Oxygen uptake does not increase linearly at high power outputs during incremental exercise test in humans

A group of 12 healthy non-smoking men [mean age 22.3 (SD 1.1)?years], performed an incremental exercise test. The test started at 30?W, followed by increases in power output (P) of 30?W every 3 min, until exhaustion. Blood samples were taken from an antecubital vein for determination of plasma concentration lactate [La^?]_pl and acid-base balance variables. Below the lactate threshold (LT) defined in this study as the highest P above which a sustained increase in [La^?]_pl was observed (at least 0.5 mmol?·?l^?1 within 3 min), the pulmonary oxygen uptake (V˙O₂) measured breath-by-breath, showed a linear relationship with P. However, at P above LT [in this study 135 (SD 30)?W] there was an additional accumulating increase in V˙O₂ above that expected from the increase in P alone. The magnitude of this effect was illustrated by the difference in the final P observed at maximal oxygen uptake (V˙O_2max) during the incremental exercise test (P _max,obs at V˙O_2max) and the expected power output at V˙O_2max(P _max,exp at V˙O_2max) predicted from the linear V˙O₂-P relationship derived from the data collected below LT. The P _max,obs at V˙O_2max amounting to 270 (SD 19)?W was 65.1 (SD 35)?W (19%) lower (P<0.01) than the P _max,exp at V˙O_{2max .} The mean value of V˙O_2max reached at P _max,obs amounted to 3555 (SD 226)?ml?·?min^?1 which was 572 (SD 269)?ml?·?min^?1 higher (P<0.01) than the V˙O₂ expected at this P, calculated from the linear relationship between V˙O₂ and P derived from the data collected below LT. This fall in locomotory efficiency expressed by the additional increase in V˙O₂, amounting to 572 (SD 269) ml O₂?·?min^?1, was accompanied by a significant increase in [La^?]_pl amounting to 7.04 (SD 2.2)?mmol?·?l^?1, a significant increase in blood hydrogen ion concentration ([H⁺]_b) to 7.4 (SD 3)?nmol?·?l^?1 and a significant fall in blood bicarbonate concentration to 5.78 (SD 1.7)?mmol?·?l^?1, in relation to the values measured at the P of the LT. We also correlated the individual values of the additional V˙O₂ with the increases (Δ) in variables [La^?]_pl and Δ[H⁺]_b. The Δ values for [La^?]_pl and Δ[H⁺]_b were expressed as the differences between values reached at the P _max,obs at V˙O_2max and the values at LT. No significant correlations between the additional V˙O₂ and Δ[La^?]_pl on [H⁺]_b were found. In conclusion, when performing an incremental exercise test, exceeding P corresponding to LT was accompanied by a significant additional increase in V˙O₂ above that expected from the linear relationship between V˙O₂ and P occurring at lower P. However, the magnitude of the additional increase in V˙O₂ did not correlate with the magnitude of the increases in [La^?]_pl and [H⁺]_b reached in the final stages of the incremental test.     

Energetics of kayaking at submaximal and maximal speeds

The energy cost of kayaking per unit distance (C_k, kJ?·?m^?1) was assessed in eight middle- to high-class athletes (three males and five females; 45–76?kg body mass; 1.50–1.88?m height; 15–32 years of age) at submaximal and maximal speeds. At submaximal speeds, C_k was measured by dividing the steady-state oxygen consumption (V˙O₂, l?·?s^?1) by the speed (v, m?·?s^?1), assuming an energy equivalent of 20.9?kJ?·?l O^?1 ₂. At maximal speeds, C_k was calculated from the ratio of the total metabolic energy expenditure (E, kJ) to the distance (d, m). E was assumed to be the sum of three terms, as originally proposed by Wilkie (1980): E?=?AnS?+?αV˙O_2max?·?t?αV˙O_2max?·?τ(1?e ^?t·τ?1), were α is the energy equivalent of O₂ (20.9?kJ?·?l?O₂ ^?1), τ is the time constant with which V˙O_2max is attained at the onset of exercise at the muscular level, AnS is the amount of energy derived from anaerobic energy utilization, t is the performance time, and V˙O_2max is the net maximal V˙O₂. Individual V˙O_2max was obtained from the V˙O₂ measured during the last minute of the 1000-m or 2000-m maximal run. The average metabolic power output (E˙, kW) amounted to 141% and 102% of the individual maximal aerobic power (V˙O_2max) from the shortest (250?m) to the longest (2000?m) distance, respectively. The average (SD) power provided by oxidative processes increased with the distance covered [from 0.64 (0.14) kW at 250?m to 1.02 (0.31) kW at 2000?m], whereas that provided by anaerobic sources showed the opposite trend. The net C_k was a continuous power function of the speed over the entire range of velocities from 2.88 to 4.45?m?·?s^?1: C _k ?=?0.02?·?v ^2.26 (r?=?0.937, n?=?32).     

Effects of hydroxyl radicals on KATP channels in guinea-pig ventricular myocytes

 We studied the effects of oxygen free radicals on the ATP-sensitive potassium channel (K_ATP channel) of guinea-pig ventricular myocytes. Single K_ATP channel currents were recorded from inside-out patches in the presence of symmetrical K⁺ concentrations (140 mM in both bath and pipette solutions). Reaction of xanthine oxidase (0.1 U/ml) on hypoxanthine (0.5 mM) produced superoxide anions (·O₂ ^-) and hydrogen peroxide (H₂O₂). Exposure of the patch membrane to ·O₂ ^- and H₂O₂ increased the opening of K_ATP channels, but this activation was prevented by adding 1 μM glibenclamide to the bath solution. In the presence of ferric iron (Fe³⁺: 0.1 mM), the same procedure produced hydroxyl radicals (·OH) via the iron-catalysed Haber-Weiss reaction. ·OH also activated K_ATP channels; however, this activation could not be prevented by, even very high concentrations of glibenclamide (10 μM). These different effects of glibenclamide suggest that the mode of action of these oxygen free radicals on K_ATP channels is different and that ·OH is more potent than ·O₂ ^-/H₂O₂ in activating K_ATP channels in the heart. Received: 14 July 1998 / Received after revision: 5 September 1998 / Accepted: 14 September 1998     

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+? _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 ? _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).     

Gender comparison of peak oxygen uptake: repetitive box lifting versus treadmill running

The gender differences in peak oxygen uptake (V˙O_2peak) for various modes of exercise have been examined previously; however, no direct gender comparisons have been made during repetitive lifting (RL). In the present study the V˙O_2peak between RL and treadmill running (TR) was compared between 20 men [mean (SD) age, height, body mass and body fat: 21 (3) years, 1.79 (0.06)?m, 81 (9)?kg, 19 (6)%, respectively] and 20 women [mean (SD) age, height, body mass and body fat: 21 (3) years, 1.63 (0.05)?m, 60 (7)?kg, 27 (6)%, respectively]. V˙O_2peak (l?·?min^?1), defined as the highest value obtained during exercise to volitional fatigue, was determined using discontinuous protocols with treadmill grade or box mass incremented to increase exercise intensity. For RL V˙O_2peak, a pneumatically driven shelf was used to lower a loaded box to the floor, and subjects then lifted the box, at a rate of 15 lifts?·?min^?1. V˙O_2peak (l?·?min^?1 and ml?·?kg^?1?·?min^?1) and minute ventilation (V˙ _E, l?·?min^?1) were determined using an on-line gas analysis system. A two-way repeated measures analysis of variance revealed significant gender effects, with men having higher values for V˙O_2peak (l?·?min^?1 and ml?·?kg^?1?·?min^?1) and V˙ _E, but women having higher values of the ventilatory equivalent for oxygen (V˙ _E/V˙O₂). There were also mode of exercise effects, with TR values being higher for V˙O_2peak (l?·?min^?1 and ml?·?kg^?1?·?min^?1) and V˙ _E and an interaction effect for V˙O_2peak {1?·?min^?1 and ml?·?kg^?1?·?min^?1) and V˙ _E/V˙O₂. The women obtained a greater percentage (≈84%) of their TR V˙O_2peak during RL than did the men (≈79%). There was a marginal tendency for women to decrease and men to increase their V˙ _E/V˙O₂ when comparing TR with RL. The magnitude of the gender differences between the two exercise modalities appeared to be similar for heart rate, V˙ _E and R, but differed for V˙O_2peak (1?·?min^?1 and ml?·?kg^?1?·?min^?1). Lifting to an absolute height (1.32?m for the RL protocol) may present a different physical challenge to men and women with respect to the degree of involvement of the muscle groups used during lifting and ventilation.     

Carbon dioxide storage and nonbicarbonate buffering in the human body before and after an Himalayan expedition

Before and 7–12 days after an Himalayan expedition CO₂ equilibration curves were determined in the blood plasma of 12 mountaineers by in vitro and in vivo CO₂ titration; in vivo osmolality changes (ΔOsm?·?ΔPCO₂ ^?1, ΔOsm?·?ΔpH^?1, where PCO₂ is the partial pressure of CO₂) during the latter experiments yielded estimates of whole body CO₂ storage. In vitro ?Δ[HCO₃ ^?]?·?ΔpH^?1 [nonbicarbonate buffer capacity (β) of blood] was increased 7 days after descent [before 31.3 (SEM 0.4) mmol?·?kgH₂O^?1, after?38.3?(SEM 3.9)?mmol?·?kgH₂O^?1; P<0.05] resulting from an increased proportion of young erythrocytes; in additional experiments an augmented β was found in young (low density cells) compared to old cells [<1.097 g?·?ml^?1: 0.216 (SEM 0.028) mmol?·?gHb^?1, >1.100?g?·?ml^?1: 0.145?(SEM 0.013)?mmol?·?gHb^?1, where Hb is haemoglobin; P<0.02]. In spite of increased Hb mass in vivo Δ[CO_2total]?·?ΔPCO₂ ^?1 [0.192?(SEM 0.010)?mmol?·?kgH₂O^?1?·?mmHg^?1] and ?Δ[HCO₃ ^?]?·?ΔpH^?1 [17.9?(SEM 1.0)?mmol?·?kgH₂O^?1] as indicators of extracellular β rose only slightly after altitude (7 days +16%, P<0.02; +7%, NS) because of haemodilution. The ΔOsm?·?ΔPCO₂ ^?1 [0.230?(SEM 0.015) mosmol?·?kgH₂O^?1?·?mmHg^?1] remained unchanged. Prealtitude differences in ΔOsm?·?ΔpH^?1 between hypercapnia [?41?(SEM 5)?mosmol?·?kgH₂O^?1] and hypo-capnia [?20?(SEM 3)?mosmol?·?kgH₂O^?1; P<0.01] disappeared temporarily after return since the former slope was reduced. The high value during hypercapnia before ascent probably resulted from mechanisms stabilizing intracellular pH during moderate hypercapnia which were attenuated after descent.     

Thiourea and dimethylthiourea decrease human neutrophil bactericidal function in vitro

Addition of thiourea (TU) or dimethylthiourea (DMTU) decreased killing ofStaphylococcus aureus, 502A, and decreased concentrations of hydrogen peroxide (H₂O₂), and hydroxyl radical (·OH), but not Superoxide anion (O₂ ^–) or lysozyme concentrations, in mixtures containing human neutrophilsin vitro. Addition of TU or DMTU also decreased concentrations of H₂O₂, · OH, or hypochlorous acid (HOCl) in neutrophil-free mixtures exposed to-D-glucose and glucose oxidase, gamma irradiation, or HOCl, respectively. Our results suggest that TU or DMTU can decrease neutrophil-mediated killing of bacteria by inhibiting O₂ metabolite-dependent bactericidal mechanisms.     

Aluminum induces oxidative burst,cell wall NADH peroxidase activity,and DNA damage in root cells of Allium cepa L

Plants under stress incur an oxidative burst that involves a rapid and transient overproduction of reactive oxygen species (ROS: O₂^??, H₂O₂, ^?OH). We hypothesized that aluminum (Al), an established soil pollutant that causes plant stress, would induce an oxidative burst through the activation of cell wall‐NADH peroxidase (NADH‐PX) and/or plasma membrane‐associated NADPH oxidase (NADPH‐OX), leading to DNA damage in the root cells of Allium cepa L. Growing roots of A. cepa were treated with Al³⁺ (800 μM of AlCl₃) for 3 or 6 hr without or with the pretreatment of inhibitors specific to NADH‐PX and NADPH‐OX for 2 hr. At the end of the treatment, the extent of ROS generation, cell death, and DNA damage were determined. The cell wall‐bound protein (CWP) fractions extracted from the untreated control and the Al‐treated roots under the aforementioned experimental conditions were also subjected to in vitro studies, which measured the extent of activation of peroxidase/oxidase, generation of ^?OH, and DNA damage. Overall, the present study demonstrates that the cell wall‐bound NADH‐PX contributes to the Al‐induced oxidative burst through the generation of ROS that lead to cell death and DNA damage in the root cells of A. cepa. Furthermore, the in vitro studies revealed that the CWP fraction by itself caused DNA damage in the presence of NADH, supporting a role for NADH‐PX in the stress response. Altogether, this study underscores the crucial function of the cell wall‐bound NADH‐PX in the oxidative burst‐mediated cell death and DNA damage in plants under Al stress. Environ. Mol. Mutagen., 2012. © 2012 Wiley Periodicals, Inc.     

Effect of intense interval workouts on running economy using three recovery durations

The purposes of this study were to determine whether running economy (RE) is adversely affected following intense interval bouts of 10?×?400-m running, and whether there is an interaction effect between RE and recovery duration during the workouts. Twelve highly trained male endurance athletes [maximal oxygen consumption; V˙O_{2 max} =72.5 (4.3) ml·kg^?1·min^?1; mean (SD)] performed three interval running workouts of 10?×?400 m with a minimum of 4 days between runs. Recovery duration between the repetitions was randomly assigned at 60, 120 or 180 s. The velocity for each 400-m run was determined from a treadmill V˙O_{2 max} test. The average running velocity was 357.9 (9.0) m?·?min^?1. Following the workout, the rating of perceived exertion (RPE) increased significantly (P??1. Changes in RE from pre- to post-workout, as well as heart rate (HR) and respiratory exchange ratio (R) were similar for the three recovery conditions. When averaged across conditions, oxygen consumption (V˙O₂) increased significantly (P??1?·?min^?1 at 200?m?·?min^?1, and from 53.1 to 54.5?ml?·?kg^?1?·?min^?1 at 268 m?·?min^?1, respectively). HR increased (from 124 to 138, and from 151 to 157 beats?·?min^?1 respectively) and R decreased (from 0.90 to 0.78, and from 0.93 to 0.89, respectively) at 200 and 268 m?·?min^?1, respectively (P?V˙O₂, HR and R were independent of the recovery duration between the repetitions.     

Relationship between isocapnic buffering and maximal aerobic capacity in athletes

This study was performed to clarify the relationship between isocapnic buffering and maximal aerobic capacity (V˙O_{2 max} ) in athletes. A group of 15 trained athletes aged 21.1 (SD 2.6) years was studied. Incremental treadmill exercise was performed using a modified version of Bruce's protocol for determination of the anaerobic threshold (AT) and the respiratory compensation point (RC). Ventilatory and gas exchange responses were measured with an aeromonitor and expressed per unit of body mass. Heart rate and ratings of perceived exertion were recorded continuously during exercise. The mean V˙O_{2 max} , oxygen uptake (V˙O₂) at AT and RC were 58.2 (SD 5.8)?ml?·?kg^?1?·?min^?1, 28.0 (SD 3.3)?ml?·?kg^?1?·?min^?1 and 52.4 (SD 6.7)?ml?· kg^?1?·?min^?1, respectively. The mean values of AT and RC, expressed as percentages of V˙O_{2 max} , were 48.3 (SD 4.2)% and 90.0 (SD 5.2)%, respectively. The mean range of isocapnic buffering defined as V˙O₂ between AT and RC was 24.4 (SD 4.5) ml?·?kg^?1?·?min^?1, and the mean range of hypocapnic hyperventilation (HHV) defined as V˙O₂ between RC and the end of exercise was 5.8 (SD 3.0)?ml?·?kg^?1?·?min^?1. The V˙O_{2 max} per unit mass was significantly correlated with AT (r?=?0.683, P?V˙O_{2 max} /mass was closely correlated with both the range of isocapnic buffering (r?=?0.803, P?r?=?0.878, P?V˙O_{2 max} per unit mass and the range of HHV (r?=?0.011, NS.). These findings would suggest that the prominence of isocapnic buffering, in addition to the anaerobic threshold, may have been related to V˙O_{2 max} of the athletes. The precise mechanisms underlying this proposed relationship remain to be elucidated.     

Energetics of swimming at maximal speeds in humans

The energy cost per unit of distance (C _s, kilojoules per metre) of the front-crawl, back, breast and butterfly strokes was assessed in 20 elite swimmers. At sub-maximal speeds (v), C _s was measured dividing steady-state oxygen consumption (V˙O₂) by the speed (v, metres per second). At supra-maximal v, C _s was calculated by dividing the total metabolic energy (E, kilojoules) spent in covering 45.7, 91.4 and 182.9?m by the distance. E was obtained as: E = E _an+V˙O_2max t _p?V˙O_2max(1?e^{?( t p/)}), where E _an was the amount of energy (kilojoules) derived from anaerobic sources, V˙O_2max litres per second was the maximal oxygen uptake, α (=20.9 kJ?·?l O₂ ^?1) was the energy equivalent of O₂, τ (24 s) was the time constant assumed for the attainment of V˙O_2max at muscle level at the onset of exercise, and t _p (seconds) was the performance time. The lactic acid component was assumed to increase exponentially with t _p to an asymptotic value of 0.418?kJ?·?kg^?1 of body mass for t _p?≥?120 s. The lactic acid component of E _an was obtained from the net increase of lactate concentration after exercise (Δ[La]_b) assuming that, when Δ[La]_b?=?1?mmol?·?l^?1 the net amount of metabolic energy released by lactate formation was 0.069 kJ?·?kg^?1. Over the entire range of v, front crawl was the least costly stroke. For example at 1?m?·?s^?1, C _s amounted, on average, to 0.70, 0.84, 0.82 and 0.124?kJ?·?m^?1 in front crawl, backstroke, butterfly and breaststroke, respectively; at 1.5?m?·?s^?1, C _s was 1.23, 1.47, 1.55 and 1.87?kJ?·?m^?1 in the four strokes, respectively. The C _s was a continuous function of the speed in all of the four strokes. It increased exponentially in crawl and backstroke, whereas in butterfly C _s attained a minimum at the two lowest v to increase exponentially at higher v. The C _s in breaststroke was a linear function of the v, probably because of the considerable amount of energy spent in this stroke for accelerating the body during the pushing phase so as to compensate for the loss of v occurring in the non-propulsive phase.     

The effect of a thiamin derivative on exercise performance

The purpose of this study was to investigate the effect of a thiamin derivative, thiamin tetrahydrofurfuryl disulfide (TTFD), on oxygen uptake (˙VO₂), lactate accumulation and cycling performance during exercise to exhaustion. Using a randomized, double-blind, cross-over design with a 10-day washout between trials, 14 subjects ingested either 1 g?·?day^?1 of TTFD or a placebo (PL) for 4 days. On day 3, subjects performed a progressive exercise test to exhaustion on a cycle ergometer for the determination of ˙VO_2submax, ˙VO_2peak, lactate concentration ([La^??]), lactate threshold (Th_La) and heart rate (?f _c). On day 4, subjects performed a maximal 2000-m time trial on a cycle ergometer. A one-way analysis of variance (ANOVA) with repeated measures was used to determine significant differences between trials. There were no significant differences detected between trials for serial measures of ˙VO_2submax, [La^?] or f _c. Likewise, ˙VO_2peak [PL 4.06 (0.19) TTFD 4.12 (0.19) l?·?min^?1, P?=?0.83], Th_La [PL 2.47 (0.17), TTFD 2.43 (0.16) l?·?min^?1, P?=?0.86] and 2000-m performance time [PL 204.5 (5.5), TTFD 200.9 (4.3)?s, P?=?0.61] were not significantly different between trials. The results of this study suggest that thiamin derivative supplementation does not influence high-intensity exercise performance.     

Impaired tracheal mucus transport in allergic bronchoconstriction: Effect of terbutaline pretreatment

The transport velocity of mucus within the trachea, pulmonary resistance, and arterial blood gas composition were measured in intubated conscious sheep with Ascaris suum sensitivity before and during allergic bronchoconstriction. Inhalation of A. suum extract for 15 min increased mean pulmonary resistance significantly from 1.9 cm H₂O · L^?1 sec^?1 to 5.1 cm H₂O · L^?1 sec^?1 after 60 min and to 4.5 cm H₂O · L^?1 sec^?1 after 120 min, while it decreased mean arterial P_O2 from 85 to 59 and 53 mm Hg, respectively, without altering arterial P_CO2 or pH. This was associated with a decrease in mean mucus velocity from 11.2 to 6.0 and 5.7 mm min^?1, respectively. The decrease in mucus velocity was accompanied by endoscopically visible increases in the quantity of tracheal mucus. No alterations in mucus velocity or pulmonary resistance were observed in animals who inhaled a control antigen (ragweed) or breathed a mixture of 10% oxygen 90% nitrogen, which produced a mean arterial P_O2 of 51 mm Hg. The administration of 0.25 mg terbutaline sulfate by subcutaneous injection prior to A. suum challenge prevented the changes in mucus velocity, pulmonary resistance, and arterial P_O2. We conclude that the decreased mucus velocity in the trachea during antigen-induced bronchoconstriction in conscious sheep is related to the allergic response, and can be prevented by the subcutaneous administration of terbutaline sulfate, a beta adrenergic agonist. This suggests that the protective effect of terbutaline sulfate in antigen-induced bronchoconstriction includes the effect on the associated impairment of mucociliary function.     

Oxygen uptake during high-intensity running: response following a single bout of interval training

Elevated oxygen uptake (V˙O₂) during moderate-intensity running following a bout of interval running training has been studied previously. To further investigate this phenomenon, the V˙O₂ response to high-intensity exercise was examined following a bout of interval running. Well-trained endurance runners were split into an experimental group [maximum oxygen uptake, V˙O_{2 max} 4.73 (0.39) l?·?min^?1] and a reliability group [V˙O_{2 max} 4.77 (0.26) l?·?min^?1]. The experimental group completed a training session (4?×?800?m at 1?km?·?h^?1 below speed at V˙O_{2 max} , with 3?min rest between each 800-m interval). Five minutes prior to, and 1?h following the training session, subjects completed 6?min 30?s of constant speed, high-intensity running designed to elicit 40% Δ (where Δ is the difference between V˙O₂ at ventilatory threshold and V˙O_{2 max} ; tests 1 and 2, respectively). The slow component of V˙O₂ kinetics was quantified as the difference between the V˙O₂ at 6?min and the V˙O₂ at 3?min of exercise, i.e. ΔV˙O₂₍₆₃₎. The ΔV˙O₂₍₆₃₎ was the same in two identical conditions in the reliability group [mean (SD): 0.30 (0.10) l?·?min^?1 vs 0.32 (0.13) l?·?min^?1]. In the experimental group, the magnitude of the slow component of V˙O₂ kinetics was increased in test 2 compared with test 1 by 24.9% [0.27 (0.14) l?·?min^?1 vs 0.34 (0.08)?l?·?min^?1, P?V˙O₂₍₆₃₎ in the experimental group was observed in the absence of any significant change in body mass, core temperature or blood lactate concentration, either at the start or end of tests 1 or 2. It is concluded that similar mechanisms may be responsible for the slow component of V˙O₂ kinetics and for the fatigue following the training session. It has been suggested previously that this mechanism may be linked primarily to changes within the active limb, with the recruitment of alternative and/or additional less efficient fibres.     

Relationship between maximal oxygen uptake on different ergometers, lean arm volume and strength in paraplegic subjects

The present experiment was designed to study the importance of strength and muscle mass as factors limiting maximal oxygen uptake (V˙O_{2 max} ) in wheelchair subjects. Thirteen paraplegic subjects [mean age 29.8 (8.7) years] were studied during continuous incremental exercises until exhaustion on an arm-cranking ergometer (AC), a wheelchair ergometer (WE) and motor-driven treadmill (TM). Lean arm volume (LAV) was estimated using an anthropometric method based upon the measurement of various circumferences of the arm and forearm. Maximal strength (MVF) was measured while pushing on the rim of the wheelchair for three positions of the hand on the rim (?30°, 0° and +30°). The results indicate that paraplegic subjects reached a similar V˙O_{2 max} [1.23 (0.34) l?·?min^?1, 1.25 (0.38) l?·?min^?1, 1.22?(0.18) l?·?min^?1 for AC, TM and WE, respectively] and V˙O_{2 max} /body mass [19.7?(5.2)?ml?·?min^?1?·?kg^?1, 19.5 (6.14) ml?·?min^?1?·?kg^?1, 19.18 (4.27) ml?·?min^?1?·?kg^?1 for AC, TM and WE, respectively on the three ergometers. Maximal heart rate f _{c max} during the last minute of AC (173 (17) beats?·?min^?1], TM [168 (14) beats?·?min^?1], and WE [165 (16) beats?·?min^?1], were correlated, but f _{c max} was significantly higher for AC than for TM (P<0.03). There were significant correlations between MVF and LAV (P<0.001) and between the MVF data obtained at different angles of the hand on the rim [311.9 (90.1) N, 313.2 (81.2) N, 257.1 (71) N, at ?30°, 0° and +30°, respectively]. There was no correlation between V˙O_{2 max} and LAV or MVF. The relatively low values of f _{c max} suggest that V˙O_{2 max} was, at least in part, limited by local aerobic factors instead of central cardiovascular factors. On the other hand, the lack of a significant correlation between V˙O_{2 max} and MVF or muscle mass was not in favour of muscle strength being the main factor limiting V˙O_{2 max} in our subjects.     

Roles of Reactive Oxygen Species-Degrading Enzymes of Francisella tularensis SCHU S4

Francisella tularensis is a facultative intracellular bacterium utilizing macrophages as its primary intracellular habitat and is therefore highly capable of resisting the effects of reactive oxygen species (ROS), potent mediators of the bactericidal activity of macrophages. We investigated the roles of enzymes presumed to be important for protection against ROS. Four mutants of the highly virulent SCHU S4 strain with deletions of the genes encoding catalase (katG), glutathione peroxidase (gpx), a DyP-type peroxidase (FTT0086), or double deletion of FTT0086 and katG showed much increased susceptibility to hydrogen peroxide (H₂O₂) and slightly increased susceptibility to paraquat but not to peroxynitrite (ONOO⁻) and displayed intact intramacrophage replication. Nevertheless, mice infected with the double deletion mutant showed significantly longer survival than SCHU S4-infected mice. Unlike the aforementioned mutants, deletion of the gene coding for alkyl-hydroperoxide reductase subunit C (ahpC) generated a mutant much more susceptible to paraquat and ONOO⁻ but not to H₂O₂. It showed intact replication in J774 cells but impaired replication in bone marrow-derived macrophages and in internal organs of mice. The live vaccine strain, LVS, is more susceptible than virulent strains to ROS-mediated killing and possesses a truncated form of FTT0086. Expression of the SCHU S4 FTT0086 gene rendered LVS more resistant to H₂O₂, which demonstrates that the SCHU S4 strain possesses additional detoxifying mechanisms. Collectively, the results demonstrate that SCHU S4 ROS-detoxifying enzymes have overlapping functions, and therefore, deletion of one or the other does not critically impair the intracellular replication or virulence, although AhpC appears to have a unique function.     

Peroxidase-mediated Oxygenation and Microbicidal Activity

It is known that a peroxidase, H₂O₂, and a halide form a "cytotoxic triad." As a result of the interactions of the components of the triad, reactive oxygen intermediates (ROI) are formed that help to destroy various invading pathogens including Candida. The present study was undertaken to determine if equivalent units of peroxidase induced equivalent levels of macrophage-mediated killing of Candida. Murine peritoneal macrophages were exposed to various concentrations of eosinophil peroxidase (EPO), myeloperoxidase (MPO), and horseradish peroxidase (HRP). Luminol-dependent chemiluminescence studies showed that equivalent units of peroxidase, as determined by oxidation of guaiacol, demonstrated a hierarchical pattern of ROI production. Macrophage phagocytosis and candidicidal activity, as measured by a fluorescence acridine orange assay, also demonstrated the same hierarchical pattern of EPO > MPO > HRP. Therefore, enzymatically equivalent peroxidases do not demonstrate equivalent candidicidal activity. These data indicate a distinct order of peroxidases relative to their ability to stimulate chemiluminescence and macrophage-mediated killing.     

Studies on aqueous polymerization of acrylamide, 2. Potassium persulfate/2-mercaptoethanol redox system

The polymerization of acrylamide in aqueous media initiated by the potassium persulfate/2-mercaptoethanol redox pair was studied at 30°C under nitrogen atmosphere. The initial rate of polymerization was found to be proportional to nearly the 1,5th power of the potassium persulfate concentration within the range of 0,6 to 2,0 mmol l^?1 and to the first power of acrylamide concentration in the range of 0,1 to 0,14 mol l^?1. The rate was also found to be proportional to the first power of the 2-mercaptoethanol concentration within the range 4,0 to 8,0 mmol l^?1. The overall activation energy was found to be 134 kJ mol^?1. Further the effect of salts (NaCl, KCl, NH₄Cl, Na₂C₂O₄, K₂C₂O₄·H₂O, (NH₄)₂C₂O₄,MnSO₄·4H₂O, and NaF) and aliphatic alcohols (methanol, ethanol, and propanol) was tested.     

Aqueous polymerization of methacrylamide initiated by the redox system K2S2O8/ascorbic acid

The polymerization of methacrylamide initiated by the redox system K₂S₂O₈/ascorbic acid has been studied at 35 ± 0,2°C under the influence of atmospheric oxygen. The molecular oxygen autocatalyses the polymerization rate. The rate of polymerization is independent of the activator (ascorbic acid) concentration within the range 2,83 · 10^?3 to 11,3 · 10^?3 mol · l^?1, this does not hold below or above the given concentration range. The rate varies linearly at low monomer concentration (up to 17,76 · 10^?2 mol · l^?1). The catalyst exponent decreases from nearly unity (0,94) to 0,57 with increasing concentration of the catalyst probably due to participation of primary radicals in the termination of growing chain. The initial rate is not changed by the addition of a strong acid (H₂SO₄) within the range 15 · 10^?5 to 30 · 10^?5 mol · l^?1. With the activator (ascorbic acid) alone, an optimum is observed within the pH range 2,9–3,5. The initial rate and the limiting conversion increases with increasing polymerization temperature. The overall energy of activation as calculated from the ARRHENIUS plot has been found to be 16,0 kcal.mol^?1 within the temperature range 30–45°C. Organic solvents (water miscible only) and small amounts of neutral salts, (KCl, Na₂SO₄) depress the initial rate and the maximum conversion. The addition of small amounts of catalysts like Cu^2⊕, Mn^2⊕, Ag^oplus; increases the initial rate but no appreciable increase in the limiting conversion is observed.     

Effects of indomethacin and polyunsaturated fatty acid diet on exercise-induced hypoxaemia in master athletes

We have previously reported a reduction in exercise-induced hypoxaemia following polyunsaturated fatty acid supplementation (PUFA). Although this might have been explained by increases in membrane fluidity, a clear explanation could not be provided due to potentially confounding influences of series-2 prosta- glandin mediated effects resulting from PUFA. In this investigation, ten master athletes [mean age 48.1 (SEM 6) years, maximal oxygen uptake (V˙O_{2 max} ) 3.39 (SEM 0.21) l?·?min^?1] completed a maximal cycling test (Ctrl) which was repeated after the administration of 150 mg of indomethacin to inhibit prostaglandin synthesis, both before and after 6 weeks of 3.66-g PUFA?·?day^?1. Cardiorespiratory parameters were obtained simultaneously with brachial arterial blood sampling for partial pressure of oxygen in arterial blood (P _aO₂), partial pressure of carbon dioxide in arterial blood (P _aCO₂), pH, oxygen saturation in arterial blood and lactate concentration determinations. A significant decrease in P _aO₂ (mmHg) from rest [93 (SEM 1.5)] was observed for exercise intensities of more than 40% V˙O_{2 max} in Ctrl reaching 75.9 (SEM 2.1) at V˙O_{2 max} . PUFA resulted in a 5.0 (SEM 0.68) mmHg upward shift (P?P _aO₂–oxygen uptake relationship, reducing the difference in partial pressure of oxygen between alveolar air and arterial blood (P _(A?a)O₂) at V˙O_{2 max} [Ctrl 36 (SEM 1.6) vs PUFA 33 (SEM 2.2) mmHg] while P _aCO₂, remained unchanged. Indomethacin had no effect on either P _aO₂, ideal partial pressure of oxygen in alveolar gas or P _(A?a)O₂ in either Ctrl or after PUFA. In contrast, the fall in pH was significantly reduced after indomethacin while V˙CO₂, P _aCO₂ and lactacidaemia remained unchanged. These observations confirm an effect of PUFA on exercise P _aO₂ behaviour which does not appear to be mediated by the influence of a series-2 prostaglandin.