Comparison of oxygen uptake at the onset of decrement-load and constant-load exercise

The purpose of the present study was to examine whether the level of oxygen uptake (V(.)(O2) at the onset of decrement-load exercise (DLE) is lower than that at the onset of constant-load exercise (CLE), since power output, which is the target of V(.)(O2) response, is decreased in DLE. CLE and DLE were performed under the conditions of moderate and heavy exercise intensities. Before and after these main exercises, previous exercise and post exercise were performed at 20 watts. DEL was started at the same power output as that for CLE and power output was decreased at a rate of 15 watts per min. V(.)(O2) in moderate CLE increased at a fast rate and showed a steady state, while V(.)(O2) in moderate DLE increased and decreased linearly. V(.)(O2) at the increasing phase in DLE was at the same level as that in moderate CLE. V(.)(O2) immediately after moderate DLE was higher than that in the previous exercise by 98+/-77.5 ml/min. V(.)(O2) in heavy CLE increased rapidly at first and then slowly increased, while V(.)(O2) in heavy DLE increased rapidly, showing a temporal convexity change, and decreased linearly. V(.)(O2) at the increasing phase of heavy DLE was the same level as that in heavy CLE. V(.)(O2) immediately after heavy DLE was significantly higher than that in the previous exercise by 156+/-131.8 ml/min. Thus, despite the different modes of exercise, V(.)(O2) at the increasing phase in DLE was at the same level as that in CLE due to the effect of the oxygen debt expressed by the higher level of V(.)(O2) at the end of DLE than that in the previous exercise.     

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.     

Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans

We tested the hypothesis that the slowerincrease in alveolar oxygen uptake(O₂) at the onset ofsupine, compared with upright, exercise would be accompanied by aslower rate of increase in leg blood flow (LBF). Seven healthy subjectsperformed transitions from rest to 40-W knee extension exercise in theupright and supine positions. LBF was measured continuously with pulsedand echo Doppler methods, andO₂ was measured breath bybreath at the mouth. At rest, a smaller diameter of thefemoral artery in the supine position(P < 0.05) was compensated by agreater mean blood flow velocity (MBV) (P < 0.05) so that LBF was not different in the two positions. At the end of6 min of exercise, femoral artery diameter was larger in the uprightposition and there were no differences inO₂, MBV, or LBF betweenupright and supine positions. The rates of increase ofO₂ and LBF in thetransition between rest and 40 W exercise, as evaluated by the meanresponse time (time to 63% of the increase), were slower in the supine[O₂ = 39.7 ± 3.8 (SE) s, LBF = 27.6 ± 3.9 s] than in the uprightpositions (O₂ = 29.3 ± 3.0 s, LBF = 17.3 ± 4.0 s;P < 0.05). These data support ourhypothesis that slower increases in alveolarO₂ at the onset of exercisein the supine position are accompanied by a slower increase in LBF.

     

Relationship between cardiac output and oxygen uptake at the onset of exercise

The purpose of the present study was to assess the relationship between the rapidity of increased gas exchange (i.e. oxygen uptake ) and increased cardiac output ( ) during the transient phase following the onset of exercise. Five healthy male subjects performed multiple rest-exercise or light exercise (25 W)-exercise transitions on an electrically braked ergometer at exercise intensities of 50, 75, or 100 W for 6 min, respectively. Each transition was performed at least eight times for each load in random order. The was obtained by a breath-by-breath method, and was measured by an impedance method during normal breathing, using an ensemble average. On transitions from rest to exercise, rapidly increased during phase I with time constants of 6.8–7.3 s. The also showed a similar rapid increment with time constants of 6.0–6.8 s with an apparent increase in stroke volume (SV). In this phase I, increased to about 29.7%–34.1% of the steady-state value and increased to about 58.3%–87.0%. Thereafter, some 20 s after the onset of exercise a mono-exponential increase to steady-state occurred both in and with time constants of 26.7–32.3 and 23.7–34.4 s, respectively. The insignificant difference between and time constants in phase I and the abrupt increase in both and SV at the onset of exercise from rest provided further evidence for a cardiodynamic contribution to following the onset of exercise from rest.     

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.     

Cardiac output and oxygen uptake kinetics at the onset and offset of exercise

1. 1. The aim of the present study is to assess the relationship between rapidity of oxygen uptake (V_O2 and cardiac output (Q) kinetics at the transient phase of the onset and offset of exercise.

2. 2. Five healthy male subjects performed multiple rest-exercise-recovery transitions on an electrically braked ergometer, work rate was 50, 75, or 100 W for 6 min, respectively.

3. 3. V_O2 was obtained by a breath-by-breath method, and Q was measured by an impedance method during normal breath, using an ensemble averaged method.

4. 4. On transition from rest to exercise, V_O2 rapidly increased as phase I with a time constant of 7.0–7.8 s. Q also showed a similar rapid increment with a time constant of 6.3–6.8 s in phase I.

5. 5. In this phase I, V_O2 increased approx. 42–68% of steady state value and Q increased 71–84%. Thereafter, V_O2 and Q increased monoexponentially up to steady state with a time constant of 26.7–32.3 and 23.7–34.4 s, respectively.

6. 6. During recovery, V_O2 (with a time constant of 35.7–38.1 s and time delay (TD) of −1 to −2 s), while Q remained to sustain the value of steady state exercise with a couple of time delay (TD = 2–7 s), and thereafter decreased monoexponentially (with a time constant of 18.9–31.6 s).

7. 7. The stroke volume showed the similar behavior to the Q kinetics after exercise, while heart rate rapidly decreased (time constant = 10.6–21.2 s).

8. 8. It is suggested that the delayed Q kinetics after exercise might be attributable to the sustained level of venous return and that Q kinetics is not linked with V_O2 kinetics after exercise.

Interaction of factors determining oxygen uptake at the onset of exercise.

Considerable debate surrounds the issue of whether the rate of adaptation of skeletal muscle O2 consumption (QO2) at the onset of exercise is limited by 1) the inertia of intrinsic cellular metabolic signals and enzyme activation or 2) the availability of O2 to the mitochondria, as determined by an extrinsic inertia of convective and diffusive O2 transport mechanisms. This review critically examines evidence for both hypotheses and clarifies important limitations in the experimental and theoretical approaches to this issue. A review of biochemical evidence suggests that a given respiratory rate is a function of the net drive of phosphorylation potential and redox potential and cellular mitochondrial PO2 (PmitoO2). Changes in both phosphorylation and redox potential are determined by intrinsic metabolic inertia. PmitoO2 is determined by the extrinsic inertia of both convective and diffusive O2 transport mechanisms during the adaptation to exercise and the rate of mitochondrial O2 utilization. In a number of exercise conditions, PmitoO2 appears to be within a range capable of modulating muscle metabolism. Within this context, adjustments in the phosphate energy state of the cell would serve as a cytosolic "transducer," linking ATP consumption with mitochondrial ATP production and, therefore, O2 consumption. The availability of reducing equivalents and O2 would modulate the rate of adaptation of QO2.     

Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare theO₂ uptake(O₂) kinetics at the onsetof heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cyclingtask to determine peak O₂(O_{2 peak}).On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice bycycling at 50%O_{2 peak} for 3.5 min,once by cycling at 100%O_{2 peak} for 2 min,and once by cycling at 130%O_{2 peak} for 75 s.O₂ deficit was not significantlydifferent between boys and men (respectively, 50%O_{2 peak} task: 6.6 ± 11.1 vs. 5.5 ± 7.3 ml · min¹ · kg¹;100% O_{2 peak} task:28.5 ± 8.1 vs. 31.8 ± 6.3 ml · min¹ · kg¹;and 130%O_{2 peak}task: 30.1 ± 5.7 vs. 35.8 ± 5.3 ml · min¹ · kg¹).To assess the kinetics, phase I was excluded from analysis. Phase IIO₂ kinetics could bedescribed in all cases by a monoexponential function. ANOVA revealed nodifferences in time constants between boys and men (respectively, 50%O_{2 peak}task: 22.8 ± 5.1 vs. 26.4 ± 4.1 s; 100%O_{2 peak} task: 28.0 ± 6.0 vs. 28.1 ± 4.4 s; and 130%O_{2 peak} task: 19.8 ± 4.1 vs. 20.7 ± 5.7 s). In conclusion, O₂ deficit and fast-componentO₂ on-transientsare similar in boys and men, even at high exercise intensities, whichis in contrast to the findings of other studies employing simplermethods of analysis. The previous interpretation that children relyless on nonoxidative energy pathways at the onset of heavy exercise isnot supported by our findings.

     

Kinetics of oxygen uptake and heart rate at onset of exercise in children

Requirements for cellular homeostasis appear to be unchanged between childhood and maturity. We hypothesized, therefore, that the kinetics of O2 uptake (VO2) in the transition from rest to exercise would be the same in young children as in teenagers. To test this, VO2 and heart rate kinetics from rest to constant work rate (75% of the subject's anaerobic threshold) in 10 children (5 boys and 5 girls) aged 7-10 yr were compared with values found in 10 teenagers (5 boys and 5 girls) aged 15-18 yr. Gas exchange was measured breath to breath, and phases I and II of the transition and phase III (steady-state exercise) were evaluated from multiple transitions in each child. Phase I (the VO2 at 20 s of exercise expressed as percent rest-to-steady-state exercise VO2) was not significantly correlated with age or weight [mean value 42.5 +/- 8.9% (SD)] nor was the phase II time constant for VO2 [mean 27.3 +/- 4.7 (SD) s]. The older girls had significantly slower kinetics than the other children but were also found to be less fit. When the teenagers exercised at work rates well below 75% of their anaerobic threshold, phase I VO2 represented a higher proportion of the overall response, but the phase II kinetics were unchanged. The temporal coupling between the cellular production of mechanical work at the onset of exercise and the uptake of environmental O2 appears to be controlled throughout growth in children.     

Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise.

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2)kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to VO2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to approximately 105% of the predetermined Vo2 peak, separated by 3 x 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means +/- SD: MAX1: 1.3 +/- 0.4 mM vs. MAX2: 7.7 +/- 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 +/- 5.5 s vs. MAX2: 33.2 +/- 7.7 s). Rather, the asymptotic "gain" of the primary Vo2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 +/- 0.9 ml.min(-1).W(-1) vs. MAX2: 9.0 +/- 0.7 ml.min(-1).W(-1); P < 0.05), such that VO2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component VO2 response but does increase the amplitude to which VO2 may rise following the onset of perimaximal-intensity cycle exercise.     

Muscle chemoreflex elevates muscle blood flow and O2 uptake at exercise onset in nonischemic human forearm.

We tested the hypothesis that increases in forearm blood flow (FBF) during the adaptive phase at the onset of moderate exercise would allow a more rapid increase in muscle O2 uptake (VO2 mus). Fifteen subjects completed forearm exercise in control (Con) and leg occlusion (Occ) conditions. In Occ, exercise of ischemic calf muscles was performed before the onset of forearm exercise to activate the muscle chemoreflex evoking a 25-mmHg increase in mean arterial pressure that was sustained during forearm exercise. Eight subjects who increased FBF during Occ compared with Con in the adaptation phase by >30 ml/min were considered "responders." For the responders, a higher VO2 mus accompanied the higher FBF only during the adaptive phase of the Occ tests, whereas there was no difference in the baseline or steady-state FBF or VO2 mus between Occ and Con. Supplying more blood flow at the onset of exercise allowed a more rapid increase in VO2 mus supporting our hypothesis that, at least for this type of exercise, O2 supply might be limiting.     

Sympathetic restraint of muscle blood flow at the onset of dynamic exercise.

Little attention has focused on sympathetic influences on skeletal muscle blood flow at the onset of exercise. We hypothesized that 1) the sympathetic nervous system constrains muscle blood flow and 2) the decline from peak blood flow is mediated by increasing sympathetic vasoconstrictor tone. Mongrel dogs (n = 7) ran on a treadmill after intra-arterial infusion of saline (control) or combined alpha(1)- and alpha(2)-adrenergic blockade (prazosin and rauwolscine). Immediate and rapid increases in hindlimb blood flow occurred at commencement of exercise with peak iliac blood flows averaging 933 +/- 79 and 1,227 +/- 90 ml/min during control and blockade conditions, respectively. At 1 min of exercise, hindlimb blood flow had decreased to 629 +/- 54 and 1,057 +/- 89 ml/min. In the absence of sympathetic vasoconstrictor tone, there was an enhanced peak blood flow at the onset of exercise. In addition, alpha-blockade attenuated the overshoot of hindlimb blood flow compared with the control condition. These data suggest that an immediate and sustained increase in sympathetic outflow restrains hindlimb blood flow at the onset of exercise and is responsible, at least in part, for an overshoot of blood flow to exercising skeletal muscle.