Effect of exercise modality on oxygen uptake kinetics during heavy exercise

The mechanisms responsible for the oxygen uptake (VO2) slow component during high-intensity exercise have yet to be established. In order to explore the possibility that the VO2 slow component is related to the muscle contraction regimen used, we examined the pulmonary VO2 kinetics during constant-load treadmill and cycle exercise at an exercise intensity that produced the same level of lactacidaemia for both exercise modes. Eight healthy subjects, aged 22-37 years, completed incremental exercise tests to exhaustion on both a cycle ergometer and a treadmill for the determination of the ventilatory threshold (defined as the lactate threshold, Th1a) and maximum VO2 (VO2max). Subsequently, the subjects completed two "square-wave" transitions from rest to a running speed or power output that required a VO2 that was halfway between the mode-specific Th1a and VO2max. Arterialised blood lactate concentration was determined immediately before and after each transition. The VO2 responses to the two transitions for each exercise mode were time-aligned and averaged. The increase in blood lactate concentration produced by the transitions was not significantly different between cycling [mean (SD) 5.9 (1.5) mM] and running [5.5 (1.6) mM]. The increase in VO2 between 3 and 6 min of exercise; (i.e. the slow component) was significantly greater in cycling than in running, both in absolute terms [290 (102) vs 200 (45) ml x min(-1); P<0.05] and as a proportion of the total VO2 response above baseline [10 (3)% vs 6 (1)%; P < 0.05]. These data indicate that: (a) a VO2 slow component does exist for high-intensity treadmill running, and (b) the magnitude of the slow component is less for running than for cycling at equivalent levels of lactacidaemia. The greater slow component observed in cycling compared to running may be related to differences in the muscle contraction regimen that is required for the two exercise modes.     

Kinetics of oxygen uptake during supine and upright heavy exercise.

It is presently unclear how the fast and slow components of pulmonary oxygen uptake (VO(2)) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (VO(2) equal to 50% of the difference between LT and peak VO(2)) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in VO(2) was similar in the two positions, but VO(2) kinetics were slower in the supine position. During heavy exercise, the rate of adjustment of VO(2) to the 6-min value was also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component of VO(2), without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exercise VO(2) was the same in the two positions. The changes in VO(2) kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component for VO(2) but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position.     

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.     

Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise.

We assessed the linearity of oxygen uptake (VO2) kinetics for several work intensities in four trained cyclists. VO2 was measured breath by breath during transitions from 33 W (baseline) to work rates requiring 38, 54, 85, and 100% of maximal aerobic capacity (VO2max). Each subject repeated each work rate four times over 8 test days. In every case, three phases (phases 1, 2, and 3) of the VO2 response could be identified. VO2 during phase 2 was fit by one of two models: model 1, a double exponential where both terms begin together close to the start of phase 2, and model 2, a double exponential where each of the exponential terms begins independently with separate time delays. VO2 rose linearly for the two lower work rates (slope 11 ml.min-1 W-1) but increased to a greater asymptote for the two heavier work rates. In all four subjects, for the two lighter work rates the double-exponential regression reduced to a single value for the time constant (average across subjects 16.1 +/- 7.7 s), indicating a truly monoexponential response. In addition, one of the responses to the heaviest work rate was monoexponential. For the remaining seven biexponential responses to the two heaviest work rates, model 2 produced a significantly better fit to the responses (P less than 0.05), with a mean time delay for the slow component of 105 +/- 46 s.(ABSTRACT TRUNCATED AT 250 WORDS)     

Forearm oxygen uptake during maximal forearm dynamic exercise

This study was undertaken in an attempt to determine the maximal oxygen uptake in a small muscle group by measuring directly the oxygen expenditure of the forearm. Five healthy medical students volunteered. The subjects' maximal forearm work capacity was determined on a spring-loaded hand ergometer. Exercise was continued until exhaustion by pain or fatigue. Two weeks later intra-arterial and intravenous catheters were placed in the dominant arm. Blood samples for measurement of oxygen concentration were collected via the catheters. Forearm blood flow was measured by means of the indicator dilution technique. Oxygen uptake was determined according to the Fick principle. The forearm oxygen uptake attained at maximal work loads was a mean of 201 (SD +/- 56) mumol.min-1.100 ml-1. It was impossible at maximal exercise to discern a plateau of the oxygen uptake curve in relation to work output. It is suggested that a plateau in the oxygen uptake curve is not a useful criterion for maximal oxygen uptake in a small muscle group. Skeletal muscle may have an unused capacity for oxygen consumption even at maximal exercise intensity where muscle work cannot be continued due to muscle pain and fatigue.     

Mean myoglobin oxygen tension during exercise at maximal oxygen uptake.

Changes in intracellular Po2 in myoglobin containing skeletal muscle during exercise were estimated in normal nonathlete subjects from measurements of shifts of CO between blood and muscle under conditions where the total body CO stores remained constant. Exercise was performed on a bicycle ergometer. In 1.5-2 and 6-7 min runs at Vo2 max with the subject breathing 21% O2, mean MbCO/HbCO increased 146 +/- 7 and 163 +/- 11% of resting values, respectively (P less than 0.05). With the subjects breathing 13-14% O2, in 1.5-2 and 6-7 min runs, Vo2 max fell an average of 4.3 +/- 5.1% and 12.0 +/- 5.2%, respectively, and mean MbCO/HbCO increased to 233 +/- 18% and 210 +/- 52% of resting value, respectively (P less than 0.05). These findings suggest that mean myoglobin Po2 fell during exercise at Vo2 max, with the subjects breathing 21% O2 and the decrease in mean myoglobin Po2 was greater with the subject breathing 13-14% O2. There was considerable variability in different subjects and in some, the data were not consistent with intracellular O2 availability limiting aerobic metabolism. The data support a postulate that there are several limiting factors for the aerobic capacity, including intracellular O2 availability.     

Cardiac output estimated noninvasively from oxygen uptake during exercise

Stringer, William W., James E. Hansen, and K. Wasserman.Cardiac output estimated noninvasively from oxygen uptake duringexercise. J. Appl. Physiol. 82(3):908-912, 1997.Because gas-exchange measurements duringcardiopulmonary exercise testing allow noninvasive measurement ofoxygen uptake (O₂), whichis equal to cardiac output (CO) × arteriovenous oxygencontent difference [C(a-vD_O2)],CO and stroke volume could theoretically be estimated if theC(a-vD_O2)increased in a predictable fashion as a function of %maximumO₂(O_{2 max}) duringexercise. To investigate the behavior ofC(a-vD_O2)during progressively increasing ramp pattern cycle ergometry exercise,5 healthy subjects performed 10 studies to exhaustion while arterialand mixed venous blood were sampled. Samples were analyzed forblood gases (pH, PCO₂,PO₂) and oxyhemoglobin and hemoglobinconcentration with a CO-oximeter. TheC(a-vD_O2)(ml/100 ml) could be estimated with a linear regression [C(a-vD_O2) = 5.72 + 0.105 × %O_{2 max};r = 0.94]. The CO estimated fromthe C(a-vD_O2)by using the above linear regression was well correlated withthe CO determined by the direct Fick method(r = 0.96). The coefficient ofvariation of the estimated CO was small (7-9%) between the lacticacidosis threshold and peakO₂. The behaviorof C(a-vD_O2),as related to peakO₂, was similar regardless of cardiac function compared with similar measurements fromstudies in the literature performed in normal and congestive heartfailure patients. In summary, CO and stroke volume can be estimatedduring progressive work rate exercise testing from measured O₂ (in normal subjects andpatients with congestive heart failure), and the resultant linearregression equation provides a good estimate ofC(a-vD_O2).

     

Comparison of oxygen uptake kinetics during knee extension and cycle exercise

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O(2) uptake (pVo(2)) kinetics and 2) to characterize the muscle blood flow, muscle Vo(2) (mVo(2)), and pVo(2) kinetics during KE to investigate the rate-limiting factor(s) of pVo(2) on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pVo(2) during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mVo(2) at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pVo(2) for both moderate and heavy exercise was higher during KE ( approximately 12 ml.W(-1).min(-1)) compared with CE ( approximately 10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mVo(2) during heavy KE [25.8 +/- 9.0 s (SD)] was not significantly different from that of the phase II pVo(2). Moreover, the slow component of pVo(2) evident for the heavy KE reflected the gradual increase in mVo(2). The initial LBF kinetics after onset of KE were significantly faster than the phase II pVo(2) kinetics (moderate: time constant LBF = 8.0 +/- 3.5 s, pVo(2) = 32.7 +/- 5.6 s, P < 0.05; heavy: LBF = 9.7 +/- 2.0 s, pVo(2) = 29.9 +/- 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pVo(2). These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pVo(2), consistent with an intramuscular limitation to Vo(2) kinetics, i.e., a microvascular O(2) delivery-to-O(2) requirement mismatch or oxidative enzyme inertia.     

Metaboreceptor-mediated muscle oxygen saturation during recovery following isometric handgrip exercise

The aim of the present study was to determine whether oxygen supply to non-exercised muscle during recovery following fatiguing exercise is influenced by accumulated metabolites within exercised muscle. Twelve healthy male subjects performed 2-min isometric handgrip exercise at 40% maximal voluntary contraction with their right hand and the exercise was followed by a 3-min recovery period. Muscle oxygen saturation (SmO(2)) determined by near-infrared spatially resolved spectroscopy was used as an index of oxygen supply to non-exercised muscle and was measured in biceps brachii and tibialis anterior muscles on the left side. Compared to the pre-exercise baseline level, SmO(2) in the biceps brachii muscle (SmO(2BB)) increased significantly from 30 sec to 1 min after the start of exercise, while SmO(2) in the tibialis anterior muscle (SmO(2TA)) remained stable during the initial 1 min of exercise. Both SmO(2BB) and SmO(2TA) began to decrease at about 1 min and continued to decrease thereafter. Due to the initial increase in SmO(2BB), only SmO(2TA) showed a significant decrease during exercise. During recovery, SmO(2BB) did not differ significantly from the pre-exercise baseline level, whereas SmO(2TA) remained significantly lower until about 1.5 min of recovery and then it did not differ significantly from the baseline level. In another bout, subjects performed handgrip exercise of the same intensity, but post-exercise arterial occlusion (PEAO) of the exercised muscle was imposed for 2 min immediately after the end of exercise. During PEAO, SmO(2BB) decreased significantly compared to the baseline level, whereas SmO(2TA) remained significantly lower until the end of PEAO. The significant decrease in SmO(2BB) and the prolongation of decrease in SmO(2TA) by PEAO suggests that the recovery of SmO(2) in the non-exercised arm and leg is mediated by muscle metaboreceptors.     

EMG versus oxygen uptake during cycling exercise in trained and untrained subjects.

The aim of this study was to test the hypothesis that bicycle training may improve the relationship between the global SEMG energy and VO2. We already showed close adjustment of the root mean square (RMS) of the surface electromyogram (SEMG) to the oxygen uptake (VO2) during cycling exercise in untrained subjects. Because in these circumstances an altered neuromuscular transmission which could affect SEMG measurement occurred in untrained individuals only, we searched for differences in the SEMG vs. VO2 relationship between untrained subjects and well-trained cyclists. Each subject first performed an incremental exercise to determine VO2max and the ventilatory threshold, and second a constant-load threshold cycling exercise, continued until exhaustion. SEMG from both vastus lateralis muscles was continuously recorded. RMS was computed. M-Wave was periodically recorded. During incremental exercise: (1) a significant non-linear positive correlation was found between RMS increase and VO2 increase in untrained subjects, whereas the relationship was best fitted by a straight line in trained cyclists; (2) the RMS/VO2 ratio decreased progressively throughout the incremental exercise, its decline being significantly and markedly accentuated in trained cyclists; (3) in untrained subjects, significant M-wave alterations occurred at the end of the trial. These M-wave alterations could explain the non-linear RMS increase in these individuals. During constant-load exercise: (1) after an initial increase, the VO2 ratio decreased progressively to reach a plateau after 2 min of exercise, but no significant inter-group differences were noted; (2) no M-wave changes were measured in the two groups. We concluded that the global SEMG energy recorded from the vastus lateralis muscle is a good estimate of metabolic energy expenditure during incremental cycling exercise only in well-trained cyclists.     

Maximum oxygen uptake and arterial blood oxygenation during hypoxic exercise in rats.

The objectives of these experiments were 1) to describe the effect of maximum treadmill exercise on gas exchange, arterial blood gases, and arterial blood oxygenation in rats acclimated for 3 wk to simulated altitude (SA, barometric pressure 370-380 Torr) and 2) to determine the contribution of acid-base changes to the changes in arterial blood oxygenation of hypoxic exercise. Maximum O2 uptake (VO2max) was measured in four groups of rats: 1) normoxic controls run in normoxia (Nx), 2) normoxic controls run in acute hypoxia [AHx inspiratory PO2 (PIO2) approximately 70 Torr], 3) SA rats run in hypoxia (3WHx, PIO2 approximately 70 Torr), and 4) SA rats run in normoxia (ANx). VO2max (ml STPD.min-1.kg-1) was 70.8 +/- 0.9 in Nx, 46.4 +/- 1.9 in AHx, 52.6 +/- 1.1 in 3WHx, and 70.0 +/- 2.4 in ANx. Exercise resulted in acidosis, hypocapnia, and elevated blood lactate in all groups. Although blood lactate increased less in 3WHx and ANx, pH was the same or lower than in Nx and AHx, reflecting the low buffer capacity of SA. In AHx and 3WHx, arterial PO2 increased with exercise; however, O2 saturation of hemoglobin in arterial blood (SaO2) decreased. In vitro measurements of the Bohr shift suggest that SaO2 decreased as a result of a decrease in hemoglobin O2 affinity. The data indicate that several features of hypoxic exercise in this model are similar to those seen in humans, with the exception of the mechanism of decrease in SaO2, which, in humans, appears to be due to incomplete alveolar-capillary equilibration.     

Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise

Barstow, Thomas J., Andrew M. Jones, Paul H. Nguyen, andRichard Casaburi. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.J. Appl. Physiol. 81(4):1642-1650, 1996.We tested the hypothesis that the amplitude ofthe additional slow component ofO₂ uptake(O₂) during heavy exerciseis correlated with the percentage of type II (fast-twitch) fibers inthe contracting muscles. Ten subjects performed transitions to a workrate calculated to require aO₂ equal to 50% betweenthe estimated lactate (Lac) threshold and maximalO₂ (50%).Nine subjects consented to a muscle biopsy of the vastus lateralis. Toenhance the influence of differences in fiber type among subjects,transitions were made while subjects were pedaling at 45, 60, 75, and90 rpm in different trials. Baseline O₂ was designed to besimilar at the different pedal rates by adjusting baseline work ratewhile the absolute increase in work rate above the baseline was thesame. The O₂ response after the onset of exercise was described by a three-exponential model. Therelative magnitude of the slow component at the end of 8-min exercisewas significantly negatively correlated with %type I fibers at everypedal rate (r = 0.64 to 0.83, P < 0.05-0.01). Furthermore,the gain of the fast component forO₂ (asml ^· min^{1 ·} W¹)was positively correlated with the %type I fibers across pedal rates(r = 0.69-0.83). Increase inpedal rate was associated with decreased relative stress of theexercise but did not affect the relationships between%fiber type and O₂parameters. The relative contribution of the slow component was alsosignificantly negatively correlated with maximalO₂(r = 0.65), whereas the gainfor the fast component was positively associated(r = 0.68-0.71 across rpm). Theamplitude of the slow component was significantly correlated with netend-exercise Lac at all four pedal rates(r = 0.64-0.84), but Lac was notcorrelated with %type I (P > 0.05).We conclude that fiber type distribution significantly affects both thefast and slow components ofO₂ during heavy exerciseand that fiber type and fitness may have both codependent andindependent influences on the metabolic and gas-exchange responses toheavy exercise.

     

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.