Skeletal muscle fiber type-specific expressions of mechanosensors integrin-linked kinase, talin, and vinculin and their modulation by loading and environmental conditions in humans.

Mechanosensors control muscle integrity as demonstrated in mice. However, no information is available in human muscle about the distribution of mechanosensors and their adaptations to mechanical loading and environmental conditions (hypoxia). Here, we hypothesized that mechanosensors show fiber-type-specific distributions and that loading and environmental conditions specifically regulate mechanosensors. We randomly subjected 28 healthy males to one of the following groups (n = 7 each) consisting of nine loading sessions within 3 weeks: normoxia moderate (NM), normoxia intensive (NI), hypoxia moderate (HM), and hypoxia intensive (HI). We took six biopsies: pre (T0), 4 h (T1), and 24 h (T2) after the third as well as 4 h (T3), 24 h (T4), and 72 h (T5) after the ninth training session. We analyzed subjects' maximal oxygen consumption (V̇O2 max), maximal power output (Pmax), muscle fiber types and cross-sectional areas (CSA), fiber-type-specific integrin-linked kinase (ILK) localizations as well as ILK, vinculin and talin protein and gene expressions in dependence on loading and environmental conditions. V̇O2 max increased upon NM and HM, Pmax upon all interventions. Fiber types did not change, whereas CSA increased upon NI and HI, but decreased upon HM. ILK showed a type 2-specific fiber type localization. ILK, vinculin, and talin protein and gene expressions differed depending on loading and environmental conditions. Our data demonstrate that mechanosensors show fiber type-specific distributions and that exercise intensities rather than environmental variables influence their profiles in human muscles. These data are the first of their kind in human muscle and indicate that mechanosensors manage the mechanosensing at a fiber-type-specific resolution and that the intensity of mechanical stimulation has a major impact.

The magnitude and time-course of physiological responses to 9 weeks of incremental ramp testing.

PURPOSE: The aims of this study were to assess (1) the day-to-day variability in, and (2) the magnitude and time-course of adaptation of physiological parameters (i.e., maximal oxygen uptake [VO2 max], heart rate [HR], blood lactate concentration, respiratory exchange ratio [RER], ratings of perceived exertion [RPE], and time-to-exhaustion [TTE]) in response to an intervention involving three incremental ramp tests per week for 9 weeks. METHODS: Twelve participants (25 ± 4 yrs, VO2 max, 47.8 ± 5.2 mL∙min-1 ∙kg-1 (means ± SD)) completed the entire experimental procedure. The tests comprised a 5-min constant workload to obtain submaximal parameters followed by an incremental protocol until exhaustion. RESULTS: The mean day-to-day variability for the maximal value of VO2 was 2.8%, 1.1% for HR, 18.1% for blood lactate concentration, 2.1% for RER, 1.1% for RPE, and 5.0% for TTE. The values for the corresponding submaximal variables were 3.8% for VO2 , 2.1% for HR, 15.6% for blood lactate concentration, 2.6% for RER and 6.0% for RPE. VO2 max (+4.7% ± 3.5%), TTE (+17.9% ± 8.6%), and submaximal HR (-3.2 ± 3.5%) improved significantly. Except for RPE (p < 0.01), there were no alterations in the coefficient of variation for any parameter. On the group level, the first changes greater than the day-to-day variability in VO2 max, TTE, and submaximal HR were observed after 21, 12, and 9 training sessions, respectively. CONCLUSION: Based on our findings, we recommend that training studies include assessment of the reliability of the measurements, for example, the CVs in the specific laboratory to be able to judge if the changes detected are actually physiological.

Repeated and Interrupted Resistance Exercise Induces the Desensitization and Re-Sensitization of mTOR-Related Signaling in Human Skeletal Muscle Fibers.

The acute resistance exercise (RE)-induced phosphorylation of mTOR-related signaling proteins in skeletal muscle can be blunted after repeated RE. The time frame in which the phosphorylation (p) of mTORS2448, p70S6kT421/S424, and rpS6S235/236 will be reduced during an RE training period in humans and whether progressive (PR) loading can counteract such a decline has not been described. (1) To enclose the time frame in which pmTORS2448, prpS6S235/236, and pp70S6kT421/S424 are acutely reduced after RE occurs during repeated RE. (2) To test whether PR will prevent that reduction compared to constant loading (CO) and (3) whether 10 days without RE may re-increase blunted signaling. Fourteen healthy males (24 ± 2.8 yrs.; 1.83 ± 0.1 cm; 79.3 ± 8.5 kg) were subjected to RE with either PR (n = 8) or CO (n = 6) loading. Subjects performed RE thrice per week, conducting three sets with 10−12 repetitions on a leg press and leg extension machine. Muscle biopsies were collected at rest (T0), 45 min after the first (T1), seventh (T7), 13th (T13), and 14th (X-T14) RE session. No differences were found between PR and CO for any parameter. Thus, the groups were combined, and the results show the merged values. prpS6S235/236 and pp70s6kT421/S424 were increased at T1, but were already reduced at T7 and up to T13 compared to T1. Ten days without RE re-increased prpS6S235/236 and pp70S6kT421/S424 at X-T14 to a level comparable to that of T1. pmTORS2448 was increased from T1 to X-T14 and did not decline over the training period. Single-fiber immunohistochemistry revealed a reduction in prpS6S235/236 in type I fibers from T1 to T13 and a re-increase at X-T14, which was more augmented in type II fibers at T13 (p < 0.05). The entity of myofibers revealed a high heterogeneity in the level of prpS6S235/236, possibly reflecting individual contraction-induced stress during RE. The type I and II myofiber diameter increased from T0 and T1 to T13 and X-T14 (p < 0.05) prpS6S235/236 and pp70s6kT421/S424 reflect RE-induced states of desensitization and re-sensitization in dependency on frequent loading by RE, but also by its cessation.

Effects of Endurance Exercise Bouts in Hypoxia, Hyperoxia, and Normoxia on mTOR-Related Protein Signaling in Human Skeletal Muscle.

Przyklenk, A, Aussieker, T, Gutmann, B, Schiffer, T, Brinkmann, C, Strüder, HK, Bloch, W, Mierau, A, and Gehlert, S. Effects of endurance exercise bouts in hypoxia, hyperoxia, and normoxia on mTOR-related protein signaling in human skeletal muscle. J Strength Cond Res 34(8): 2276-2284, 2020-This study investigated the effects of short-term hypoxia (HY), hyperoxia (PER), and normoxia on anabolic signaling proteins in response to an acute bout of moderate endurance exercise (EEX) before and after an endurance exercise training intervention. Eleven healthy male subjects conducted one-legged cycling endurance exercise (3 × 30 min·wk for 4 weeks). One leg was trained under hypoxic (12% O2) or hyperoxic conditions (in a randomized cross-over design), and the other leg was trained in normoxia (20.9% O2) at the same relative workload. Musculus vastus lateralis biopsies were taken at baseline (T0) as well as immediately after the first (T1) and last (T2) training session to analyze anabolic signaling proteins and the myofiber cross-sectional area (FCSA). No significant differences were detected for FCSA between T0 and T2 under all oxygen conditions (p > 0.05). No significant differences (p > 0.05) were observed for BNIP3, phosphorylated RSK1, ERK1/2, FoxO3a, mTOR, and S6K1 between all conditions and time points. Phosphorylated Akt/PKB decreased significantly (p < 0.05) at T1 in PER and at T2 in HY and PER. Phosphorylated rpS6 decreased significantly (p < 0.05) at T1 only in PER, whereas nonsignificant increases were shown in HY at T2 (p = 0.10). Despite no significant regulations, considerable reductions in eEF2 phosphorylation were detected in HY at T1 and T2 (p = 0.11 and p = 0.12, respectively). Short-term hypoxia in combination with moderate EEX induces favorable acute anabolic signaling responses in human skeletal muscle.

Endurance training alters YKL40, PERM1, and HSP70 skeletal muscle protein contents in men with type 2 diabetes mellitus.

BACKGROUND: The fight against type 2 diabetes mellitus (T2DM) is tremendously challenging. This pilot study investigates whether endurance training (3 times per week for 3 months, moderate intensity) can change the skeletal muscle protein contents of chitinase-3-like protein-1 (YKL40), peroxisome proliferator-activated receptor y coactivator-1 and estrogen-related receptor-induced regulator in muscle-1 (PERM1) and heat-shock protein-70 (HSP70), which have been discussed as novel therapeutically relevant targets. METHODS: Muscle biopsies were obtained from overweight/obese men with T2DM (n = 7, years = 63 ± 9) at T1 (6 weeks pre-training), T2 (1 week pre-training) and T3 (3 to 4 days post-training). The protein levels of YKL40, PERM1, and HSP70 were determined by immunohistochemistry. RESULTS: YKL40, PERM1, and HSP70 were significantly upregulated following endurance training (T2-T3: +103%, +61%, +89%, p = 0.012, p = 0.010, p = 0.028). There was a fiber type-specific distribution of HSP70 with increased protein contents in type I fibers. A significant change in the fiber type distribution with an increase in type I fibers and a decrease in type II fibers was observed post-training. There were no significant differences for YKL40, PERM1, HSP70, or the fiber type distribution between T1 and T2. CONCLUSION: The training-induced upregulation of YKL40, PERM1, and HSP70 could help manage the diabetic disease and reduce its complications.

Influence of endurance training on skeletal muscle mitophagy regulatory proteins in type 2 diabetic men.

BACKGROUND: Mitophagy is a form of autophagy for the elimination of mitochondria. Mitochondrial content and function are reduced in the skeletal muscle of patients with type 2 diabetes mellitus (T2DM). Physical training has been shown to restore mitochondrial capacity in T2DM patients, but the role of mitophagy has not been examined in this context. This study analyzes the impact of a 3-month endurance training on important skeletal muscle mitophagy regulatory proteins and oxidative phosphorylation (OXPHOS) complexes in T2DM patients. METHODS: Muscle biopsies were obtained from eight overweight/obese T2DM men (61±10 years) at T1 (6 weeks pre-training), T2 (1 week pre-training), and T3 (3 to 4 days post-training). Protein contents were determined by Western blotting. RESULTS: The training increased mitochondrial complex II significantly (T2-T3: +29%, p = 0.037). The protein contents of mitophagy regulatory proteins (phosphorylated form of forkhead box O3A (pFOXO3A), mitochondrial E3 ubiquitin protein ligase-1 (MUL1), Bcl-2/adenovirus E1B 19-kD interacting protein-3 (BNIP3), microtubule-associated protein 1 light chain-3B (the ratio LC3B-II/LC3B-I was determined)) did not differ significantly between T1, T2, and T3. CONCLUSIONS: The results imply that training-induced changes in OXPHOS subunits (significant increase in complex II) are not accompanied by changes in mitophagy regulatory proteins in T2DM men. Future studies should elucidate whether acute exercise might affect mitophagic processes in T2DM patients (and whether a transient regulation of mitophagy regulatory proteins is evident) to fully clarify the role of physical activity and mitophagy for mitochondrial health in this particular patient group.

Endurance Exercise in Hypoxia, Hyperoxia and Normoxia: Mitochondrial and Global Adaptations.

We hypothesized short-term endurance exercise (EN) in hypoxia (HY) to exert decreased mitochondrial adaptation, peak oxygen consumption (VO2peak) and peak power output (PPO) compared to EN in normoxia (NOR) and hyperoxia (PER). 11 male subjects performed repeated unipedal cycling EN in HY, PER, and NOR over 4 weeks in a cross-over design. VO2peak, PPO, rate of perceived exertion (RPE) and blood lactate (Bla) were determined pre- and post-intervention to assess physiological demands and adaptation. Skeletal muscle biopsies were collected to determine molecular mitochondrial signaling and adaptation. Despite reduced exercise intensity (P<0.05), increased Bla and RPE levels in HY revealed higher metabolic load compared to PER (P<0.05) and NOR (n.s.). PPO increased in all groups (P<0.05) while VO2peak and mitochondrial signaling were unchanged (P>0.05). Electron transport chain complexes tended to increase in all groups with the highest increase in HY (n.s.). EN-induced mitochondrial adaptability and exercise capacity neither decreased significantly in HY nor increased in PER compared to NOR. Despite decreased exercise intensity, short term EN under HY may not necessarily impair mitochondrial adaptation and exercise capacity while PER does not augment adaptation. HY might strengthen adaptive responses under circumstances when absolute training intensity has to be reduced.

Intense Resistance Exercise Promotes the Acute and Transient Nuclear Translocation of Small Ubiquitin-Related Modifier (SUMO)-1 in Human Myofibres.

Protein sumoylation is a posttranslational modification triggered by cellular stress. Because general information concerning the role of small ubiquitin-related modifier (SUMO) proteins in adult skeletal muscle is sparse, we investigated whether SUMO-1 proteins will be subjected to time-dependent changes in their subcellular localization in sarcoplasmic and nuclear compartments of human type I and II skeletal muscle fibers in response to acute stimulation by resistance exercise (RE). Skeletal muscle biopsies were taken at baseline (PRE), 15, 30, 60, 240 min and 24 h post RE from 6 male subjects subjected to a single bout of one-legged knee extensions. SUMO-1 localization was determined via immunohistochemistry and confocal laser microscopy. At baseline SUMO-1 was localized in perinuclear regions of myonuclei. Within 15 and up to 60 min post exercise, nuclear SUMO-1 localization was significantly increased (p < 0.01), declining towards baseline levels within 240 min post exercise. Sarcoplasmic SUMO-1 localization was increased at 15 min post exercise in type I and up to 30 min post RE in type II myofibres. The changing localization of SUMO-1 proteins acutely after intense muscle contractions points to a role for SUMO proteins in the acute regulation of the skeletal muscle proteome after exercise.

High force development augments skeletal muscle signalling in resistance exercise modes equalized for time under tension.

How force development and time under tension (TUT) during resistance exercise (RE) influence anabolic signalling of skeletal muscle is incompletely understood. We hypothesized that high force development during RE is more important for post-exercise-induced signalling than submaximal and fatiguing RE with lower force development but similar TUT. Twenty-two male subjects (24 ± 6 years, 181 ± 9 cm, 79 ± 2 kg) performed three distinct RE modes in the fed state with equal TUT but distinct force output: (i) maximal eccentric RE (ECC, n = 7) three sets, eight reps, 100% eccentric dynamic force; (ii) standard RE (STD, n = 7), three sets, 10 reps, 75% dynamic force; and (iii) high fatiguing single-set RE (HIT, n = 8), 20 reps, 100% eccentric-concentric force; vastus lateralis biopsies were collected at baseline, 15, 30, 60, 240 min and 24 h after RE, and the signalling of mechanosensitive and mammalian target of rapamycin (mTOR)-related proteins was determined. The phosphorylation levels of pFAK(Tyr397), pJNK(Thr183/Tyr185), pAKT(Thr308/Ser473), pmTOR(Ser2448), p4E-BP1(Thr37/46), p70s6k(Thr389)/(Ser421/Thr424) and pS6(Ser235/236) were significantly higher in ECC than those in STD and HIT at several time points (P < 0.01). pJNK(Thr183/Tyr185) and pS6(Ser235/236) levels were significantly higher in type II myofibres in ECC compared with STD and HIT. HIT exerted throughout the weakest signalling response. We conclude that high force development during acute RE is superior for anabolic skeletal muscle signalling than fatiguing RE with lower force output but similar TUT. Our results suggest that this response is substantially driven by the higher activation of type II myofibres during RE.

Early functional outcome of two different orthotic concepts in ankle sprains: a randomized controlled trial.

INTRODUCTION: Purpose of the study was the evaluation of the early functional outcome of patients with an acute ankle sprain treated either with a semirigid, variable, phase-adapted modular ankle orthosis or an invariable orthotic reference device. MATERIALS AND METHODS: Forty-seven patients with acute ankle sprain grade II or more were included. In addition, 77 healthy controls as a reference were investigated. The injured subjects were treated with one of the two devices by random for 6 weeks. Ankle scores (FAOS, AOFAS) were taken at baseline after injury, 1 and 3 months after injury. Functional performance tests (balance platform, zig zag run, shuttle run, vertical drop jump) were performed at 1 and 3 months after injury. RESULTS: No significant score differences could be found between the two intervention groups except for achieving a preinjury activity level after 3 months only in the modular orthosis group. Postural functional performances (balance test) also showed no significant differences whereas the results of the agility tests revealed small but significant better results in the modular orthosis group in comparison to the invariable orthosis group. Cohen's effect sizes were high. CONCLUSION: Differences between the two intervention groups were marginal and very small but significant and--regarding Cohen's effect sizes--effective. Especially relating to functional performance, this might be a careful indication that a more effective strategy for promoting a protected, rapid recovery to physical activity after ankle sprains might be achieved by applying a phase-adapted ankle orthosis. Especially in athletic patients, phase-adapted orthosis should be further investigated and considered to ensure fully protected ligament healing as well as to regain early functional recovery.

Kinesio taping and jump performance in elite female track and field athletes and jump performance in elite female track and field athletes.

CONTEXT: The application of kinesio tape (KT) to lower-extremity muscles as an ergogenic aid to improve muscle-strength-related parameters such as jumping is controversial. OBJECTIVE: To test the hypothesis that the application of KT enhances the jumping performance of healthy uninjured elite female track and field athletes. DESIGN: A double 1-legged jump test was performed before and after the application of blue K-Active tape without traction on the maximally stretched gastrocnemius, hamstrings, rectus femoris, and iliopsoas muscles according to the generally accepted technique. PARTICIPANTS: 18 German elite female track and field athletes (age 21 ± 2 y, height 172 ± 4 cm, body mass 62 ± 5 kg, active time in their sport 13 ± 4 y). RESULTS: Factorial analysis of variance with repeated measures (ANOVA, Bonferroni) revealed no significant differences in jumping performance between the tests (P > .05, d = 0.26). CONCLUSIONS: These findings suggest that the application of KT has no influence on jumping performance in healthy, uninjured female elite athletes. The authors do not recommend the use of KT for the purpose of improving jump performance.

Evaluation of changes in the haemoglobin of skin and muscle tissue of the calf, as induced by topical application of a nonivamide/nicoboxil cream.

Topical agents like nonivamide and nicoboxil induce hyperaemisation and increase cutaneous blood flow and temperature. This study aimed to determine the effects of a nonivamide-nicoboxil cream on haemodynamics in the skin and calf muscle, via optical spectroscopy, discriminating between the changes for skin and muscle. Optical spectroscopy was applied in the visible (VIS) and near-infrared (NIR) wavelength range. The study determined the effect of the cream on changes in oxygenated (ΔoxyHb) and deoxygenated (ΔdeoxyHb) haemoglobin in skin and muscle, as well as on tissue oxygen saturation (SO2) in the skin of 14 healthy subjects. The left and right calves of the subjects were either treated with nonivamide-nicoboxil cream or were sham-administered. NIR spectroscopy allows noninvasive in-vivo examination of the oxygenation of human skeletal muscle. Topical administration of the nonivamide-nicoboxil cream significantly increased the concentration of oxygenated haemoglobin and tissue oxygen saturation in the skin, as well as the concentration of oxygenated haemoglobin in the muscle of the treated legs after 15 min, but with stronger and faster effects in the skin. The topical application of the nonivamide-nicoboxil cream increased blood flow in (smaller vessels of) the skin and muscle tissues.

The impact of increased blood lactate on serum S100B and prolactin concentrations in male adult athletes.

S100B is an astroglial protein that is increased in the peripheral bloodstream after traumatic brain injury (TBI). Elevated serum levels of S100B have been shown to be predictive of mild TBI. Furthermore, physical activity (PA) can affect S100B levels. Interestingly, increased serum S100B concentrations have been detected in athletes without apparent TBI. Such increases could be attributed to tissue hypoperfusion reflected by blood lactate concentrations [BLa(-)] and/or increased serotonergic activity reflected by prolactin (PRL). The impact of increased blood lactates on peripheral S100B levels per se are yet unknown. The purpose of our study was to investigate if increased blood lactate induced by sodium lactate infusion, without the "side effects" of PA, resulted in changes in serum S100B and PRL. Twelve male adults were given a sodium lactate infusion for a period of 24 min by a perfusor with an infusion rate of 0.01 mL kg(-1) min(-1), increased every 3 min. The main outcome measures showed no increase in serum S100B (p > 0.05). Prolactin increased significantly (p < 0.05) after [BLa(-)] exceeded a concentration of 4 mmol L(-1). Furthermore, the expected values of blood lactate achieved peak values ranging from 11 to 15 mmol L(-1). We conclude that neither increased blood lactate nor serum PRL play an exclusive role in the regulation of S100B. Nevertheless, PA should be surveyed in medical history and critically assessed in determining the severity of TBI, especially in sports. Further studies are needed to clarify the impact of PA on the biomarker S100B.

Training-induced alterations of skeletal muscle mitochondrial biogenesis proteins in non-insulin-dependent type 2 diabetic men.

This study investigates whether regular physical activity (moderate endurance or resistance training twice a week for 3 months) influences the key regulatory molecules of mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α), nuclear respiratory factor-1 (NRF1), and mitochondrial transcription factor A (TFAM)) in patients suffering from non-insulin-dependent type 2 diabetes mellitus (T2DM) (n = 16, years = 62 ± 7, body mass index (BMI) = 30 ± 4 kg/m(2)). Seven T2DM men took part in endurance training, and 9 men participated in resistance training. BMI-matched non-diabetic male control subjects (CON) (n = 7, years = 53 ± 6, BMI = 30 ± 4 kg/m(2)) were studied for comparison. The protein contents of PGC1α, NRF1, and TFAM were determined using immunohistochemical staining methods on biopsies taken from the musculus vastus lateralis. At baseline, no differences were observed in NRF1-density between the T2DM men and the CON, while the contents of PGC1α and TFAM were decreased in the T2DM men. PGC1α and TFAM contents were not changed in the T2DM patients after the training period, but NRF1 was decreased. The down-regulation of mitochondrial signaling molecules might explain the patho-physiological reduction in mitochondrial biogenesis found in T2DM. Physical training, as performed in our study, did not reverse the down-regulation of mitochondrial signaling molecules--at least not after 3 months. [corrected].

Mechanical and physiological effects of varying pole weights during Nordic walking compared to walking.

The study investigated the effect of varying pole weights on energy expenditure, upper limb muscle activation and on forces transmitted to the poles during Nordic walking (NW). Twelve women [age = 21 (2) years, body mass = 60.8 (6) kg, height = 1.71 (0.06) m] participated in five 7-min walking tests randomly chosen without poles (W), with normal NW poles (NW) or with added masses of 0.5 kg (NW + 0.5) 1.0 kg (NW + 1.0) or 1.5 kg (NW + 1.5) at a speed of 2 m s(-1). Heart rate (HR), relative oxygen uptake ([Formula: see text]), blood lactate (La) and rate of perceived exertion (RPE) were registered along with surface EMG (SEMG) from biceps brachii, triceps brachii, trapecius and deltoideus muscles. Inbuilt force transducers measured reaction forces along the long axes of the poles. NW + 0.5 and NW + 1.5 showed significant increases for [Formula: see text] and RPE compared with W (p < 0.05) but with no respective differences within NW. SEMG revealed higher activation of biceps brachii for all NW tests plus added masses compared to W (p < 0.05). Additionally the activation of biceps brachii was higher for NW + 1.5 compared to NW (p < 0.05). The contribution to overall activation duration of triceps brachii became lower but increased for biceps brachii with heavier poles. The increased energy expenditure during NW can be attributed to intensified muscle activation during forward swing of the poles. Heavier poles have no effect on energy expenditure compared to NW with usual poles but enhance muscular activity. Since there are no benefits concerning physiological and biomechanical parameters we do not recommend the use of heavier NW poles.

The influence of resistance training on patients with metabolic syndrome--significance of changes in muscle fiber size and muscle fiber distribution.

People who are afflicted with "metabolic syndrome" exhibit multiple coronary disease risk factors such as insulin resistance, hypertension, hyperlipidemia, or obesity. Twenty-six volunteers (13 women and 13 men) with such disease risk factors (56 ± 5 years) participated in a 14-week resistance training program. Given the fact that resistance training may improve cardiometabolic parameters, the fasting total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides, insulin, glucose value, homeostatic model assessment (HOMA) index, and blood pressure and body mass index (BMI) were measured before and after the training intervention. In addition, muscle biopsies from the vastus lateralis muscle of 11 of the men and 5 of the women were analyzed to determine whether changes in the muscle morphology influence the cardiometabolic parameters. Resistance training resulted in a significant increase in fasting HDL for the entire group (from 44.35 ± 9.43 to 48.57 ± 10.96 mg·dl(-1), p = 0.016). No other blood parameter changed significantly. No change was observed in the HOMA index, blood pressure, or BMI. The muscle fiber type distribution did not change, but a significant hypertrophy of muscle fibers was evident (an increase of the ellipse minor axis of 67.3 ± 16.6 to 72.1 ± 12.3 µm, p = 0.004). Moderate intensity resistance training, as was performed in our study, induces hypertrophic impulses but does not seem to have a clear positive influence on cardiometabolic risk factors. However, 2 sessions of moderate intensity resistance training per week can enhance the fasting HDL cholesterol in middle-aged subjects.

Pre-exposure to hyperoxic air does not enhance power output during subsequent sprint cycling.

Previous studies have indicated that aerobic pathways contribute to 13-27% of the energy consumed during short-term (10-20 s) sprinting exercise. Accordingly, the present investigation was designed to test the hypothesis that prior breathing of oxygen-enriched air (F(in)O(2) = 60%) would enhance power output and reduce fatigue during subsequent sprint cycling. Ten well-trained male cyclists (mean +/- SD age, 25 +/- 3 years; height, 186.1 +/- 6.9 cm; body mass, 79.1 +/- 8.2 kg; maximal oxygen uptake [VO(2max)]: 63.2 +/- 5.2 ml kg(-1) min(-1)) took 25 breaths of either hyperoxic (HO) or normoxic (NO) air before performing 15 s of cycling at maximal exertion. During this performance, the maximal and mean power outputs were recorded. The concentration of lactate, pH, partial pressure of and saturation by oxygen, [H(+)] and base excess in arterial blood were assessed before and after the sprint. The maximal (1,053 +/- 141 for HO vs. 1,052 +/- 165 W for NO; P = 0.77) and mean power outputs (873 +/- 123 vs. 876 +/- 147 W; P = 0.68) did not differ between the two conditions. The partial pressure of oxygen was approximately 2.3-fold higher after inhaling HO in comparison to NO, while lactate concentration, pH, [H(+)] and base excess (best P = 0.32) after sprinting were not influenced by exposure to HO. These findings demonstrate that the peak and mean power outputs of athletes performing short-term intense exercise cannot be improved by pre-exposure to oxygen-enriched air.

Three Weeks of Detraining Does Not Decrease Muscle Thickness, Strength or Sport Performance in Adolescent Athletes.

The purpose of this study was to examine the effects of detraining following a block (BLOCK) or daily undulating periodized (DUP) resistance training (RT) on hypertrophy, strength, and athletic performance in adolescent athletes. Twenty-one males (age = 16 ± 0.7 years; range 15-18 years) were randomly assigned to one of two 12-week intervention groups (three full-body RT sessions per week): BLOCK (n = 9); DUP (n = 12). Subsequently a three-week detraining period was applied. Body mass, fat mass (FM), fat-free mass (FFM), muscle mass, muscle thickness (rectus femoris, vastus lateralis and triceps brachii), one-repetition maximum squat and bench press, countermovement jump (CMJ), peak power calculated from CMJ (Ppeak), medicine ball put distance, and 36.58m sprint were recorded before and after RT as well as after detraining. BLOCK and DUP were equally effective for improvements of athletic performance in young athletes. Both groups displayed significantly (ρ ≤ 0.05) higher values of all measures after RT except FM, which was unchanged. Only FM increased (p = 0.010; ES = 0.14) and FFM decreased (p = 0.018; ES = -0.18) after detraining. All other measurements were unaffected by the complete cessation of training. Values were still elevated compared to pre-training. Linear regression showed a strong correlation between the percentage change by resistance training and the decrease during detraining for CMJ (R2 = 0.472) and MBP (R2 = 0.629). BLOCK and DUP RT seem to be equally effective in adolescent athletes for increasing strength, muscle mass, and sport performance. In addition, three weeks of detraining did not affect muscle thickness, strength, or sport performance in adolescent athletes independent of previous resistance training periodization model used.

Evidence for Training-Induced Changes in miRNA Levels in the Skeletal Muscle of Patients With Type 2 Diabetes Mellitus.

Physical training can improve glycemic control in patients with type 2 diabetes mellitus (T2DM). However, the underlying mechanisms are not entirely clear. An interesting piece of the puzzle could be the regulation of micro-RNAs (miRNAs). They are important modulators of protein expression. Some miRNAs were found to be both linked to poor glycemic control/insulin resistance (with evidence from in vivo and/or in vitro studies) and dysregulated in the skeletal muscle of T2DM patients. This pilot study examines whether a 3-month endurance training program [three times a week, 70-80% peak heart rate (HRpeak)] can down-regulate their levels in T2DM men (n = 7). One skeletal muscle biopsy sample was obtained from each patient at T1 (6 weeks pre-intervention), one at T2 (1 week pre-intervention) and one at T3 (3-4 days post-intervention). miRNA-27a-3p, -29a-3p, -29b-3p, -29c-3p, -106b-5p, -135a-5p, -143-3p, -144-3p, -194-5p, and - 206 levels were determined by RT-qPCR. Friedman ANOVA and post-hoc tests showed that miRNA-29b-3p, -29c-3p and -135a-5p levels were significantly reduced post-training (T3 vs. T2 and/or T1). Glycated hemoglobin (HbA1c) and HOMA insulin resistance index did not change significantly. However, HbA1c was reduced in 6 of 7 patients post-training. Furthermore, Spearman's rank correlation analyses with all values from all time points showed significant negative associations between miRNA-29c-3p, -106b-5p, -144-3p and -194-5p levels and cardiorespiratory fitness (VO2peak). The study results imply that regular exercise and improving one's physical fitness is helpful for the regulation of skeletal muscle miRNAs in T2DM patients. Whether or not changes in the miRNA profile can affect the clinical situation of T2DM patients warrants further research.