooled within-subject data. Analysis of variance on the individual MRT estimates showed 53.9% of the variability was attributable to the slope of the regression, whereas only 2.4% could be attributed to baseline VO2. It was concluded that several repetitions of the ramp work rate tests should be pooled prior to estimation of kinetics parameters.
The immediate storage of CO2 at the onset of exercise was estimated in 5 subjects as the difference between measured and predicted CO2 production at work rates of 33, 53 and 75% VO2max. Three time varying models of respiratory exchange ratio (RER) were used to obtain an expected range of predicted CO2 production. Calculated CO2 storage in the transition from rest to 33% VO2max ranged from 0.33 to 0.38 ml X kg-1 X torr-1; from 33 to 53% VO2max, corresponding values were -0.04 to 0.14 ml X kg-1 X torr-1; and, from 53 to 75% VO2max, values ranged from -0.25 to 0.16 ml X kg-1 X torr-1. In two models, CO2 storage decreased significantly at the highest work rate. Estimates of CO2 storage by hyperventilation in the steady state of exercise yielded significantly greater storage. It was concluded that immediate CO2 storage at the onset of exercise was less than hyperventilation estimates, and that it tended to decrease with metabolic acidosis.
Cardiac output (Q) was estimated in supine rest and in upright cycling at several work rates up to 200 W in five male and one female subjects. At least four repetitions of both the CO2-rebreathing plateau method (Collier, J. Appl. Physiol. 9:25-29, 1956) and the Kim et al. (J. Appl. Physiol. 21: 1338-1344, 1966) single-breath method were performed at each work rate, in a steady state of O2 consumption and heart rate. At supine rest and low work rates, estimates of Q were similar by the two methods. However, at higher work rates, the single-breath method significantly (P less than 0.05) underestimated the value obtained by CO2 rebreathing. The reason for the difference in estimates of Q by the two methods was traced to the determination of arterial partial pressure of CO2 (PaCO2) and mixed venous partial pressure of CO2 (PvCO2). The estimate of PaCO2 from the single-breath method was approximately 88.5% of the estimate from end-tidal PCO2 used with the rebreathing method (P less than 0.001). The oxygenated PvCO2 calculated from the single-breath Q averaged approximately 92.5% of the PvCO2 from CO2 rebreathing (P less than 0.0001). The difference in estimates of Q was not eliminated by using a logarithmic form of the CO2 dissociation curve with the single-breath method.
Chronic, as well as acute, exercise increases circulating PRL in females. The response of males to repeated exercise, however, is unknown. The purpose of the present study was to examine the effects of acute and chronic exercise on plasma PRL levels in untrained males. Eight male subjects performed cycle ergometer exercise at 50% of their maximal oxygen uptake on 10 consecutive days. The subjects exercised in an environmental chamber maintained at 39 degrees C and 30% relative humidity. PRL levels were measured on days 1, 5, and 10 before exercise, and after 20 and 45 minutes of exercise. Acute exercise increased PRL levels. However, plasma levels did not significantly increase during exercise on days 5 and 10. This suggests a similarity in the PRL response to acute exercise in males and females, but a sex difference in the response to chronic exercise.
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The power-endurance time curve described for cycle ergometry has been examined with respect to high velocity treadmill running to exhaustion. On a cycle ergometer, a hyperbolic function has been described that can be linearized by expressing power relative to the inverse of time to exhaustion. The mathematical relationship of this linear function is P = W'/t + theta f, where P = power output, W' = slope of regression, and theta f = fatigue threshold (intercept of power output). Six cross-country runners took part as subjects. Each ran to exhaustion with the treadmill at 6 different velocities between 19.2 and 22.4 km/h. The linear regressions fitted to velocity versus 1/time had correlation coefficients between r = 0.979 and 0.997. It was concluded that the treadmill velocity-endurance time relationship for runs of 2-12 min duration conformed to a similar hyperbolic function as that described for cycle ergometry. The two parameters W' and theta f might provide valuable indices of physical performance potential, which can be used to monitor training responses in competitive runners.
The effects of beta-adrenergic receptor blockade (100 mg oral metoprolol) or matched placebo on gas exchange kinetics were studied in six males. Ventilation and gas exchange were monitored in four transitions for each treatment from loadless pedalling (0 W) to a selected work rate (100 W) and back to 0 W. Breath-by-breath data were averaged for analysis. Oxygen uptake (VO2) kinetics were significantly slowed at the onset of exercise and recovery by beta-blockade. This resulted in larger oxygen deficit and oxygen debt (671 +/- 115, 586 +/- 87 ml O2, respectively) for beta-blockade than for placebo (497 +/- 87, 474 +/- 104 ml O2). In addition, oxygen deficit was significantly larger than oxygen debt during beta-blockade tests. These results can be explained by greater utilization of oxygen and creatine phosphate stores as well as anaerobic glycolysis at the onset of 100 W exercise with beta-blockade. Carbon dioxide output (VCO2) kinetics were significantly slowed by beta-blockade only at the onset of exercise. Expired ventilation (VE) kinetics were not affected by beta-blockade. At 0 W, VE was significantly reduced by beta-blockade. Heart rate was lower at all times with beta-blockade. Kinetics of heart rate were not affected. These data for VO2 kinetics at the start and end of exercise indicate that even in moderate-intensity exercise, lactic acid production can contribute significantly to energy supply. The use of the term ' alactic ' to describe the deficit and debt associated with this exercise is not appropriate.
To investigate the role of high-intensity intermittent exercise on adaptations in blood volume and selected hematological measures, four male subjects aged 19-23 yr [peak O2 consumption (VO2max) = 53 ml X min-1 X kg-1] performed supramaximal (120% VO2max) cycle exercise on 3 consecutive days. Each exercise session consisted of intermittent work performed as bouts of 1-min work to 4-min rest until fatigue or until a maximum of 24 repetitions had been completed. Measurements on blood samples were made before the exercise period and 24 h after the last exercise session. Plasma volume (PV) estimated using 131I-human serum albumin increased by 11.6% (3,504 vs. 3,912 ml; P less than 0.05). Total blood volume (TBV) based on PV and hematocrit (Hct) values increased by 4.5% (5,798 vs. 6,059 ml; P less than 0.05), whereas red cell volume (RCV) decreased by 6.4% (2,294 vs. 2,147 ml; P less than 0.05). Measurements of hematological indices indicated significant reductions (P less than 0.05) in whole-blood Hct (39.7 vs. 35.5%), hemoglobin concentration (15.5 vs. 13.9 g/100 ml), hemoglobin content (897 vs. 839 g), and red blood cell count (5.15 vs. 4.55 X 10(6) X mm-3). The findings of this study suggest that exercise intensity is a major factor in promoting exercise-induced hypervolemia and that rapid elevations in PV can be induced early in training.
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The kinetics of oxygen uptake (VO2) were assessed in 17 normal subjects with beta-blockade and placebo. beta-blockade was achieved with either 50 mg oral metoprolol or 40 mg oral propranolol, each twice per day. Tests were conducted on the cycle ergometer at work rates approximating 80% of the work rate at ventilatory anaerobic threshold. Work rate was initiated as a square wave starting from prior rest. Data obtained 48 h, 1 week, and 4 weeks after starting drug or placebo were pooled to increase the number of points for regression analysis of kinetic parameters. While there were no differences in the plateau values for VO2 with and without beta-blockade, the rate of adaptation to steady state was significantly slower with beta-blockade than with placebo (P less than 0.05). This resulted in an increase of oxygen deficit by approximately 200 ml O2. Cardiac output measured by CO2 rebreathing was significantly reduced by beta-blockade (metoprolol by 4.1%, propranolol by 12.2%, both P less than 0.05). Blood lactate concentration was unaffected by beta-blockade. It was concluded that the influence of beta-blockade on the oxygen transport system was responsible for the significantly slower increase of VO2 to steady state in submaximal exercise.
The influence of prior exercise state on the kinetics of VO2, VE, and HR was studied in six subjects. The exercise conditions tested were square wave increases in work rate from rest to 80% of the work rate at anaerobic threshold (AT), from O W loadless pedaling to 80% AT, from rest to 40% AT, and from 40% to 80% AT. The kinetic response was evaluated by the time constant (tau) and mean response time (MRT = time to achieve 63% response) as determined by nonlinear regression. For both VO2 and HR, tau and MRT were not significantly different in the rest or O W to 80% AT tests, but were significantly faster in the rest to 40% AT test and significantly slower in the 40% to 80% AT test than the rest and O W to 80% AT tests. The tau for VE was significantly slower in the 40% to 80% AT tests than in the other tests. The coincident variation of HR and VO2 kinetics is taken as support for the hypothesis that VO2 kinetics are controlled by oxygen transport. Evidence from the literature that supports both the oxygen transport and the oxygen utilization for the control of VO2 kinetics is reviewed.
The exercise responses to two different progressive, upright cycle ergometer tests were studied in nine healthy, young subjects either with no drug (ND) or following 48 h or oral propranolol (P) (40 mg q.i.d.). The ergometer tests increased work rate by 30 W either every 30 s or every 4 min. Propranolol caused a significant (p less than 0.05) reduction in peak oxygen uptake (VO2) during both the 30-s and 4-min tests (30-s ND, 3949 +/- 718 mL X min-1 (means +/- SD); 30-s P, 3408 +/- 778 mL X min-1; 4-min ND, 4058 +/- 409 mL X min-1; 4-min P, 3725 +/- 573 mL X min-1). There was no difference between 30-s ND and 4-min ND for peak VO2. The ventilatory anaerobic threshold was not significantly different between any test (30-s ND, 2337 +/- 434 mL O2 X min-1; 30-s P, 2174 +/- 406 mL O2 X min-1; ND, 2433 +/- 685 mL O2 X min-1; 4-min P, 2296 +/- 604 mL O2 X min-1). The VO2 at which blood lactate had increased by 0.5 mM above resting levels was significantly lower than the ventilatory anaerobic threshold for the 4-min ND (1917 +/- 489) and the 4-min P (1978 +/- 412) tests, but was not different for the 30-s ND and 30-s P tests. At exhaustion in the progressive tests, the blood PCO2 was higher (p less than 0.05) in both 30-s tests than 4-min tests.(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to investigate the interrelationship between the ventilatory anaerobic threshold (VAT), the blood lactate anaerobic threshold (LAT), and the alteration in muscle metabolism. Ten subjects (5 men and 5 women) performed progressive exercise to exhaustion on two occasions for determination of the VAT and the LAT. For both AT criteria, the initial breakpoints (P less than 0.05) in the relationship between ventilation (VE) and O2 uptake (VO2VAT) and lactate (La) and power output (POLAT) were determined by multisegmental linear regression. During three subsequent tests the subjects performed progressive exercise to various percentages of the VO2VAT. Biopsies were obtained from the musculus vastus lateralis for determination of selected glycolytic intermediates at the cessation of exercise. It was found that the VO2VAT, expressed in terms of power output (POVAT), occurred at a higher value (P less than 0.05) than the POLAT (1,004 vs. 621 kg X min-1). Blood La values at these power outputs were 2.09 and 1.25 mM, respectively. Determination of the muscle La concentration at 79, 94, and 110% of VO2VAT indicated significant increases (P less than 0.05) from rest values of 1.59 to 4.49, 6.37, and 11.3 mmol X kg wet wt-1, respectively. It is concluded that the gas exchange AT as determined by the relationship between VE and VO2VAT and the AT as determined by blood La accumulation (LAT) are not coincidental. In addition the elevation in muscle anaerobic glycolysis precedes both the VAT and the blood LAT in this progressive exercise test.
The kinetics of oxygen uptake (VO2), carbon dioxide output (VCO2), and expired ventilation (VE) in the transition from rest or from prior exercise were studied in response to step increases in power output (PO). The data were modeled with a single-component exponential function incorporating a time delay (TD). Each subject exercised on four occasions. Test 1 was an incremental test for determination of ventilatory anaerobic threshold (AT). Step increase tests were rest to 80% of PO at AT (test 2), rest-40% AT (3a), 40-80% AT (3b), rest-40% AT (4a), and 40-120% AT (4b). Respiratory gas exchange was monitored by open-circuit techniques. The VO2 kinetics showed the time constant (tau) to be longer in the transitions from prior exercise [tests 3b and 4b were 60.6 +/- 10.8 (SD) and 79.2 +/- 17.4 s] than from rest (tests 2, 3a, and 4a were 37.8 +/- 7.2, 30.0 +/- 7.8, and 39.6 +/- 17.4 s). The mean response time (MRT = tau + TD) was also longer for these tests. Kinetic analysis for VCO2 showed a tendency for tau to be shorter for the tests from prior exercise, but neither tau nor tau + TD were significantly different between tests. In contrast to VCO2, VE kinetics showed a significantly longer tau + TD for test 3b (P less than 0.05) and test 4b (P less than 0.01). This study has shown the VO2 kinetics to be delayed when a given increment in PO occurred from prior exercise, whether the final PO was below or above the AT. Further, the dissociation of VCO2 and VE kinetics does not support a direct link between these two variables as the sole control factor in exercise hyperpnea.
The anaerobic threshold has generally been determined by simple visual inspection of ventilation or other gas-exchange data obtained during incremental exercise. To establish objective criteria for the determination of anaerobic threshold, a computer algorithm has been developed that models the ventilatory response to exercise using multisegment linear regression. The best-fit regression model is chosen by minimizing the pooled residual sum of squares . The anaerobic threshold is reported as the first break point in that model. The computer-determined anaerobic threshold values for 37 subjects were compared with subjectively determined values as chosen by four independent observers. The observers' estimates, when pooled to yield a single a single value for each subject, gave a mean value for the gas-exchange anaerobic threshold of 2.26 +/- 0.69 l/min. The estimates by the computer method averaged 2.21 +/- 0.65 l/min. The correlation coefficient for these two methods was 0.94.
The effect of work rate increase in ramp work tests was studied in six healthy subjects. Each subject exercised on a cycle ergometer with the work rate incremented by either 65.4 W . min-1 and 49.0 W . min-1 for the fast ramps or 8.2 W . min-1 and 6.1 W . min-1 for the slow ramps for male and female subjects, respectively. Gas exchange was monitored by open-circuit spirometry. Arterialized venous blood samples were obtained from a dorsal hand vein. The peak VO2 was not significantly different for fast (3218 +/- 602 ml . min-1, X +/- SD) and slow (3237 +/- 601 ml . min-1) ramp tests. Gas-exchange anaerobic threshold, determined by multi-segment linear regression of VE vs VO2, was similar for fast and slow ramp tests (1742 +/- 415 and 1925 +/- 639 ml O2 . min-1, P greater than 0.05). The VO2 at which blood lactate increased 0.5 mM above resting levels was lower (1463 +/- 259 ml . min-1, P less than 0.05) than the gas-exchange anaerobic threshold for the slow ramp test. The VO2 at which blood lactate reached 2.0 mM was greater (2383 +/- 247 ml . min-1, P less than 0.05) than the gas-exchange anaerobic threshold for the fast ramp test. In addition to these lactate differences, blood pH and HCO3- did not change in direct proportion to the lactate concentration in either test. Blood PCO2 was significantly (P less than 0.05) greater at the point of exhaustion in the fast ramp test (42.2 +/- 2.3 mmHg) than in the slow ramp test (26.7 +/- 2.1 mmHg). It is concluded that the gas-exchange anaerobic threshold can be clearly dissociated from the blood lactate threshold by altering the work rate forcing function. Other mechanisms, such as H+ efflux and CO2 storage capacity, are more likely explanations for the gas-exchange anaerobic threshold.
The coupling between ventilation (VE) and oxygen uptake (VO2) or carbon dioxide production (VCO2) was tested during constant-load cycle ergometry in five healthy, young female volunteers. The ratio of VCO2/VO2 (respiratory quotient, RQ) was altered during exercise by prior dietary manipulation involving three diets: (a) low carbohydrate (L), (b) high carbohydrate (H) and (c) normal, mixed (M) diet. The constant power output selected for a 10-min exercise period approximated 80% of the power output at the anaerobic threshold. At rest and during exercise, the RQ and blood lactate concentration were lower following the L diet than either the H or M diets. All measurements for the H and M diets were similar. In exercise, the VO2 was higher in the L diet (1428 ml/min) than the H diet (1293 ml/min) (P less than 0.05). Although the VCO2 tended to be lower and the VE higher during exercise in the L diet, these values were not significantly different from the H dit. The ratio of VE/VO2 was not different fro the two diets. In the L diet, VE/VCO2 was greater than the H diet (P less than 0.05). A kinetic analysis showed no differences as a consequence of the diets in the rate of adaptation of VO2, VCO2 or VE to the plateau levels. This study has demonstrated an uncoupling of the constant relationship between VE and VCO2 by prior dietary manipulation; however, the relationship between VE and VO2 remained constant in spite of a change in the metabolic RQ which altered VO2 and VCO2 at a constant power output.