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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.
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.
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