Lactate acidosis and the increase in VE/VO2 during incremental exercise

The purpose of this investigation was to determine whether the onset of lactate acidosis is responsible for the increase in ventilatory equivalent (VE/VO2) during exercise of increasing intensity. Eight male subjects performed maximal incremental exercise tests on a cycle ergometer on two separate occasions. For the control (C) treatment, the initial work rates consisted of 4 min of unloaded pedaling (60 rpm) and 1 min of pedaling at a work rate of 30 W. Thereafter, the work rate was increased each minute by 22 W until volitional fatigue. Venous blood samples were taken before the onset of exercise and at the end of each work rate for determination of pH and lactate. Ventilatory parameters at each work rate were also monitored. Before the experimental treatment (E), the subjects performed two 3-min work bouts at high intensity (210-330 W) on the cycle ergometer in order to prematurely raise blood lactate levels and lower blood pH. The same incremental exercise test as C was then performed. The results indicated that the increase in VE/VO2 occurred at similar work rates and %VO2max although the venous H+ and lactate concentrations were significantly elevated during the E treatment. These results suggest that a decrease in the blood pH resulting from blood lactate accumulation is not responsible for the increase in VE/VO2 during incremental exercise.     

Muscle oxidative metabolism accelerates with mild acidosis during incremental intermittent isometric plantar flexion exercise

BACKGROUND: It has been thought that intramuscular ADP and phosphocreatine (PCr) concentrations are important regulators of mitochondorial respiration. There is a threshold work rate or metabolic rate for cellular acidosis, and the decrease in muscle PCr is accelerated with drop in pH during incremental exercise. We tested the hypothesis that increase in muscle oxygen consumption (o2mus) is accelerated with rapid decrease in PCr (concomitant increase in ADP) in muscles with drop in pH occurs during incremental plantar flexion exercise. METHODS: Five male subjects performed a repetitive intermittent isometric plantar flexion exercise (6-s contraction/4-s relaxation). Exercise intensity was raised every 1 min by 10% maximal voluntary contraction (MVC), starting at 10% MVC until exhaustion. The measurement site was at the medial head of the gastrocnemius muscle. Changes in muscle PCr, inorganic phosphate (Pi), ADP, and pH were measured by 31P-magnetic resonance spectroscopy. o2mus was determined from the rate of decrease in oxygenated hemoglobin and/or myoglobin using near-infrared continuous wave spectroscopy under transient arterial occlusion. Electromyogram (EMG) was also recorded. Pulmonary oxygen uptake (o2pul ) was measured by the breath-by-breath gas analysis. RESULTS: EMG amplitude increased as exercise intensity progressed. In contrast, muscle PCr, ADP, o2mus, and o2pul did not change appreciably below 40% MVC, whereas above 40% MVC muscle PCr decreased, and ADP, o2mus, and o2pul increased as exercise intensity progressed, and above 70% MVC, changes in muscle PCr, ADP, o2mus, and o2pul accelerated with the decrease in muscle pH (~6.78). The kinetics of muscle PCr, ADP, o2mus, and o2pul were similar, and there was a close correlation between each pair of parameters (r = 0.969~0.983, p < 0.001). CONCLUSION: With decrease in pH muscle oxidative metabolism accelerated and changes in intramuscular PCr and ADP accelerated during incremental intermittent isometric plantar flexion exercise. These results suggest that rapid changes in muscle PCr and/or ADP with mild acidosis stimulate accelerative muscle oxidative metabolism.     

Effect of exercise duration during incremental exercise on the determination of anaerobic threshold and the onset of blood lactate accumulation

To determine the effect of the duration of incremental exercise on the point at which arterial blood lactate concentration (HLa) increases above the resting value (anaerobic threshold: AT) and on the point at which HLa reaches a constant value of 4 mM (onset of blood lactate accumulation: OBLA), eight male students performed two different kinds of incremental exercise. A comparison of arterial HLa and venous HLa was made under both conditions of incremental exercise. The incremental bicycle exercise tests consisted of 25 W increase every minute (1-min test) and every 4 min (4-min test). At maximal exercise, there were no significant differences in either gas exchange parameters or HLa values for the two kinds of incremental exercise. However, the peak workloads attained during the two exercises were significantly different (P less than 0.01). At OBLA and AT, there were no significant differences in gas exchange parameters during the 1-min and 4-min tests except for the workload (at OBLA P less than 0.01; at AT P less than 0.05). When venous blood HLa was used instead of arterial HLa for a 4-min test, AT was not significantly different from that obtained by arterial HLa, but OBLA was significantly different from that obtained by arterial HLa (P less than 0.05). On the other hand, for the 1-min test, venous HLa values yielded significantly higher AT and OBLA compared with those obtained using arterial HLa (P less than 0.01). It was concluded that when arterial blood was used, there was no effect of duration of workload increase in an incremental exercise test on the determination of the AT and OBLA expressed in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Skeletal muscle oxygenation during incremental exercise

The purpose of this study was to investigate the relationship between muscle oxygenation level at exhaustion and maximal oxygen uptake (VO2max) in an incremental cycling exercise. Nine male subjects took part in an incremental exhaustive cycling exercise, and then cuff occlusion was performed. Changes in oxy-(deltaHbO2) and deoxy-(deltaHb) hemoglobin concentrations in the vastus lateralis muscle were measured with a near infrared spectroscopy (NIRS). Muscle oxygenation during incremental exercise was expressed as a percentage (%Moxy) of the maximal range observed during an arterial occlusion as the lower reference point. A systematic decrease was observed in %Moxy with increasing intensity. A significant relationship was observed between %Moxy at exhaustion and VO2max (p < 0.01). We concluded that the one of the limiting factor of VO2max is the muscle oxygen diffusion capacity, and %Moxy during exercise could be one of the indexes of muscle oxygen diffusion capacity.     

Blood lactate accumulation and muscle deoxygenation during incremental exercise.

Near-infrared spectroscopy (NIRS) could allow insights into controversial issues related to blood lactate concentration ([La](b)) increases at submaximal workloads (). We combined, on five well-trained subjects [mountain climbers; peak O(2) consumption (VO(2peak)), 51.0 +/- 4.2 (SD) ml. kg(-1). min(-1)] performing incremental exercise on a cycle ergometer (30 W added every 4 min up to voluntary exhaustion), measurements of pulmonary gas exchange and earlobe [La](b) with determinations of concentration changes of oxygenated Hb (Delta[O(2)Hb]) and deoxygenated Hb (Delta[HHb]) in the vastus lateralis muscle, by continuous-wave NIRS. A "point of inflection" of [La](b) vs. was arbitrarily identified at the lowest [La](b) value which was >0.5 mM lower than that obtained at the following. Total Hb volume (Delta[O(2)Hb + HHb]) in the muscle region of interest increased as a function of up to 60-65% of VO(2 peak), after which it remained unchanged. The oxygenation index (Delta[O(2)Hb - HHb]) showed an accelerated decrease from 60- 65% of VO(2 peak). In the presence of a constant total Hb volume, the observed Delta[O(2)Hb - HHb] decrease indicates muscle deoxygenation (i.e., mainly capillary-venular Hb desaturation). The onset of muscle deoxygenation was significantly correlated (r(2) = 0.95; P < 0.01) with the point of inflection of [La](b) vs., i.e., with the onset of blood lactate accumulation. Previous studies showed relatively constant femoral venous PO(2) levels at higher than approximately 60% of maximal O(2) consumption. Thus muscle deoxygenation observed in the present study from 60-65% of VO(2 peak) could be attributed to capillary-venular Hb desaturation in the presence of relatively constant capillary-venular PO(2) levels, as a consequence of a rightward shift of the O(2)Hb dissociation curve determined by the onset of lactic acidosis.     

Use of arterialized venous blood sampling during incremental exercise tests.

Close agreement between arterialized venous and arterial pH, PCO2, and lactate has previously been demonstrated during steady-state exercise. The purpose of the present study was to compare arterialized venous and arterial pH, PCO2, K+, lactate, pyruvate, and epinephrine during the constantly changing circumstances of an incremental exercise test. Eight normal subjects undertook an incremental exercise test (increasing by 20 W/min) to exhaustion on a cycle ergometer during which simultaneous arterial and arterialized venous samples were drawn over the last 20 s of each work load. Linear regression of arterialized venous on arterial values showed that r varied from 0.97 to 0.99 for the variables examined and, therefore, showed that accurate estimates of arterial values could be made from the arterialized venous results during incremental testing. For many purposes it could be assumed that arterialized venous values equaled arterial values without serious error.     

Prior heavy-intensity exercise speeds VO2 kinetics during moderate-intensity exercise in young adults.

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (tauVO2) was examined in young adults exhibiting relatively fast (FK; tauVO2 < 30 s; n = 6) and slow (SK; tauVO2 > 30 s; n = 6) VO2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak VO2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). tauVO2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 +/- 5 s vs. 26 +/- 5 s, respectively) and SK (30 +/- 8 s vs. 45 +/- 11 s, respectively); linear regression analysis showed a greater "speeding" of VO2 kinetics in subjects exhibiting a greater Mod1 tauVO2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced (P <0.05) in Mod2, whereas the HHb mean response time was reduced (P <0.05) in FK (Mod2, 22 +/- 3 s; Mod1, 32 +/- 11 s) but not different in SK (Mod2, 36 +/- 13 s; Mod1, 34 +/- 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of VO2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.     

Independence of exercise hyperpnea and acidosis during high-intensity exercise in ponies

We investigated arterial PCO2 (PaCO2) and pH (pHa) responses in ponies during 6-min periods of high-intensity treadmill exercise. Seven normal, seven carotid body-denervated (2 wk-4 yr) (CBD), and five chronic (1-2 yr) lung (hilar nerve)-denervated (HND) ponies were studied during three levels of constant load exercise (7 mph-11%, 7 mph-16%, and 7 mph-22% grade). Mean pHa for each group of ponies became alkaline in the first 60 s (between 7.45 and 7.52) (P less than 0.05) at all work loads. At 6 min pHa was at or above rest at 7 mph-11%, moderately acidic at 7 mph-16% (7.32-7.35), and markedly acidic at 7 mph-22% (7.20-7.27) for all groups of ponies. Yet with no arterial acidosis at 7 mph 11%, normal ponies decreased PaCO2 below rest (delta PaCO2) by 5.9 Torr at 90 s and 7.8 Torr by 6 min of exercise (P less than 0.05). With a progressively more acid pHa at the two higher work loads in normal ponies, delta PaCO2 was 7.3 and 7.8 Torr by 90 s and 9.9 and 11.4 Torr by 6 min, respectively (P less than 0.05). CBD ponies became more hypocapnic than the normal group at 90 s (P less than 0.01) and tended to have greater delta PaCO2 at 6 min. The delta PaCO2 responses in normal and HND ponies were not significantly different (P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Change in double product during stepwise incremental exercise

The purpose of this study was to observe the change in double product with increases in the intensity of bicycle exercise. Eleven young male adults participated in this study. The subjects performed graded bicycling exercise increasing 20 watts every 2 min from 0 watts until the heart rate (HR) reached 170 beats.min(-1). During exercise systolic blood pressure (SBP) and HR were continuously measured. Initially SBP gradually increased with the increase in workload, but when the intensity of exercise became even higher, the rate of increase slowed. On the other hand, the increase in HR was very small during the initial 5 min of exercise and when the intensity of exercise increased, the rate of increase of HR became higher. The polygonal regression analyses on the relation of double product to elapsed time revealed clear break-points. On average, the break-point of double product was 6.6 min (56 watts). These results clearly showed that the break-point of double product with an increase in workload appeared even though the workload was relatively low.     

Influence of moderate cold exposure on blood lactate during incremental exercise.

This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30 degrees C or at 10 degrees C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO2) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la-]b. The VO2 was identical under both environments. At 10 degrees C, as compared to 30 degrees C, the lactate anaerobic threshold (Than,la-) occurred at an exercise intensity 15 W higher and [la-]b was lower for submaximal intensities above the Than,la-. Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10 degrees C [15.60 (SEM 3.15) nmol.l-1] than at 30 degrees C [8.64 (SEM 2.37) nmol.l-1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la-]b observed for submaximal high intensities during severe cold exposure.     

Potassium and ventilation during incremental exercise in trained and untrained men.

The present investigation was undertaken to examine the relationship between plasma potassium (K+) and ventilation (VE) during incremental exercise. Blood lactate (La-) was also measured, and its relationship with VE was similarly examined. Eight endurance-trained triathletes (ET) and eight active but untrained men (UT) performed an incremental cycling test to volitional fatigue. Maximal oxygen uptake (VO2max) and oxygen uptake (VO2) at lactate threshold (LT) were higher (P < 0.05) in ET (VO2max 4.60 +/- 0.10 l/min, LT 2.77 +/- 0.85 l/min) than in UT (VO2max 3.79 +/- 0.11 l/min, LT 1.94 +/- 0.60 l/min). There were significant (P < 0.05) correlations between VE and K+ (UT 0.87, ET 0.77) and between VE and La- (UT 0.88, ET 0.85). In ET compared with UT, VE was lower (P < 0.05) at 330 W, K+ was lower at 300 and 330 W, and La- was lower at all work loads > 90 W. These results suggest that K+ may make an important contribution to the regulation of ventilation during incremental exercise and that endurance training attenuates the K+ response to that exercise.     

Effects of acute hypoxia on cerebral and muscle oxygenation during incremental exercise.

To determine if fatigue at maximal aerobic power output was associated with a critical decrease in cerebral oxygenation, 13 male cyclists performed incremental maximal exercise tests (25 W/min ramp) under normoxic (Norm: 21% Fi(O2)) and acute hypoxic (Hypox: 12% Fi(O2)) conditions. Near-infrared spectroscopy (NIRS) was used to monitor concentration (microM) changes of oxy- and deoxyhemoglobin (Delta[O2Hb], Delta[HHb]) in the left vastus lateralis muscle and frontal cerebral cortex. Changes in total Hb were calculated (Delta[THb] = Delta[O2Hb] + Delta[HHb]) and used as an index of change in regional blood volume. Repeated-measures ANOVA were performed across treatments and work rates (alpha = 0.05). During Norm, cerebral oxygenation rose between 25 and 75% peak power output {Power(peak); increased (inc) Delta[O2Hb], inc. Delta[HHb], inc. Delta[THb]}, but fell from 75 to 100% Power(peak) {decreased (dec) Delta[O2Hb], inc. Delta[HHb], no change Delta[THb]}. In contrast, during Hypox, cerebral oxygenation dropped progressively across all work rates (dec. Delta[O2Hb], inc. Delta[HHb]), whereas Delta[THb] again rose up to 75% Power(peak) and remained constant thereafter. Changes in cerebral oxygenation during Hypox were larger than Norm. In muscle, oxygenation decreased progressively throughout exercise in both Norm and Hypox (dec. Delta[O2Hb], inc. Delta [HHb], inc. Delta[THb]), although Delta[O2Hb] was unchanged between 75 and 100% Power peak. Changes in muscle oxygenation were also greater in Hypox compared with Norm. On the basis of these findings, it is unlikely that changes in cerebral oxygenation limit incremental exercise performance in normoxia, yet it is possible that such changes play a more pivotal role in hypoxia.     

Breathing pattern in highly competitive cyclists during incremental exercise

The purpose of our investigation was to analyse the breathing patterns of professional cyclists during incremental exercise from submaximal to maximal intensities. A group of 11 elite amateur male road cyclists [E, mean age 23 (SD 2) years, peak oxygen uptake (VO2peak) 73.8 (SD 5.0) ml kg(-1) min(-1)] and 14 professional male road cyclists [P, mean age 26 (SD 2) years, (VO2peak) 73.2 (SD 6.6) ml kg(-1) min(-1)] participated in this study. Each of the subjects performed an exercise test on a cycle ergometer following a ramp protocol (exercise intensity increases of 25 W x min(-1)) until the subject was exhausted. For each subject, the following parameters were recorded during the tests: oxygen consumption (VO2), carbon dioxide output (VCO2), pulmonary ventilation (VE), tidal volume (VT), breathing frequency (fb), ventilatory equivalents for oxygen (VE x VO2(-1)) and carbon dioxide (VE x VCO2(-1)), end-tidal partial pressure of oxygen and partial pressure of carbon dioxide, inspiratory (tI) and expiratory (tE) times, inspiratory duty cycle (tI/tTOT, where tTOT is the time for one respiratory cycle), and mean inspiratory flow rate (VT/tI). Mean values of VE were significantly higher in E at 300, 350 and 400 W (P < 0.05, P < 0.05 and P < 0.01, respectively); fb was also higher in E in most moderate-to-maximal intensities. On the other hand, VT showed a different pattern in both groups at near-to maximal intensities, since no plateau was observed in P. The response of tI and tE was also different. Finally, VT/tI and tI/tTOT showed a similar response in both P and E. It was concluded that the breathing pattern of the two groups differed mainly in two aspects: in the professional cyclists, VE increased at any exercise intensity as a result of increases in both VT and fb, with no evidence of tachypnoeic shift, and tE was prolonged in this group at high exercise intensities. In contrast, neither the central drive nor the timing component of respiration seem to have been significantly altered by the training demands of professional cycling.     

Prior heavy exercise increases oxygen cost during moderate exercise without associated change in surface EMG.

The aim of this study was to test the hypothesis that prior heavy exercise results in a higher oxygen cost during a subsequent bout of moderate exercise due to changes in muscle activity. Eight male subjects (25+/-2 yr, +/-SE) performed moderate-moderate and moderate-heavy-moderate transitions in work rate (cycling intensity, moderate=90% LT, heavy=80% VO(2) peak). The second bout of moderate exercise was performed after 6 min (C) or 30s (D) of recovery. Pulmonary gas exchange was measured breath-by-breath and surface electromyography was obtained from the vastus lateralis and medialis muscles. Root mean square (RMS) and median power frequency (MDPF) were computed. Prior heavy exercise increased DeltaVO(2)/DeltaWR (C: +2.0+/-0.8 ml min(-1)W(-1), D: +3.4+/-0.8 ml min(-1)W(-1); P<0.05) and decreased exercise efficiency (C: -13.3+/-5.6%, D: -22.2 +/-4.9%; P<0.05) during the second bout of moderate exercise in the absence of changes in RMS. MDPF was slightly elevated ( approximately 2%) during the second bout of moderate exercise, but MDPF was not correlated with V O(2) (r=0.17). These findings suggest that the increased oxygen cost during moderate exercise following heavy exercise is not due to increased muscle activity as assessed by surface electromyography.     

Electromyogram as an indicator of neuromuscular fatigue during incremental exercise

This study analysed the changes in the electromyographic activity (EMG) of the vastus lateralis muscle (VL) during an incremental maximal oxygen uptake test on a treadmill. A breakpoint in the integrated electromyogram (iEMG)-velocity relationship has already been interpreted in two ways: either as a sign of neuromuscular fatigue or as an expression of the iEMG-velocity relationship characteristics. The aim of this study was to test a method of distinguishing fatigue effects from those due to increases in exercise power. Eight well-trained male runners took part in the study. They completed a running protocol consisting of 4-min stages of increments in power output. Between each stage (about 15 s after the start of a minute at rest), the subjects had to maintain a standard effort: a 10-s isometric leg extension contraction [50% isometric maximal voluntary contraction (IMVC)]. The EMG was recorded during the running and isometric protocols, a change in the EMG signal during the isometric exercise being considered as the sign of fatigue. The iEMG-velocity relationships were strongly fitted by a second-order polynomial function for data taken at both the start (r = 0.98) and the end (r = 0.98) of the stage. Based on the stability of the 50%IMVC-iEMG relationship noted between stages, the start-iEMG has been identified as expressing the iEMG-velocity relationship without fatigue. The stage after which end-iEMG increased significantly more steeply than start-iEMG was considered as the iEMG threshold and was simultaneous with the ventilatory equivalent for carbon dioxide threshold. The parallel changes of minute ventilation and iEMG would suggest the existence of common regulation stimuli linked either to effort intensity and/or to metabolic conditions. The fall in intracellular [K⁺] has been discussed as being one of the main factors in regulating ventilation. Accepted: 16 December 1997     

Mathematical analysis of the heart rate performance curve during incremental exercise testing

In this study we performed laboratory treadmill protocols of increasing load. Heart rate was continuously recorded and blood lactate concentration was measured for determination of lactate threshold by means of LTD-max and LT4.0 methods.Our results indicate that the shape of heart rate performance curve (HRPC) during incremental testing depends on the applied exercise protocol (change of initial speed and the step of running speed increase, with the constant stage duration). Depending on the applied protocol, the HRPC can be described by linear, polynomial (S-shaped), and exponential mathematical expression.We presented mathematical procedure for estimation of heart rate threshold points at the level of LTD-max and LT4.0, by means of exponential curve and its relative deflection from the initial trend line (tangent line to exponential curve at the point of starting heart rate). The relative deflection of exponential curve from the initial trend line at the level of LTD-max and/or LT4.0 can be defined, based on the slope of the initial trend line. Using originally developed software that allows mathematical analysis of heart rate-load relation, LTD-max and/or LT4.0 can be estimated without direct measurement of blood lactate concentration.