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It is well documented that physical activity can induce a number of various stimuli which are able to enhance the strength and endurance performance of muscles. Moreover, regular physical activity can preserve or delay the appearance of several metabolic disorders in the human body. Physical exercise is also known to enhance the mood and cognitive functions of active people, although the physiological backgrounds of these effects remain unclear. In recent years, since the pioneering study in the past showed that physical activity increases the expression of the brain derived neurothophic factor (BDNF) in the rat brain, a number of studies were undertaken in order to establish the link between that neurothrophin and post-exercise enhancement of mood and cognitive functions in humans. It was recently demonstrated that physical exercise can increase plasma and/or serum BDNF concentration in humans. It was also reported that physical exercise or electrical stimulation can increase the BDNF expression in the skeletal muscles. In the present review, we report the current state of research concerning the effect of a single bout of exercise and training on the BDNF expression in the brain, in both the working muscles as well as on its concentrations in the blood. We have concluded that there may be potential benefits of the exercise-induced enhancement of the BDNF expression and release in the brain as well as in the peripheral tissues, resulting in the improvement of the functioning of the body, although this effect, especially in humans, requires more research.
We have examined the effect of 5 week cycling endurance training program on the sarco(endo)plasmic reticulum Ca2+ ATPase isoforms (SERCA1 and 2) and myosin heavy chain (MyHC) in the vastus lateralis muscle as well as on the oxygen uptake to power output ratio (VO2/PO) during incremental cycling. Fifteen untrained men performed an incremental cycling exercise until exhaustion before and after moderate intensity training. Muscle biopsies were taken from vastus lateralis before and after training program. Training resulted in higher (P = 0.048) maximal oxygen uptake (VO2max) as well as in higher power output reached at VO2max (P = 0.0001). Moreover, lower (P = 0.02) VO2/PO ratio determined during incremental moderate intensity cycling (i.e. 30-120 W) as well as lower (P = 0.003) VO2/PO ratio reached at VO2max were observed after the training. A significant down regulation of SERCA2 protein (P = 0.03) and tendency (P = 0.055) to lower SERCA1 content accompanied by lower (P<10-4) plasma thyroid hormone concentration, with no changes (P = 0.67) in MyHC composition in vastus lateralis muscle were found after training. We have concluded that the increase in mechanical efficiency of cycling occurring during first weeks of endurance training is not related to changes in MyHC composition but it may be due to down-regulation of SERCA pumps.
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.
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.
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.
It has been reported that various types of mammalian muscle fibers differ regarding the content of several metabolites at rest. However, to our knowledge no data have been reported in the literature, concerning the muscle energetic status at rest in high class athletes when considering the dominant and non-dominant leg separately. We have hypothesised that due to higher mechanical loads on the dominant leg in athletes, the metabolic profile in the dominant leg at rest in the calf muscles, characterized by [PCr], [ADPfree], [AMPfree] and GATP, will significantly differ among endurance athletes, sprinters and untrained individuals. In this study we determined the GATP and adenine phosphates concentrations in the dominant and non-dominant legs in untrained subjects (n = 6), sprinters (n = 10) and endurance athletes (n = 7) at rest. The (mean ± SD) age of the subjects was 23.4 ± 4.3 years. Muscle metabolites were measured in the calf muscles at rest, by means of 31P-MRS, using a 4.7 T superconducting magnet (Bruker). When taking into account mean values in the left and right leg, phosphocreatine concentration ([PCr]) and GATP were significantly lower (p<0.05, Wilcoxon-Mann-Whitney test), and [ADPfree] was significantly higher (p = 0.04) in endurance athletes than in untrained subjects. When considering the differences between the left and right leg, [PCr] in the dominant leg was significantly lower in endurance athletes than in sprinters (p = 0.01) and untrained subjects (p = 0.02) (25.91 ± 2.87 mM; 30.02 ± 3.12 mM and 30.71 ± 2.88 mM, respectively). The [ADPfree] was significantly higher (p = 0.02) in endurance athletes than in sprinters and untrained subjects (p = 0.02) (42.19 ± 13.44 µM; 27.86 ± 10.19 µM; 25.35 ± 10.97 µM, respectively). The GATP in the dominant leg was significantly lower (p = 0.02) in endurance athletes than in sprinters and untrained subjects (p = 0.01) (-60.53 ± 2.03 kJ·M-1; -61.82 ± 1.05 kJ·M-1, -62.29 ± 0.73 kJ·M-1, respectively). No significant differences were found when comparing [PCr], [ADPfree], [AMPfree], [Mg2+free], GATP in the dominant leg and the mean values for both legs in sprinters and untrained subjects. Moreover, no significant differences were found when comparing the metabolites in non-dominant legs in all groups of subjects. We postulate that higher [ADPfree] and lowerGATP at rest is a feature of endurance-trained muscle. Moreover, when studying the metabolic profile of the locomotor muscles in athletes one has to consider the metabolic differences between the dominant and non-dominant leg.
Strenuous exercise was reported to involve the alteration in the release of some "stress" hormones such as growth hormone (GH), cortisol, catecholamines and appropriate adjustment of energy metabolism but the relative contribution of these hormones to metabolic response, to cycling exercise performed at different muscle shortening velocities, has not been clarified. Aims: The purpose of this experiment was to assess the effect of applying different pedalling rates during a prolonged incremental cycling exercise test on the changes in the plasma levels of growth hormone, cortisol, insulin, glucagon and leptin in humans. Material and Methods: Fifteen healthy non-smoking men (means ± SD: age 22.9 ± 2.4 years; body mass 71.9 ± 8.2 kg; height 178 ± 6 cm; with VO2max of 3.896 ± 0.544 l . min-1), assessed in laboratory tests, were subjects in this study. The subjects performed in two different days a prolonged incremental exercise tests at two different pedalling rates, one of them at 60 and another at 120 rev . min-1. During this tests the power output has increased by 30 W every 6 minutes. The tests were stopped when the subject reached about 70 % of the VO2max. Results and conclusions: We have found that choosing slow or fast pedalling rates (60 or 120 rev . min-1), while generating the same external mechanical power output, had no effect on the pattern of changes in plasma cortisol, insulin, glucagon, glucose and leptin concentrations. But, generation of the same external mechanical power output at 120 rev . min-1 causes more stepper increase (p < 0.01) in the plasma growth hormone concentration [GH]pl and plasma lactate concentrations [La]pl when compared to that observed during cycling at 60 rev . min-1. We have also found that the onset of a significant increase in [GH]pl during cycling at 60 rev . min-1 was not accompanied by significant increase in [La]pl. While during cycling at 120 rev . min-1 the onset of a significant increase in [La]pl occurred without increase in [GH]pl, but with continuation of exercise when plasma [La]pl increased, there was also a parallel rise in plasma [GH]pl, as reported before. This results indicates that the increase in [GH]pl during exercise is not closely related to the increase in [La]pl.
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