Effects of endurance training under calorie restriction on energy substrate metabolism in mouse skeletal muscle and liver.

We investigated whether calorie restriction (CR) enhances metabolic adaptations to endurance training (ET). Ten-week-old male Institute of Cancer Research (ICR) mice were fed ad libitum or subjected to 30% CR. The mice were subdivided into sedentary and ET groups. The ET group performed treadmill running (20-25 m/min, 30 min, 5 days/week) for 5 weeks. We found that CR decreased glycolytic enzyme activity and monocarboxylate transporter (MCT) 4 protein content, while enhancing glucose transporter 4 protein content in the plantaris and soleus muscles. Although ET and CR individually increased citrate synthase activity in the plantaris muscle, the ET-induced increase in respiratory chain complex I protein content was counteracted by CR. In the soleus muscle, mitochondrial enzyme activity and protein levels were increased by ET, but decreased by CR. It has been suggested that CR partially interferes with skeletal muscle adaptation to ET.

Better maintenance of enzymatic capacity and higher levels of substrate transporter proteins in skeletal muscle of aging female mice.

This study investigated sex-specific differences in high-energy phosphate, glycolytic, and mitochondrial enzyme activities and also metabolite transporter protein levels in the skeletal muscles of adult (5 months old), middle-aged (12 months old), and advanced-aged (24 months old) mice. While gastrocnemius glycogen content increased with age regardless of sex, gastrocnemius triglyceride levels increased only in advanced-aged female mice. Aging decreased creatine kinase and adenylate kinase activities in the plantaris muscle of both sexes and in the soleus muscle of male mice but not in female mice. Irrespective of sex, phosphofructokinase and lactate dehydrogenase (LDH) activities decreased in the plantaris and soleus muscles. Additionally, hexokinase activity in the plantaris muscle and LDH activity in the soleus muscle decreased to a greater extent in aged male mice compared with those in aged female mice. Mitochondrial enzyme activities increased in the plantaris muscle of aged female mice but did not change in male mice. The protein content of the glucose transporter 4 in the aged plantaris muscle and fatty acid translocase/cluster of differentiation 36 increased in the aged plantaris and soleus muscles of both sexes, with a significantly higher content in female mice. These findings suggest that females possess a better ability to maintain metabolic enzyme activity and higher levels of metabolite transport proteins in skeletal muscle during aging, despite alterations in lipid metabolism. Our data provide a basis for studying muscle metabolism in the context of age-dependent metabolic perturbations and diseases that affect females and males differently.

Identifying physiological determinants of 800 m running performance using post-exercise blood lactate kinetics.

PURPOSE: The aims of the present study were to investigate blood lactate kinetics following high intensity exercise and identify the physiological determinants of 800 m running performance. METHODS: Fourteen competitive 800 m runners performed two running tests. First, participants performed a multistage graded exercise test to determine physiological indicators related to endurance performance. Second, participants performed four to six 30-s high intensity running bouts to determine post-exercise blood lactate kinetics. Using a biexponential time function, lactate exchange ability (γ1), lactate removal ability (γ2), and the quantity of lactate accumulated (QLaA) were calculated from individual blood lactate recovery data. RESULTS: 800 m running performance was significantly correlated with peak oxygen consumption (r = -0.794), γ1 and γ2 at 800 m race pace (r = -0.604 and -0.845, respectively), and QLaA at maximal running speed (r = -0.657). V ˙ O2peak and γ2 at 800 m race pace explained 83% of the variance in 800 m running performance. CONCLUSION: Our results indicate that (1) a high capacity to exchange and remove lactate, (2) a high capacity for short-term lactate accumulation and, (3) peak oxygen consumption, are critical elements of 800 m running performance. Accordingly, while lactate has primarily been utilized as a performance indicator for long-distance running, post-exercise lactate kinetics may also prove valuable as a performance determinant in middle-distance running.

Metabolomic responses to high-intensity interval exercise in equine skeletal muscle: effects of rest interval duration.

High-intensity interval training has attracted considerable attention as a time-efficient strategy for inducing physiological adaptations, but the underlying mechanisms have yet to be elucidated. By using metabolomics techniques, we investigated changes in the metabolic network responses in Thoroughbred horses to high-intensity interval exercise performed with two distinct (15 min or 2 min) rest intervals. The peak plasma lactate level was higher during high-intensity exercise with a 2 min rest duration than that with a 15 min rest duration (24.5±6.8 versus 13.3±2.7 mmol l-1). The arterial oxygen saturation was lower at the end of all exercise sessions with a 2 min rest duration than that with a 15 min rest duration. Metabolomic analysis of skeletal muscle revealed marked changes in metabolite concentrations in the first and third bouts of the 15 min rest interval conditions. In contrast, there were no metabolite concentrations or pathways that significantly changed during the third bout of exercise performed with a 2 min rest interval. Our findings suggest that the activity of each energy production system is not necessarily reflected by apparent changes in metabolite concentrations, potentially due in part to a better match between metabolite flux into and out of the pathway and cycle, as well as between metabolite production and disposal. This study provides evidence that changes in metabolite concentrations vary greatly depending on the number of repetitions and the length of rest periods between exercises, even if the exercises themselves are identical.

Stride-to-stride variability and fluctuations at intensities around lactate threshold in distance runners.

Stride-to-stride variability and fluctuations in running have been widely investigated in relation to fatigue, injury, and other factors. However, no studies have examined the relationship of stride-to-stride variability and fluctuations with lactate threshold (LT), a well-known performance indicator for distance runners that represents the threshold at which fast-twitch muscle fibers are activated and the glycolytic system is hyperactivated. In this study, we examined a relationship between LT and stride-to-stride variability and fluctuations in trained middle- and long-distance runners (n = 33). All runners were asked to perform multistage graded exercise tests while wearing accelerometers on the upper surface of their shoes. The LT was determined by measuring blood lactate concentrations after each stage. Three gait parameters for each step were calculated based on the acceleration data: stride time (ST), ground contact time (CT), and peak acceleration (PA). The coefficient of variation (CV) and the long-range correlations (α) for each parameter were also calculated. The effects of the runner's group and the relative intensity for CV and α on gait parameters were evaluated using a two-way repeated measures analysis of variance. Although no significant effect was observed in the CV and α of ST, significant intensity main effects were observed for the CV and α of CT and PA. The lack of significant changes in ST might be the result of runners' adequate control of ST to minimize energy cost. All the parameters showing significant changes with increasing intensity decreased dramatically when they were close to LT. This might have been caused by an increase in physiological load near LT and be interpreted as a variation in motor control because of alternations in the mobilized muscle fibers and physiological changes around the LT. The α should be useful for non-invasive LT detection.

Sex-specific differences in the metabolic enzyme activity and transporter levels in mouse skeletal muscle during postnatal development.

Although sex-associated differences in energy metabolism in adults are well-characterized, developmental sex-specific changes in skeletal muscle metabolism are largely unknown. This study investigated sex differences in high-energy phosphate, glycolytic, and mitochondrial enzyme activities and metabolite transporter protein levels in mouse skeletal muscles during the early postnatal period (day 10), post-weaning (day 28), sexual maturity (day 56), and adult life (day 140). No significant sex-specific differences were observed on days 10 and 28, except for glucose transporter (GLUT) 4 level. The hexokinase, phosphofructokinase, and lactate dehydrogenase activities of skeletal muscle were higher and the citrate synthase, cytochrome c oxidase, and ß-hydroxyacyl-CoA dehydrogenase activities were lower in female mice than those in male mice on days 56 and 140. The GLUT4 and FAT/CD36 protein levels were higher and the monocarboxylate transporter 4 level was lower in the skeletal muscles of female mice than those of male mice, particularly on days 56 and 140. At 140 days of age, the respiratory exchange ratio during treadmill running (15 m/min, 60 min) was lower in females than that in males, despite no sex differences at rest. In summary, sex differences were not evident in the early postnatal and post-weaning periods but became apparent after the mice reached sexual maturity. These findings indicate that sexually mature animals are a better model for investigating sex differences, particularly in the context of studying energy metabolism in mice.

Effects of Endurance Training on Metabolic Enzyme Activity and Transporter Proteins in Skeletal Muscle of Ovariectomized Mice.

PURPOSE: Estrogen deficiency or insufficiency can occur under several conditions, leading to negative health outcomes. To establish an effective countermeasure against estrogen loss, we investigated the effects of endurance training on ovariectomy (OVX)-induced metabolic disturbances. METHODS: Female Institute of Cancer Research mice underwent OVX or sham operations. On day 7 of recovery, the mice were randomized to remain either sedentary or undergo 5 wk of treadmill running (15-20 m·min -1 , 60 min, 5 d·wk -1 ). During week 5 of the training, all animals performed a treadmill running test (15 m·min -1 , 60 min). RESULTS: After the experimental period, OVX resulted in greater gains in body mass, fat mass, and triglyceride content in the gastrocnemius muscle. OVX enhanced phosphofructokinase activity in the plantaris muscle and decreased lactate dehydrogenase activity in the plantaris and soleus muscles. OVX decreased the protein content of NDUFB8, a mitochondrial respiratory chain subunit, but did not decrease other mitochondrial proteins or enzyme activities. Endurance training significantly enhanced mitochondrial enzyme activity and protein content in the skeletal muscles. Although OVX increased the respiratory exchange ratio during the treadmill running test, and postexercise blood lactate levels, endurance training normalized these parameters. CONCLUSIONS: The present findings suggest that endurance training is a viable strategy to counteract the negative metabolic consequences in hypoestrogenism.

Branched-chain amino acid supplementation suppresses the detraining-induced reduction of mitochondrial content in mouse skeletal muscle.

Exercise training enhances oxidative capacity whereas detraining reduces mitochondrial content in skeletal muscle. The strategy to suppress the detraining-induced reduction of mitochondrial content has not been fully elucidated. As previous studies reported that branched-chain amino acid (BCAA) ingestion increased mitochondrial content in skeletal muscle, we evaluated whether BCAA supplementation could suppress the detraining-induced reduction of mitochondrial content. Six-week-old male Institute of Cancer Research (ICR) mice were randomly divided into four groups as follows: control (Con), endurance training (Tr), detraining (DeTr), and detraining with BCAA supplementation (DeTr + BCAA). Mice in Tr, DeTr, and DeTr + BCAA performed treadmill running exercises [20-30 m/min, 60 min, 5 times/week, 4 weeks]. Then, mice in DeTr and DeTr + BCAA were administered with water or BCAA [0.6 mg/g of body weight, twice daily] for 2 weeks of detraining. In whole skeletal muscle, mitochondrial enzyme activities and protein content were decreased after 2 weeks of detraining, but the reduction was suppressed by BCAA supplementation. Peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein content, a master regulator of mitochondrial biogenesis, was decreased by detraining irrespective of BCAA ingestion. Regarding mitochondrial degradation, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), a mitophagy-related protein, was significantly higher in the Tr group than in the DeTr + BCAA group, but not different from in the DeTr group. With respect to mitochondrial quality, BCAA ingestion did not affect oxygen consumption rate (OCR) and reactive oxygen species (ROS) production in isolated mitochondria. Our findings suggest that BCAA ingestion suppresses the detraining-induced reduction of mitochondrial content partly through inhibiting mitophagy.

Inhibition of monocarboxylate transporters (MCT) 1 and 4 reduces exercise capacity in mice.

The concept of lactate shuttle is widely accepted in exercise physiology. Lactate transport is mediated by monocarboxylate transporters (MCT), which enable cells to take up and release lactate. However, the role of lactate during exercise has not yet been fully elucidated. In this study, we investigated the effects of lactate transport inhibition on exercise capacity and metabolism in mice. Here, we demonstrated that MCT1 inhibition by α-cyano-4-hydroxycinnamate administration (4-CIN, 200 mg/g of body weight) reduced the treadmill running duration at 20 m/min. The administration of 4-CIN increased the blood lactate concentration immediately after exercise. With matched exercise duration, the muscle lactate concentration was higher while muscle glycogen content was lower in 4-CIN-administered mice. Further, we showed that MCT4 inhibition by bindarit administration (50 mg/kg of body weight) reduced the treadmill running duration at 40 m/min. Bindarit administration increased the muscle lactate but did not alter the blood lactate and glucose concentrations, as well as muscle glycogen content, immediately after exercise. A negative correlation was observed between exercise duration at 40 m/min and muscle lactate concentration immediately after exercise. Our results suggest that lactate transport via MCT1 and MCT4 plays a pivotal role in sustaining exercise.

Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle.

Recent evidence has shown that mitochondrial respiratory function contributes to exercise performance and metabolic health. Given that lactate is considered a potential signaling molecule that induces mitochondrial adaptations, we tested the hypothesis that lactate would change mitochondrial respiratory function in skeletal muscle. Male ICR mice (8 weeks old) received intraperitoneal injection of PBS or sodium lactate (1 g/kg BW) 5 days a week for 4 weeks. Mitochondria were isolated from freshly excised gastrocnemius muscle using differential centrifugation and were used for all analyses. Lactate administration significantly enhanced pyruvate + malate- and glutamate + malate-induced (complex I-driven) state 3 (maximal/ATP synthesis-coupled) respiration, but not state 2 (basal/proton conductance) respiration. In contrast, lactate administration significantly decreased succinate + rotenone-induced (complex II-driven) state 3 and 2 respiration. No significant differences were observed in malate + octanoyl-l-carnitine-induced state 3 or 2 respiration. The enzymatic activity of complex I was tended to increase and those of complexes I + III and IV were significantly increased after lactate administration. No differences were observed in the activities of complexes II or II + III. Moreover, lactate administration increased the protein content of NDUFS4, a subunit of complex I, but not those of the other components. The present findings suggest that lactate alters mitochondrial respiratory function in skeletal muscle.

Effects of endurance training on metabolic enzyme activity and transporter protein levels in the skeletal muscles of orchiectomized mice.

This study investigated whether endurance training attenuates orchiectomy (ORX)-induced metabolic alterations. At 7 days of recovery after sham operation or ORX surgery, the mice were randomized to remain sedentary or undergo 5 weeks of treadmill running training (15-20 m/min, 60 min, 5 days/week). ORX decreased glycogen concentration in the gastrocnemius muscle, enhanced phosphofructokinase activity in the plantaris muscle, and decreased lactate dehydrogenase activity in the plantaris and soleus muscles. Mitochondrial enzyme activities and protein content in the plantaris and soleus muscles were also decreased after ORX, but preserved, in part, by endurance training. In the treadmill running test (15 m/min, 60 min) after 4 weeks of training, orchiectomized sedentary mice showed impaired exercise performance, which was restored by endurance training. Thus, endurance training could be a potential therapeutic strategy to prevent the hypoandrogenism-induced decline in muscle mitochondrial content and physical performance.

Effects of glucose ingestion at different frequencies on glycogen recovery in mice during the early hours post exercise.

BACKGROUND: When a high-carbohydrate diet is ingested, whether as small frequent snacks or as large meals, there is no difference between the two with respect to post-exercise glycogen storage for a period of 24 h. However, the effect of carbohydrate intake frequency on glycogen recovery a few hours after exercise is not clear. Athletes need to recover glycogen quickly after physical exercise as they sometimes exercise multiple times a day. The aim of this study was to determine the effect of carbohydrate intake at different frequencies on glycogen recovery during the first few hours after exercise. METHODS: After 120 min of fasting, 6-week-old male ICR mice were subjected to treadmill running exercise (20 m/min for 60 min) to decrease the levels of muscle and liver glycogen. Mice were then given glucose as a bolus (1.2 mg/g of body weight [BW], immediately after exercise) or as a pulse (1.2 mg/g of BW, every 15 min × 4 times). Following this, the blood, tissue, and exhaled gas samples were collected. RESULTS: In the bolus group, blood glucose concentration was significantly lower and plasma insulin concentration was significantly higher than those in the pulse group (p < 0.05). The plantaris muscle glycogen concentration in the bolus group was 25.3% higher than that in the pulse group at 60 min after glucose ingestion (p < 0.05). Liver glycogen concentration in the pulse group was significantly higher than that in the bolus group at 120 min after glucose ingestion (p < 0.05). CONCLUSIONS: The present study showed that ingesting a large amount of glucose immediately after exercise increased insulin secretion and enhanced muscle glycogen recovery, whereas frequent and small amounts of glucose intake was shown to enhance liver glycogen recovery.

Effects of post-exercise glucose ingestion at different solution temperatures on glycogen repletion in mice.

Carbohydrate ingestion is essential for glycogen recovery after exercise. Although studies have investigated methods for enhancement of glycogen repletion with regard to nutrients and their amounts, no studies have examined the effect of temperature of the ingested solution on glycogen recovery. Therefore, this study aimed to investigate the effect of the temperature of glucose solution ingested after exercise on glycogen recovery. Seven-week-old male ICR mice were fasted for 16 h and subjected to treadmill running exercise (20 m/min for 60 min) to decrease glycogen storage. Then, the mice were administered glucose (1.5 mg/g body weight) at three different solution temperatures: 4°C, cold solution group (Cold); 37°C, mild solution group (Mild); and 55°C, hot solution group (Hot). Our results revealed that blood glucose, plasma insulin, and muscle glycogen concentrations did not differ among the three groups. In contrast, liver glycogen concentration in the Hot group was significantly higher than that in the post-exercise and Cold groups (p < 0.05). Furthermore, portal glucose concentration was significantly higher in the Hot group than in the Cold group (p < 0.01). These observations suggest that postexercise muscle glycogen repletion occurs regardless of glucose solution temperature, and that ingesting hot glucose solution after exercise can be an effective means for liver glycogen repletion compared with cold glucose solution ingestion.

Lactate administration does not affect denervation-induced loss of mitochondrial content and muscle mass in mice.

Lactate is considered to be a signaling molecule that induces mitochondrial adaptation and muscle hypertrophy. The purpose of this study was to examine whether lactate administration attenuates denervation-induced loss of mitochondrial content and muscle mass. Eight-week-old male Institute of Cancer Research mice underwent unilateral sciatic nerve transection surgery. The contralateral hindlimb served as a sham-operated control. From the day of surgery, mice were injected intraperitoneally with PBS or sodium lactate (equivalent to 1 g·kg-1 body weight) once daily for 9 days. After 10 days of denervation, gastrocnemius muscle weight decreased to a similar extent in both the PBS- and lactate-injected groups. Denervation significantly decreased mitochondrial enzyme activity, protein content, and MCT4 protein content in the gastrocnemius muscle. However, lactate administration did not have any significant effects. The current observations suggest that daily lactate administration for 9 days does not affect denervation-induced loss of mitochondrial content and muscle mass.

High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery.

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

Enhanced skeletal muscle glycogen repletion after endurance exercise is associated with higher plasma insulin and skeletal muscle hexokinase 2 protein levels in mice: comparison of level running and downhill running model.

To identify factors that influence post-exercise muscle glycogen repletion, we compared the glycogen recovery after level running with downhill running, an experimental model of impaired post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice performed endurance level running (no inclination) or downhill running (-5° inclination) on a treadmill. In Experiment 1, to determine whether these two types of exercise resulted in different post-exercise glycogen repletion patterns, tissues were harvested immediately post-exercise or 2 days post-exercise. Compared to the control (sedentary) group, level running induced significant glycogen supercompensation in the soleus muscle at 2 days post-exercise (p = 0.002). Downhill running did not induce glycogen supercompensation. In Experiment 2, mice were orally administered glucose 1 day post-exercise; this induced glycogen supercompensation in soleus and plantaris muscle only in the level running group (soleus: p = 0.005, plantaris: p = 0.003). There were significant positive main effects of level running compared to downhill running on the plasma insulin (p = 0.017) and C-peptide concentration (p = 0.011). There was no difference in the glucose transporter 4 level or the phosphorylated states of proteins related to insulin signaling and metabolism in skeletal muscle. The level running group showed significantly higher hexokinase 2 (HK2) protein content in both soleus (p = 0.046) and plantaris muscles (p =0.044) at 1 day after exercise compared to the downhill running group. Our findings suggest that post-exercise skeletal muscle glycogen repletion might be partly influenced by plasma insulin and skeletal muscle HK2 protein levels.

Performance, Metabolic, and Neuromuscular Consequences of Repeated Wingates in Hypoxia and Normoxia: A Pilot Study.

BACKGROUND: Compared with normoxia, repeated short (5-10 s) sprints (>10 efforts) with incomplete recovery (≤30 s) in hypoxia likely cause substantial performance reduction accompanied by larger metabolic disturbances and magnitude of neuromuscular fatigue. However, the effects of hypoxia on performance of repeated long (30 s) "all-out" efforts with near complete recovery (4.5 min) and resulting metabolic and neuromuscular adjustments remain unclear. PURPOSE: The intention was to compare acute performance, metabolic, and neuromuscular responses across repeated Wingates between hypoxia and normoxia. METHODS: On separate visits, 6 male participants performed 4 × 30-second Wingate efforts with 4.5-minute recovery in either hypoxia (fraction of inspired oxygen: 0.145) or normoxia. Responses to exercise (muscle and arterial oxygenation trends, heart rate, and blood lactate concentration) and the integrity of neuromuscular function in the knee extensors were assessed for each exercise bout. RESULTS: Mean (P = .80) and peak (P = .92) power outputs, muscle oxygenation (P = .88), blood lactate concentration (P = .72), and perceptual responses (all Ps > .05) were not different between conditions. Arterial oxygen saturation was significantly lower, and heart rate higher, in hypoxia versus normoxia (P < .001). Maximal voluntary contraction force and peripheral fatigue indices (peak twitch force and doublets at low and high frequencies) decreased across efforts (all Ps < .001) irrespective of conditions (all Ps > .05). CONCLUSION: Despite heightened arterial hypoxemia and cardiovascular solicitation, hypoxic exposure during 4 repeated 30-second Wingate efforts had no effect on performance and accompanying metabolic and neuromuscular adjustments.

No Influence of Acute Moderate Normobaric Hypoxia on Performance and Blood Lactate Concentration Responses to Repeated Wingates.

BACKGROUND: Training in hypoxia versus normoxia often induces larger physiological adaptations, while this does not always translate into additional performance benefits. A possible explanation is a reduced oxygen flux, negatively affecting training intensity and/or volume (decreasing training stimulus). Repeated Wingates (RW) in normoxia is an efficient training strategy for improving both physiological parameters and exercise capacity. However, it remains unclear whether the addition of hypoxia has a detrimental effect on RW performance. PURPOSE: To test the hypothesis that acute moderate hypoxia exposure has no detrimental effect on RW, while both metabolic and perceptual responses would be slightly higher. METHODS: On separate days, 7 male university sprinters performed 3 × 30-s Wingate efforts with 4.5-min passive recovery in either hypoxia (FiO2: 0.145) or normoxia (FiO2: 0.209). Arterial oxygen saturation was assessed before the first Wingate effort, while blood lactate concentration and ratings of perceived exertion were measured after each bout. RESULTS: Mean (P = .92) and peak (P = .63) power outputs, total work (P = .98), and the percentage decrement score (P = .25) were similar between conditions. Arterial oxygen saturation was significantly lower in hypoxia versus normoxia (92.0% [2.8%] vs 98.1% [0.4%], P < .01), whereas blood lactate concentration (P = .78) and ratings of perceived exertion (P = .51) did not differ between conditions. CONCLUSION: In sprinters, acute exposure to moderate hypoxia had no detrimental effect on RW performance and associated metabolic and perceptual responses.

Short-Term Repeated Wingate Training in Hypoxia and Normoxia in Sprinters.

Repeated Wingate efforts (RW) represent an effective training strategy for improving exercise capacity. Living low-training high altitude/hypoxic training methods, that upregulate muscle adaptations, are increasingly popular. However, the benefits of RW training in hypoxia compared to normoxia on performance and accompanying physiological adaptations remain largely undetermined. Our intention was to test the hypothesis that RW training in hypoxia provides additional performance benefits and more favorable physiological responses than equivalent training in normoxia. Twelve male runners (university sprinters) completed six RW training sessions (3 × 30-s Wingate "all-out" efforts with 4.5-min recovery) in either hypoxia (FiO2: 0.145, n = 6) or normoxia (FiO2: 0.209, n = 6) over 2 weeks. Before and after the intervention, participants underwent a RW performance test (3 × 30-s Wingate "all-out" efforts with 4.5-min recovery). Peak power output, mean power output, and total work for the three exercise bouts were determined. A capillary blood sample was taken for analyzing blood lactate concentration (BLa) 3 min after each of the three efforts. Peak power output (+ 11.3 ± 23.0%, p = 0.001), mean power output (+ 6.6 ± 6.8%, p = 0.001), and total work (+ 6.3 ± 5.4% p = 0.016) significantly increased from pre- to post-training, independently of condition. The time × group × interval interaction was significant (p = 0.05) for BLa. Compared to Pre-tests, BLa values during post-test were higher (+ 8.7 ± 10.3%) after about 2 in the normoxic group, although statistical significance was not reached (p = 0.08). Contrastingly, BLa values were lower (albeit not significantly) during post- compared to pre-tests after bout 2 (-9.3 ± 8.6%; p = 0.08) and bout 3 (-9.1 ± 10.7%; p = 0.09) in the hypoxic group. In conclusion, six RW training sessions over 2 weeks significantly improved RW performance, while training in hypoxia had no additional benefit over normoxia. However, accompanying BLa responses tended to be lower in the hypoxic group, while an opposite pattern was observed in the normoxic group. This indicates that different glycolytic and/or oxidative pathway adaptations were probably at play.

Short-term hypoxic training increases monocarboxylate transporter 4 and phosphofructokinase activity in Thoroughbreds.

The aim of this study was to investigate effects of short-term hypoxic training on lactate metabolism in the gluteus medius muscle of Thoroughbreds. Using crossover design (3 months washout), eight Thoroughbred horses were trained for 2 weeks in normoxia (FI O2  = 21%) and hypoxia (FI O2  = 18%) each. They ran at 95% maximal oxygen consumption (V̇O2max ) on a treadmill inclined at 6% for 2 min (3 days/week) measured under normoxia. Before and after each training period, all horses were subjected to an incremental exercise test (IET) under normoxia. Following the 2-week trainings, V̇O2max in IET increased significantly under both oxygen conditions. The exercise duration in IET increased significantly only after hypoxic training. The monocarboxylate transporter (MCT) 1 protein levels remained unchanged after training under both oxygen conditions, whereas MCT4 protein levels increased significantly after training in hypoxia but not after training in normoxia. Phosphofructokinase activity increased significantly only after hypoxic training, whereas cytochrome c oxidase activity increased significantly only after normoxic training. Our results suggest that hypoxic training efficiently enhances glycolytic capacity and levels of the lactate transporter protein MCT4, which facilitates lactate efflux from the skeletal muscle.