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Purpose: This study aimed to investigate the impact of sprint interval training (SIT) on both the acute and 3-week modulations of cell-free DNA (cfDNA), as well as its association with neuromuscular fatigue and physical performance in healthy young and old men. Methods: Ten young (20–25 year old) and nine elderly (63–72 year old) healthy men performed nine SIT sessions consisting of 4-to-6-all-out cycling repetitions of 30 s interspaced with 4-min rest intervals. We compared the maximal voluntary contractions torque, central activation ratio, low-frequency fatigue (LFF), and cfDNA concentrations between the groups before, immediately after, 1 h after, and 24 h after the first and ninth SIT sessions. Results: The plasma cfDNA levels were increased post-exercise (from 1.4 ± 0.258 to 1.91 ± 0.278 ng/ml (P < 0.01) on a log10 scale), without significant differences between the groups. However, older individuals showed a slight decrease in the baseline cfDNA values, from 1.39 ± 0.176 to 1.29 ± 0.085 ng/ml on a log10 scale, after 3 weeks (P = 0.043). Importantly, the elevation of the post-exercise cfDNA values was correlated with an increase in LFF in both groups. Three weeks of SIT induced an improvement in the recovery of LFF (main session effect, P = 0.0029); however, only the young group showed an increase in aerobic capacity (VO2max) (from 40.8 ± 6.74 to 43.0 ± 5.80 ml/kg/min, P = 0.0039). Conclusion: Three weeks of SIT diminished the baseline cfDNA values in the old group, together with an improvement in the recovery of LFF. However, VO2max was increased only in the young group. [ABSTRACT FROM AUTHOR]

Cigarette smoking is associated with a lower exercise capacity and lower muscle fatigue resistance. This is at least partly attributable to carboxyhaemoglobin (HbCO) in the blood that via reduction in the oxygen-carrying capacity, and the left-shift of the Hb-dissociation curve would reduce tissue oxygenation. On the other hand, a reduced oxygen uptake due to mitochondrial dysfunction would result in improved oxygenation. We used previously collected capillarisation, myoglobin and estimated cellular maximal muscle oxygen consumption data derived from succinate dehydrogenase-stained sections from the vastus lateralis muscle from six smokers and five non-smokers. These data were fed into an expanded Krogh tissue oxygenation model to assess whether an impaired muscle fatigue resistance in smokers is primarily due to HbCO or impaired mitochondrial respiration. The model showed that in smokers with 6% and 20% HbCO (causing a left-shift of the Hb-dissociation curve) average muscle oxygenation was reduced by 1.9% and 7.2%, respectively. Muscle oxygenation was increased by 13.3% when maximal mitochondrial respiration was reduced by 29%. A combination of a 29% reduction in maximal mitochondrial respiration and 20% HbCO led to no significant difference in muscle oxygenation from that in non-smokers. This indicates that while HbCO may explain the reduced exercise capacity after just one smoking session, in chronic smokers impaired mitochondrial respiration appears more important in reducing oxygen extraction and exercise capacity with only a small contribution of the left-shift of the Hb-dissociation curve. [ABSTRACT FROM AUTHOR]

The application of post-exercise cooling (e.g., cold water immersion) and post-exercise heating has become a popular intervention which is assumed to increase functional recovery and may improve chronic training adaptations. However, the effectiveness of such post-exercise temperature manipulations remains uncertain. The aim of this comprehensive review was to analyze the effects of post-exercise cooling and post-exercise heating on neuromuscular function (maximal strength and power), fatigue resistance, exercise performance, and training adaptations. We focused on three exercise types (resistance, endurance and sprint exercises) and included studies investigating (1) the early recovery phase, (2) the late recovery phase, and (3) repeated application of the treatment. We identified that the primary benefit of cooling was in the early recovery phase (< 1 h post-exercise) in improving fatigue resistance in hot ambient conditions following endurance exercise and possibly enhancing the recovery of maximal strength following resistance exercise. The primary negative impact of cooling was with chronic exposure which impaired strength adaptations and decreased fatigue resistance following resistance training intervention (12 weeks and 4–12 weeks, respectively). In the early recovery phase, cooling could also impair sprint performance following sprint exercise and could possibly reduce neuromuscular function immediately after endurance exercise. Generally, no benefits of acute cooling were observed during the 24–72-h recovery period following resistance and endurance exercises, while it could have some benefits on the recovery of neuromuscular function during the 24–48-h recovery period following sprint exercise. Most studies indicated that chronic cooling does not affect endurance training adaptations following 4–6 week training intervention. We identified limited data employing heating as a recovery intervention, but some indications suggest promise in its application to endurance and sprint exercise. [ABSTRACT FROM AUTHOR]

Purpose: Unaccustomed eccentric contractions generally result in a long-lasting contractile impairment, referred to as prolonged low-frequency force depression (PLFFD), and delayed-onset muscle soreness (DOMS). We here used repeated drop jumps (DJs) as an eccentric contraction model and studied the effects of increasing the time between DJs from 20 s to 5 min. We hypothesized that both PLFFD and DOMS would be less marked at the longer DJ interval due to the longer time to restore structural elements between DJs. Methods: Young men (n = 12) randomly performed 50 DJs with either 20-s (DJ-20 s) or 5-min (DJ-5 min) rest between DJs. Voluntary, 20 Hz and 100 Hz electrically stimulated isometric knee extension torques and muscle soreness were monitored before and for 7 days after DJs; serum CK activity was measured to assess muscle fibre protein leakage. In additional experiments, changes in mRNA levels were assessed in muscle biopsies collected before and 1 h after exercise. Results: A marked PLFFD was observed with both protocols and the extent of 20 Hz torque depression was smaller immediately and 1 day after DJ-5 min than after DJ-20 s (p < 0.05), whereas the MVC and 100 Hz torques were similarly decreased with the two protocols. Markedly larger differences between the two protocols were observed for the muscle soreness score, which 1–4 days after exercise was about two times larger with DJ-20 s than with DJ-5 min (p < 0.01). Conclusions: The larger protective effect of the longer DJ interval against DOMS than against PLFFD indicates that their underlying mechanisms involve different structural elements. [ABSTRACT FROM AUTHOR]

While concurrent training is regularly used in older populations, the inverse relationship between fibre size and oxidative capacity suggests that endurance training in resistance-trained individuals may result in some loss of resistance training-induced gains in muscle mass, which may be more pronounced in older people. We investigated the impact of superimposed endurance training in younger (28.5 ± 4.8 years; n = 8) and older (67.5 ± 5.5 years; n = 7) highly resistance-trained men. Participants underwent a 10-week endurance cycling training programme consisting of five 6-min intervals at 75% max heart rate (HRmax) separated by 4-min intervals at 90% HRmax. The anatomical cross-sectional area (ACSA) of the thigh muscles, as determined with MRI, was 24% smaller in older compared to younger participants (p < 0.001). Although maximal oxygen consumption (VO2max) was also lower in the older group (p < 0.001), VO2max per kg body mass did not differ significantly between younger and older participants. Histological analyses of biopsies of the m. vastus lateralis showed that endurance training induced an increase in succinate dehydrogenase activity in both younger and older participants (p ≤ 0.043), and an increase in the number of capillaries around type I fibres (p = 0.017). The superimposed endurance training did not induce a significant decrease in thigh ACSA, fibre cross-sectional area, or knee extensor maximum voluntary isometric force. These observations indicate that adding endurance training to resistance training can lead to positive endurance-related adaptations without negative consequences for muscle size and strength in older and younger resistance-trained people. [ABSTRACT FROM AUTHOR]

Purpose: Carbohydrate (CHO) restriction could be a potent metabolic regulator of endurance exercise-induced muscle adaptations. Here, we determined whether post-exercise CHO restriction following strenuous exercise combining continuous cycling exercise (CCE) and sprint interval exercise could affect the gene expression related to mitochondrial biogenesis and oxidative metabolism in human skeletal muscle. Methods: In a randomized cross-over design, 8 recreationally active males performed two cycling exercise sessions separated by 4 weeks. Each session consisted of 60-min CCE and six 30-s all-out sprints, which was followed by ingestion of either a CHO or placebo beverage in the post-exercise recovery period. Muscle glycogen concentration and the mRNA levels of several genes related to mitochondrial biogenesis and oxidative metabolism were determined before, immediately after, and at 3 h after exercise. Results: Compared to pre-exercise, strenuous cycling led to a severe muscle glycogen depletion (> 90%) and induced a large increase in PGC1A and PDK4 mRNA levels (~ 20-fold and ~ 10-fold, respectively) during the acute recovery period in both trials. The abundance of the other transcripts was not changed or was only moderately increased during this period. CHO restriction during the 3-h post-exercise period blunted muscle glycogen resynthesis but did not increase the mRNA levels of genes associated with muscle adaptation to endurance exercise, as compared with abundant post-exercise CHO consumption. Conclusion: CHO restriction after a glycogen-depleting and metabolically-demanding cycling session is not effective for increasing the acute mRNA levels of genes involved in mitochondrial biogenesis and oxidative metabolism in human skeletal muscle. [ABSTRACT FROM AUTHOR]

It has been observed that there is an inverse relationship between fiber size and oxidative capacity due to oxygen, ADP, and ATP diffusion limitations. We aimed to see if regular endurance exercise alongside a hypertrophic stimulus would lead to compromised adaptations to both, particularly in older animals. Here we investigated the effects of combining overload with regular endurance exercise in young (12 months) and old (26 months) male mice. The plantaris muscles of these mice were overloaded through denervation of synergists to induce hypertrophy and the mice ran on a treadmill for 30 min per day for 6 weeks. The hypertrophic response to overload was not blunted by endurance exercise, and the increase in fatigue resistance with endurance exercise was not reduced by overload. Old mice demonstrated less hypertrophy than young mice, which was associated with impaired angiogenesis and a reduction in specific tension. The data of this study suggest that combining endurance exercise and overload induces the benefits of both types of exercise without compromising adaptations to either. Additionally, the attenuated hypertrophic response to overload in old animals may be due to a diminished capacity for capillary growth. [ABSTRACT FROM AUTHOR]

This correction notice is for an article titled "A modelling approach to disentangle the factors limiting muscle oxygenation in smokers" published in the European Journal of Applied Physiology. The correction addresses an error in the affiliation details for one of the authors, Tomas Venckunas. The correct affiliation should be Lithuanian Sports University in Kaunas, Lithuania, not the Department of Life Sciences at Manchester Metropolitan University in the UK. The publisher, Springer Nature, emphasizes their neutrality regarding jurisdictional claims and institutional affiliations. The authors of the article are Hans Degens, Tomas Venckunas, and Rob Cl Wüst. [Extracted from the article]

We hypothesized that endurance athletes have lower muscle power than power athletes due to a combination of weaker and slower muscles, while their higher endurance is attributable to better oxygen extraction, reflecting a higher muscle oxidative capacity and larger stroke volume. Endurance (n = 87; distance runners, road cyclists, paddlers, skiers), power (n = 77; sprinters, throwers, combat sport athletes, body builders), team (n = 64; basketball, soccer, volleyball) and non-athletes (n = 223) performed a countermovement jump and an incremental running test to estimate their maximal anaerobic and aerobic power (VO2max), respectively. Dynamometry and M-mode echocardiography were used to measure muscle strength and stroke volume. The VO2max (L min-1) was larger in endurance and team athletes than in power athletes and non-athletes (p < 0.05). Athletes had a larger stroke volume, left ventricular mass and left ventricular wall thickness than non-athletes (p < 0.02), but there were no significant differences between athlete groups. The higher anaerobic power in power and team athletes than in endurance athletes and non-athletes (p < 0.001) was associated with a larger force (p < 0.001), but not faster contractile properties. Endurance athletes (20.6%) had a higher (p < 0.05) aerobic:anaerobic power ratio than controls and power and team athletes (14.0-15.3%). The larger oxygen pulse, without significant differences in stroke volume, in endurance than power athletes indicates a larger oxygen extraction during exercise. Power athletes had stronger, but not faster, muscles than endurance athletes. The similar VO2max in endurance and team athletes and similar jump power in team and power athletes suggest that concurrent training does not necessarily impair power or endurance performance. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to examine the effect of acute blood flow restriction during the late recovery phase between two resistance exercise bouts on muscular endurance and oxygenation.Methods: Amateur male middle- and long-distance runners performed two bouts of one-leg dynamic plantar flexion exercise to failure with the load equivalent to 75% of maximum. Subjects were randomly assigned into two experimental groups with thigh occlusion pressure between bouts at either 120 or 200 mmHg with 20 min of passive rest in between, and two control groups without any blood flow restriction separated by either 5 or 20 min of rest. Blood flow restriction in the experimental groups was implemented during the last 15 min of recovery. Calf arterial blood flow and muscle oxygenation were measured by venous occlusion plethysmography and near-infrared spectroscopy, respectively.Results: Decrease of muscular oxygenation and blood flow during recovery between exercise bouts depended on the applied occlusion pressure. When compared with bout 1, work capacity in the experimental groups during bout 2 was reduced by 9.3 ± 2.2% with 120 mmHg and by 10.5 ± 3.1% (p < 0.05) with 200 mmHg occlusion pressure. In the control groups, work capacity was restored after 20 min (- 3.9 ± 3.2%, p > 0.05) but not after 5-min recovery (- 20.0 ± 1.8%, p < 0.05).Conclusions: Blood flow restriction late in recovery after a heavy resistance exercise bout decreased muscle oxygenation and work capacity during the subsequent heavy resistance exercise bout. [ABSTRACT FROM AUTHOR]

Competitive athletics is often associated with moderate left ventricular (LV) hypertrophy. The aim of this study was to shed more light on the extent and type of cardiac hypertrophic response to different athletic conditioning in females. Standard two-dimensional M-mode and Doppler echocardiography was performed at rest in Caucasian female sprinters (n = 10) and long-distance runners (n = 10) of similar age (range 16-34 years), training experience (5-18 years) and competitive level, and in age-matched healthy female sedentary controls (n = 10). No differences in echocardiographic parameters were detected between female sprinters and sedentary controls (p > 0.05). Interventricular septum and LV wall (p < 0.05) were thicker, and LV mass was greater (p < 0.01) in long-distance runners as compared with sprinters or sedentary controls. Absolute LV diameter was not increased in long-distance runners (p > 0.05), though relative LV diameter was higher in long-distance runners as compared to sprinters (p < 0.05). As compared with controls, relative wall thickness (the sum of LV wall thickness and interventricular septum thickness divided by LV diameter) was higher (p = 0.004) in long-distance runners. Neither systolic nor diastolic LV parameters were different among the groups (p > 0.05). In conclusion, sprint running training has not been found to induce alterations in cardiac morphology or function at rest in female athletes. Cardiac mass in female long-distance runners is higher mainly due to myocardial wall thickening, while integral myocardial function at rest is not affected as a consequence of either this hypertrophy or sprint training. [ABSTRACT FROM AUTHOR]

The coactivator PGC-1α1 is activated by exercise training in skeletal muscle and promotes fatigue-resistance. In exercised muscle, PGC-1α1 enhances the expression of kynurenine aminotransferases (Kats), which convert kynurenine into kynurenic acid. This reduces kynurenine-associated neurotoxicity and generates glutamate as a byproduct. Here, we show that PGC-1α1 elevates aspartate and glutamate levels and increases the expression of glycolysis and malate-aspartate shuttle (MAS) genes. These interconnected processes improve energy utilization and transfer fuel-derived electrons to mitochondrial respiration. This PGC-1α1-dependent mechanism allows trained muscle to use kynurenine metabolism to increase the bioenergetic efficiency of glucose oxidation. Kat inhibition with carbidopa impairs aspartate biosynthesis, mitochondrial respiration, and reduces exercise performance and muscle force in mice. Our findings show that PGC-1α1 activates the MAS in skeletal muscle, supported by kynurenine catabolism, as part of the adaptations to endurance exercise. This crosstalk between kynurenine metabolism and the MAS may have important physiological and clinical implications. PGC-1α is activated by exercise and promotes resistance to fatigue in muscles. Here, the authors show that PGC-1α activates the malate-aspartate shuttle, and allows muscle to utilise kynurenine, leading to more efficient glucose oxidation and mitochondrial respiration. [ABSTRACT FROM AUTHOR]