Physiological background of the change point in VO2 and the slow component of oxygen uptake kinetics.

It is generally believed that oxygen uptake during incremental exercise--until VO2max, increases linearly with power output (see eg. Astrand & Rodahl, 1986). On the other hand, it is well established that the oxygen uptake reaches a steady state only during a low power output exercise, but during a high power output exercise, performed above the lactate threshold (LT), the oxygen uptake shows a continuous increase until the end of the exercise. This effect has been called the slow component of VO2 kinetics (Whipp & Wasserman, 1972). The presence of a slow component in VO2 kinetics implies that during an incremental exercise test, after the LT has been exceeded, the VO2 to power output relationship has to become curvilinear. Indeed, it has recently been shown that during the incremental exercise, the exceeding of the power output, at which blood lactate begins to accumulate (LT), causes a non-proportional increase in VO2 (Zoladz et al. 1995) which indicates a drop in muscle mechanical efficiency. The power output at which VO2 starts to rise non-proportionally to the power output has been called "the change point in VO2" (Zoladz et al. 1998). In this paper, the significance of the factors most likely involved in the physiological mechanism responsible for the change point in oxygen uptake (CP-VO2) and for the slow component of VO2 kinetics, including: increase of activation of additional muscle groups, intensification of the respiratory muscle activity, recruitment of type II muscle fibres, increase of muscle temperature, increase of the basal metabolic rate, lactate and hydrogen ion accumulation, proton leak through the inner mitochondrial membrane, slipping of the ATP synthase and a decrease in the cytosolic phosphorylation potential, are discussed. Finally, an original own model describing the sequence of events leading to the non-proportional increase of oxygen cost of work at a high exercise intensity is presented.     

Plasma ammonia concentrations and the slow component of oxygen uptake kinetics during cycle ergometry

The purposes of this study were to 1) compare the patterns of responses for plasma ammonia concentration ([NH3]) during moderate- vs. heavy-intensity cycle ergometry, and 2) examine the relationship between the V O2 slow component (V O 2SC) and plasma [NH3]. Thirteen healthy, untrained men (mean +/- SEM age = 24.8 +/- 0.6 years) performed a total of eight constant power output exercises (7 minutes in duration) at two different intensities (moderate, 60% gas exchange threshold [GET] = 60% of the gas exchange threshold; and heavy, Delta 50% = 50% of the difference between GET and V O2 max). Blood was collected from an antecubital vein before the exercise, during the last 3 minutes of the 6-minute warm-up, and during each minute of the 7-minute constant power output workbout. The time course of changes in plasma [NH3] and V O2 during the two constant power output exercise intensities were assessed separately using 2 (intensity) x 7 (time) repeated-measures analyses of variance. For 60% GET, there were no significant differences in the mean normalized plasma [NH3] during the 7-minute workbout. For Delta 50%, there was a significant increase in the mean normalized plasma [NH3] during the 7-minute workbout. These findings suggest a potential relationship between exercise-induced hyperammonemia and the V O 2SC during heavy-intensity exercise.     

Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance

The purpose of this study was to develop a method to determine the power output at which oxygen uptake (V˙O₂) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1 (SD 1.4) years, body mass 73.6 (SD 7.4) kg, height 179.4 (SD 7.5) cm, maximal oxygen uptake (V˙O_2max) 3.726 (SD 0.363) l · min⁻¹], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70 rev · min⁻¹. The test started at a power output of 30 W, followed by increases amounting to 30 W every 3 min. At 5 min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1 ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]_pl, partial pressure of O₂ and CO₂ and hydrogen ion concentration [H⁺]_b. The lactate threshold (LT) in this study was defined as the highest power output above which [La⁻]_pl showed a sustained increase of more than 0.5 mmol · l⁻¹ · step⁻¹. The V˙O₂ was measured breath-by-breath. In the analysis of the change point (CP) of V˙O₂ during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: X _i =at _i +b+ɛ _i for i=1,2,…,T, and E(X _i )>at _i +b for i =T+1,…,n, where X ₁, … , X _n are independent and ɛ _i ∼N(0,σ²). In the first phase, a linear relationship between V˙O₂ and power output was assumed, whereas in the second phase an additional increase in V˙O₂ above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-V˙O₂). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP-O₂ as described in our model. The power output at CP-V˙O₂ amounted to 136.8 (SD 31.3) W. It was only 11 W – non significantly – higher than the power output corresponding to LT. The V˙O₂ at CP-V˙O₂ amounted to 1.828 (SD 0.356) l · min⁻¹ was [48.9 (SD 7.9)% V˙O_{2 max} ]. The [La⁻]_pl at CP-V˙O₂, amounting to 2.57 (SD 0.69) mmol · l⁻¹ was significantly elevated (P<0.01) above the resting level [1.85 (SD 0.46) mmol · l⁻¹], however the [H⁺]_b at CP-V˙O₂ amounting to 45.1 (SD 3.0) nmol · l⁻¹, was not significantly different from the values at rest which amounted to 44.14 (SD 2.79) nmol · l⁻¹. An increase of power output of 30 W above CP-V˙O₂ was accompanied by a significant increase in [H⁺]_b above the resting level (P=0.03). Accepted: 25 March 1998     

Physiological responses during prolonged exercise at the power output corresponding to the blood lactate threshold

Heart rate (HR) and oxygen uptake (VO2) at the mechanical power (W) corresponding to the capillary blood lactate ([la]cap) of 4 mmol.l-1 (Wlt) were measured in 34 healthy male subjects during incremental exercise (Winc). On the basis of these measurements, the subjects were asked to cycle at Wlt for 60 min (steady-state exercise, Wss). Twenty subjects could not reach the target time (mean exhaustion time, te, 38.2 min, SD 5.3), while 6 of the 14 remaining subjects declared themselves exhausted at the end of exercise. The final [la]cap if the two groups of exhausted subjects were 5.3 mmol.l-1, SD 2.3 and 4.3 mmol.l-1, SD 1.1, respectively. At the end of Wss, [la]cap and HR were significantly lower in the 8 unexhausted subjects than in the other subjects. This group also had a lower HR at Wlt during Winc. The HR and VO2 appeared to be higher during Wss than during Winc. When all subjects were ranked according to their te during Wss, Wlt (expressed per kilogram of body mass) was found to be negatively related to te. In conclusion, during Winc, measurements of physiological variables at fixed [la]cap give a poor prediction of their trends during Wss and of the relative te; at the same work load [la]cap can be quite different in the two experimental conditions. Furthermore, resistance to exercise fatigue at Wlt seems lower in the fitter subjects.     

Mechanical muscular power output and work during ergometer cycling at different work loads and speeds

The aim of the study was to calculate the magnitude of the instantaneous muscular power output at the hip, knee and ankle joints during ergometer cycling at different work loads and speeds. Six healthy subjects pedalled a weight-braked cycle ergometer at 0, 120 and 240 W at a constant speed of 60 rpm. The subjects also pedalled at 40, 60, 80 and 100 rpm against the same resistance, giving power outputs of 80, 120, 160 and 200 W respectively. The subjects were filmed with a cine-film camera, and pedal reaction forces were recorded from a force transducer mounted in the pedal. The muscular work for the hip, knee and ankle joint muscles was calculated using a model based upon dynamic mechanics and described elsewhere. The total work during one pedal revolution significantly increased with increased work load but did not increase with increased pedalling rate at the same braking force. The relative proportions of total positive work at the hip, knee and ankle joints were also calculated. Hip and ankle extension work proportionally decreased with increased work load. Pedalling rate did not change the relative proportion of total work at the different joints.     

Effect of blood lactate concentration and the level of oxygen uptake immediately before a cycling sprint on neuromuscular activation during repeated cycling sprints

The purpose of this study was to determine whether neuromuscular activation is affected by blood lactate concentration (La) and the level of oxygen uptake immediately before a cycling sprint (preVO(2)). The tests consisted of ten repeated cycling sprints for 10 sec with 35-sec (RCS(35)) and 350-sec recovery periods (RCS(350)). Peak power output (PPO) was not significantly changed despite an increase in La concentration up to 12 mmol/L in RCS(350). Mean power frequency (MPF) of the power spectrum calculated from a surface electromyogram on the vastus lateralis showed a significantly higher level in RCS(350). In RCS(35), preVO(2) level and La were higher than those in RCS(350) in the initial stage of the RCS and in the last half of the RCS, respectively. Thus, neuromuscular activation during exercise with maximal effort is affected by blood lactate concentration and the level of oxygen uptake immediately before exercise, suggesting a cyclic system between muscle recruitment pattern and muscle metabolites.     

Blood flow and oxygen uptake increase with total power during five different knee-extension contraction rates.

Controversies exist regarding quantification of internal power (IP) generated by the muscles to overcome energy changes of moving body segments when external power (EP) is performed. The aim was to 1) use a kinematic model for estimation of IP during knee extension, 2) validate the model by independent calculation of IP from metabolic variables (IP(met)), and 3) analyze the relationship between total power (TP = EP + IP) and physiological responses. IP increased in a curvilinear manner (5, 7, 13, 21, and 34 W) with contraction rate (45, 60, 75, 90, and 105 contractions/min), but it was independent of EP. Correspondingly, IP(met) was 5, 7, 10, 19, and 28 W, supporting the kinematic model. Heart rate, pulmonary oxygen uptake, and leg blood flow plotted vs. TP fell on the same line independent of contraction rate, and muscular mechanical efficiency as well as delta efficiency remained remarkably constant across contraction rates. It is concluded that the novel metabolic validation of the kinematic model supports the model assumptions, and physiological responses proved to be closely related to TP, supporting the legitimacy of IP estimates.     

Effect of exercise to rest ratio on plasma lactate concentration at work rates above and below maximum oxygen uptake

The metabolic and physiological responses to different exercise to rest ratios (E:R) (2:1, 1:1, 1:2) of eight subjects exercising at work rates approximately 10% above and below maximum oxygen uptake (VO2max) were assessed. Each of the six protocols consisted of 15 1-min-long E:R intervals. Total work (kJ), oxygen uptake (VO2), heart rate (fc) and plasma lactate concentrations were monitored. With increases in either E:R or work rate, VO2 and fc increased (P < 0.05). The average (15 min) VO2 and fc ranged from 40 to 81%, and from 62 to 91% of maximum, respectively. Plasma lactate concentrations nearly doubled at each E:R when work rate was increased from 90 to 110% of VO2max and ranged from a low of 1.8 mmol.l-1 (1:2-90) to a high of 10.7 mmol.l-1 (2:1-110). The 2:1-110 protocol elicited plasma lactate concentrations which were approximately 15 times greater than that of rest. These data suggest that plasma lactate concentrations during intermittent exercise are very sensitive to both work rate and exercise duration.     

Hemodynamic responses to 30-min cycling exercise at 70% VO2 max both in ambiant air and during chest-immersion

The aim of this study was to examine the influence of water immersion to the chest on cardio-vascular adaptation to exercise. Upright or sitting immersion causes an increase in central blood volume, but it remains controversial whether central blood volume remains elevated during dynamic exercise in water and facilitates cardiac adaptation, depending particularly on the intensity of exercise which can be matched for O2 consumption (metabolic range) or for mechanical intensity (work load). We have compared hemodynamic variables measured during two cycling exercises at the same mechanical intensity, performed both in ambiant air and during immersion up to the chest.     

Contributions in astrocytes of SMIT1/2 and HMIT to myo-inositol uptake at different concentrations and pH

myo-Inositol is important for cell signaling both in cytoplasm and in intracellular organelles. It is required in the plasma membrane and cytoplasm for maintained synthesis of the second messengers, inositoltrisphosphate (IP(3)) and diacylglycerol (DAG) from phosphatidylinositol bisphosphate (PIP(2)), and in organelles as precursor for synthesis of complex signaling phospholipids and inositolphosphates from IP(3) and PIP(2). myo-Inositol must be taken up into the cell where its is used, because neither neurons nor astrocytes synthesize it. It is also an osmolyte, taken up in response to surrounding hyperosmolarity and released during hypo-osmolarity. There are three myo-inositol transporters, the Na(+)-dependent SMIT1 and SMIT2, and HMIT, which co-transports myo-inositol with H(+). Their relative expressions in astrocytes and neurons are unknown. Uptake kinetics for myo-inositol in astrocytes has repeatedly been determined, but always on the assumption of only one component, leaving kinetics for the individual transporters unknown. This paper demonstrates that astrocytes obtained directly from the brain express SMIT1 and HMIT, but little SMIT2, and that all three transporters are expressed in neurons. Cultured mouse astrocytes show a high-affinity/low-capacity myo-inositol uptake (V(max): 60.0 ± 3.0 pmol/min per mg protein; K(m): 16.7 ± 2.6 μM), mediated by SMIT1 and perhaps partly by SMIT2. It was determined in cells pre-treated with HMIT-siRNA and confirmed by specific inhibition of SMIT. However at physiologically relevant myo-inositol concentrations most uptake is by a lower-affinity/higher-capacity uptake, mediated by HMIT (V(max): 358 ± 60 pmol/min per mg protein; K(m): 143 ± 36 μM) and determined by subtraction of SMIT-mediated from total uptake. At high myo-inositol concentrations, its uptake is inhibited by incubation in medium with increased pH, and increased during intracellular acidification with NH(4)Cl. This is in agreement with literature data for HMIT alone. At low concentration, where SMIT1/2 activity gains importance, myo-inositol uptake is reduced by ammonia-induced intracellular acidification, consistent with the transporter's pH sensitivity reported in the literature.     

Growth, contents of K+ and kinetics of K+(86Rb) uptake in barley cultured at different low supply rates of potassium

Plants of barley ( Hordeum vulgare L. cv. Salve) were grown with 6.5–35% relative increase of K⁺ supply per day (RKR) using a special computer-controlled culture unit. After a few days on the culture solution the plants adapted their relative growth rate (RGR) to the rate of nutrient supply. The roots of the plants remained in a low salt status irrespective of the rate of nutrient supply, whereas the concentration of K⁺ in shoots increased with RKR. Both V_max and K_m for K⁺(⁸⁶Rb) influx increased with RKR. It is concluded that with a continuous and stable K⁺ stress, the K⁺ uptake system is adjusted to provide an effective K⁺ uptake at each given RKR. Allosteric regulation of K⁺ influx does not occur and efflux of K⁺ is very small.