Myoglobin deficiency impairs maximal oxygen uptake and exercise performance: a lesson from Mb-/- mice.

Myoglobin (Mb) plays an important role at rest and during exercise as a reservoir of oxygen and has been suggested to regulate NO• bioavailability under hypoxic/acidic conditions. However, its ultimate role during exercise is still a subject of debate. We aimed to study the effect of Mb deficiency on maximal oxygen uptake ( V ̇ O 2 max ${\dot V_{{{\mathrm{O}}_2}\max }}$ ) and exercise performance in myoglobin knockout mice (Mb-/- ) when compared to control mice (Mb+/+ ). Furthermore, we also studied NO• bioavailability, assessed as nitrite (NO2 - ) and nitrate (NO3 - ) in the heart, locomotory muscle and in plasma, at rest and during exercise at exhaustion both in Mb-/- and in Mb+/+ mice. The mice performed maximal running incremental exercise on a treadmill with whole-body gas exchange measurements. The Mb-/- mice had lower body mass, heart and hind limb muscle mass (P < 0.001). Mb-/- mice had significantly reduced maximal running performance (P < 0.001). V ̇ O 2 max ${\dot V_{{{\mathrm{O}}_2}\max }}$ expressed in ml min-1 in Mb-/ - mice was 37% lower than in Mb+/+ mice (P < 0.001) and 13% lower when expressed in ml min-1  kg body mass-1 (P = 0.001). Additionally, Mb-/- mice had significantly lower plasma, heart and locomotory muscle NO2 - levels at rest. During exercise NO2 - increased significantly in the heart and locomotory muscles of Mb-/- and Mb+/+ mice, whereas no significant changes in NO2 - were found in plasma. Our study showed that, contrary to recent suggestions, Mb deficiency significantly impairs V ̇ O 2 max ${\dot V_{{{\mathrm{O}}_2}\max }}$ and maximal running performance in mice. KEY POINTS: Myoglobin knockout mice (Mb-/- ) possess lower maximal oxygen uptake ( V ̇ O 2 max ${\dot V_{{{\mathrm{O}}_2}\max }}$ ) and poorer maximal running performance than control mice (Mb+/+ ). Respiratory exchange ratio values at high running velocities in Mb-/- mice are higher than in control mice suggesting a shift in substrate utilization towards glucose metabolism in Mb-/- mice at the same running velocities. Lack of myoglobin lowers basal systemic and muscle NO• bioavailability, but does not affect exercise-induced NO2 - changes in plasma, heart and locomotory muscles. The present study demonstrates that myoglobin is of vital importance for V ̇ O 2 max ${\dot V_{{{\mathrm{O}}_2}\max }}$ and maximal running performance as well as explains why previous studies have failed to prove such a role of myoglobin when using the Mb-/- mouse model.

Exercise Training Decreases Nitrite Concentration in the Heart and Locomotory Muscles of Rats Without Changing the Muscle Nitrate Content.

BACKGROUND: Skeletal muscles are postulated to be a potent regulator of systemic nitric oxide homeostasis. In this study, we aimed to evaluate the impact of physical training on the heart and skeletal muscle nitric oxide bioavailability (judged on the basis of intramuscular nitrite and nitrate) in rats. METHODS AND RESULTS: Rats were trained on a treadmill for 8 weeks, performing mainly endurance running sessions with some sprinting runs. Muscle nitrite (NO2-) and nitrate (NO3-) concentrations were measured using a high-performance liquid chromatography-based method, while amino acids, pyruvate, lactate, and reduced and oxidized glutathione were determined using a liquid chromatography coupled with tandem mass spectrometry technique. The content of muscle nitrite reductases (electron transport chain proteins, myoglobin, and xanthine oxidase) was assessed by western immunoblotting. We found that 8 weeks of endurance training decreased basal NO2- in the locomotory muscles and in the heart, without changes in the basal NO3-. In the slow-twitch oxidative soleus muscle, the decrease in NO2- was already present after the first week of training, and the content of nitrite reductases remained unchanged throughout the entire period of training, except for the electron transport chain protein content, which increased no sooner than after 8 weeks of training. CONCLUSIONS: Muscle NO2- level, opposed to NO3-, decreases in the time course of training. This effect is rapid and already visible in the slow-oxidative soleus after the first week of training. The underlying mechanisms of training-induced muscle NO2- decrease may involve an increase in the oxidative stress, as well as metabolite changes related to an increased muscle anaerobic glycolytic activity contributing to (1) direct chemical reduction of NO2- or (2) activation of muscle nitrite reductases.

Training-induced impairment of endothelial function in track and field female athletes.

Professional athletes are often exposed to high training loads that may lead to overfatigue, overreaching and overtraining that might have a detrimental effects on vascular health. We determined the effects of high training stress on endothelial function assessed by the flow-mediated dilation (FMD) and markers of glycocalyx shedding. Vascular examination as well as broad biochemical, hormonal and cardiometabolic evaluation of sprint and middle-distance female runners were performed after 2 months of preparatory training period and compared to age-matched control group of women. Female athletes presented with significantly reduced FMD (p < 0.01) and higher basal serum concentrations of hyaluronan (HA) and syndecan-1 (SDC-1) (p < 0.05 and p < 0.001, respectively), that was accompanied by significantly lower basal serum testosterone (T) and free testosterone (fT) concentrations (p < 0.05) and higher cortisol (C) concentration (p < 0.05). It resulted in significantly lower T/C and fT/C ratios in athletes when compared to controls (p < 0.01). Moreover, fT/C ratio were significantly positively correlated to FMD and negatively to HA concentrations in all studied women. Accordingly, the training load was significantly negatively correlated with T/C, fT/C and FMD and positively with the concentrations of HA and SDC-1. We concluded that young female track and field athletes subjected to physical training developed impairment of endothelial function that was associated with anabolic-catabolic hormone balance disturbances. Given that training-induced impairment of endothelial function may have a detrimental effects on vascular health, endothelial status should be regularly monitored in the time-course of training process to minimalize vascular health-risk in athletes.

Age-related decrease in serum dihydrotestosterone concentration is accompanied by impaired vascular status.

INTRODUCTION: The effect of androgens on the cardiovascular system in humans is ambiguous. Moreover, still little is known about the effects of the most potent androgen, dihydrotestosterone, on arterial stiffness and endothelial function. The aim of this study was to evaluate whether age-dependent alterations in serum concentration of dihydrotestosterone and its circulating metabolite are accompanied by changes in endothelial function and arterial stiffness. METHODS: In 12 young and 11 older men, basal serum concentrations of testosterone, dehydroepiandrosterone sulfate (DHAE-S), androstenedione (AE), dihydrotestosterone (DHT) and androstanediol glucuronide (ADG) were analyzed in relation to vascular status including cIMT - carotid intima media thickness, cAI - central augmentation index, crPWV - carotid radial pulse wave velocity, SI - stiffness index, endothelial and inflammatory markers. RESULTS: Although concentration of testosterone was not different between young and older group, it was demonstrated that DHT, DHEA-S, AE and ADG were significantly lower in older men in comparison to young men (p < 0.01). Interestingly the most surprising difference was found for DHT concentration, that was as much as 61 % lower in aged men that displayed significantly higher values of cIMT, AI, crPWV and SI (p < 10-4), suggestive of arterial stiffness. Furthermore, DHT was negatively correlated to all arterial wall parameters (cAI, crPWV, SI and cIMT), c-reactive protein (CRP) and hyaluronic acid (HA) concentration, as well as positively correlated to markers of endothelial function (MNA and 6-keto-PGF1α) in all studied individuals (n = 23). CONCLUSIONS: We have shown that ageing leads to a significant decrease in DHT concentration that is accompanied by impaired arterial wall characteristics and worsened endothelial function. Therefore more attention should be paid to the DHT, DHEA-S and ADG concentrations as a biomarkers for vascular dysfunction in ageing men.

Endurance Training Increases the Running Performance of Untrained Men without Changing the Mitochondrial Volume Density in the Gastrocnemius Muscle.

The activity and quantity of mitochondrial proteins and the mitochondrial volume density (MitoVD) are higher in trained muscles; however, the underlying mechanisms remain unclear. Our goal was to determine if 20 weeks' endurance training simultaneously increases running performance, the amount and activity of mitochondrial proteins, and MitoVD in the gastrocnemius muscle in humans. Eight healthy, untrained young men completed a 20-week moderate-intensity running training program. The training increased the mean speed of a 1500 m run by 14.0% (p = 0.008) and the running speed at 85% of maximal heart rate by 9.6% (p = 0.008). In the gastrocnemius muscle, training significantly increased mitochondrial dynamics markers, i.e., peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) by 23%, mitochondrial transcription factor A (TFAM) by 29%, optic artrophy-1 (OPA1) by 31% and mitochondrial fission factor (MFF) by 44%, and voltage-dependent anion channel 1 (VDAC1) by 30%. Furthermore, training increased the amount and maximal activity of citrate synthase (CS) by 10% and 65%, respectively, and the amount and maximal activity of cytochrome c oxidase (COX) by 57% and 42%, respectively, but had no effect on the total MitoVD in the gastrocnemius muscle. We concluded that not MitoVD per se, but mitochondrial COX activity (reflecting oxidative phosphorylation activity), should be regarded as a biomarker of muscle adaptation to endurance training in beginner runners.

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•) stored in the form of nitrite [NO2-] and nitrate [NO3-] (NOx). Nitrite, which can be reduced to NO• under hypoxic and acidotic conditions, is considered a physiologically relevant, direct source of bioactive NO•. 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-] compared to fast-twitch muscles with a lower content of those proteins. The muscle type had no observed effect on the [NO3-]. Our results demonstrated that fast-twitch muscles possess greater potential to generate NO• 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• provision (acidic/hypoxic vasodilation) and delay muscle fatigue.

Lowered Serum Testosterone Concentration Is Associated With Enhanced Inflammation and Worsened Lipid Profile in Men.

The negative relationship between testosterone and inflammatory cytokines has been reported for decades, although the exact mechanisms of their interactions are still not clear. At the same time, little is known about the relation between androgens and acute phase proteins. Therefore, in this investigation, we aimed to study the relationship between androgen status and inflammatory acute phase reactants in a group of men using multi-linear regression analysis. Venous blood samples were taken from 149 men ranging in age from 18 to 77 years. Gonadal androgens [testosterone (T) and free testosterone (fT)], acute phase reactants [C-reactive protein (CRP), ferritin (FER), alpha-1-acid glycoprotein (AAG), and interleukin-6 (IL-6)], cortisol (C), and lipid profile concentrations were determined. It was demonstrated that the markers of T and fT were negatively correlated with all acute phase proteins (CRP, FER, and AAG; p < 0.02) and the blood lipid profile [total cholesterol (TC), low-density lipoprotein (LDL), and triglycerides (TG); p < 0.03]. Multivariate analysis showed that T, fT, and the fT/C ratio were inversely correlated with the CRP, AAG, and FER concentrations independently of age and blood lipids. When adjustment for BMI was made, T, fT, and the fT/C ratio were negatively correlated with the AAG concentrations only. In addition, it was demonstrated that gonadal androgens were positively correlated with physical activity level (p < 0.01). We have concluded that a lowered serum T concentration may promote inflammatory processes independently of adipose tissue and age through a reduced inhibition of inflammatory cytokine synthesis, which leads to enhanced acute phase protein production. Therefore, a low serum T concentration appears to be an independent risk factor in the development of atherosclerosis and cardiovascular diseases. Moreover, the positive correlation between testosterone and physical activity level suggests that exercise training attenuates the age-related decrease in gonadal androgens and, in this way, may reduce the enhancement of systemic low-grade inflammation in aging men.

Plasma BCAA concentrations during exercise of varied intensities in young healthy men-the impact of endurance training.

BACKGROUND: Branched-chain amino acids (BCAA) i.e., leucine (Leu), isoleucine (Ile) and valine (Val) are important amino acids, which metabolism play a role in maintaining system energy homeostasis at rest and during exercise. As recently shown lowering of circulating BCAA level improves insulin sensitivity and cardiac metabolic health. However, little is known concerning the impact of a single bout of incremental exercise and physical training on the changes in blood BCAA. The present study aimed to determine the impact of a gradually increasing exercise intensity-up to maximal oxygen uptake (VO2max) on the changes of the plasma BCAA [∑BCAA]pl, before and after 5-weeks of moderate-intensity endurance training (ET). METHODS: Ten healthy young, untrained men performed an incremental cycling exercise test up to exhaustion to reach VO2max, before and after ET. RESULTS: We have found that exercise of low-to-moderate intensity (up to ∼50% of VO2max lasting about 12 min) had no significant effect on the [∑BCAA]pl, however the exercise of higher intensity (above 70% of VO2max lasting about 10 min) resulted in a pronounced decrease (p < 0.05) in [∑BCAA]pl. The lowering of plasma BCAA when performing exercise of higher intensity was preceded by a significant increase in plasma lactate concentration, showing that a significant attenuation of BCAA during incremental exercise coincides with exercise-induced acceleration of glycogen utilization. In addition, endurance training, which significantly increased power generating capabilities at VO2max (p = 0.004) had no significant impact on the changes of [∑BCAA]pl during this incremental exercise. CONCLUSION: We have concluded that an exercise of moderate intensity of relatively short duration generally has no effect on the [∑BCAA]pl in young, healthy men, whereas significant decrease in [∑BCAA]pl occurs when performing exercise in heavy-intensity domain. The impact of exercise intensity on the plasma BCAA concentration seems to be especially important for patients with cardiometabolic risk undertaken cardiac rehabilitation or recreational activity.

Age-Dependent Impairment in Endothelial Function and Arterial Stiffness in Former High Class Male Athletes Is No Different to That in Men With No History of Physical Training.

Background Physical activity is generally considered to exert positive effects on the cardiovascular system in humans. However, surprisingly little is known about the delayed effect of professional physical training performed at a young age on endothelial function and arterial stiffness in aging athletes. The present study aimed to assess the impact of long-lasting professional physical training (endurance and sprint) performed at a young age on the endothelial function and arterial stiffness reported in older age in relation to glycocalyx injury, prostacyclin and nitric oxide production, inflammation, basal blood lipid profile, and glucose homeostasis. Methods and Results This study involved 94 male subjects with varied training backgrounds, including young athletes (mean age ∼25 years), older former high class athletes (mean age ∼60 years), and aged-matched untrained control groups. Aging increased arterial stiffness, as reflected by an enhancement in pulse wave velocity, augmentation index, and stiffness index (P<10-4), as well as decreased endothelial function, as judged by the attenuation of flow-mediated vasodilation (FMD) in the brachial artery (P=0.03). Surprisingly, no effect of the training performed at a young age on endothelial function and arterial stiffness was observed in the former athletes. Moreover, no effect of training performed at a young age (P>0.05) on blood lipid profile, markers of inflammation, and glycocalyx shedding were observed in the former athletes. Conclusions Our study clearly shows that aging, but not physical training history, represents the main contributing factor responsible for decline in endothelial function and increase in arterial stiffness in former athletes.

Endurance training-induced changes in the GH-IGF-I axis influence maximal muscle strength in previously untrained men.

OBJECTIVE: In this study we have determined the effects of 20weeks of endurance running training on the GH-IGF-I axis changes in the context of the skeletal muscle performance and physical capacity level. DESIGN: Before and after the endurance training program a maximal incremental exercise tests, a 1500m race and a muscle strength measurements were performed and the blood samples were taken to determine both resting as well as end-exercise serum growth hormone (GH), insulin-like growth hormone-I (IGF-I), insulin-like growth hormone binding protein-3 (IGFBP-3) and plasma interleukin-6 (IL-6) concentrations. RESULTS: 20weeks of endurance running training improved power output generated at the end of the maximal incremental test by 24% (P<0.012), 1500m running time by 13% (P<0.012) and maximal muscle strength by 9% (P<0.02). End-exercise IGF-I/IGFBP-3 ratio was decreased by 22% after the training (P<0.04) and the magnitude of IGF-I/IGFBP-3 ratio decrease (ΔIGF-I/IGFBP-3ex) was 2.3 times higher after the training (P<0.04). The magnitude of the exercise-induced changes in IGFBP-3 concentration was also significantly higher (P<0.04) and there was a trend toward lower end-exercise IGF-I concentration (P=0.08) after the training. These changes were accompanied by a significantly higher (30%) end-exercise IL-6 concentration (P<0.01) as well as by a 3.4 times higher magnitude of IL-6 increase (P<0.02) after the training. Moreover, there were strong positive correlations between changes in resting serum IGF-I concentration (ΔIGF-Ires) and IGF-I/IGFBP-3 ratio (ΔIGF-I/IGFBP-3res) and changes in muscle strength (ΔMVC) (r=0.95, P=0.0003 and r=0.90, P=0.002, respectively). CONCLUSIONS: The training-induced changes in the components of the GH-IGF-I axis may have additive effects on skeletal muscle performance and physical capacity improvement.

Moderate-intensity endurance training improves endothelial glycocalyx layer integrity in healthy young men.

NEW FINDINGS: What is the central question of this study? The main aim of the present study was to determine the effect of prolonged moderate-intensity endurance training on the endothelial glycocalyx layer integrity in relationship to the training-induced changes in oxidative stress and antioxidant defence in humans. What is the main finding and its importance? We have shown, for the first time, a protective effect of prolonged moderate-intensity endurance training on endothelial glycocalyx layer integrity, as judged by significantly lower basal and end-exercise serum concentrations of glycocalyx damage markers, i.e. syndecan-1 and heparan sulfate, accompanied by attenuation of oxidative stress and enhancement of antioxidant defence after training in previously untrained healthy young men. In this study, we evaluated the effect of 20 weeks of moderate-intensity endurance training (ET) on the endothelial glycocalyx layer integrity in relationship to the training-induced changes in antioxidant defence. Eleven healthy young, untrained men performed an incremental cycling exercise bout until exhaustion before and after 20 weeks of ET. Endurance training consisted of 40 min sessions, mainly of moderate intensity (∼50% of maximal oxygen uptake), performed four times per week. Venous blood samples were taken at rest and at the end of the maximal exercise test. Muscle biopsies from vastus lateralis were taken before and after the training. Endurance training resulted in a significant increase in physical capacity (P < 0.05) as reflected by an increase in power output reached at the lactate threshold and at maximal oxygen uptake. Training led to a decrease (P < 0.05) in basal and end-exercise concentrations of blood markers of glycocalyx damage (syndecan-1 and heparan sulfate). The lowering of glycocalyx shedding after the ET was accompanied by an attenuation of oxidative stress, as evidenced by a decrease in the basal plasma concentration of isoprostanes, and by an increase in antioxidant defence, reflected by an enhancement in superoxide dismutase 2 protein content in vastus lateralis (P < 0.05). In contrast, training did not induce a significant increase in basal nitrite/nitrate plasma concentration (P > 0.05). Moderate-intensity ET exerts a pronounced protective effect on endothelial glycocalyx integrity at rest and during exercise, probably through an improvement of antioxidant defence that may represent the vasoprotective mechanisms highly responsive to moderate-intensity endurance training.

Mechanisms of Attenuation of Pulmonary V'O2 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±SD: age 22.33±1.44 years, V'O2peak 3198±458 mL ∙ min-1) performed an endurance training composed mainly of moderate-intensity cycling, lasting 20 weeks. Training resulted in a decrease (by ~5%, P = 0.027) in V'O2 during prior low-intensity exercise (20 W) and in shortening of τp of the V'O2 on-kinetics (30.1±5.9 s vs. 25.4±1.5 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 ~5% (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.

Mechanisms responsible for the acceleration of pulmonary V̇O2 on-kinetics in humans after prolonged endurance training.

The effect of prolonged endurance training on the pulmonary V̇O2 on- and off-kinetics in humans, in relation to muscle mitochondria biogenesis, is investigated. Eleven untrained physically active men (means±SD: age 22.4±1.5 years, V̇O2peak 3,187±479 ml/min) performed endurance cycling training (4 sessions per week) lasting 20 wk. Training shortened τp of the pulmonary V̇O2 on-kinetics during moderate-intensity cycling by ∼19% from 28.3±5.2 to 23.0±4.0 s (P=0.005). τp of the pulmonary V̇O2 off-kinetics decreased by ∼11% from 33.7±7.2 to 30.0±6.6 (P=0.02). Training increased (in vastus lateralis muscle) mitochondrial DNA copy number in relation to nuclear DNA (mtDNA/nDNA) (+53%) (P=0.014), maximal citrate synthase (CS) activity (+38%), and CS protein content (+38%) (P=0.004), whereas maximal cytochrome c oxidase (COX) activity after training tended to be only slightly (+5%) elevated (P=0.08). By applying to the experimental data, our computer model of oxidative phosphorylation (OXPHOS) and using metabolic control analysis, we argue that COX activity is a much better measure of OXPHOS intensity than CS activity. According to the model, in the present study a training-induced increase in OXPHOS activity accounted for about 0-10% of the decrease in τp of muscle and pulmonary V̇O2 for the on-transient, whereas the remaining 90-100% is caused by an increase in each-step parallel activation of OXPHOS.

Skeletal muscle myosin heavy chain isoform content in relation to gonadal hormones and anabolic-catabolic balance in trained and untrained men.

Gonadal hormones and anabolic-catabolic hormone balance have potent influence on skeletal muscle tissue, but little is known about their action with regard to myosin heavy chain (MHC) transformation in humans. We investigated the relationship between skeletal muscle MHC isoform content in the vastus lateralis muscle and basal testosterone (T) concentration in 3 groups of subjects: endurance trained (E), sprint/strength trained (S), and untrained (U) young men. We have also determined basal sex hormone-binding globulin and cortisol (C) concentrations in untrained subjects to examine the relationship between MHC composition and the anabolic-catabolic hormone balance. Moreover, basal free testosterone (fT) and bioavailable testosterone (bio-T) concentrations were calculated for this subgroup. Despite significant differences in MHC isoform content (69.4 ± 2.39%, 61.4 ± 8.04%, and 37.5 ± 13.80% of MHC-2 for groups S, U, and E, respectively, Kruskal-Wallis: H = 18.58, p < 0.001), the T concentration was similar in the three groups of subjects (18.84 ± 5.73 nmol·L(-1), 18.60 ± 5.73 nmol·L(-1), and 20.73 ± 4.06 nmol·L(-1) for U, E, and S groups, respectively, Kruskal-Wallis: H = 1.11, p > 0.5). We have also found that in the U group, type 2 MHC in the vastus lateralis muscle is positively correlated with basal fT:C ratio (r = 0.63, p = 0.01). It is concluded that the differences in the training history and training specificity can be distinguished with regard to the MHC composition but not with regard to the basal T concentration. Simultaneously, it has been shown that MHC isoform content in human vastus lateralis muscle may be related to basal anabolic-catabolic hormone balance, and this hypothesis needs further investigation.

Isometric strength training lowers the O2 cost of cycling during moderate-intensity exercise.

The effect of maximal voluntary isometric strength training of knee extensor muscles on pulmonary V'O(2) on-kinetics, the O(2) cost of cycling and peak oxygen uptake (V'O(2peak)) in humans was studied. Seven healthy males (mean ± SD, age 22.3 ± 2.0 years, body weight 75.0 ± 9.2 kg, V'O(2peak) 49.5 ± 3.8 ml kg(-1) min(-1)) performed maximal isometric strength training lasting 7 weeks (4 sessions per week). Force during maximal voluntary contraction (MVC) increased by 15 % (P < 0.001) after 1 week of training, and by 19 % (P < 0.001) after 7 weeks of training. This increase in MVC was accompanied by no significant changes in the time constant of the V'O(2) on-kinetics during 6 min of moderate and heavy cycling intensities. Strength training resulted in a significant decrease (by ~7 %; P < 0.02) in the amplitude of the fundamental component of the V'O(2) on-kinetics, and therefore in a lower O(2) cost of cycling during moderate cycling intensity. The amplitude of the slow component of V'O(2) on-kinetics during heavy cycling intensity did not change with training. Training had no effect on the V'O(2peak), whereas the maximal power output reached at V'O(2peak) was slightly but significantly increased (P < 0.05). Isometric strength training rapidly (i.e., after 1 week) decreases the O(2) cost of cycling during moderate-intensity exercise, whereas it does not affect the amplitude of the slow component of the V'O(2) on-kinetics during heavy-intensity exercise. Isometric strength training can have beneficial effects on performance during endurance events.

Gonadal hormone status in highly trained sprinters and in untrained men.

It is a common view that strength and sprint trained athletes are characterized by high plasma/serum testosterone (T) concentration, which is believed to be partly responsible for their performance level. This opinion, however, has poor scientific background. The aim of this study was to give evidence-based information on this issue. We examined gonadal hormone status at rest after overnight fasting in high and top-class track and field sprinters (n = 16) and in untrained men (n = 15). It was shown that basal T, free testosterone (fT), bioavailable testosterone (bio-T), and sex hormone-binding globulin concentrations were not significantly different (p > 0.05) in sprinters vs. untrained subjects. Further comparison of the results of the basal serum T concentration in 8 sprinters showed its significant changes during an annual training period. Significantly higher T concentration during a low-intensity training period (beginning of December) than during heavy sprint specific training period (end of March) was observed in these athletes (n = 8) (mean ± SD; 23.37 ± 5.28 vs. 20.99 ± 4.74 nmol · L(-1), respectively, p = 0.04). We have concluded that basal gonadal hormone concentration in high and top-class athletes (sprinters and jumpers) did not appear to be significantly different when compared with untrained subjects. Moreover, basal T concentration in sprinters can differ significantly during an annual training period. This fact should be taken into consideration when interpreting the results of gonadal hormone status in athletes at varied training stages.

[Ventilatory efficiency during incremental exercise in relation to various types of myosin heavy chain content in vastus lateralis m. quadricipitis femoris in healthy young men]. / Efektywnosc wentyiacji pluc w wysilku fizycznym a zawartosc róznych typów ciwzkich lancuchów miozyny w miesniu czworoglowym uda u mlodych zdrowych mezczyzn.

The main aim of this study was to determine whether ventilatory efficiency during incremental exercise is related to various types of myosin heavy chain (MyHC) content in vastus lateralis in. quadricipitis femoris in young healthy men. The respiratory efficiency was expressed by VE/VCO2 slope, determined during sublactate threshold power outputs of the incremental exercise. A significant negative correlation between V(E)/VCO2 and P(ET)CO2 (amounting to: at rest r = -0.43 p < 0.05; at the LT r = -0.87 p < 0.01; at the VO2 max r = -0.95 p < 0.01) was observed. Moreover, the level of PETCO2 at rest and during exercise was not related to the MyHC content of the vastus lateralis muscle. No relationship between the content of various types of MyHC and respiratory efficiency was found.

Heart rate variability during incremental cycling exercise in healthy untrained young men.

BACKGROUND: Linear relationship between the increase of heart rate (HR) and the power output (PO) during sub-maximal exercise is well documented. However the study considering the effect of progressive increase of PO on the parameters of heart rate variability (HRV) remain scarce. AIM: This study investigated changes of the HRV time and spectral parameters in young, untrained men during incremental cycling exercise. METHODS: Fifteen young, untrained men aged 21 +/- 1.5 years participated in our study. Preliminary medical examination excluded any cardiovascular diseases. The examined individuals were cycling on the cycle ergometer (Monark 824E, Sweden) with constant frequency, amounting to 60 rev x min(-1). PO was increased by 30 W every 3 minutes. ECG was recorded via shortened limb lead I, using Dual BIO Amp (AD Instruments, Castle Hill, Australia) hardware and Power Lab (AD Instruments) software. Spectral analysis of HRV was based on the fast Fourier transformation (FFT). The time (HR, RMSSD) and spectral (LF, HF) parameters were analysed within 3 minutes time periods, before the exercise and on each level of the generated power output. RESULTS: The exercise was performed until the subjects reached 80% of the HR max expected for their age. This has occurred at the PO = 202 +/- 33 W (mean +/- SD). Mean HR in this group showed linear increase (p < 0.001) with power output (90 +/- 7 bt x min(-1) at 30 W vs. 166 +/- 11 bt x min(-1) at the power output of 202 +/- 33 W). Significant decrease of time parameters of the HRV (0 W vs. 202 +/- 33 W)--SDNN (p < 0.001) and RMSSD (p < 0.001) were observed in the analysed group. Spectral parameters of the HRV also presented significant reduction. Decreases of total power of the HRV spectrum (TP, p < 0.001), low frequency (LF, p < 0.01) and high frequency (HF, p < 0.01)) spectra as well as LF/HF ratio (p < 0.01) were noted. CONCLUSIONS: In the light of the present study, the applicability of the HRV power spectrum, with its present interpretation, to the assessment of the sympatho-vagal interaction during incremental exercise is indeed very questionable.