Kinetics of oxygen uptake at the onset of exercise near or above peak oxygen uptake.

We tested the hypothesis that kinetics of O(2) uptake (VO(2)) measured in the transition to exercise near or above peak VO(2) (VO(2 peak)) would be slower than those for subventilatory threshold exercise. Eight healthy young men exercised at approximately 57, approximately 96, and approximately 125% VO(2 peak). Data were fit by a two- or three-component exponential model and with a semilogarithmic transformation that tested the difference between required VO(2) and measured VO(2). With the exponential model, phase 2 kinetics appeared to be faster at 125% VO(2 peak) [time constant (tau(2)) = 16.3 +/- 8.8 (SE) s] than at 57% VO(2 peak) (tau(2) = 29. 4 +/- 4.0 s) but were not different from that at 96% VO(2 peak) exercise (tau(2) = 22.1 +/- 2.1 s). VO(2) at the completion of phase 2 was 77 and 80% VO(2 peak) in tests predicted to require 96 and 125% VO(2 peak). When VO(2) kinetics were calculated with the semilogarithmic model, the estimated tau(2) at 96% VO(2 peak) (49.7 +/- 5.1 s) and 125% VO(2 peak) (40.2 +/- 5.1 s) were slower than with the exponential model. These results are consistent with our hypothesis and with a model in which the cardiovascular system is compromised during very heavy exercise.     

Maximal oxygen uptake in Chilean workers of normal nutritional status

Maximum oxygen uptake (VO2max) was measured directly and predicted from cardiac frequency measurements in 54 healthy Chilean industrial workers aged 20 to 55 years, together with assessment of their dietary intake, body composition and blood chemistry. Measurement of VO2 was performed on a motor-driven treadmill. The predicted VO2max was obtained using a cycle ergometer by two methods: 1) the Astrand-Ryhming nomogram and 2) the linear relationship between "steady state" heart rate (HR) and submaximum work, with subsequent extrapolation to "maximum" heart rate. Extrapolation of the HR/load regression line to 170 bpm permitted determination of the physical working capacity at 170 bpm (W170). VO2max for the 20-29 year group (Group I) averaged 3624 ml.min-1 and decreased to 3066 ml.min-1 in the 50-55 year group (Group IV). Lower values were obtained using the Astrand-Ryhming nomogram and HR/load regression (-15% and -9% respectively). W170 was also affected by age (Group I: 190.6 W and Group IV: 158.5 W). No significant correlation were found between VO2max and plasma variables, with the exception of cholesterol (r = 0.59). On the contrary, anthropometric variables showed significant correlations with VO2max, which permitted the prediction of VO2max using multiple regression equations. The two best correlations were: 1. VO2max = 0.800 - 0.0225.(A) +0.0189.(W)+1.26.(H) (r = 0.87; p less than 0.001) 2. VO2max = 0.996 - 0.0176.(A) + 0.025.(W) + 0.838.(H) + 0.0255.(LBM) (r = 0.88; p less than 0.001) where A = years of age; W = body weight in kg; H = height in m and LBM = lean body mass in kg.     

Determination of maximal oxygen consumption in exercising pregnant sheep.

Previous work with pregnant ewes has shown that acute bouts of exercise may cause changes in plasma hormone concentrations, blood flow distribution, and maternal and fetal temperatures. However, most of these studies do not quantify the chosen exercise intensity through measurement of oxygen consumption (VO2). Therefore the purpose of this study was to statistically model the VO2 response of pregnant sheep to treadmill (TM) exercise to determine the exercise intensities (% maximal VO2) of previous studies. Ewes with either single (n = 9) or twin (n = 5) fetuses were studied from 100 to 130 days of gestation. After 1-2 wk of TM habituation, maximal VO2 (VO2max) was determined by measurements of VO2 (open flow-through method) and blood lactate concentration. VO2 was measured as a function of TM incline (0, 3, 5, and 7 degree) and speed (0.8-3.4 m/s). VO2max averaged 57 +/- 7 (SD) ml.min-1.kg-1, and peak lactate concentration during exercise averaged 22 +/- 2 mmol/l. The relationship between VO2 (ml.min-1.kg-1) and incline (INC) and speed (SP) [VO2 = 0.70(INC) + 13.95(SP) + 1.07(INC x SP) - 1.18] was linear (r2 = 0.94). Our findings suggest that most previous research used exercise intensities less than 60% VO2max and indicate the need for further research that examines the effect of exercise during pregnancy at levels greater than 60% VO2max.     

Errors in predicting maximal oxygen consumption in pregnant women.

This study was designed to determine the accuracy of estimated values of maximal heart rate (HRmax) and oxygen consumption (VO2) during pregnancy. We measured HR and maximal VO2 (VO2max) at rest and during cycle (CE) and treadmill exercise (TE) tests with rapidly increasing exercise intensities during gestation and after delivery. Pregnancy was found to affect the linear relationship of HR and %VO2max so that the intercept increases with advancing gestation and the slope decreases. Estimated maximal HR (HRmax, est), 220 - age (yr) x beats/min, overestimated measured HRmax by 8% (CE) and 5% (TE). For VO2max estimated by Astrand's nomogram (VO2max, est1) and by linear extrapolation of submaximal values of HR and VO2 to HRmax, est (VO2max, est2), individual errors were large (SD 17-28%). Mean VO2max, est1 overestimated measured VO2max by 20% during CE but not during TE (-2%) and elicited the erroneous impression that VO2max decreases during CE in pregnancy. Mean VO2max, est2 values were not significantly different from measured VO2max values. This apparent accuracy resulted from two opposing errors: 1) HRmax, est overestimated HRmax, and 2) above 70% VO2max the slope of the HR-%VO2max relationship was significantly reduced. Therefore neither method to estimate VO2max can replace the measurement of VO2max.     

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.     

Characterization of the cortisol response to incremental exercise in physically active young men

This study examined the cortisol response to incremental exercise; specifically to see if there was an increase in blood cortisol levels at low intensity exercise (i.e., < 60% VO2 intensity threshold) and determine whether a linear relationship existed between the blood cortisol responses and exercise of increasing workloads (i.e., intensity). Healthy, physically active young men (n = 11) completed exercise tests involving progressive workload stages (3 min) to determine peak oxygen uptake responses (VO2). Blood specimens were collected at rest and at the end of each stage and analyzed for cortisol. Results showed cortisol was significantly increased from resting levels at the end of the first exercise stage (80 W; 41.9 +/- 5.4% peak VO2) and remained significantly elevated from rest until the exercise ended. Interestingly, however, the cortisol concentrations observed at 80 W through 200 W did not significantly differ from one another. Thereafter, during the final two stages of exercise the cortisol concentrations increased further (p < 0.01). The subjects exceeded their individual lactate thresholds over these last two stages of exercise. Regression modeling to characterize the cortisol response resulted in significant regression coefficients (r = 0.415 [linear] and r = 0.655 [3rd order polynominal], respectively; p < 0.05). Comparative testing (Hotelling test) between the two regression coefficents revealed the polynominal model (sigmoidal curve) was the significantly stronger of the two (p = 0.05). In conclusion, the present findings refute the concept that low intensity exercise will not provoke a significant change in blood cortisol levels and suggest the response to incremental exercise involving increasing exercise workloads (i.e., intensities) are not entirely linear in nature. Specifically, a sigmoid curve more highly accurately characterizes the cortisol response to such exercise.     

Relationship between arterial oxygen desaturation and ventilation during maximal exercise.

The purpose of the present study was to investigate the contribution of ventilation to arterial O2 desaturation during maximal exercise. Nine untrained subjects and 22 trained long-distance runners [age 18-36 yr, maximal O2 uptake (VO2max) 48-74 ml.min-1 x kg-1] volunteered to participate in the study. The subjects performed an incremental exhaustive cycle ergometry test at 70 rpm of pedaling frequency, during which arterial O2 saturation (SaO2) and ventilatory data were collected every minute. SaO2 was estimated with a pulse oximeter. A significant positive correlation was found between SaO2 and end-tidal PO2 (PETO2; r = 0.72, r2 = 0.52, P < 0.001) during maximal exercise. These statistical results suggest that approximately 50% of the variability of SaO2 can be accounted for by differences in PETO2, which reflects alveolar PO2. Furthermore, PETO2 was highly correlated with the ventilatory equivalent for O2 (VE/VO2; r = 0.91, P < 0.001), which indicates that PETO2 could be the result of ventilation stimulated by maximal exercise. Finally, SaO2 was positively related to VE/VO2 during maximal exercise (r = 0.74, r2 = 0.55, P < 0.001). Therefore, one-half of the arterial O2 desaturation occurring during maximal exercise may be explained by less hyperventilation, specifically for our subjects, who demonstrated a wide range of trained states. Furthermore, we found an indirect positive correlation between SaO2 and ventilatory response to CO2 at rest (r = 0.45, P < 0.05), which was mediated by ventilation during maximal exercise. These data also suggest that ventilation is an important factor for arterial O2 desaturation during maximal exercise.     

Relationship between muscle fatigue and oxygen uptake during cycle ergometer exercise with different ramp slope increments.

The surface electromyogram (EMG) from active muscle and oxygen uptake (VO2) were studied simultaneously to examine changes of motor unit (MU) activity during exercise tests with different ramp increments. Six male subjects performed four exhausting cycle exercises with different ramp slopes of 10, 20, 30 and 40 W.min-1 on different days. The EMG signals taken from the vastus lateralis muscle were stored on a digital data recorder and converted to obtain the integrated EMG (iEMG). The VO2 was measured, with 20-s intervals, by the mixing chamber method. A non-linear increase in iEMG against work load was observed for each exercise in all subjects. The break point of the linear relationship of iEMG was determined by the crossing point of the two regression lines (iEMGbp). Significant differences were obtained in the exercise intensities corresponding to maximal oxygen uptake (VO2max) and the iEMGbp between 10 and 30, and 10 and 40 W.min-1 ramp exercises (P < 0.05). However, no significant differences were obtained in VO2max and VO2 corresponding to the iEMGbp during the four ramp exercises. With respect to the relationship between VO2 and exercise intensity during the ramp increments, the VO2-exercise intensity slope showed significant differences only for the upper half (i.e. above iEMGbp). These results demonstrated that the VO2max and VO2 at which a nonlinear increase in iEMG was observed were not varied by the change of ramp slopes but by the exercise intensity corresponding to VO2max and the iEMGbp was varied by the change of ramp slopes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of sampling on variability and plateau in oxygen uptake

To evaluate the effect of the gas exchange sampling interval on variability and plateau in O2 uptake (VO2), 10 subjects underwent steady-state treadmill exercise at 50% maximal VO2 and 6 subjects underwent maximal testing using a ramp protocol. During steady-state exercise, gas exchange data were acquired by using 10 different sampling intervals. The variability in VO2 was greater as the sampling interval shortened (SD = 4.5 ml.kg-1.min-1 for breath-by-breath vs. 0.8 ml.kg-1.min-1 for 60-s samples). The breath-by-breath data suggested a Gaussian distribution, and most of the variability was attributable to tidal volume (51%). During ramp testing, the slope of the change in VO2 (for each sample) was regressed with time. Considerable variability in the slopes was observed throughout exercise, and in each subject the slopes varied about zero, demonstrating both positive and negative values throughout submaximal effort. These observations were made despite the use of large sampling intervals. Shortening the sample resulted in even greater variability. We conclude that 1) the sampling interval can have a major impact on gas exchange data during exercise and 2) considerable variability exists in the slope of the change in VO2 with a consistent change in external work regardless of the sample used, suggesting that a plateau (defined as the slope of a VO2 sample at peak exercise that does not differ significantly from a slope of zero) in VO2 is not a reliable physiological marker for maximal effort.     

Effect of creatine supplementation on oxygen uptake kinetics during submaximal cycle exercise.

The purpose of this study was to test the effect of oral creatine (Cr) supplementation on pulmonary oxygen uptake (VO(2)) kinetics during moderate [below ventilatory threshold (VT)] and heavy (above VT) submaximal cycle exercise. Nine subjects (7 men; means +/- SD: age 28 +/- 3 yr, body mass 73.2 +/- 5.6 kg, maximal VO(2) 46.4 +/- 8.0 ml. kg(-1). min(-1)) volunteered to participate in this study. Subjects performed transitions of 6-min duration from unloaded cycling to moderate (80% VT; 8-12 repeats) and heavy exercise (50% change; i.e., halfway between VT and maximal VO(2); 4-6 repeats), both in the control condition and after Cr loading, in a crossover design. The Cr loading regimen involved oral consumption of 20 g/day of Cr monohydrate for 5 days, followed by a maintenance dose of 5 g/day thereafter. VO(2) was measured breath by breath and modeled by using two (moderate) or three (heavy) exponential terms. For moderate exercise, there were no differences in the parameters of the VO(2) kinetic response between control and Cr-loaded conditions. For heavy exercise, the time-based parameters of the VO(2) response were unchanged, but the amplitude of the primary component was significantly reduced with Cr loading (means +/- SE: control 2.00 +/- 0.12 l/min; Cr loaded 1.92 +/- 0.10 l/min; P < 0.05) as was the end-exercise VO(2) (control 2.19 +/- 0.13 l/min; Cr loaded 2.12 +/- 0.14 l/min; P < 0.05). The magnitude of the reduction in submaximal VO(2) with Cr loading was significantly correlated with the percentage of type II fibers in the vastus lateralis (r = 0.87; P < 0.01; n = 7), indicating that the effect might be related to changes in motor unit recruitment patterns or the volume of muscle activated.     

Intersubject variability in cardiac output-O2 uptake relation of men during exercise

Intersubject variability in the relation between cardiac output (Q) and O2 uptake (VO2) was examined during supine cycling up to the maximum level in 40 normal untrained men age 27 +/- 4 (SD) yr. In individual subjects, Q increased linearly against VO2 in the submaximum exercise range. The SD of Q on VO2 was so small (0.47 +/- 0.25 l/min) that Q could be given by a linear function of VO2 as Q = K(VO2 - VO2 r) + Qr, where K, VO2 r, and Qr are the slope of the regression line, the resting VO2, and resting Q, respectively. K varied widely among the subjects studied, ranging from 5.5 to 10.3 and was independent of both physical characteristics and Qr, which ranged from 3.7 to 8.3 l/min. However, K correlated significantly with changes in heart rate, stroke volume, mean arterial pressure, and systemic vascular conductance. From these results, we concluded that the intersubject variability in the Q-VO2 relation was caused independently by individual variations in resting hemodynamics and in cardiovascular response to exercise.     

Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise.

We tested the hypothesis that heavy-exercise phase II oxygen uptake (VO(2)) kinetics could be speeded by prior heavy exercise. Ten subjects performed four protocols involving 6-min exercise bouts on a cycle ergometer separated by 6 min of recovery: 1) moderate followed by moderate exercise; 2) moderate followed by heavy exercise; 3) heavy followed by moderate exercise; and 4) heavy followed by heavy exercise. The VO(2) responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms. Neither moderate- nor heavy-intensity exercise had an effect on the VO(2) kinetic response to subsequent moderate exercise. Although heavy-intensity exercise significantly reduced the mean response time in the second heavy exercise bout (from 65.2 +/- 4.1 to 47.0 +/- 3.1 s; P < 0.05), it had no significant effect on either the amplitude or the time constant (from 23.9 +/- 1.9 to 25.3 +/- 2.9 s) of the VO(2) response in phase II. Instead, this "speeding" was due to a significant reduction in the amplitude of the VO(2) slow component. These results suggest phase II VO(2) kinetics are not speeded by prior heavy exercise.     

Day-to-day changes in oxygen uptake kinetics at the onset of exercise during strenuous endurance training.

The aim of this study was to assess the effect of strenuous endurance training on day-to-day changes in oxygen uptake (VO2) on-kinetics (time constant) at the onset of exercise. Four healthy men participated in strenuous training for 30 min.day-1, 6 days.week-1 for 3 weeks. The VO2 was measured breath-by-breath every day except Sunday at exercise intensities corresponding to the lactate threshold (LT) and the onset of blood lactate accumulation (OBLA) which were obtained before training. Furthermore, an incremental exercise test was performed to determine LT, OBLA and maximal oxygen uptake (VO2max) before and after the training period and every weekend. The 30-min heavy endurance training was performed on a cycle ergometer 5 days.week-1 for 3 weeks. Another six men served as the control group. After training, significant reductions of the VO2 time constant for exercise at the pretraining LT exercise intensity (P less than 0.05) and at OBLA exercise intensity (P less than 0.01) were observed, whereas the VO2 time constants in the control group did not change significantly. A high correlation between the decrease in the VO2 time constant and training day was observed in exercise at the pretraining LT exercise intensity (r = -0.76; P less than 0.001) as well as in the OBLA exercise intensity (r = -0.91; P less than 0.001). A significant reduction in the blood lactate concentration during submaximal exercise and in the heart rate on-kinetics was observed in the training group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise.

Prior heavy exercise markedly alters the O2 uptake (VO2) response to subsequent heavy exercise. However, the time required for VO2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the VO2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second VO2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary VO2 time constant (from 25.9 +/- 4.7 s to 23.9 +/- 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary VO2 amplitude (from 2.42 +/- 0.39 to 2.53 +/- 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the VO2 slow component (from 0.44 +/- 0.13 to 0.21 +/- 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20-45 min, but not after 60 min, of recovery. The increase in the primary VO2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 +/- 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20-60 min of recovery. The priming effect of prior heavy exercise on the VO2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.     

Comparison of oxygen uptake kinetics during concentric and eccentric cycle exercise.

O2 uptake (VO2) kinetics and electromyographic (EMG) activity from the vastus medialis, rectus femoris, biceps femoris, and medial gastrocnemius muscles were studied during constant-load concentric and eccentric cycling. Six healthy men performed transitions from baseline to high-intensity eccentric (HE) exercise and to high-intensity (HC), moderate-intensity (MC), and low-intensity (LC) concentric exercise. For HE and HC exercise, absolute work rate was equivalent. For HE and LC exercise, VO2 was equivalent. VO2 data were fit by a two- or three-component exponential model. Surface EMG was recorded during the last 12 s of each minute of exercise to obtain integrated EMG and mean power frequency. Only in the HC exercise did VO2 increase progressively with evidence of a slow component (phase 3), and only in HC exercise was there evidence of a coincident increase with time in integrated EMG of the vastus medialis and rectus femoris muscles (P < 0.05) with no change in mean power frequency. The phase 2 time constant was slower in HC [24.0 +/- 1.7 (SE) s] than in HE (14.7 +/- 2.8 s) and LC (16.7 +/- 2.2 s) exercise, while it was not different from MC exercise (20.6 +/- 2.1 s). These results show that the rate of increase in VO2 at the onset of exercise was not different between HE and LC exercise, where the metabolic demand was similar, but both had significantly faster kinetics for VO2 than HC exercise. The VO2 slow component might be related to increased muscle activation, which is a function of metabolic demand and not absolute work rate.     

Oxygen cost and oxygen uptake dynamics and recovery with 1 min of exercise in children and adults.

To test the hypothesis that O2 uptake (VO2) dynamics are different in adults and children, we examined the response to and recovery from short bursts of exercise in 10 children (7-11 yr) and 13 adults (26-42 yr). Each subject performed 1 min of cycle ergometer exercise at 50% of the anaerobic threshold (AT), 80% AT, and 50% of the difference between the AT and the maximal O2 uptake (VO2max) and 100 and 125% VO2max. Gas exchange was measured breath by breath. The cumulative O2 cost [the integral of VO2 (over baseline) through exercise and 10 min of recovery (ml O2/J)] was independent of work intensity in both children and adults. In above-AT exercise, O2 cost was significantly higher in children [0.25 +/- 0.05 (SD) ml/J] than in adults (0.18 +/- 0.02 ml/J, P less than 0.01). Recovery dynamics of VO2 in above-AT exercise [measured as the time constant (tau VO2) of the best-fit single exponential] were independent of work intensity in children and adults. Recovery tau VO2 was the same in both groups except at 125% VO2max, where tau VO2 was significantly smaller in children (35.5 +/- 5.9 s) than in adults (46.3 +/- 4 s, P less than 0.001). VO2 responses (i.e., time course, kinetics) to short bursts of exercise are, surprisingly, largely independent of work rate (power output) in both adults and children. In children, certain features of the VO2 response to high-intensity exercise are, to a small but significant degree, different from those in adults, indicating an underlying process of physiological maturation.     

V(O2) recovery kinetics in the horse following moderate, heavy, and severe exercise.

At the onset of exercise, horses exhibit O2 uptake (VO2) kinetics that are qualitatively similar to those of humans. In humans, there is a marked dissymmetry between on- and off-kinetics for VO2. This investigation sought to formally characterize the off-transient (recovery) VO2 kinetics in the horse within the moderate (M), heavy (H), and severe (S) exercise domains. Six horses were run on a high-speed treadmill at M, H, and S exercise intensities (i.e., that speed which yielded approximately 50, 85, 100% peak VO2, respectively, on the maximal incremental test). The time courses for the recovery were modeled by using a three-phase model with a single-exponential (fast component) or double-exponential (fast and slow component) phase 2. The single-exponential phase 2 model provided an excellent fit to the off-transient data, with the exception of one horse in the H domain which was best modeled by a double exponential. The time delay elicited no domain dependency (M, 18.0 +/- 1.0; H, 17.6 +/- 1.1; S, 17.8 +/- 2.0 s; P > 0.05), as was the case for the fast-component time constants (M, 16.3 +/- 2.0 s; H, 13.5 +/- 1.0 s; S, 14.6 +/- 0.3 s; P > 0.05). In the H and S (but not M) domains, the VO2 following resolution of the fast component was elevated above the preexercise baseline (H, 3.0 +/- 1.0 l/min; S, 5.7 +/- 1.1 l/min). This additional postexercise VO2 was correlated to the end-exercise increase in lactate (r = 0.94, P < 0.001) but not the end-exercise pulmonary arterial blood temperature (r = 0.45, P > 0.05). These data indicate that the time delay and subsequent kinetic response of the primary (fast-component) phase of exercise VO2 recovery in the horse is independent of the preceding exercise-intensity domain. However, in the H and S domains, the fast component resolves to an elevated baseline.     

Blood flow and muscle oxygen uptake at the onset and end of moderate and heavy dynamic forearm exercise

We hypothesized that forearm blood flow (FBF) during moderate intensity dynamic exercise would meet the demands of the exercise and that postexercise FBF would quickly recover. In contrast, during heavy exercise, FBF would be inadequate causing a marked postexercise hyperemia and sustained increase in muscle oxygen uptake (VO(2musc)). Six subjects did forearm exercise (1-s contraction/relaxation, 1-s pause) for 5 min at 25 and 75% of peak workload. FBF was determined by Doppler ultrasound, and O(2) extraction was estimated from venous blood samples. In moderate exercise, FBF and VO(2musc) increased within 2 min to steady state. Rapid recovery to baseline suggested adequate O(2) supply during moderate exercise. In contrast, FBF was not adequate during heavy dynamic exercise. Immediately postexercise, there was an approximately 50% increase in FBF. Furthermore, we observed for the first time in the recovery period an increase in VO(2musc) above end-exercise values. During moderate exercise, O(2) supply met requirements, but with heavy forearm exercise, inadequate O(2) supply during exercise caused accumulation of a large O(2) deficit that was repaid during recovery.     

Use of recovery VO2 to predict running economy

The purpose of this study was to determine whether running economy (RE) could be predicted accurately using recovery VO2 values. Twelve runners (means VO2max = 61.9, SD 4.9 ml.kg-1.min-1) completed three treadmill RE sessions over a 2-week period. During each session, subjects performed three 6-min runs at 69%, 78%, and 87% VO2max. RE was calculated from a single 2-min gas collection during the last 2 min of running. Immediately following each run, recovery VO2 data obtained during randomly assigned 15-s, 20-s, or 25-s gas collections were used to predict exercise VO2. Correlations and mean absolute percentage variation (% VAR) between actual and predicted VO2 at each relative intensity and recovery period are reported. Although the relationship between actual and predicted VO2 was significant and more pronounced at higher exercise intensities, the overall magnitude of the association was low to moderate (r range = 0.50-0.81). The range of % VAR between actual and predicted aerobic demands also obscured marked underprediction (-6.5% to -12.5%) and overprediction (+10.1% to +17.4%) of actual VO2 in some subjects. These data suggest that 15-, 20-, and 25-s recovery VO2 values do not correlate strongly with steady-state VO2, nor do they adequately account for variation in individual economy profiles.     

Effects of standing cycling and the use of toe stirrups on maximal oxygen uptake

Twenty-eight subjects (6 normal men, 14 distance runners, and 8 rowers) were tested for maximal oxygen uptake (VO2max) and associated physiological measures during bicycle ergometer exercise with toe stirrups while standing (BEts) and during treadmill exercise (TM). Correlation between BEts VO2max and TM VO2max was high (r = 0.901, p less than 0.05). No significant difference existed between the two VO2max values (60.3 +/- 8.9 vs. 60.5 +/- 9.7 ml.kg-1.min-1; n = 28). No differences were found even when three different subgroups were separately compared. It is concluded that the higher VO2max elicited during BEts as compared with normal sitting cycling may be attributed to the increased muscle blood flow and/or involvement of a larger muscle mass, the latter being partly evidenced by the observation of greater electromyographic activity during BEts.