Cardiac output and oxygen release during very high-intensity exercise performed until exhaustion

Our objectives were firstly, to study the patterns of the cardiac output () and the arteriovenous oxygen difference [(a–)O₂] responses to oxygen uptake (O₂) during constant workload exercise (CWE) performed above the respiratory compensation point (RCP), and secondly, to establish the relationships between their kinetics and the time to exhaustion. Nine subjects performed two tests: a maximal incremental exercise test (IET) to determine the maximal O₂ ( V ̇O₂peak), and a CWE test to exhaustion, performed at p 50 (intermediate power between RCP and O₂peak). During CWE, V ̇O₂ was measured breath-by-breath, Q ̇ was measured beat-by-beat with an impedance device, and blood lactate (LA) was sampled each minute. To calculate ( a–v ̄)O₂, the values of V ̇O₂ and Q ̇ were synchronised over 10 s intervals. A fitting method was used to describe the V ̇O₂, Q ̇ and ( a–v ̄)O₂ kinetics. The ( a–v ̄)O₂ difference followed a rapid monoexponential function, whereas both V ̇O₂ and Q ̇ were best fitted by a single exponential plus linear increase: the time constant () V ̇O₂ [57 (20 s)] was similar to ( a–v ̄)O₂, whereas for Q ̇ was significantly higher [89 (34) s, P <0.05] (values expressed as the mean and standard error). LA started to increase after 2 min CWE then increased rapidly, reaching a similar maximal value as that seen during the IET. During CWE, the rapid component of O₂ uptake was determined by a rapid and maximal ( a–)O₂ extraction coupled with a two-fold longer Q ̇ increase. It is likely that lactic acidosis markedly increased oxygen availability, which when associated with the slow linear increase of Q ̇, may account for the V ̇O₂ slow component. Time to exhaustion was larger in individuals with shorter time delay for ( a–v ̄)O₂ and a greater for .     

Physiological responses to intermittent and continuous exercise at the same relative intensity in older men

We investigated the physiological responses in older men to continuous (CEx) and intermittent (IEx) exercise. Nine men [70.4 (1.2) years, O_2peak: 2.21 (0.20) l min^–1; mean (SE)] completed eight exercise tests (two CEx and six IEx) on an electronically braked cycle ergometer in random order. CEx and IEx were performed at 50% and 70% O_2peak. IEx was performed using 60sE:60sR, 30sE:30sR and 15sE:15sR exercise to rest ratios. The duration of exercise was adjusted so that the total amount of work completed was the same for each exercise test. Oxygen uptake (O₂), minute ventilation (_E) and heart rate (HR) were measured at the mid-point of each exercise test. Arterialised blood samples were obtained at rest and during exercise and analysed for pH and PCO₂. At the same relative intensity (50% or 70% O_2peak), IEx resulted in a significantly lower (P<0.01) O₂, _E and HR than CEx. There were no significant differences (P>0.05) in O₂, _E and HR measured at the mid point of the three exercise to rest ratios at 50% and 70% O_2peak. pH and PCO₂ during CEx and IEx at 50% O_2peak were not significantly different from rest. CEx performed at 70% O_2peak resulted in significant decreases (P<0.05) in pH and PCO₂. There was a significant decrease (P<0.05) in pH only during the 60sE:60sR IEx at 70% O_2peak. Changes in arterialised PCO₂ during the 60sE:60sR, 30sE:30sR and 15sE:15sR at both 50% and 70% O_2peak exercise tests were not significant. When exercising at the same percentage of O_2peak and with the total amount of work fixed, IEx results in significantly lower physiological responses than CEx in older men. All results are given as mean (SE).     

Effect of order of exercise intensity upon cardiorespiratory,metabolic, and perceptual responses during exercise of mixed intensity

Exercise of mixed intensities can be of benefit in many different ways. However, whether physiological interaction exists between exercises of different intensity is questionable. As such, the primary aim of this study was to examine the effect of order of exercise intensity upon cardiorespiratory, metabolic, and perceptual responses during exercise of mixed intensity. Eight males and four females volunteered to serve as subjects for the study. They were informed of the purpose of the experiment and gave their written consent to participate. Each subject completed a peak oxygen uptake (O_2peak) test and two submaximal exercises of mixed intensity on three separate laboratory visits. During each submaximal exercise trial, subjects performed a 15-min (high intensity) exercise at 70%O_2peak that was followed by another 15-min (low intensity) exercise at 50%O_2peak (high/low, H/L), or a 15-min exercise at 50%O_2peak that was followed by another 15-min exercise at 70%O_2peak (low/high, L/H). Oxygen uptake (O₂), respiratory exchange ratio (R), expired ventilation (_E), heart rate (HR) and ratings of perceived exertion (RPE) were measured every 5 min throughout exercise. Energy expenditure and carbohydrate and fat oxidation were calculated from O₂ adjusted for substrate metabolism using R and then accumulated for each phase of exercise intensity as well as for the entire exercise session. O₂ and HR were higher (P<0.05), while R was lower (P<0.05) at the lower intensity in H/L than in L/H. _E and RPE were lower (P<0.05) at the higher intensity in H/L than in L/H. While no differences in caloric expenditure and carbohydrate oxidation between the two trials were observed, fat oxidation was higher (P<0.05) both at the lower intensity and for the entire trial in H/L than in L/H. It appears that during exercise of mixed intensity, placing some periods of moderate intensity exercise prior to a milder one is a more favorable sequence in that it can elicit a greater fat oxidation while being felt less stressful.     

Effect of intermittent hypoxia on oxygen uptake during submaximal exercise in endurance athletes

The purpose of the present study was to clarify the following: (1) whether steady state oxygen uptake (O₂) during exercise decreases after short-term intermittent hypoxia during a resting state in trained athletes and (2) whether the change in O₂ during submaximal exercise is correlated to the change in endurance performance after intermittent hypoxia. Fifteen trained male endurance runners volunteered to participate in this study. Each subject was assigned to either a hypoxic group (n=8) or a control group (n=7). The hypoxic group spent 3 h per day for 14 consecutive days in normobaric hypoxia [12.3 (0.2)% inspired oxygen]. The maximal and submaximal exercise tests, a 3,000-m time trial, and resting hematology assessments at sea level were conducted before and after intermittent normobaric hypoxia. The athletes in both groups continued their normal training in normoxia throughout the experiment. O₂ during submaximal exercise in the hypoxic group decreased significantly (P<0.05) following intermittent hypoxia. In the hypoxic group, the 3,000-m running time tended to improve (P=0.06) after intermittent hypoxia, but not in the control group. Neither peak O₂ nor resting hematological parameters were changed in either group. There were significant (P<0.05) relationships between the change in the 3,000-m running time and the change in O₂ during submaximal exercise after intermittent hypoxia. The results from the present study suggest that the enhanced running economy resulting from intermittent hypoxia could, in part, contribute to improved endurance performance in trained athletes.     

Aerobic exercise performance correlates with post-ischemic flow-mediated dilation of the brachial artery in young healthy men

In older healthy men, aerobic exercise capacity is related to postischemic flow-mediated dilation of the brachial artery (FMD), but corresponding data in a younger population is not available. In addition, whether submaximal aerobic exercise performance also correlates with this kind of vasomotor reactivity is not known. Therefore, in 15 nonsmoking young healthy men [age 27 (5) years; body mass index: 24 (2) kg/m²; mean (SD)] with different levels of ordinary physical activity, but not performing upper-extremity training, we measured FMD at 1 min after reactive hyperemia, and pulmonary oxygen uptake (O₂) at ventilatory anaerobic threshold (O₂AT) and at peak effort (peak O₂) during an incremental exercise on a treadmill. In our participants, FMD was 9.1 (3.4)%, O₂AT was 40.72 (5.92) ml/kg per min, and peak O₂ was 52.95 (8.13) ml/kg per min. Using bivariate Pearsons correlation, and in separate multivariate regression analyses, O₂AT and peak VO₂ showed a significant and reasonably good correlation with FMD (r=0.84, P<0.001 and r=0.77, P=0.001, respectively), independent of age, body mass index and serum total cholesterol (=0.77, P<0.001, R² of the overall model=0.79 and =0.70, P<0.005, R² of the overall model=0.69, respectively). Our data provide evidence suggesting that in young healthy men a higher submaximal and maximal aerobic exercise performance is associated with a greater FMD of peripheral conduit arteries.     

Effects of training in normoxia and normobaric hypoxia on time to exhaustion at the maximum rate of oxygen uptake

The effects of endurance training in normoxia or in hypoxia on time to exhaustion (T_lim) at the work rate corresponding to peak oxygen uptake (O_2peak) were examined at sea level in 13 healthy subjects. Before and after training the subjects performed the following: (1) incremental exercises up to exhaustion to determine peak oxygen uptake in normoxia (O_2peakN), the percentage of this value at the 4 mmol l^–1 blood lactate concentration (O₂4%N) and the work rate corresponding to O_2peakN (Pa_peakN), (2) a 5-min 90% Pa_peakN exercise followed by a 10-min passive recovery to determine the maximal blood lactate concentration (La_max) measured during the recovery, and (3) a T_lim at Pa_peakN. Training consisted of pedalling 2 h a day, 6 days a week, for 4 weeks. Five subjects trained in normobaric hypoxia [HT; partial pressure of inhaled oxygen (P_IO₂) 89 mmHg] and eight subjects trained at the same relative work rates in normoxia (NT; P_IO₂ 141 mmHg). The training-induced improvement of all the measured parameters were closely matched between the HT and the NT (P>0.05). Training increased T_lim by 59.7% [164(40) s]. The value of T_lim was related to O₂4%N and to La_max before and after training. Also, the training-induced improvement of T_lim was related to the concomitant decrease in La_max. It is concluded that: (1) endurance training including continuous high-intensity exercises improves T_lim for exercises performed at the same relative (higher absolute) work rate after training, (2) intermittent hypoxic training has no potentiating effect on T_lim as compared with training in normoxia, and (3) the intra-individual training-induced improvement of T_lim was associated with metabolic alteration in relation to lactate accumulation.     

Peak exercise oxygen uptake and left ventricular systolic and diastolic function and arterial mechanics in healthy young men

Echocardiography can be used to estimate myocardial contractility by the assessment of the circumferential end-systolic stress-corrected left ventricular (LV) fractional shortening measured at midwall level (stress-corrected MWS). Whether stress-corrected MWS at rest predicts exercise peak oxygen uptake (peak O₂) is unknown. Also, it is not known whether the propagation rate of the early LV filling wave (E wave propagation rate, _p), a new pre-load insensitive index of LV diastolic function, and echocardiographically assessed indices of arterial stiffness correlate to peak O₂. Accordingly, we performed echocardiographic studies and exercise tests with respiratory gas analysis in 15 young healthy male subjects (mean age 27 years, range 18–36). Neither stress-corrected-MWS (r=0.20, P=NS) nor ejection fraction (r=–0.05, P=NS) correlated significantly with peak O₂. Adjustment for age and resting heart rate had no effect on the results. In separate multiple regression models adjusting for standard covariates (age, LV size and heart rate), peak O₂ correlated with _p (beta=0.98, P<0.01), as well as with E/A (beta=0.85, P<0.01), and with the isovolumic relaxation time (indicator of LV relaxation) (beta=–0.59, P<0.05). Arterial stiffness indices showed no significant relation to peak O₂. We conclude that in young healthy male subjects, resting myocardial contractility and arterial stiffness are not significant correlates of peak O₂, whereas LV diastolic function, and in particular _p, influences the variability of peak O₂.     

The V̇O2 response for an exhaustive treadmill run at 800-m pace: a breath-by-breath analysis

Recent research in which data were averaged over 10 or 30 s suggests that the O₂ response of aerobically fit individuals plateaus below O_{2 max} in an exhaustive square-wave run lasting ~2 min. To investigate this phenomenon we examined the breath-by-breath O₂ response of trained runners to an exhaustive treadmill run at 800 m pace. Eight male competitive runners completed two treadmill tests on separate days: a ramp test to exhaustion and an exhaustive square-wave run at 800-m pace. For the ramp test, the breath-by-breath data were smoothed with a 15-s moving average and the highest of the smoothed values was taken as O_{2 peak} [mean (SD): 68.9 (5.6) ml kg^–1 min^–1]. For the square-wave, the breath-by-breath data were interpolated to give one value per second and modelled using a monoexponential function. Following a delay of 11.2 (1.5) s, O₂ increased quickly [phase-2 time constant of 10.7 (2.7) s] towards an asymptote that represented just 85 (6)% of O_{2 peak} from the ramp test. Expressed in ml kg^–1 min^–1, this asymptote was independent of O_{2 peak} (r=0.04, P=0.94). However, as a percentage of O_{2 peak} it was negatively correlated with O_{2 peak} itself (r=–0.96, P<0.001). It is concluded that in an exhaustive square-wave treadmill run lasting ~2 min the O₂ of aerobically fit runners increases quickly to plateau at a level that is lower than, but independent of, O_2max     

Decrease in peak heart rate with acute hypoxia in relation to sea level VO(2max)

The aim of this study was to evaluate the influence of arterial oxygen saturation (SaO₂) on maximal heart rate during maximal exercise under conditions of acute hypoxia compared with normoxia. Forty-six males were divided into three groups depending on their sea level maximal oxygen consumption (O_2max): high [GH, O_2max=64.2 (3.3) ml.min^–1.kg^–1], medium [GM, 50.8 (3.9) ml.min^–1.kg^–1] and low [GL, 41.0 (1.9) ml.min^–1.kg^–1]. All subjects performed a maximal exercise test in two conditions of inspired oxygen tension (PIO₂, (149 mmHg and 70 mmHg). Among the GM group, seven subjects performed five supplementary incremental exercise tests at PIO₂ 136, 118, 104, 92, and 80 mmHg. Measurements of O_2max and SaO₂ using an ear-oxymeter were carried out at all levels of PIO₂. The decrease in SaO₂ and peak heart rate (HR_peak) with PIO₂ became significant from 104 and 92 mmHg. SaO₂ correlated with the decrease in HR_peak. For PIO₂=70 mmHg, the decrease in O_2max, SaO₂ and HR_peak was, respectively, 44%, 62%, and 17.0 bpm for GH, 38%, 68%, and 14.7 bpm for GM, and 34%, 68%, and 11.8 bpm for GL. During maximal exercise in hypoxia, SaO₂ was lower for GH than GM and GL (p<0.01). Among subjects in GH, five presented exercise-induced hypoxemia (EIH) when exercising in normoxia. The EIH group exhibited a greater decrement in HR_peak than the non-EIH group at maximal hypoxic exercise (21.2 bpm vs. 15.0 bpm; p<0.05). When subjects are exposed to acute hypoxia, the lower SaO₂, due either to lower PIO₂ or to training status, is associated with lower HR_peak.     

Kinetics of oxygen uptake during arm cranking with the legs inactive or exercising at moderate intensities

The purpose of this study was to compare the kinetics of oxygen uptake (O₂) during arm cranking with the legs inactive or exercising. Each subject (n=8) performed three exercise protocols: 6-min arm cranking at an intensity of 60% of peak oxygen uptake (O_2peak, AC₆₀) and 6-min combined arm cranking and leg cycling in which AC₆₀ was added to on-going leg cycling at an intensity of 20% or 40% of O_2peak (LC₂₀ and LC₄₀: AC₆₀LC₂₀ and AC₆₀LC₄₀, respectively). After the onset of arm cranking, O₂ tended to increase until the end of arm cranking in all of the three exercise modes. The amplitudes of this increase in O₂ were 0.98 (0.18), 0.93 (0.16) and 0.84 (0.12) l.min^–1 during AC₆₀, AC₆₀LC₂₀ and AC₆₀LC₄₀, respectively, and there were significant differences between values for each exercise. The data are presented as means and standard deviations. There were no significant differences in the effective O₂ time constant, partial O₂ deficit, and the difference between the values of O₂ measured at 3 and 6 min in the three exercise modes. The present results indicate that the amplitude of the increase in O₂ is reduced during arm cranking with the legs exercising, that this reduction becomes greater with increases in the intensity of leg cycling, and that the rate of increase in O₂ is not affected by the additional muscle mass of the legs exercising below moderate intensities. The decrease in the amplitude of increase in O₂ might be caused by reduction in oxygen supply to the exercising arms due to large muscle mass and/or overlaps of activity of stabilizing muscles during combined arm and leg exercise.     

Overshoot in <Emphasis Type="Italic">V̇</Emphasis>O<Subscript>2</Subscript> following the onset of moderate-intensity cycle exercise in trained cyclists

We have previously observed that following the onset of moderate intensity cycle ergometry, the pulmonary O₂ uptake (O₂) in trained cyclists often does not increase towards its steady-state value with the typical mono-exponential characteristics; rather, there is a transient overshoot. The purpose of this study was to systematically examine this phenomenon by comparing the O₂responses to two moderate-intensity work rates and one high-intensity work rate in trained and untrained subjects. Following a ramp exercise test to the limit of tolerance for the determination of the gas exchange threshold (GET) and O_2peak, seven trained cyclists [mean (SD); O_2peak 66.6 (2.5) ml·kg^–1·min^–1] and eight sedentary subjects [O_2peak 42.9 (5.1) ml·kg^–1·min^–1] completed six step transitions from baseline cycling to work rates requiring 60% and 80% GET and three step transitions from baseline cycling to a work rate requiring 50% of the difference between GET and O_2peak (50%). O₂ was measured breath-by-breath and modelled using standard techniques. The sedentary subjects did not overshoot the steady-state O₂ at any intensity. At 60% GET, six of the seven cyclists overshot the steady-state O₂ [by an integral volume of 164 (44) ml between ~45 and 125 s]. At 80% GET, four of the seven cyclists overshot the steady-state O₂ [by an integral volume of 185 (92) ml between ~55 and 140 s]. None of the cyclists showed an overshoot at 50%. These results indicate that trained cyclists evidence an overshoot in O₂ before steady-state is reached in the transition to moderate-intensity exercise. The mechanism(s) responsible for this effect remains to be elucidated, as does whether the overshoot confers any functional or performance benefit to the trained cyclist.     

Peak oxygen uptake during running and arm cranking normalized to total and regional skeletal muscle mass measured by magnetic resonance imaging

The purposes of our study were to determine the peak oxygen uptake ( O_2peak) per total or regional skeletal muscle (SM) mass using magnetic resonance imaging (MRI) and to investigate the relationships between SM mass and O_2peak during running and arm cranking. Eight male college swimmers aged 18–22 years [mean (SD) age 20.0 (1.3) years] were recruited to participate in this study. O₂ during running and arm cranking were measured using an automated breath-by-breath mass spectrometry system. Contiguous MRI slices were obtained from the first vertebra cervicale to the malleolus lateralis (1.0-cm slice thickness, 0-cm inter-slice gap), resulting in a total of approximately 156 images for each subject. The absolute O_2peak and the O_2peak per body mass during running and arm cranking were 3.6 (0.6) l.min^-1, 54.4 (5.9) ml.min^-1.kg^-1 and 2.5 (0.5) l.min^-1, 36.9 (5.3) ml.min^-1.kg^-1, respectively. The absolute O_2peak was higher ( P <0.05) during running than during arm cranking, but not the O_2peak per regional area SM mass. The lower body SM mass was correlated to the O_2peak during running ( r =0.95, P <0.001). All measurements and calculated values were expressed as the mean (SD) for the eight subjects. To eliminate the influence of body mass and fat-free mass (FFM), a regression analysis was performed on the mass-residuals of the O_2peak during running and the lower body SM mass. The residuals of lower body SM mass were correlated to the residuals of O_2peak during running, with respect to body mass ( r =0.90, P <0.001) and FFM ( r =0.82, P <0.05). These results suggest that the MRI-measured lower body SM mass was closely associated to the absolute O_2peak during running, independently of body mass or FFM, and that the O_2peak per regional SM mass corresponded, regardless of the type of exercise (upper or lower body).     

Non-linear cardiac output dynamics during ramp-incremental cycle ergometry

Published literature asserts that cardiac output (=O₂×1/C_(a-v)O₂) increases as a linear function of oxygen uptake with a slope of approximately 5–6 during constant work rate exercise. However, we have previously demonstrated that C_(a-v)O₂ has a linear relationship as a function of O₂ during progressively increasing work rate incremental exercise. Therefore, we hypothesized that may indeed have a non-linear relationship with respect to O₂ during incremental, non-steady state exercise. To investigate this hypothesis, we performed five maximal progressive work rate exercise studies in healthy human subjects. was determined every minute during exercise using measured breath-by-breath O₂, and arterial and pulmonary artery measurements of PO₂, hemoglobin saturation, and content. was plotted as a function of O₂ and the linear and non-linear (first order exponential and hyperbolic) fits determined for each subject. Tests for linearity were performed by assessing the significance of the quadratic terms added to the linear relation using least squares estimation in linear regression. Linearity was inadequate in all cases (group P<0.0001). We conclude that cardiac output is a non-linear function of O₂ during ramp-incremental exercise; the pattern of non-linearity suggests that while the kinetics of are faster than those of O₂ they progressively slow as work rate (and O₂) increases.     

Dichloroacetate does not speed phase-II pulmonary V̇O2 kinetics following the onset of heavy intensity cycle exercise

We hypothesised that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) by dichloroacetate (DCA) would speed phase-II pulmonary O₂ uptake (O₂) kinetics following the onset of high-intensity, sub-maximal exercise. Eight healthy males (aged 19–33 years) completed two square-wave transitions of 6 min duration from unloaded cycling to a work-rate equivalent to ~80% of peak O₂ either with or without prior i.v. infusion of DCA (50 mg kg^–1 body mass in 50 ml saline). Pulmonary O₂ was measured breath-by-breath throughout all tests, and O₂ kinetics were determined using non-linear regression techniques from the averaged individual response to each of the conditions. Infusion of DCA resulted in significantly lower blood [lactate] during the baseline cycling period (means±SEM: control 0.9±0.1, DCA 0.5±0.1 mM; P<0.01) consistent with successful activation of PDC. However, DCA had no discernible effect on the rate at which O₂ increased towards the initially anticipated steady state following the onset of exercise as reflected in the time constant of the fundamental O₂ response (control 26.7±4.1, DCA 27.7±2.8 s). These results indicate that the principal limitation to oxidative metabolism following the onset of high-intensity, sub-maximal cycle exercise lies downstream from PDC and/or that muscle O₂ consumption is primarily under feedback control via the concentration of one or more of the reactants associated with ATP hydrolysis.     

Prediction of sprint triathlon performance from laboratory tests

This study investigated whether sprint triathlon performance can be adequately predicted from laboratory tests. Ten triathletes [mean (SEM), age 21.8 (0.3) years, height 179 (2) cm, body mass 67.5 (2.5) kg] performed two graded maximal exercise test in random order, either on their own bicycle which was mounted on an ergometer or on a treadmill, to determine their peak oxygen consumption (O₂peak). Furthermore, they participated in two to three 30-min constant-load tests in both swimming, cycling and running to establish their maximal lactate steady state (MLSS) in each exercise mode. Swim tests were performed in a 25-m swimming pool (water temperature 27°C). During each test heart rate (HR), power output (PO) or running/swimming speed and blood lactate concentration (BLC) were recorded at regular intervals. Oxygen uptake (O₂) was continuously measured during the graded tests. Two weeks after the laboratory tests all subjects competed in a triathlon race (500 m swim, 20-km bike, 5-km run) [1 h 4 min 45 s (1 min 38 s)]. Peak HR was 7 beats·min^–1 lower in the graded cycle test than in the treadmill test (p<0.05) at similar peak BLC (~10 mmol·l^–1) and O₂peak (~5 L·min^–1). High correlations were found between O₂peak during cycling (r=–0.71, p<0.05) or running (r=–0.69, p<0.05) and triathlon performance. Stepwise multiple regression analysis showed that running speed and swimming speed at MLSS, together with BLC in running at MLSS, yielded the best prediction of performance [1 h 5 min 18 s (1 min 49 s)]. Thus, our data indicate that exercise tests aimed to determine MLSS in running and swimming allow for a precise estimation of sprint triathlon performance.     

Limitation of muscle deoxygenation in the triceps during incremental arm cranking in women

The present study investigated the difference in oxygen kinetics in the exercising muscle between arm cranking and leg cycling in women. Twenty-seven females completed incremental arm cranking and leg cycling tests on separate days. During each exercise, spatially resolved near-infrared spectroscopy was used to measure changes in the tissue oxygen saturation (SO₂), oxygenated (oxy-) hemoglobin and/or myoglobin (Hb/Mb), deoxygenated (deoxy-) Hb/Mb, and total Hb/Mb in the triceps during arm cranking and in the vastus lateralis during leg cycling. During arm cranking, there was a rapid increase in the respiratory exchange ratio and a lower ventilatory threshold compared to leg cycling, which confirmed accelerated anaerobic glycolysis in this mode of exercise. During leg cycling, SO₂ remained decreased near to or until approaching peak oxygen uptake (O_2peak). During arm cranking, however, the decrease in oxy-Hb/Mb and increase in deoxy-Hb/Mb stopped at the middle of O_2peak (mean 51.4%), consequently resulting in a leveling off in the SO₂ decrease, although total Hb/Mb continued to increase. These results might suggest that the oxygen demand in the triceps attained the maximum at that intensity, despite an adequate oxygen supply during arm cranking.     

Effects of brief leg cooling after moderate exercise on cardiorespiratory responses to subsequent exercise in the heat

We investigated the effects of brief leg cooling after moderate exercise on the cardiorespiratory responses to subsequent exercise in the heat. Following 40 min of ergometer cycling [65% peak oxygen uptake (O_2peak)] at 35°C (Ex. 1), seven male subjects [21.9 (1.1) years of age; 170.9 (1.9) cm height; 66.0 (2.0) kg body mass; 46.7 (2.0) ml kg^–1 min^–1 O_2peak] immersed their legs in 35°C (control condition, CONT) or 20°C (cooling condition, COOL) water for 5 min and then repeated the cycling (as before, but for 10 min) (Ex. 2). Just before Ex. 2, esophageal temperature (T _es) was lower in COOL than in CONT [36.9 (0.2) vs 37.5 (0.1)°C] (P<0.01), as also were both mean skin temperature [33.9 (0.2) vs 35.2 (0.2)°C] (P<0.01), and heart rate (HR) [93.2 (6.0) vs 102.7 (4.9) beats min^–1] (P<0.05). During Ex. 2, no differences between CONT and COOL were observed in oxygen uptake, arterial blood pressure, blood lactate concentration, or ratings of perceived exertion; however, T _es, skin temperature, and HR were lower in COOL than in CONT. Further, during the first 5 min of Ex. 2, minute ventilation was significantly lower in COOL than in CONT [50.3 (2.0) vs 53.4 (2.6) l min^–1] (P<0.01). These results suggest that brief leg cooling during the recovery period may be effective at reducing thermal and cardiorespiratory strain during subsequent exercise in the heat.     

The VO2 response to exhaustive square wave exercise: influence of exercise intensity and mode

We investigated the oxygen uptake (O₂) response to exhaustive square wave exercise of approximately 2, 5 and 8 min duration in cycling and running. Nine males completed a ramp test and three square wave tests on a motorised treadmill and the same four tests on a cycle ergometer, throughout which gas exchange was assessed (Douglas bag method). The peak O₂ from the ramp test was higher for running than for cycling [mean (SD): 58.4 (2.8) vs. 55.9 (3.7) ml.kg^–1.min^–1; P=0.04]. However O_2max (defined as the highest O₂ achieved in any of the four tests) did not differ between running and cycling [60.0 (2.9) vs. 58.5 (3.3) ml.kg^–1.min^–1; P=0.15]. The peak O₂ was similar (P>0.1) for the 5 and 8 min square wave tests [98.5 (1.8) and 99.2 (2.3) %O_2max for running; 97.0 (4.2) and 97.5 (2.0) %O_2max for cycling] but lower (P<0.001) for the 2-min test [91.8 (2.5) and 89.9 (5.5) %O_2max for running and cycling respectively]. O₂ increased over the final two 30-s collection periods of the 2-min test for cycling [O₂=0.18 (0.15) l.min^–1; P<0.01] but not running [O₂=0.00 (0.09) l.min^–1; P=0.98]. We conclude that in the aerobically fit the peak O₂ for square wave running or cycling at an intensity severe enough to result in exhaustion in approximately 2 min is below O_2max. In running, O₂ plateaus at this sub-maximal rate.     

New acquisitions in the assessment of breath-by-breath alveolar gas transfer in humans

We summarise recent results obtained in testing some of the algorithms utilised for estimating breath-by-breath (BB) alveolar O₂ transfer (VO_2A) in humans. VO_2A is the difference of the O₂ volume transferred at the mouth minus the alveolar O₂ stores changes. These are given by the alveolar volume change at constant O₂ fraction (F _AiO₂ V _Ai) plus the O₂ alveolar fraction change at constant volume [V _Ai–1(F _Ai–F _Ai–1)O₂], where V _Ai–1 is the alveolar volume at the beginning of the breath i. All these quantities can be measured BB, with the exception of V _Ai–1, which is usually set equal to the subjects functional residual capacity (FRC) (Auchincloss algorithm, AU). Alternatively, the respiratory cycle can be defined as the time elapsing between two equal O₂ fractions in two subsequent breaths (Grønlund algorithm, GR). In this case, F _AiO₂=F _Ai–1O₂ and the term V _Ai–1(F _Ai–F _Ai–1)O₂ disappears. BB alveolar gas transfer was first determined at rest and during exercise at steady-state. AU and GR showed the same accuracy in estimating alveolar gas transfer; however GR turned out to be significantly more precise than AU. Secondly, the effects of using different V _Ai–1 values in estimating the time constant of alveolar O₂ uptake (O_2A) kinetics at the onset of 120 W step exercise were evaluated. O_2A was calculated by using GR and by using (in AU) V _Ai–1 values ranging from 0 to FRC +0.5 l. The time constant of the phase II kinetics (₂) of O_2A increased linearly, with V _Ai–1 ranging from 36.6 s for V _Ai–1=0 to 46.8 s for V _Ai–1=FRC+0.5 l, whereas ₂ amounted to 34.3 s with GR. We concluded that, when using AU in estimating O_2A during step exercise transitions, the ₂ value obtained depends on the assumed value of V _Ai–1.     

Effects of shortening velocity and of oxygen consumption on efficiency of contraction in dog gastrocnemius

Previous observations have shown that, in isolated perfused dog gastrocnemii in situ, stimulated to aerobic rhythmic isotonic tetanic contractions (at about 40% of maximal isometric force), only about 20% of the overall metabolic power (proportional to the rate of O₂ consumption, O₂) was converted into mechanical power (Ẇ). Here we report that, in the same preparation, the maximal velocity during the shortening phase of each tetanus (v, mm s^–1) increased with the rate of energy dissipation, as given by the difference between O₂ and Ẇ (W kg^–1). The relationship between these variables was described by: v=2.85(O₂–Ẇ)^1.24 (R ²=0.85; n=17). A mathematical analysis of this equation shows that the overall mechanical efficiency (=ẆO₂ ^–1) decreased with increasing v (at constant O₂), whereas it increased with increasing O₂ (at constant v). The net effect of this state of affairs was that the decrease of over the entire range of work intensities was relatively minor (from 0.22 to 0.15), in spite of a large increase of v, (from 40 to 120 mm s^–1), thanks to the concomitant increase of O₂ (from 10 to 25 W kg^–1). So, under these experimental conditions, the energetics of work performance seems to be governed by two conflicting needs. The need for a sufficiently high shortening speed (and hence power output), itself requiring a sufficiently large energy dissipation rate, which, however, brings about a fall in . This is counteracted by the increased O₂, which in turn leads to an increased efficiency at the expense of a fall in shortening speed.This article was published in Human Muscular Function during Dynamic Exercise, Marconnet P, Saltin B, Komi P, Poortmans J (eds) Med Sport Sci 41 (series editors: M. Hebbelink, R.J. Shephard) pp. 1–9, Karger, Basel, 1996. It is reproduced with minor editorial modifications. Permission from Karger is gratefully acknowledged.