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The paper sought to determine the exercise intensity where the slow component of oxygen uptake (o2) first appears in decremental work load exercise (DLE). Incremental work load exercise (ILE) was performed with an increment rate of 15 watts (W) per minute. In DLE, power outputs were decreased by 15 W per minute, from 120 (DLE120), 160 (DLE160), 200 (DLE200) and 240 (DLE240) W, respectively. The slopes of o2 against the power output were obtained in the lower section from 0 to 50 W in all DLEs, and in the upper section from 80 to 120 W in DLE160 and from 100 to 150 W in DLE200 and DLE240. The power output at exhaustion in ILE was 274 ± 20 W. The power output at the ventilatory threshold (VT) obtained in ILE was 167 ± 22 W. The initial power output in DLE160 was near the power output at VT. The slopes obtained in the upper sections were 11.4 ± 0.9 ml • min-1 • W-1 in DLE160, 12.8 ± 0.8 ml • min-1 • W-1 in DLE200, and 14.8 ± 1.1 ml • min-1 • W-1 in DLE240. The slope obtained in DLE120 was 10.9 ± 0.6 ml • min-1. There were no differences in slope between the upper and lower sections in DLE160 but there were significant differences in slopes between the upper and lower sections in DLE200 and DLE240. Thus, the slow component, which could be observed as a steeper slope in DLE, began to increase when the initial power output in DLE was near to VT.
For the last decade there have been considerable discussion concerning the linearity / non-linearity of the oxygen uptake (O2) - power output (W) relationship with strong experimental evidence of non-linearity provided mainly by breath-by-breath measurements. In this study, we attempted to answer the question whether the O2 - W relationship in the Åstrand nomogram, as presented in the Textbook of Work Physiology, P.-O. Åstrand et al. (2003), page 281, based on the Douglas bag method, is indeed linear, as stated by the authors before, or if a change point in O2, described by Zoladz et al. (1998) Eur J Appl Physiol 78: 369-377, can possibly be detected in those data. The O2 - W data were taken from the Åstrand nomogram referenced above and from the Table 9.5 on page 282 in the same reference and tested for the presence of the change point in O2, using our two-phase model (see the reference above). In the first phase, a linear O2 - W relationship was assumed, whereas in the second one (above the so-called change point) an additional increase in O2 above the values expected from the linear model was allowed. It was found that in the data taken from the Åstrand nomogram (data for men), as well as in the data taken from the Table 9.5, statistically significant change points in O2 were present at the power output of 150 W. The documentation of the presence of a change point in the O2 - W relationship in the Åstrand data provides further evidence for the existence of a non-linearity in the O2 - W relationship in incremental exercise tests of humans, also in O2 data based upon the Douglas bag method.
The aim of this study was to examine the relationship between the content of various types of myosin heavy chain isoforms (MyHC) in the vastus lateralis muscle and pulmonary oxygen uptake during moderate power output incremental exercise, performed at low and at high pedalling rates. Twenty one male subjects (mean ± SD) aged 24.1 ± 2.8 years; body mass 72.9 ± 7.2 kg; height 179.1 ± 4.8 cm; BMI 22.69 ± 1.89 kg . m-2; VO2max 50.6 ± 5.3 ml . kg . min-1, participated in this study. On separate days, they performed two incremental exercise tests at 60 rev . min-1 and at 120 rev . min-1, until exhaustion. Gas exchange variables were measured continuously breath by breath. Blood samples were taken for measurements of plasma lactate concentration prior to the exercise test and at the end of each step of the incremental exercise. Muscle biopsies were taken from the vastus lateralis muscle, using Bergström needle, and they were analysed for the content of MyHC I and MyHC II using SDS - PAGE and two groups (n=7, each) were selected: group H with the highest content of MyHC II (60.7 % ± 10.5 %) and group L with the lowest content of MyHC II (27.6 % ± 6.1 %). We have found that during incremental exercise at the power output between 30 - 120 W, performed at 60 rev . min-1, oxygen uptake in the group H was significantly greater than in the group L (ANCOVA, p=0.003, upward shift of the intercept in VO2 / power output relationship). During cycling at the same power output but at 120 rev . min-1, the oxygen uptake was also higher in the group H, when compared to the group L (i.e. upward shift of the intercept in VO2 / power output relationship, ANCOVA, p=0.002). Moreover, the increase in pedalling rate from 60 to 120 rev . min-1 was accompanied by a significantly higher increase of oxygen cost of cycling and by a significantly higher plasma lactate concentration in subjects from group H. We concluded that the muscle mechanical efficiency, expressed by the VO2 / PO ratio, during cycling in the range of power outputs 30 - 120 W, performed at 60 as well as 120 rev . min-1, is significantly lower in the individuals with the highest content of MyHC II, when compared to the individuals with the lowest content of MyHC II in the vastus lateralis.
Data concerning cardiovascular effects of peripherally and centrally located histamine H3 receptor stimulation are contradictory, and despite excessive studies their role in the control of the cardiovascular function have not been cleared yet. Effect of histamine H3 receptors activation have been attributed to modulation of sympathetic system activity but exact role of peripherally and centrally located histamine H3 receptors stimulation in the modulation of vascular tone of the mesentery and intestinal metabolism remains unexplored. Aim of the present study was to evaluate the role of centrally and peripherally located histamine H3 receptors in the modulation of vascular tone of the mesentery and metabolic activity of intestinal tissue. In anesthetized rats total mesenteric blood flow (MBF), mucosal intestinal blood flow (LDBF), intestinal oxygen uptake (VO2) and arterial pressure (AP) were determined. Intestinal arterial conductance (C) was also calculated. Administration of the selective histamine H3 receptor agonist imetit (10 µmol/kg i.a) evoked marked changes in hemodynamic and metabolic parameters; MBF, LDBF, C and VO2 were significantly increased, whereas AP was significantly decreased. Pretreatment with histamine H3 receptor antagonist clobenpropit (4 µmol/kg i.a.) abolished imetit-induced circulatory and oxygen uptake responses. Clobenpropit (4 µmol/kg i.a.) alone failed to affect the MBF, LDBF, AP, C and VO2 values. Central administration of imetit (0.1 µmol i.c.v.) markedly increased AP and decreased MBF, LDBF, C and VO2. Pretreatment with histamine H3 receptor antagonist clobenpropit (0,4 µmol i.c.v.) diminished circulatory and metabolic responses to centrally injected imetit. Central histamine H3 receptors blockade by clobenpropit evoked no significant changes in the mesenteric arterial and mucosal microcirculatory blood flow, intestinal metabolism and mean arterial pressure. We conclude that, peripheral histamine H3 receptors when stimulated decreases vasoconstrictory tone of the mesenteric artery and precapillary structures and evokes increase of intestinal oxygen uptake. This might be in part due to inhibition of sympathetic postganglionic fibers vasopressor activity. Central histamine H3 receptor stimulation activates vasoconstrictory sympathetic adrenergic system with possible involvement of other, presumably non-histaminergic receptors system. At basal conditions neither central nor peripheral histamine H3 receptors are involved in the control of mesenteric macro - and microcirculation and intestinal oxygen consumption.
Introduction. Numerous studies have focused on the association between I/D ACE and physical fi tness; however, this association in professional hockey players has never been recognized. Aim of the Study. The study examined the distribution of Alu insertion (I)/deletion (D) angiotensin converting enzyme (ACE) genotypes in elite male professional fi eld hockey players. Material and Methods. The effect of Alu insertion (I)/deletion (D) angiotensin converting enzyme (ACE) genotypes on motor skills and maximal oxygen uptake (VO₂max) in 47 elite male fi eld hockey players was studied. Genotyping for ACE I/D was performed using a polymerase chain reaction on DNA from leucocytes. The studied motor skills such as speed – 20 m run, power – vertical jump, recovery – step-test, speed endurance (15 x 20 m) shuttle run, were established using functional tests. The VO₂max was measured during progressive exercise test till exhaustion. Results. The authors do not confi rm some literature data that D allele favours endurance ability. We did not detect signifi cant genotype effects of ACE on the analyzed traits; how-ever a tendency for decreased performance of individuals with the DD genotype was noted for vertical jump, power peak and power. Conclusions. Analysis of the genetic profi le of ACE I/D may provide supplemetary information on a player’s predispositions to exercise with specifi c energy requirements.
Kruk. В., Szczypaczewska M., Opaszowski В., Kaciuba Uściłko H., Nazar K. Thermoregulatory and metabolic responses to repeated bouts of prolonged cycle-ergometer exercise in man. Acta Physiol. Pol., Changes in body temperature, oxygen uptake (VO₂ ), heart rate (HR), sweating rate and plasma osmolality were examined in 10 human subjects, performing four successive 30 min exercise-bouts of the same intensity (50% VO₂ max) separated by 30 min rest periods. In spite of the rest intervals and replacement of body fluid loss there was a progressive increase in VO₂ . HR, rectal (Tre) and mean body (Tb) temperatures in consecutive exercise bouts. The thermoregulatory efficiency showed an increasing tendency, and a delay in the sweating response at the beginning of each exercise was shortened. It is concluded that a drift in metabolic and temperature responses to exercise, reported throughout a long-term continuous work, occurs also in the euhydrated subjects performing a prolonged intermittent exercise. It is not caused by an impaired thermoregulation during exercise but rather by insufficient restitution of metabolic processes during rest intervals.
It is well known that the oxygen uptake kinetics during rest-to-work transition (O2 on-kinetics) in trained subjects is significantly faster than in untrained individuals. It was recently postulated that the main system variable that determines the transition time (t1/2) of the O2 on-kinetics in skeletal muscle, at a given moderate ATP usage/work intensity, and under the assumption that creatine kinase reaction works near thermodynamic equilibrium, is the absolute (in mM) decrease in [PCr] during rest-to-work transition. Therefore we postulate that the training-induced acceleration of the O2 on-kinetics is a marker of an improvement of absolute metabolic stability in skeletal muscles. The most frequently postulated factor responsible for enhancement of muscle metabolic stability is the training-induced increase in mitochondrial proteins. However, the mechanism proposed by Gollnick and Saltin (1982) can improve absolute metabolic stability only if training leads to a decrease in resting [ADPfree]. This effect is not observed in many examples of training causing an acceleration of the O2 on-kinetics, especially in early stages of training. Additionally, this mechanism cannot account for the significant training-induced increase in the relative (expressed in % or as multiples of the resting values) metabolic stability at low work intensities, condition in which oxidative phosphorylation is not saturated with [ADPfree]. Finally, it was reported that in the early stage of training, acceleration in the O2 on-kinetics and enhancement of muscle metabolic stability may precede adaptive responses in mitochondrial enzymes activities or mitochondria content. We postulate that the training-induced acceleration in the O2 on-kinetics and the improvement of the metabolite stability during moderate intensity exercise in the early stage of training is mostly caused by an intensification of the “parallel activation” of ATP consumption and ATP supply pathways. A further acceleration in O2 on-kinetics, resulting from prolonged periods of training, may be caused by a further and more pronounced improvement in the muscles’ absolute metabolic stability, caused by an intensification of the “parallel activation” as well as by an increase in mitochondrial proteins.
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Oxygen uptake kinetics: Why are they so slow? And what do they tell us?

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O2 kinetics and O2 deficit are important determinants of exercise tolerance. In "normal" conditions convective and diffusive O2 delivery to skeletal muscle fibers do not represent important determinants of O2 kinetics, whose limiting factors seem mainly located within muscle fibers. Whereas a limiting role by PDH has not been confirmed, the role of inhibition of mitochondrial respiration by NO needs further investigations. Important determinants of skeletal muscle O2 kinetics likely reside in the interplay between bioenergetic mechanisms at exercise onset. By acting as high-capacitance energy buffers, PCr hydrolysis and anaerobic glycolysis would delay or attenuate the increase in [ADP] within muscle fibers following rapid increases in ATP demand, preventing a more rapid activation of oxidative phosphorylation. The different "localization" of the main limiting factors for O2 kinetics and O2max offers the opportunity to perform a functional evaluation of oxidative metabolism at two different levels of the pathway for O2, from ambient air to mitochondria. WhereasO2max is mainly limited by the capacity of the cardiovascular system to deliver O2 to exercising muscles, by analysis of O2 kinetics the functional evaluation is mainly related to skeletal muscle. In pathological conditions the situation may be less clear, and warrants further investigations.
In this study we have examined the relationship between the content of different isoforms of MyHC in the vastus lateralis m. quadricipitis femoris and the VO2 / power output relationship during incremental cycling exercise. Twenty-one male subjects: aged 24.0 ± 2.5 years, body mass 73.0 ± 7.2 kg, height 179 ± 5 cm, BMI 22.78 ± 1.84 kg . m-2 , VO2 max 3697 ± 390 ml . min-1 , 50.9 ± 5.2 ml . kg-1 . min-1 , participated in this experiment. The subjects performed an incremental exercise test until exhaustion. The exercise test started at power output of 30 W, followed by an increase amounting to 30 W every 3 minutes. The pedalling rate was maintained at 60 rev . min-1 . Gas exchange variables were measured continuously using breath-by- breath system Oxycon Jaeger. At the end of each step blood samples were taken for lactate concentration. Muscle biopsy samples taken from the vastus lateralis m. quadricipitis femoris, using the Bergstrom needle, were analysed for the content of different MyHC (I, IIa, IIx) using SDS-PAGE and Western blotting. The pre-exercise VO2, as a mean value of six-minute measurements, expressed both in ml . min-1 , and in ml . kg -1 . min-1 , was positively correlated with the content of MyHC II in the vastus lateralis (p < 0.01). We have also found that the pre-exercise values of VO2 in the group of subjects with a high proportion of MyHC II (59.9 ± 11.2 %) were significantly higher (p < 0.02, when VO2 was expressed in ml . min-1 , and p < 0.01 when VO2 was expressed in ml . kg-1 . min-1 ) than in the group with low content of MyHC II (27.5 ± 6.0 %) in the vastus lateralis. Moreover, we have found a significant negative correlation (r = -0.562, p < 0.01) between the slope in the VO2/PO relationship below the lactate threshold (LT) and the content of MyHC IIa in the vastus lateralis. The most interesting finding of our study was that the magnitude of the non-linear increase in the VO2 / power output relationship present above the LT was positively correlated ( r = 0.510, p < 0.02) with the content of MyHC II in the vastus lateralis. Our results show, that there is no simple relationship between the content of different types of MyHC in the vastus lateralis and the oxygen cost of work during incremental exercise test. Individuals with a high content of MyHC II in the vastus lateralis m. quadricipitis femoris consume more oxygen in the pre-exercise conditions than subjects with a low content of MyHC II in their muscles. Subjects with a high content of MyHC II require a smaller increase in VO2 for maintaining a linear increase in power output up to the lactate threshold (lower slope in this relationship), but after exceeding the LT, they consume more oxygen above that expected from the linear relationship below the LT, than the subjects with a low content of MyHC II in their muscles. Therefore, non-linear increase in the VO2 / power output relationship, present above the LT, is more pronounced in subjects with a higher content of MyHC II in the vastus lateralis m. quadricipitis femoris.
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