Running performance at high running velocities is impaired but V'O_{2max} and peripheral endothelial function are preserved in IL-6^{−/−} mice

It has been reported that IL-6 knockout mice (IL-6^{−/−}) possess lower endurance capacity than wild type mice (WT), however the underlying mechanism is poorly understood. The aim of the present work was to examine whether reduced endurance running capacity in IL-6^{−/−} mice is linked to impaired maximal oxygen uptake (V′O_{2max}), decreased glucose tolerance, endothelial dysfunction or other mechanisms. Maximal running velocity during incremental running to exhaustion was significantly lower in IL-6−/− mice than in WT mice (13.00±0.97 m.min^{-1} vs. 16.89±1.15 m.min^{-1}, P<0.02, respectively). Moreover, the time to exhaustion during running at 12 m.min^{-1} in IL-6^{−/−} mice was significantly shorter (P<0.05) than in WT mice. V′O_{2max} in IL-6^{−/−} (n = 20) amounting to 108.3±2.8 ml.kg^{-1}.min^{-1} was similar as in WT mice (n = 22) amounting to 113.0±1.8 ml.kg^{-1}.min^{-1}, (P = 0.16). No difference in maximal COX activity between the IL-6^{−/−} and WT mice in m. soleus and m. gastrocnemius was found. Moreover, no impairment of peripheral endothelial function or glucose tolerance was found in IL-6^{−/−} mice. Surprisingly, plasma lactate concentration during running at 8 m.min−1 as well at maximal running velocity in IL-6^{−/−} mice was significantly lower (P<0.01) than in WT mice. Interestingly, IL-6^{−/−} mice displayed important adaptive mechanisms including significantly lower oxygen cost of running at a given speed accompanied by lower expression of sarcoplasmic reticulum Ca^{2+}-ATPase and lower plasma lactate concentrations during running at submaximal and maximal running velocities. In conclusion, impaired endurance running capacity in IL-6^{−/−} mice could not be explained by reduced V′O_{2max}, endothelial dysfunction or impaired muscle oxidative capacity. Therefore, our results indicate that IL-6 cannot be regarded as a major regulator of exercise capacity but rather as a modulator of endurance performance. Furthermore, we identified important compensatory mechanism limiting reduced exercise performance in IL-6^{−/−} mice

Mechanisms of attenuation of pulmonary V'O_{2} slow component in humans after prolonged endurance training

In this study we have examined the effect of prolonged endurance training program on the pulmonary oxygen uptake (V'O2 ) kinetics during heavy-intensity cycling-exercise and its impact on maximal cycling and running performance. Twelve healthy, physically active men (mean\ub1SD: age 22.33\ub11.44 years, V'O2peak 3198\ub1458 mL \ub7 min-1 ) performed an endurance training composed mainly of moderate-intensity cycling, lasting 20 weeks. Training resulted in a decrease (by 3c5%, P = 0.027) in V'O2 during prior low-intensity exercise (20 W) and in shortening of \u3c4 p of the V'O2 on-kinetics (30.1\ub15.9 s vs. 25.4\ub11.5 s, P = 0.007) during subsequent heavy-intensity cycling. This was accompanied by a decrease of the slow component of V'O2 on-kinetics by 49% (P = 0.001) and a decrease in the end-exercise V'O2 by 3c5% (P = 0.005). An increase (P = 0.02) in the vascular endothelial growth factor receptor 2 mRNA level and a tendency (P = 0.06) to higher capillary-to-fiber ratio in the vastus lateralis muscle were found after training (n = 11). No significant effect of training on the V'O2peak was found (P = 0.12). However, the power output reached at the lactate threshold increased by 19% (P = 0.01). The power output obtained at the V'O2peak increased by 14% (P = 0.003) and the time of 1,500-m performance decreased by 5% (P = 0.001). Computer modeling of the skeletal muscle bioenergetic system suggests that the training-induced decrease in the slow component of V'O2 on-kinetics found in the present study is mainly caused by two factors: an intensification of the each-step activation (ESA) of oxidative phosphorylation (OXPHOS) complexes after training and decrease in the "additional" ATP usage rising gradually during heavy-intensity exercise

Nitrite Concentration in the Striated Muscles Is Reversely Related to Myoglobin and Mitochondrial Proteins Content in Rats

Skeletal muscles are an important reservoir of nitric oxide (NO&bull;) stored in the form of nitrite [NO2&minus;] and nitrate [NO3&minus;] (NOx). Nitrite, which can be reduced to NO&bull; under hypoxic and acidotic conditions, is considered a physiologically relevant, direct source of bioactive NO&bull;. The aim of the present study was to determine the basal levels of NOx in striated muscles (including rat heart and locomotory muscles) with varied contents of tissue nitrite reductases, such as myoglobin and mitochondrial electron transport chain proteins (ETC-proteins). Muscle NOx was determined using a high-performance liquid chromatography-based method. Muscle proteins were evaluated using western-immunoblotting. We found that oxidative muscles with a higher content of ETC-proteins and myoglobin (such as the heart and slow-twitch locomotory muscles) have lower [NO2&minus;] compared to fast-twitch muscles with a lower content of those proteins. The muscle type had no observed effect on the [NO3&minus;]. Our results demonstrated that fast-twitch muscles possess greater potential to generate NO&bull; via nitrite reduction than slow-twitch muscles and the heart. This property might be of special importance for fast skeletal muscles during strenuous exercise and/or hypoxia since it might support muscle blood flow via additional NO&bull; provision (acidic/hypoxic vasodilation) and delay muscle fatigue

Tempo restytucji częstości skurczów serca jako czuły wskaźnik zmian stopnia aktywności fi zycznej u kobiet w wieku około i pomenopauzalnym

Heart rate recovery (HRR), which is defined as the rate of heart rate decline after cessation of exercise, is an important indicator of exercise tolerance. The aim of this study was to investigate the effect of a 4-month moderate reduction in physical activity on pre-exercise and exercise heart rate (HR) as well as HRR after exercise cessation in perimenopausal and postmenopausal women. 10 physically active females, 62.5±3.0 years old, participated in this study. They performed an 8-min constant power output (~50W) cycling exercise at an intensity corresponding to about 65% of maximal heart rate. Heart rate was measured continuously starting from 1 minute before exercise, during the exercise test and 3 min after exercise cessation. Furthermore, before and after exercise, blood pressure (BP) and tympanic temperature (Tt) were measured. The exercise test was performed twice, before and after a 4-month reduction in physical activity. 4 months of the slight reduction in physical activity (by ~16%) did not cause any changes in pre-exercise and exercise HR, however, significantly higher HR during the 1st min after exercise (p=0.03), as well slower HRR (p=0.03), were reported. No effects of the reduction in physical activity were observed in resting and post-exercise BP and Tt. Even a slight reduction in physical activity is accompanied by a lower rate of HRR , which indicates a decrease in exercise tolerance. These results indicate that HRR is a sensitive indicator of physical capacity also in peri- and postmenopausal women, since the changes in HRR in response to physical activity level occur earlier than changes in pre-exercise and exercise heart rate. heart rate, heart rate recovery, physical activity in the elderlyWstęp: Szybkość spadku częstości skurczów serca po zakończonym wysiłku, czyli tempo restytucji częstości skurczów serca (HRR) jest ważnym wskaźnikiem tolerancji wysiłku. Celem niniejszej pracy było zbadanie wpływu umiarkowanej redukcji aktywności fizycznej na przedwysiłkową, wysiłkową częstość skurczów serca (HR) oraz na przebieg HRR po wysiłku w grupie kobiet w wieku około- i pomenopauzalnym. Materiał i metody: W badaniach wzięło udział dziesięć aktywnych fizycznie kobiet w wieku 62.5±3.0 lat. Badane wykonywały 8-minutowy test wysiłkowy na cykloergometrze ze stałą intensywnością (~50W) odpowiadającą ~65% maksymalnej częstości skurczów serca. Częstość skurczów serca mierzono w sposób ciągły, począwszy od 1 minuty przed rozpoczęciem testu, w czasie jego trwania oraz przez 3 minuty od jego zakończenia. Przed rozpoczęciem testu wysiłkowego oraz tuż po jego zakończeniu wykonano pomiar ciśnienia tętniczego krwi (BP) oraz temperatury tympanalnej (Tt). Test wysiłkowy wykonano dwukrotnie przed i po 4-miesięcznym okresie zmniejszenia aktywności fizycznej. Wyniki: 4-miesięczny okres niewielkiego zmniejszenia aktywności fizycznej (o około ~16%) nie wywołał istotnych zmian w przedwysiłkowym i wysiłkowym HR, jednakże zaobserwowano istotnie wyższe HR w 1 minucie po zakończeniu wysiłku (p=0.03), jak i wolniejsze tempo HRR (p=0.03). Redukcja obciążeń treningowych nie wywołała zmian w spoczynkowych i powysiłkowych wielkościach BP i Tt. Wnioski: Nawet niewielka redukcja aktywności fizycznej prowadzi do spadku tempa restytucji częstości skurczów serca co wskazuje na pogorszenie tolerancji wysiłku. Wyniki te dowodzą, że HRR jest czułym wskaźnikiem wydolności fizycznej również u kobiet w wieku około- i pomenopauzalnym, gdyż jego zmiana w odpowiedzi na zmianę poziomu aktywności fizycznej pojawia się wcześniej niż zmiany w przedwysiłkowej i wysiłkowej częstości skurczów serca

The impact of aging and physical training on angiogenesis in the musculoskeletal system

Angiogenesis is the physiological process of capillary growth. It is strictly regulated by the balanced activity of agents that promote the formation of capillaries (pro-angiogenic factors) on the one hand and inhibit their growth on the other hand (anti-angiogenic factors). Capillary rarefaction and insufficient angiogenesis are some of the main causes that limit blood flow during aging, whereas physical training is a potent non-pharmacological method to intensify capillary growth in the musculoskeletal system. The main purpose of this study is to present the current state of knowledge concerning the key signalling molecules implicated in the regulation of skeletal muscle and bone angiogenesis during aging and physical training

Myosin heavy chain composition in the vastus lateralis muscle in relation to oxygen uptake and heart rate during cycling in humans

In this study we examined the relationship between fast myosin heavy chain (MyHC2) content in the vastus lateralis and the rate of oxygen uptake (VO2) and heart rate (HR) increase during an incremental exercise in 38, young, healthy men. Prior to the exercise test, muscle biopsies were taken in order to evaluate the MyHC composition. It was found that during cycling performed below the lactate threshold (LT), a positive relationship between MyHC2 and the intercept of the oxygen uptake and power output (VO2-PO) relationship existed (r=0.49, P=0.002), despite no correlation between MyHC2 and the slope value of the VO2-PO relationship (r= -0.18, P=0.29). During cycling performed above the LT, MyHC2 correlated positively with the magnitude of the nonlinearity in the VO2-PO relationship; i.e. with the accumulated VO2'excess' (r=0.44, P=0.006) and peak VO2'excess' (r=0.44, P=0.006), as well as with the slope of the HR-PO relationship (r=0.49, P=0.002). We have concluded that a greater MyHC2 content in the vastus lateralis is accompanied by a higher oxygen cost of cycling during exercise performed below the LT. This seems to be related to the higher energy cost of the non-cross-bridge activities in the muscles possessing a greater proportion of MyHC2 content. In the case of heavy-intensity exercise, a higher MyHC2 content in the vastus lateralis is accompanied by greater non-linearity in the VO2-PO relationship, as well as a steeper increase in HR in the function of an increase of PO. This relationship can be explained by greater disturbances in metabolic stability in type II muscle fibres during exercise, resulting in a decrease of muscle mechanical efficiency and greater increase of heart rate at a given power output. Therefore, MyHC composition has an impact on the oxygen cost of cycling both below and above the LT