Effect of different pedal rates on oxygen uptake slow component during constant-load cycling exercise

AIM: We hypothesized that an extremely high pedal rate would induce much more type II muscle fibers recruitment even at an early phase of the same absolute work rate compared with normal pedal rates, and would result in changed amplitude of the pulmonary oxygen uptake slow component (VO(2)SC) during heavy constant-load exercise. METHODS: Two square-wave transitions of constant-load exercise were carried out at an exercise intensity corresponding to a VO(2) of 130% of the ventilatory threshold. The amplitude of the VO(2)SC in phase III during heavy constant-load exercise was determined at normal (60 rpm) and extremely high pedal rates (110 rpm). The VO(2) kinetics were analyzed by nonlinear regression. RESULTS: Although the absolute work rates were almost identical in the two pedal rates cycling exercise, the amplitude of the VO(2) in phase II (phase II amplitude), end-exercise VO(2) (EEVO(2)) and blood lactate accumulation ([La]) were significantly greater at 110 rpm than at 60 rpm (2 260+/-242 vs 1.830+/-304 mL.min(-1) for phase II amplitude; P<0.01, 2 350+/-265 vs 1 709+/-342 mL.min(-1) for EEVO(2); P<0.01, 6.4+/-1.3 vs 3.2+/-1.3 mmol.L(-1) for [La]; P<0.01, respectively). The amplitude of the VO(2)SC in phase III also revealed a significantly higher value at 110 rpm compared with 60 rpm (416+/-73 vs 201+/-89 mL.min(-1), P<0.01). In spite of the appearance of greater VO(2)SC at 110 rpm, no corresponding changes in integrals of the electromyography (EMG) signal and mean power frequency were observed. CONCLUSIONS: The results of this study indicate that the amplitude of the VO(2)SC was greater in higher pedal rate during the same work rate constant-load cycling exercise, which might be associated with a progressive increase in the adenosine triphosphate requirement of already recruited muscle fibers in exercising muscle.     

Muscle glycogen depletion alters oxygen uptake kinetics during heavy exercise

PURPOSE: To test the hypothesis that muscle fiber recruitment patterns influence the oxygen uptake (VO2) kinetic response, constant-load exercise was performed after glycogen depletion of specific fiber pools. METHODS: After validation of protocols for the selective depletion of Type I and II muscle fibers, 19 subjects performed square-wave exercise at 80% VT (moderate) and at 50% of the difference between VT and VO2max (heavy) without any prior depleting exercise (CON), after HIGH (10 x 1-min exercise bouts at 120% VO2max), and after LOW (3 h of exercise at 30% VO2max) exercise. RESULTS: Differences in VO2 kinetic parameters were only observed in heavy exercise AFTER HIGH: the VO2 primary component was higher (1.75 +/- 0.12 L x min) compared with CON (1.65 +/- 0.11 L x min, P < 0.05), and the VO2 slow component was lower (0.18 +/- 0.03 L x min) compared with CON (0.24 +/- 0.04 L x min, P < 0.05). CONCLUSIONS: The results indicate that the VO2 response to heavy constant-load exercise can be altered by depletion of glycogen in the Type II muscle fibers, lending support to the theory that muscle fiber recruitment influences both the VO2 primary and slow component amplitudes during heavy intensity exercise.     

Effect of glycogen depletion on the oxygen uptake slow component in humans

Previous studies have indicated that the (.-)VO(2) slow component is related to the recruitment of type II muscle fibres. We therefore hypothesised that an exercise and dietary regimen designed to deplete type I muscle fibres of glycogen would result in a greater contribution of type II muscle fibres to the exercise power output and therefore a larger amplitude of the (.-)VO(2) slow component. Eight male subjects took part in this study. On day 1, the subjects reported to the laboratory at 8 a.m., and completed a 9 min constant-load cycling test at a work rate equivalent to 85 % (.-)VO(2) peak. On day 2 at 12 p.m., the subjects were fed a 4200 kJ meal (60 % protein, 40 % fat); at 6 p.m. they completed a 2 h cycling test at 60 % (.-)VO(2) peak. On day 3 at 8 a.m., the subjects performed an exercise test identical to that of day 1. Metabolic and respiratory measurements indicated that our experimental design was effective in reducing the muscle glycogen content. (.-)VO(2) was significantly higher (by approximately 140 ml x min (-1)) throughout exercise following glycogen depletion but no appreciable changes in (.-)VO(2) kinetics were found: neither the time constant of the primary response (from 35.4 +/- 2.5 to 33.2 +/- 4.4 s) nor the amplitude of the slow component (from 404 +/- 95 to 376 +/- 81 ml x min (-1)) was significantly altered. Therefore, we suggest that the increased (.-)VO(2) throughout exercise and the unaltered (.-)VO(2) slow component following glycogen depletion might be explained by a shift towards a greater reliance on fat metabolism in type I muscle fibres with no appreciable change in fibre type recruitment patterns.     

Effects of sodium bicarbonate on VO2 kinetics during heavy exercise

PURPOSE: Sodium bicarbonate was used to investigate the effect of blood pH on VO2 kinetics during heavy exercise. METHODS: On separate days, 10 active subjects performed two 6-min cycling bouts (208 +/- 12 W) at 25 W above their ventilatory threshold. Each subject ingested 0.3 g x kg(-1) of sodium bicarbonate with approximately 1 L of water or water alone 1 h before exercise. VO2 kinetics were examined by means of a three-component mono-exponential model. RESULTS: Bicarbonate ingestion caused a significant increase in the preexercise blood pH (7.512 +/- 0.009 vs 7.425 +/- 0.007; P < 0.001). In the bicarbonate trial, the time constant for the rapid component (27.9 +/- 3.5 s) was slower than the control trial (20.8 +/- 2.4 s; P = 0.017). The higher blood pH after bicarbonate ingestion would have diminished local blood flow and caused a leftward shift of the oxygen-hemoglobin dissociation curve both of which would slow oxygen delivery to working muscle. In addition, bicarbonate ingestion diminished the amplitude of the slow component 29% (463 +/- 43 vs 649 +/- 53 mL x min(-1); P = 0.040). The primary cause of the slow component during heavy exercise is fatigue of working fibers and an accompanying increase of motor unit recruitment. Elevated plasma bicarbonate concentration is reported to stimulate the efflux of H from muscle fibers and to increase intramuscular pH. CONCLUSIONS: The slower time constant during the rapid component suggested that oxygen delivery is a limiting factor of VO2 kinetics during the onset of heavy exercise. Also, these results imply that bicarbonate ingestion diminished fatigue in working fibers during the slow component.     

Delayed onset muscle soreness does not alter O2 uptake kinetics during heavy-intensity cycling in humans

The purpose of this study was to determine if exercise-induced delayed onset muscle soreness (DOMS) would alter O2 uptake kinetics during heavy cycling in 9 untrained females. O2 uptake kinetics were characterised during 8-min of constant-load cycling performed with and without DOMS. DOMS was caused by completing 30 min of bench-stepping at a rate of 15 steps.min(-1). Two days after bench stepping, all subjects reported significant leg muscle soreness. Both phase II kinetics (without DOMS tau1: 26.6 +/- 2.4 s; with DOMS tau1: 27.2 +/- 3.7 s) and the slow component amplitude (without DOMS: 277 +/- 15 mL.min(-1); with DOMS: 291 +/- 21 mL.min(-1)) were unaffected by DOMS. The change in blood lactate concentration from rest to end-exercise was significantly greater during exercise performed with DOMS. Eccentric exercise causing a moderate degree of DOMS does not appear to impact upon the mechanisms mediating phase II or the slow component of O2 uptake kinetics.     

Endurance training reduces end-exercise VO2 and muscle use during submaximal cycling

INTRODUCTION: End-exercise VO2 during heavy, constant-load exercise is reduced after endurance training, due to an attenuated VO2 slow component. PURPOSE/METHODS: To determine whether the training-induced reduction in end-exercise VO2 was associated with reduced muscle use, we measured VO2 and T2 changes in magnetic resonance images in the final minute of two 15-min constant-load cycle rides, one above lactate threshold and the other below lactate threshold. These measures were repeated after a 4-wk period in eight subjects who trained on a cycle ergometer and seven controls. RESULTS: There were no changes in end-exercise VO2 or active muscle after training in either group during low-intensity cycling, in which no VO2 slow component was present. During high-intensity cycling, in which there was a slow component before training, the training group experienced a significant reduction (P < 0.05) in end-exercise VO2 (2625 +/- 673; 2567 +/- 605 mL.min (-1) and the T2 of the vastus lateralis (35.6 +/- 1.4; 34.5 +/- 0.9 ms). CONCLUSION: These results support the hypothesis that reduction in end-exercise VO2 (and the VO2 slow component) after training is due to reduced muscle use during heavy, constant load cycling.     

Effect of prior exercise on VO(2) slow component is not related to muscle temperature

INTRODUCTION: It has been widely reported that the VO(2) slow component is reduced in the second of two bouts of heavy exercise. It has also been shown that an increase in muscle temperature (Tm) produced by wearing hot-water-perfused pants causes a reduction in the VO(2) slow component. Therefore, the aim of this study was to investigate whether the effect of prior heavy exercise on the VO(2) slow component of subsequent heavy exercise is related to the warming-up of the exercising limbs. METHODS: Six male subjects completed an exercise protocol consisting of two constant-load exercise bouts (EX-1 and EX-2) at 90% VO(2peak), separated by 6 min of rest. The Tm of the m. vastus lateralis was measured with an indwelling thermistor. Seven days later, the subjects completed a second exercise protocol consisting of a passive warming-up of the upper legs until the same Tm was reached as after EX-1, followed by a constant-load work bout (EX-3) identical to EX-1 and EX-2. RESULTS: Tm reached comparable levels at the start of EX-2 and EX-3 (37.3 +/- 0.6 degrees C and 37.2 +/- 0.3 degrees C, respectively). The VO(2) slow component (measured as deltaVO(2)(6-2 min)) was reduced by 57% after prior heavy exercise ( < 0.05), whereas no significant reduction was observed after prior passive warming-up. CONCLUSIONS: The results of this study indicate that the reduction in VO(2) slow component observed after prior heavy exercise cannot be explained by an increase in muscle temperature of the upper legs.     

Slow-twitch fiber glycogen depletion elevates moderate-exercise fast-twitch fiber activity and O2 uptake

PURPOSE: We tested the hypotheses that previous glycogen depletion of slow-twitch (ST) fibers enhances recruitment of fast-twitch (FT) fibers, elevates energy requirement, and results in a slow component of VO2 during moderate-intensity dynamic exercise in humans. METHODS: Twelve healthy, male subjects cycled for 20 min at approximately 50% VO2max with normal glycogen stores (CON) and with exercise-induced glycogen depleted ST fibers (CHO-DEP). Pulmonary VO2 was measured continuously and single fiber, muscle homogenate, and blood metabolites were determined repeatedly during each trial. RESULTS: ST fiber glycogen content decreased (P < 0.05) during CON (293 +/- 24 to 204 +/- 17 mmol x kg d.w.), but not during CHO-DEP (92 +/- 22 and 84 +/- 13 mmol x kg d.w.). FT fiber CP and glycogen levels were unaltered during CON, whereas FT fiber CP levels decreased (29 +/- 7%, P < 0.05) during CHO-DEP and glycogen content tended to decrease (32 +/- 14%, P = 0.07). During CHO-DEP, VO2 was higher (P < 0.05) from 2 to 20 min than in CON (0-20 min:7 +/- 1%). Muscle lactate, pH and temperature, ventilation, and plasma epinephrine were not different between trials. From 3 to 20 min of CHO-DEP, VO2 increased (P <0.05) by 5 +/- 1% from 1.95 +/- 0.05 to 2.06 +/- 0.08 L x min but was unchanged during CON. In this exercise period, muscle pH and blood lactate were unaltered in both trials. Exponential modeling revealed a slow component of VO2 equivalent to 0.12 +/- 0.04 L x min during CHO-DEP. CONCLUSION: This study demonstrates that previous glycogen depletion of ST fibers enhances FT fiber recruitment, elevates O2 cost, and causes a slow component of VO2 during dynamic exercise with no blood lactate accumulation or muscular acidosis. These findings suggest that FT fiber recruitment elevates energy requirement of dynamic exercise in humans and support an important role of active FT fibers in producing the slow component of VO2     

The effect of prior high-intensity cycling exercise on the VO2 kinetics during high-intensity cycling exercise is situated at the additional slow component

In previous studies conclusions about the effect of prior exercise on VO2 kinetics of subsequent high-intensity exercise are generally based on observed changes in the overall VO2 response without considering the effects on the VO2 fast and slow component. The aim of the present study was to examine the effect on the VO2 fast and slow component separately. Therefore 10 subjects performed an exercise protocol consisting of an initial 3 min period of unloaded cycling followed by two constant-load work bouts at a work rate corresponding to 90% VO2peak, separated by 3 min of rest and 3 min of unloaded cycling. VO2 was measured on a breath-by-breath basis, and the response curves were analysed by a biexponential model. To increase signal-to-noise ratio, subjects performed four repetitions of the exercise protocol, each separated by at least one day. There was no significant alteration in VO2 kinetic parameters of the primary, fast component after high-intensity exercise. However, there was a significant effect of prior high-intensity exercise on the VO2 kinetic parameters of the slow component. The time constant and the amplitude of the slow component were reduced by respectively 44% (from 231.0 +/- 111.7 s to 130.1 +/- 50.4 s) and 49% (from 824 +/- 270 ml x min(-1) to 417 +/- 134 ml x min(-1)). The results of this study indicate that the effect of high-intensity exercise on the VO2 kinetics of a subsequent high-intensity exercise is probably limited to an effect on the slow component.     

Muscle activation and the slow component rise in oxygen uptake during cycling

PURPOSE: During constant-rate high-intensity exercise, a steady state for oxygen uptake (VO2) is not achieved and, after the initial rapid increase, VO2 continues to increase slowly. The mechanism underlying the slow-component rise in VO2 during high-intensity exercise is unknown. It has been hypothesized that increased muscle use may be a contributing factor, but only limited electromyograph (EMG) data are available supporting this hypothesis. The purpose of this study was to determine whether there is an association between the VO2 slow component and muscle use assessed by contrast shifts in magnetic resonance images (magnetic resonance imaging (MRI)). METHODS: The VO2 slow component was measured in 16 subjects during two 15-min bouts of cycling performed at high and low intensities. EMG and MRI transverse relaxation times (T2) were obtained after 3 and 15 min to determine muscle activity at each intensity. RESULTS: Low-intensity cycling produced no VO2 slow component, and no increases in muscle activity, except for a small increase (P < 0.05) in the T2 of the vastus lateralis. During high-intensity cycling, VO2, T2 of the vastus lateralis, rectus femoris and whole leg, and EMG activity and median power frequency of the vastus lateralis rose significantly (P < 0.05) from 3 to 15 min. Percent increases in VO2 and muscle T2 were related during high-intensity cycling (r = 0.63), but not during low-intensity cycling (r = 0.00). CONCLUSION: We conclude that increased muscle use is in part responsible for the slow component rise in oxygen uptake. The results support the hypothesis that during constant-rate exercise at intensities above lactate threshold, progressively greater use of fast-twitch motor units increases energy demand and causes concomitant progressive increases in VO2 and lactate.     

Relationship between the slow component of oxygen uptake and the potential reduction in maximal power output during constant-load exercise.

BACKGROUND: The purpose of the present study was to examine the relationship between the slow component of oxygen uptake (VO2) and muscle fiber fatigue. Maximal power output (MPO) was used as an index of muscle fiber fatigue. METHODS: Two constant exercises were carried out at exercise intensities of 40% and 80% of maximal oxygen uptake (VO2max). Each exercise was repeated three times, once for the measurement for VO2, and the other two times for MPO testing, at 3 and 6 minutes after work output. RESULTS: Reproducibility of MPO at rest was assessed by correlation coefficient. Its value was 0.933. At 40% VO2max, MPO did not significantly decrease from the resting value. At 80% VO2max, MPO significantly decreased by 129+/-77 watts at 3 min and by 178+/-108 watts at 6 min. The VO2 kinetic at 40% VO2 was well described by a monoexponential function with a time constant of 0.432 min. However, at 80% VO2max, a slow component of the form of a linear drift superimposed on a monoexponential function with an essentially equal time constant (0.469 min) was unambiguously detected. This slow component was significantly related to the decrease in MPO (r=0.567). CONCLUSIONS: The present results suggested that the fatigue of muscle fibers may be one of the factors that produce the slow component of VO2 during high intensity exercise.     

A disproportionate increase in VO2 coincident with lactate threshold during treadmill exercise.

PURPOSE: The purpose of this study was to assess the relationship between pulmonary VO2 and running speed over a range of exercise intensities. During constant-load cycle exercise above the lactate threshold (Tlac), it has been shown that VO2 does not attain a steady state within 3 min but continues to rise until either a delayed but elevated steady-state VO2 is attained or exhaustion occurs. Since this greater oxygen cost of exercise (V02 slow component) has only been demonstrated at discrete exercise intensities above Tlac, it was hypothesised that the onset of the VO2 slow component would coincide with Tlac during an incremental test if the stage durations were of sufficient length. METHODS: Five male subjects (mean +/- SD age 31 +/- 2 yr: VO2peak 60.1 +/- 5.8 mL x kg(-1) x min(-1)) performed four identical treadmill tests within an 8-d period. The tests involved the completion of six stages of 7-min duration. Running speed was increased by 0.5 km x h(-1) between stages. In the first test, fingertip capillary blood was sampled at the end of each stage for determination of Tlac. For all tests expired air was collected into Douglas bags from 3.0 to 3.75 min and from 6.0 to 6.75 min of each stage to determine any increase in V02 (deltaVO2) over the duration of the stage. RESULTS: The mean deltaVO2 for each stage over the four tests was determined for each subject. Repeated measures ANOVA with post-hoc Tukey tests revealed a significant increase in deltaVO2 at running speeds above, but not below, Tlac. CONCLUSIONS: The results of this study confirm the close association between the VO2 slow component and the onset of lactic acidosis and demonstrate alinearity in the VO2-exercise intensity relationship above Tlac for incremental treadmill exercise.     

VO2 response profiles in severe intensity exercise

AIM: VO2peak can be achieved over the range of intensities that define the severe intensity domain. The purpose of this study was to help characterize the VO2 response during constant-load exercise in this domain. METHODS: Twelve participants performed cycle ergometer tests at 267+/-52 W, 238+/-45 W, and 216+/-37 W, which were individually selected to elicit VO2peak and to cause fatigue in 3 min, 5 min, and 7 min, respectively. RESULTS: Times to fatigue were 201+/-16 s, 301+/-20 s, and 448+/-51 s, respectively. VO2 responded faster at higher work rates, with VO2peak reached after 154+/-25 s, 193+/-35 s, and 206+/-24 s, respectively. Extrapolation of the times to reach VO2peak revealed that 300 W was the highest power, and 151 s was the shortest time, for which VO2peak could be elicited. TheVO2 response was described using a three-component model. Exercise intensity did not affect the speed of the primary response, with time constants of 22+/-3 s, 23+/-4 s, and 23+/-4 s, respectively. However, the size of the primary phase was greater at higher intensities, with amplitudes of 1,798+/-200 mlxmin-1, 1,739+/-267 mlxmin-1, and 1,677+/-254 mlxmin-1, respectively. The amplitude of the slow component was correspondingly smaller at higher intensities. Extrapolation of the slow component amplitudes revealed that 299 W was the highest intensity, and 152(-1)53 s was the shortest time, for which a slow component would be engendered. CONCLUSION: VO2peak is attained faster at higher intensities because the amplitude of the primary response is greater, not because the response is faster. There is a slow component to the VO2 response at all intensities within the severe domain, but not at higher intensities, in the extreme domain, where fatigue occurs before VO2peak can be elicited.     

Effects of high-intensity interval training on the response during severe exercise

This study examined the effect of high-intensity interval training on the VO2 response during severe, constant-load exercise. Prior to, and following training, 10 females (V O2 peak 37.4+/-6.0 mL kg-1 min-1) performed a graded exercise test to determine VO2 peak and lactate threshold (LT) and a 6 min cycle test (CT) at the pre-training VO2 peak intensity. Training involved high-intensity intervals (2 min work, 1 min rest) performed 3x week for 8 weeks. Breath-by-breath data from 0 to 6 min during the CT were smoothed using 5s averages and fit to a bi-exponential model starting from 20s. Training resulted in significant improvements in VO2 max (2.34+/-0.37-2.78+/-0.30 L min-1), power at VO2 max (170+/-26-204+/-25 W) and power at LT (113+/-17-136+/-20 W) (p<0.05). Following training, the VO2 response showed a significant increase in the amplitude of the primary phase (A1) (1396+/-103-1695+/-100 mL min-1; p<0.05) and end-exercise VO2 (VO2 EE), with no difference (p>0.05) in the time constants of either phase or the amplitude of the slow component (318+/-67-380+/-48 mL; p=0.15). In conjunction, accumulated oxygen deficit (AOD) (43.7+/-9.8-17.2+/-2.8 mL O2 eq kg-1) and anaerobic contribution to the CT (19.4+/-4.4-7.2+/-1.2%) were significantly reduced. In contrast to previous moderate-intensity research, a high-intensity interval training program increased A1 and VO2 EE for the same absolute exercise intensity, decreasing the AOD during a severe-intensity CT.     

Effect of prior exercise on the VO2/work rate relationship during incremental exercise and constant work rate exercise

The disproportionate increase in VO2 ("extra VO2) reported at elevated intensity during incremental exercise (IE) might result from the same physiological mechanisms as the VO2 slow component observed during heavy constant work rate exercise (CWRE). Moreover, it has been demonstrated that prior heavy exercise can diminish the VO2 slow component. The aim of this study was to evaluate whether prior heavy exercise also alters the "extra VO2" during IE. Ten trained sprinters performed three tests on a cycle ergometer: Test 1 was an IE; Test 2 consisted of six minutes of a CWRE (90% of VO2max) followed by six minutes at 35 W and by an IE and Test 3 was composed of two CWRE of six minutes separated by six minutes of exercise at 35 W. For each IE, the slope and the intercept of the VO2/work rate relationship were calculated by linear regression using data before the first Ventilatory Threshold (pre-VT1 slope). The difference between VO2max measured and VO2max expected using the pre-LT slope was calculated (deltaVO2). We also calculated the difference between VO2 at min five and VO2 at min three during CWRE of Test 3 (deltaVO2(5' - 3')). VO2max was significantly higher than VO2exp during IE of Test 1 and Test 2. deltaVO2 during IE did not differ between Test 1 and Test 2 (+ 259 +/- 229 ml x min(-1) vs. + 222 +/- 221 ml x min(-1)). During Test 3, six subjects achieved five minutes of exercise during the second CWRE and deltaVO2(5' - 3') was significantly decreased during the second CWRE (338 +/- 65 ml x min(-1) vs. 68 +/- 98 ml x min(-1), n = 6). These results demonstrate that the amplitude of the "extra VO2"during IE was not affected by prior exercise, whereas the slow component of VO2 evaluated by deltaVO2(5' - 3') during CWRE was lowered. This implies that prior exercise does not have the same effect on the slow component of VO2 and on the "extra VO2". Therefore we were unable to demonstrate a relationship between the VO2 slow component and the extra-VO2 phenomenon during IE.     

The decrease in VO(2) slow component induced by prior exercise does not affect the time to exhaustion

In previous studies decreases in the VO(2) slow component were observed after prior heavy exercise. The observed effects after prior low-intensity exercise were rather controversial. The purpose of the present study was to more thoroughly examine the effects of prior low-intensity exercise on the VO(2) slow component. Furthermore, it has been suggested that the VO(2) slow component may be a determinant of exercise tolerance. Therefore we tested the hypothesis whether an attenuated VO(2) slow component induced by prior exercise could affect the time to exhaustion. Ten subjects performed four exercise protocols consisting of heavy cycling exercise (95 % VO(2)peak) until exhaustion. This constant-load exercise was performed without prior exercise (protocol NPE), or was preceded by 6 min heavy cycling exercise (protocol 6HPE), 12 min low-intensity cycling exercise (protocol 12LPE) or 6 min low-intensity cycling exercise (protocol 6LPE). The VO(2) slow component quantified as Delta VO(2 (end-2)) (669 +/- 90 ml x min (-1) in NPE) was significantly reduced after heavy as well as low-intensity exercise (respectively 47 %, 29 % and 17 % in 6HPE, 12LPE and 6LPE). This reduction lead to a significantly lower end VO(2) in 6HPE and 12LPE. The time to exhaustion (594 +/- 139 s in NPE), however, was unaffected by prior exercise rejecting our hypothesis that the attenuated VO(2) slow component could improve the capability to sustain exercise performance.     

Prior arm exercise speeds the VO2 kinetics during arm exercise above the heart level

PURPOSE: To test the hypothesis that the initial O2 uptake kinetics during exercise where the rise in blood flow (and, by implication, O2 delivery) to the working muscles during an abrupt increase in exercise intensity is reduced (i.e., arm exercise performed above the level of the heart) would be faster when preceded by a bout of high-intensity exercise. METHODS: Eleven physically active males completed two protocols, each consisting of two consecutive bouts of 6 min of high-intensity arm crank exercise separated by 6 min of recovery. In one protocol, the arm crank exercise was performed with the arms below the level of the heart (HL). RESULTS: In the HL protocol, the amplitudes of the VO2 fast and slow component were unaffected by prior exercise, whereas the VO2 fast component time constant was significantly reduced in the second bout (49.8+/-22.1 vs 40.7+/-13.2 s; P<0.05). CONCLUSION: The results of this study demonstrate that prior high-intensity exercise caused a significant speeding of the VO2 fast component response during subsequent high-intensity arm crank exercise performed above, and not below, the level of the heart.     

Oxygen uptake kinetics during moderate and heavy intensity exercise in humans: the influence of hypoxia and training status

This study examined the influence of moderate hypoxia on the oxygen uptake (V.O(2)) kinetic response (primary time constant and slow component amplitude) during moderate and heavy cycle exercise in twenty-seven male subjects with various training status. Nine endurance trained (21.5 +/- 2.6 yr), nine sprint trained (22.9 +/- 5.7 yr), and nine untrained controls (24.0 +/- 4.4 yr) completed incremental tests to exhaustion in normoxia (inspired gas concentration or FIO (2) = 21 % O(2)) and hypoxia (FIO (2) = 13 % O(2)) to establish the FIO (2)-specific ventilatory threshold (VT) and maximal VO(2). Subsequently, the subjects performed repeated constant work rate cycling exercises during 7 min at moderate intensity (80 % of FIO (2)-specific VT) and heavy intensity (midway between the FIO (2) specific VT and maximal VO(2)). Pulmonary gas exchange was measured breath-by-breath during all exercise sessions. For both moderate and heavy intensities, the time constant of the primary VO(2) component was significantly (p < 0.05) slowed by approximately 25 to 30 % in hypoxia compared to normoxia to the same extent in the three groups. Hypoxia produced a more important decrease in the amplitude of the slow component in endurance athletes (- 36 %) than in sprinters (- 30 %) and controls (- 12 %). These results suggest that both primary and slow components of VO(2) kinetics during the adjustment to moderate- and heavy-intensity exercise are sensitive to hypoxia while training status tended to modulate partly the slow component amplitude.     

The slow component of VO2 in professional cyclists

OBJECTIVES: To analyse the slow component of oxygen uptake (VO2) in professional cyclists and to determine whether this phenomenon is due to altered neuromuscular activity, as assessed by surface electromyography (EMG). METHODS: The following variables were measured during 20 minute cycle ergometer tests performed at about 80% of VO2MAX in nine professional road cyclists (mean (SD) age 26 (2) years; VO2max 72.6 (2.2) ml/kg/min): heart rate (HR), gas exchange variables (VO2, ventilation (VE), tidal volume (VT), breathing frequency (fb), ventilatory equivalents for oxygen and carbon dioxide (VE/VO2 and VE/VCO2 respectively), respiratory exchange ratio (RER), and end tidal PO2 and PCO2 (PETO2 and PETCO2 respectively)), blood variables (lactate, pH, and [HCO3-]) and EMG data (root mean from square voltage (rms-EMG) and mean power frequency (MPF)) from the vastus lateralis muscle. RESULTS: The mean magnitude of the slow component (from the end of the third minute to the end of exercise) was 130 (0.04) ml in 17 minutes or 7.6 ml/min. Significant increases from three minute to end of exercise values were found for the following variables: VO2 (p<0.01), HR (p<0.01), VE (p<0.05), fb (p<0.01), VE/VO2 (p<0.05), VE/VCO2 (p<0.01), PETO2 (p<0.05), and blood lactate (p<0.05). In contrast, rms-EMG and MPF showed no change (p>0.05) throughout the exercise tests. CONCLUSIONS: A significant but small VO2 slow component was shown in professional cyclists during constant load heavy exercise. The results suggest that the primary origin of the slow component is not neuromuscular factors in these subjects, at least for exercise intensities up to 80% of VO2MAX.     

Circulating white blood cells affect red cell pulmonary transit times in endurance athletes during intense exercise

PURPOSE: The aim of this study was to determine the relationship between the right-to-left ventricular red cell pulmonary transit times (PTT) during intense exercise and circulating white blood cell (WBC) counts in highly trained endurance athletes. We postulated that high levels of WBCs preexercise would slow PTT. Eleven endurance-trained athletes (VO2max = 69.6 +/- 7.7 mL.kg-1.min-1; weight = 75.0 +/- 6.2 kg; height = 181.0 +/- 7.1 cm) performed 6.5 min constant-load, near-maximal cycling exercise (approximately 92% VO2max) on two different days. Preexercise WBC counts were measured in arterial blood drawn from the radial artery 30 min before exercise. PTT was measured during the 3rd min of exercise by first-pass radionuclide cardiography using centroid and deconvolution analysis, whereas cardiac output (Q) was measured during the last 2.5 min of exercise via a count-based ratio method from the MUGA technique. RESULTS: Combined mean PTT from both deconvolution and centroid analysis at minute three of exercise was 2.45 +/- 0.21 s, whereas the preexercise WBC count was 5.3 +/- 1.6 x 109.L-1. Cardiopulmonary blood volume at minute three of exercise was 1.22 +/- 0.13 L, VO2 was 4.58 +/- 0.44 L.min-1, and Q was 30.2 +/- 4.2 L.min-1. We found that PTT was negatively correlated with circulating WBC (r = -0.61; adjusted r2 = 0.30; P = 0.04; N = 11) but not with the dispersion (spread) of transit times around the mean (r = 0.19; P = 0.57). CONCLUSION: This suggests that athletes with higher circulating numbers of WBCs preexercise have faster (shorter) red cell transit times through the lung during intense exercise.