ABSTRACT
Evidence suggests that positive pacing strategy improves exercise performance and fatigue tolerance in athletic events lasting 1-5 min. This study investigated muscle metabolic responses to positive and negative pacing strategies in Thoroughbred horses. Eight Thoroughbred horses performed 2 min treadmill running using positive (1 min at 110% maximal O2 uptake [VÌO2max], followed by 1 min at 90% VÌO2max) and negative (1 min at 90% VÌO2max, followed by 1 min at 110% VÌO2max) pacing strategies. The arterial-mixed venous O2 difference did not significantly differ between the two strategies. Plasma lactate levels increased toward 2 min, with significantly higher concentrations during positive pacing than during negative pacing. Muscle glycogen level was significantly lower at 1 and 2 min of positive pacing than those of negative pacing. Metabolomic analysis showed that the sum of glycolytic intermediates increased during the first half of positive pacing and the second half of negative pacing. Regardless of pacing strategy, the sum of tricarboxylic acid cycle metabolites increased during the first half but remained unchanged thereafter. Our data suggest that positive pacing strategy is likely to activate glycolytic metabolism to a greater extent compared to negative pacing, even though the total workload is identical.
Subject(s)
Glycogen , Lactic Acid , Physical Conditioning, Animal , Animals , Horses , Physical Conditioning, Animal/physiology , Lactic Acid/blood , Lactic Acid/metabolism , Glycogen/metabolism , Oxygen Consumption , Muscle, Skeletal/metabolism , Male , Exercise Test , Glycolysis , Female , Citric Acid CycleABSTRACT
Individual variations in peripheral oxygen saturation (SpO2) during repeated sprints in hypoxia and their impact on exercise performance remain unclear despite fixed external hypoxic stimuli (inspired oxygen fraction: FiO2). This study examined SpO2 individual variations during repeated sprints in hypoxia and their impact on exercise performance. Thirteen highly-trained sprint runners performed 10 × 10-s cycle sprints with 30-s passive recoveries in normobaric hypoxia (FiO2: 0.150). Mean power output (MPO), post-sprint SpO2, and heart rate for each sprint were assessed. Sprint decrement score (Sdec), evaluating fatigue development, was calculated using MPO variables. Participants were categorized into a high saturation group (HiSat, n = 7) or a low saturation group (LowSat, n = 6) based on their mean post-sprint SpO2 (measured 10-15 s after each sprint). Individual mean post-sprint SpO2 ranged from 91.6% to 82.2%. Mean post-sprint SpO2 was significantly higher (P < 0.001, d = 1.54) in HiSat (89.1% ± 1.5%) than LowSat (84.7% ± 1.6%). A significantly larger decrease in Sdec (P = 0.008, d = 1.68) occurred in LowSat (-22.3% ± 2.3%) compared to HiSat (-17.9% ± 2.5%). MPO (P = 0.342 d = 0.55) and heart rate (P = 0.225 d = 0.67) did not differ between groups. There was a significant correlation (r = 0.61; P = 0.028) between SpO2 and Sdec. In highly-trained sprint runners, individual responses to hypoxia varied widely and significantly affected repeated sprint ability, with greater decreases in SpO2 associated with larger performance alterations (i.e., larger decrease in Sdec).
ABSTRACT
Blood lactate concentration during exercise is a reliable indicator of energy metabolism and endurance performance. Lactate is also present in sweat, and sweating plays an important role in thermoregulation, especially in hot conditions. Recently, wearable sensors have enabled the real-time and noninvasive measurement of sweat lactate concentration, potentially serving as an alternative indicator of blood lactate response. However, the evidence regarding the relationship between sweat and blood lactate responses during incremental exercise in hot conditions is lacking. In a randomized cross-over design, six highly trained male runners completed two incremental treadmill tests under normal (20°C/50%RH) or hot (30°C/50%RH) conditions. The tests include 3-min running stages and 1-min recovery, starting at 12 km/h and increasing by 1 km/h at each stage. Blood and sweat lactate concentrations were measured at each stage to determine blood and sweat lactate thresholds (LT). Blood lactate concentrations were higher under hot conditions (p < 0.01), but there was no difference in the response pattern or velocity at blood LT between conditions. Significant early increase (p < 0.01) in sweat lactate and low velocity at sweat LT (p < 0.05) were observed under hot conditions. A significant correlation between blood and sweat lactate concentrations was found under normal conditions (p < 0.001) but not under hot conditions, and no significant correlations were observed between the velocity at blood and sweat LT. In conclusion, sweat lactate concentration does not consistently reflect blood lactate concentration during incremental exercise.
ABSTRACT
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.
Subject(s)
Caloric Restriction , Energy Metabolism , Liver , Monocarboxylic Acid Transporters , Muscle, Skeletal , Physical Conditioning, Animal , Animals , Muscle, Skeletal/metabolism , Male , Mice , Caloric Restriction/methods , Liver/metabolism , Physical Conditioning, Animal/physiology , Energy Metabolism/physiology , Monocarboxylic Acid Transporters/metabolism , Mice, Inbred ICR , Endurance Training/methods , Glucose Transporter Type 4/metabolism , Adaptation, Physiological/physiology , Citrate (si)-Synthase/metabolism , Muscle ProteinsABSTRACT
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.
Subject(s)
Aging , Muscle, Skeletal , Animals , Muscle, Skeletal/metabolism , Female , Male , Aging/metabolism , Mice , Glycogen/metabolism , Glucose Transporter Type 4/metabolism , Adenylate Kinase/metabolism , L-Lactate Dehydrogenase/metabolism , Sex Factors , Creatine Kinase/metabolism , Hexokinase/metabolism , Triglycerides/metabolism , Phosphofructokinases/metabolism , Glycolysis/physiologyABSTRACT
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 Ë 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.
ABSTRACT
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 (15â min or 2â min) rest intervals. The peak plasma lactate level was higher during high-intensity exercise with a 2â min rest duration than that with a 15â min rest duration (24.5±6.8 versus 13.3±2.7â mmolâ l-1). The arterial oxygen saturation was lower at the end of all exercise sessions with a 2â min rest duration than that with a 15â min rest duration. Metabolomic analysis of skeletal muscle revealed marked changes in metabolite concentrations in the first and third bouts of the 15â 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 2â 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.
Subject(s)
Muscle, Skeletal , Physical Conditioning, Animal , Humans , Animals , Horses , Muscle, Skeletal/physiology , Exercise Therapy , Oxygen Consumption/physiology , RestABSTRACT
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.
ABSTRACT
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.
Subject(s)
Energy Metabolism , Muscle, Skeletal , Male , Mice , Female , Animals , Muscle, Skeletal/physiology , Electron Transport Complex IV/metabolism , Glycolysis , Hexokinase/metabolismABSTRACT
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.
Subject(s)
Endurance Training , Physical Conditioning, Animal , Animals , Female , Humans , Mice , Estradiol , Estrogens , Muscle, Skeletal/metabolism , Ovariectomy , Physical Conditioning, Animal/physiology , Triglycerides/metabolismABSTRACT
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.
Subject(s)
Amino Acids, Branched-Chain , Mitochondria , Male , Mice , Animals , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism , Amino Acids, Branched-Chain/metabolism , Mitochondria/metabolism , Muscle, Skeletal/metabolism , Dietary SupplementsABSTRACT
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.
Subject(s)
Monocarboxylic Acid Transporters , Symporters , Animals , Body Weight , Exercise Tolerance , Glycogen/metabolism , Lactic Acid/metabolism , Mice , Monocarboxylic Acid Transporters/metabolism , Muscle Proteins/metabolism , Muscle, Skeletal/metabolism , Symporters/metabolismABSTRACT
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.
ABSTRACT
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.
Subject(s)
Endurance Training , Physical Conditioning, Animal , Running , Animals , Glycogen/metabolism , Mice , Muscle, Skeletal/metabolism , Physical Conditioning, Animal/physiology , Physical Endurance/physiologyABSTRACT
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.
Subject(s)
Glucose , Liver Glycogen/metabolism , Physical Conditioning, Animal/physiology , Animals , Blood Glucose , Dietary Carbohydrates/administration & dosage , Glucose/administration & dosage , Insulin/blood , Male , Mice , Mice, Inbred ICR , Muscle, SkeletalABSTRACT
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.
Subject(s)
Glucose/metabolism , Glycogen/metabolism , Physical Conditioning, Animal/methods , Temperature , Animals , Eating , Glucose/administration & dosage , Liver/metabolism , Male , Mice , Mice, Inbred ICR , Muscle, Skeletal/metabolism , Muscle, Skeletal/physiologyABSTRACT
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.
Subject(s)
Lactic Acid , Muscle Denervation , Animals , Lactic Acid/metabolism , Male , Mice , Mitochondria , Muscle, Skeletal/metabolism , Sciatic Nerve/metabolismABSTRACT
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.
Subject(s)
Diet, Carbohydrate Loading/methods , Dietary Carbohydrates/pharmacology , Glucose Transport Proteins, Facilitative/metabolism , Glycogen/metabolism , Muscle, Skeletal/metabolism , Animals , Blood Glucose/metabolism , Glucose/administration & dosage , Jejunum/drug effects , Male , Mice , Models, Animal , Physical Conditioning, Animal/physiologyABSTRACT
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.
Subject(s)
Glycogen/metabolism , Hexokinase/metabolism , Insulin/blood , Muscle, Skeletal/metabolism , Physical Conditioning, Animal , Physical Exertion , Animals , Male , Mice , Mice, Inbred ICRABSTRACT
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.