Effects of electrical stimulation of the lower extremities on postprandial hyperglycemia and arterial stiffness.

PURPOSE: To compare the acute effects of electrical stimulation (ES) of the lower extremities on postprandial hyperglycemia and arterial stiffness during oral glucose tolerance testing (OGTT). METHODS: In a randomized crossover study, eight healthy young men completed three experimental trials in which they underwent ES for 30 min, starting 60 min before (Before) or 30 min after (After) ingesting 75 g of glucose; ES was not performed in the control trial (Control). The subjects' blood glucose levels and brachial-ankle pulse wave velocity (baPWV) were measured as an index of arterial stiffness at baseline and 30, 60, and 120 min after glucose ingestion. Serum insulin levels were measured at baseline and 60 min after glucose ingestion. RESULTS: The subjects' glucose intake led to an increase in their blood glucose concentration in all trials, however, in the After trial, ES resulted in significantly lower blood glucose concentrations at 60 min post glucose ingestion compared to the Control and Before trials. The area under the curve (AUC) of serum insulin concentrations during the OGTT in the After trial was significantly lower than that in the other two trials. Moreover, glucose ingestion did not increase the baPWV, however, 30 min of ES during the postprandial state acutely reduced the baPWV. CONCLUSION: These results suggest that ES is most effective in reducing postprandial hyperglycemia when administered after a meal. Thus, lower extremity ES may be an alternative exercise method to activate postprandial glucose metabolism in healthy individuals.

Effect of curcumin supplementation on inflammatory status and muscle damage in competitive female soccer players: a placebo-controlled, singleblind, nonrandomized, crossover pilot study.

PURPOSE: Curcumin, a major component of turmeric, has anti-inflammatory and antioxidative properties, which are associated with protective effects against muscle damage. This study examined the effects of dietary curcumin on inflammation and muscle damage in female competitive soccer players. METHODS: A single-blinded, placebo-controlled, nonrandomized, crossover pilot study was conducted. Six competitive female soccer players (20.0 ± 2.0 yearsold) who participated in a 2-week preseason training program were assigned to two conditions: placebo and curcumin. The participants ingested a placebo or curcumin dosage (270 mg/day) during 2 weeks of preseason training, with 1 week of washout. Fasting blood samples were collected under resting conditions before (day 0) and after (day 15) the training period to examine changes in the concentration of interleukin 6 (IL-6), an inflammatory marker, and indices reflective of muscle damage. RESULTS: Curcumin decreased the concentration of IL-6 released (mean decrease, -30.2 ± 28.1%), whereas no decrease was observed in the placebo condition (13.4 ± 17.4%). Changes in plasma IL-6 concentrations were significantly greater in the curcumin condition than in the placebo condition (p < 0.05). However, curcumin supplementation had no significant effects on muscle damage indices. CONCLUSION: The present study shows that curcumin supplementation could attenuate inflammation, as indicated by IL-6 concentrations, in competitive female soccer players during the training period.

Eccentric exercise improves myocardial oxygen supply/demand balance with decelerating aortic diastolic pressure decay: The acute and chronic studies.

Both eccentric (ECC) and concentric (CON) exercises improve energy expenditure and blood lipid profile. Although ECC exercise has a more beneficial effect on these factors than CON exercise, its benefits on vital organs are still unclear. This study investigated the mode-of-action-dependent effects on myocardial perfusion index. Seventeen healthy men (age: 26 ± 5 years) were randomly enrolled in CON (n = 9) and ECC (n = 8) groups. Transient exercise and regular training (three-day a week for 4-week) included bicep curl comprising 5-set of 10-repetition, each using 75% one-repetition maximum concentric loading. The ECC group performed one-repetition of ECC for 3-s and CON for 1-s, while the CON group performed one-repetition of CON for 3-s and ECC for 1-s. All participants were assessed for subendocardial viability ratio (SEVR, myocardial perfusion index) and aortic diastolic pressure decay. Before study, these were found to be same for both groups. Transient (ΔSEVR: 20.3 ± 13.3%, p = 0.01; Δdecay: -0.07 ± 0.02 s-1, p < .001) and regular (ΔSEVR: 18.5 ± 12.8%, p = .001; Δdecay: -0.06 ± 0.05 s-1, p = .004) ECC (but not CON) exercises significantly increased SEVR and decelerated decay. Increased SEVR with ECC exercise was associated with decelerated decay (transient ECC: r2 = 0.56, 95% confidence interval [CI] = -0.95 to -0.10, p = .03; regular ECC: r2 = 0.53, 95% CI = -0.95 to -0.05, p = .04). These findings suggest that ECC exercise improves myocardial perfusion and diastolic pressure contour is involved in physiological mechanisms.

Effects of Dietary Vitamin D Deficiency on Markers of Skeletal Muscle Mitochondrial Biogenesis and Dynamics.

We examined the effects of dietary vitamin D deficiency on markers of mitochondrial biogenesis and dynamics in rat soleus muscle. Male Wistar rats were fed a chow with no vitamin D (No-D; 0 IU/kg) or a moderate dose (Mod-D; 2,000 IU/kg) of vitamin D chow for 8 wk. Compared to the Mod-D group, at 8 wk the No-D group showed significantly lower serum 25(OH)D levels. Although vitamin D deficiency had no effect on body composition, the No-D rats showed significantly decreased levels of PGC-1α, a marker of skeletal muscle mitochondrial biogenesis, and DRP1, a marker of skeletal muscle mitochondrial fission. The change in the PGC-1α protein expression and the serum 25(OH)D concentrations were significantly correlated. The change in DRP1 protein expression and the serum 25(OH)D concentrations tended to be correlated. There was no significant between-group difference in markers of mitochondrial fusion (MFN2 and OPA1) and mitophagy (PARKIN) in soleus muscle, and no relationship with serum 25(OH)D concentrations. Collectively our findings suggest that dietary vitamin D deficiency decreased PGC-1α and DRP1 protein expression in rat soleus muscle.

Effect of Taurine on the Regulation of Glucose Uptake in the Skeletal Muscle.

Diabetes is so common in Japan as to be called a national disease. Taurine, a free amino acid found abundantly in mammalian tissues that is also a key ingredient of many "energy drinks," has been shown to be effective in improving the hyperglycemic state caused by diabetes. Taurine administration is associated with increased insulin secretion from the pancreas, higher levels of insulin signaling-related factors, and higher expression of the glucose transporter, GLUT4. Skeletal muscle is the main target organ of insulin: Via cell surface GLUT4 molecules, myocytes take up blood glucose, enabling skeletal muscle contraction. The enhancing effect of taurine on blood glucose uptake in skeletal muscle has not been fully studied, and little is known about its mechanism. This review article summarizes what is known about the effects of taurine on insulin secretion from the pancreas and especially blood glucose uptake in skeletal muscle.

Taurine supplementation enhances endurance capacity by delaying blood glucose decline during prolonged exercise in rats.

Taurine enhances physical performance; however, the underlying mechanism remains unclear. This study examined the effect of taurine on the overtime dynamics of blood glucose concentration (BGC) during endurance exercise in rats. Male F344 rats were subjected to transient treadmill exercise until exhaustion following 3 weeks of taurine supplementation or non-supplementation (TAU and CON groups). Every 10 min during exercise, BGC was measured in blood collected through cannulation of the jugular vein. Gluconeogenesis-, lipolysis-, and fatty acid oxidation-related factors in the plasma, liver, and skeletal muscles were also analyzed after 120-min run. Exercise time to exhaustion was significantly longer with taurine supplementation. BGC in the two groups significantly increased by 40 min and gradually and significantly decreased toward the respective exhaustion point. The decline in BGC from the peak at 40 min was significantly slower in the TAU group. The time when the once-increased BGC regressed to the 0-time level was significantly and positively correlated with exercise time until exhaustion. At the 120-min point, where the difference in BGC between the two groups was most significant, plasma free fatty acid concentration and acetyl-carnitine and N-acetyltaurine concentrations in skeletal muscle were significantly higher in the TAU group, whereas glycogen and glucogenic amino acid concentrations and G6Pase activity in the liver were not different between the two groups. Taurine supplementation enhances endurance capacity by delaying the decrease in BGC toward exhaustion through increases of lipolysis in adipose tissues and fatty acid oxidation in skeletal muscles during endurance exercise.

Egg White Protein Promotes Developmental Growth in Rodent Muscle Independently of Leucine Content.

BACKGROUND: Leucine has unique anabolic properties, serving as a nutrient signal that stimulates muscle protein synthesis. OBJECTIVE: We tested whether the leucine concentration is the only factor determining protein quality for muscle development. METHODS: We selected 3 dietary proteins: casein (CAS), egg white protein (EWP), and albumin (ALB), representing the leucine concentrations of ∼8.3%, 7.7%, and 6.7% of the total protein (wt:wt), respectively. In the chronic feeding experiment, these proteins were pair-fed to growing male Wistar rats [110-135 g body weight (BW)] for 14 d as a protein source, providing 10% of total energy intake, after which soleus and extensor digitorum longus (EDL) muscles were used to estimate muscle growth. In the acute administration experiment, we injected CAS, ALB, and EWP to rats by oral gavage (0.3 g protein/100 g BW), and after 1 or 3 h EDL muscle was excised for capillary electrophoresis-MS-based metabolomics. In another chronic feeding experiment, rats were pair-fed either CAS or a CAS diet supplemented with arginine to the same level as in the EWP diet for 14 d. RESULTS: At the end of the 14-d feeding, soleus and EDL muscle weight was 20% and 17% higher, respectively, when rats were fed EWP as compared with CAS (P < 0.05). In addition, the 14-d EWP diet increased the expression of p70S6K by 117% compared with CAS (P < 0.05). These results suggest the possibility that some amino acids (excluding leucine), derived from EWP, promote muscle growth. Metabolomics analysis showed that muscle arginine concentration, following acute protein administration, appeared to match muscle growth over the 14-d feeding period. In addition, 14-d arginine supplementation to a CAS diet increased EDL muscle weight by 15% when compared with the plain CAS diet (P < 0.05). CONCLUSIONS: EWP promotes rat developmental muscle growth compared with CAS, which can be partly explained by the arginine-rich EWP.

Stature is negatively associated with increased arterial stiffness after high-intensity bicep curls training in young Japanese men.

Reports have indicated that high-intensity resistance training (RT) increases or does not change arterial stiffness. Meanwhile, higher stature has been suggested to have a protective effect on cardiovascular disease and arterial stiffness. Stature could explain the disagreement in the reported effects of RT on arterial stiffness. This study was aimed at investigating whether stature is related to RT-induced change in arterial stiffness. Thirty-six young Japanese men were assigned to the control (n = 15) and training groups (n = 21). RT programme consisted of supervised bicep curls 3 days per week for 4 weeks (5 sets of 10 repetitions at 75% of 1-repetition maximum). Arterial compliance (AC) and ß-stiffness index (via combination of ultrasound and carotid pressure waveforms) were measured in all participants. To verify the effect of stature on RT-induced change in arterial stiffness, the training group was divided into tertiles of stature: lower, middle, and higher stature groups (each group, n = 7). RT significantly decreased AC and increased ß-stiffness index in only the lower stature group (both, P < 0.05). Moreover, stature was positively associated with decreased AC and negatively associated with increased ß-stiffness index, even after adjusting for confounders including changes in relative strength, pulse pressure, and arterial distension (P < 0.05). The present results suggest that short stature contributes to the increase in arterial stiffness induced by RT in young Japanese men. The present findings suggest that stature should be taken into consideration when designing/engaging in RT programme, due to potential implications for cardiovascular health. HighlightsParticipants were divided into 3 groups according to tertiles of statures, and arterial stiffness of lower stature group (range of stature: 161.0-169.8 cm) increased after resistance training in young Japanese men, but not middle and higher stature group.Stature was negatively associated with the changed arterial stiffness by resistance training.This study suggests that short stature contributes to the elevation in arterial stiffness elicited by resistance training.

N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises.

During endurance exercises, a large amount of mitochondrial acetyl-CoA is produced in skeletal muscles from lipids, and the excess acetyl-CoA suppresses the metabolic flux from glycolysis to the TCA cycle. This study evaluated the hypothesis that taurine and carnitine act as a buffer of the acetyl moiety of mitochondrial acetyl-CoA derived from the short- and long-chain fatty acids of skeletal muscles during endurance exercises. In human subjects, the serum concentrations of acetylated forms of taurine (NAT) and carnitine (ACT), which are the metabolites of acetyl-CoA buffering, significantly increased after a full marathon. In the culture medium of primary human skeletal muscle cells, NAT and ACT concentrations significantly increased when they were cultured with taurine and acetate or with carnitine and palmitic acid, respectively. The increase in the mitochondrial acetyl-CoA/free CoA ratio induced by acetate and palmitic acid was suppressed by taurine and carnitine, respectively. Elevations of NAT and ACT in the blood of humans during endurance exercises might serve the buffering of the acetyl-moiety in mitochondria by taurine and carnitine, respectively. The results suggest that blood levels of NAT and ACT indicate energy production status from fatty acids in the skeletal muscles of humans undergoing endurance exercise.

Short-term running exercise alters DNA methylation patterns in neuronal nitric oxide synthase and brain-derived neurotrophic factor genes in the mouse hippocampus and reduces anxiety-like behaviors.

Running exercise has beneficial effects on brain health. However, the effects of relatively short-term running exercise (STEx) on behavior, and its underlying signaling pathways, are poorly understood. In this study, we evaluated the possibility that the regulation by STEx of brain-derived neurotrophic factor (BDNF) and neuronal nitric oxide synthase (nNOS, encoded by NOS1), which are important molecules for anxiety regulation, might involve mechanisms of epigenetic modification, such as DNA methylation. C57BL/6J male mice were divided into sedentary (SED, n = 12) and STEx (EX, n = 15) groups; STEx was conducted with the mice for a duration of 11 days. STEx reduced anxiety-like behaviors, and STEx reduced Nos1α and increased Bdnf exon I and IV mRNA levels in the hippocampus. Interestingly, behavioral parameters were associated with Bdnf exon I and IV and Nos1α mRNA levels in the ventral, but not dorsal, hippocampal region. However, STEx had no effect on peroxisome proliferator-activated receptor-γ coactivator 1α (Pgc-1α) or fibronectin type III domain-containing 5 (Fndc5) mRNA levels, which are relatively long-term exercise-induced upstream regulators of BDNF. In parallel with gene expression changes, we found, for the first time, that STEx downregulated Bdnf promoter IV and upregulated Nos1 DNA methylation levels in the hippocampus, and these patterns were partially different between the dorsal and ventral regions. These findings suggest that the beneficial effects of running exercise on mood regulation may be controlled by alterations in epigenetic mechanisms, especially in the ventral hippocampus. These effects occur even after a relatively short-term period of exercise.

Acute bout of exercise downregulates thioredoxin-interacting protein expression in rat contracting skeletal muscles.

We previously reported that in rat skeletal muscle, disuse (i.e., decreased muscle contractile activity) rapidly increases thioredoxin-interacting protein (TXNIP), which is implicated in the reduced glucose uptake. Accordingly, we sought herein to (a) determine the effect of exercise (i.e., increased muscle contractile activity) on muscle TXNIP protein expression, and (b) elucidate the mechanisms underlying the changes of TXNIP protein expression in response to exercise. Rat epitrochlearis and soleus muscles were dissected out after an acute bout of 3-hr swimming (without weight loading) or 3-hr treadmill running (15% grade at 9m/min). In a separate protocol, the isolated epitrochlearis and soleus muscles were incubated for 3 hr with AMP-dependent protein kinase activator AICAR. Immediately after the cessation of the 3-hr swimming, the TXNIP protein was decreased in epitrochlearis but not in soleus muscle. Conversely, 3-hr treadmill running decreased the TXNIP protein in soleus but not in epitrochlearis muscle. TXNIP protein was decreased concomitantly with reduced postexercise muscle glycogen, showing that a decrease in TXNIP protein expression occurs in muscles that are recruited during exercise. In addition, 3-hr incubation with AICAR decreased TXNIP protein in both isolated epitrochlearis and soleus muscles. Our results suggest that (a) an acute bout of exercise downregulates TXNIP protein expression in rat contracting skeletal muscles, and (b) the reduction in TXNIP protein expression in contracting muscles is probably mediated by AMPK activation, at least in part.

Relationship between early-onset muscle soreness and indirect muscle damage markers and their dynamics after a full marathon.

BACKGROUND/OBJECTIVE: Muscle soreness and damage occurs after completing a full marathon. Here we refer to muscle soreness induced by prolonged running as early-onset muscle soreness (EOMS) because muscle soreness and damage markers induced after prolonged running are different from delayed-onset muscle soreness (DOMS) and muscle damage markers induced after eccentric contraction, such as resistance exercise. The dynamics and relationship between muscle damage markers and EOMS are unclear; therefore, in this study, we aimed to elucidate the relationship between EOMS and indirect muscle damage markers, and their dynamics after a full marathon. METHODS: The following measurements were performed in 19 subjects who completed a full marathon: perceived muscle soreness (using a numeric rating scale), thigh circumference (CIR), hip joint range of motion (ROM), jump height (JH) and muscle damage marker activities in the blood (CK, AST, LDH, ALD) before (Pre), after (Post) and every day for 4 days after a full marathon (D1-4). RESULTS: EOMS was induced, as determined by the numeric rating scale score peaking immediately after a full marathon. ROM and JH significantly decreased and all muscle damage markers significantly increased after a full marathon. Serum CK and AST peaked at D1. Serum LDH and ALD peaked at Post and D3. Each marker showed different dynamics. CIR significantly decreased after a full marathon. CONCLUSION: Muscle soreness peaked and muscle damage markers in the blood showed different dynamics after a full marathon. In other words, this is different from DOMS.

LDH isoenzyme 5 is an index of early onset muscle soreness during prolonged running.

BACKGROUND: Muscle soreness is also induced during prolonged running such as a full marathon, and muscle soreness and increased damage markers are detected immediately after such a running. We named this muscle soreness, early onset muscle soreness (EOMS). Additionally, lactate dehydrogenase (LDH) level which has some isoenzyme is increased immediately after prolonged exercise. However, it is unclear that EOMS is related to muscle damage markers on prolonged running. This study aimed to determine at which point EOMS, and muscle damage markers are related to EOMS during prolonged running. METHODS: We studied 11 male subjects who habitually perform aerobic exercise. They ran 30 km at 90% of ventilatory threshold intensity. Every 10 km, we estimated perceived muscle soreness, and sampled blood to measure muscle and liver damage, inflammation, and oxidative stress (d-ROM and BAP) markers. RESULTS: Muscle soreness score lower limbs were significantly appeared at 20 km compared to that at 0 km. Serum lactate dehydrogenase (LDH) level increased at 30 km compared to that at 0 km. LDH isoenzymes 3, 4, and 5, and neutrophils significantly increased at 30 km compared to those at 0 km. Serum LDH isoenzyme 5 and change in aspartate aminotransferase significantly increased at 20 km. In addition, there was a significant correlation between the thigh NRS and amount of serum LDH isoenzyme 5 from 0 km to 20 km. d-ROM and BAP increased at 10 km compared to those at 0 km. CONCLUSIONS: EOMS started to occur at 20 km during a 30 km running task. Our data suggest that LDH isoenzyme 5 is a marker of occurrence in EOMS during prolonged running.

Effects of Taurine Supplementation on Vascular Endothelial Function at Rest and After Resistance Exercise.

High-intensity resistance exercise has been shown to increase arterial stiffness and reduce vascular endothelial function. Taurine supplementation has a favorable effect on maintaining vascular function. We had previously reported that taurine supplementation attenuated increases in resistance exercise-induced arterial stiffness. In the present study, we further investigate the effects of taurine supplementation on vascular endothelial function at rest and after resistance exercise.Twenty-nine healthy men were recruited and randomly assigned to either the placebo supplement group (n = 14) or the taurine supplement group (n = 15) in a double-blinded manner. Subjects were required to ingest 6 g of either a placebo or the taurine supplement for 2 weeks prior to and 3 days following the exercise. Two weeks after the commencement of supplementation, the subjects were asked to perform 2 sets of 20 repetitive unilateral maximal-effort resistance exercise of the elbow flexors on a Biodex isokinetic dynamometer, with each contraction lasting 3 s, with 1 repetition performed every 9 s and 4 min rest in between sets. We evaluated the changes in brachial artery flow-mediated dilation (FMD) in the non-exercised arm as an index of vascular endothelial function. Relative and absolute FMDs were measured prior to supplementation, before exercise, and 24, 48, and 96 h after exercise.Two weeks of taurine supplementation significantly increased both relative and absolute FMDs. Baseline diameter significantly increased at 96 h following the exercise in both groups. However, there was no change in the peak diameter. Consequently, both relative and absolute FMDs were significantly reduced at 96 h after the exercise in both groups. Taurine supplementation does not affect resistance exercise-induced reduction in FMD.Two weeks of taurine supplementation (6 g/day) significantly increased vascular endothelial function at rest; however, taurine supplementation did not improve resistance exercise-induced reduction in FMD.

Anxiety-like behaviors and hippocampal nNOS in response to diet-induced obesity combined with exercise.

A high-fat diet (HFD) and overweight status can induce hippocampal dysfunction, leading to depression and anxiety. Exercise has beneficial effects on emotional behaviors. We previously reported that exercise training rescues HFD-induced excess hippocampal neuronal nitric oxide synthase (nNOS) expression, which is a key regulator of anxiety. Here, we investigated anxiety-like behaviors and hippocampal nNOS expression in response to HFD combined with exercise. Mice were assigned to standard diet, HFD, or HFD with exercise groups for 12 weeks. We found that exercise during the final 6 weeks of the HFD regime improved 12 weeks of HFD-induced defecation, accompanied by rescue of excess nNOS expression. However, anxiety indicators in the elevated plus maze were unchanged. These effects were not apparent after only 1 week of exercise. In conclusion, 6 weeks of exercise training reduced HFD-related anxiety according to one of our measures (defecation), and reversed changes in the hippocampal nNOS/NO pathway.

Immobilization rapidly induces thioredoxin-interacting protein gene expression together with insulin resistance in rat skeletal muscle.

Acute short duration of disuse induces the development of insulin resistance for glucose uptake in rodent skeletal muscle. Because thioredoxin-interacting protein (TXNIP) has been implicated in the downregulation of insulin signaling and glucose uptake, we examined the possibility that muscle disuse rapidly induces insulin resistance via increased TXNIP mRNA and protein expression. Male Wistar rats were subjected to unilateral 6-h hindlimb immobilization by plaster cast. At the end of this period, the soleus muscles from both immobilized and contralateral nonimmobilized hindlimbs were excised and examined. The 6-h immobilization resulted in an increase in TXNIP mRNA and protein expressions together with a decrease in insulin-stimulated 2-deoxyglucose uptake in the rat soleus muscle. Additionally, in the rats euthanized 6 h after the plaster cast removal, TXNIP protein expression and insulin-stimulated glucose uptake in the immobilized muscle had both been restored to a normal level. Various interventions (pretreatment with transcription inhibitor actinomycin D or AMP-dependent protein kinase activator 5-aminoimidazole-4-carboxamide ribonucleotide) also suppressed the increase in TXNIP protein expression in 6-h-immobilized muscle together with partial prevention of insulin resistance for glucose uptake. These results suggested the possibility that increased TXNIP protein expression in immobilized rat soleus muscles was associated with the rapid induction of insulin resistance for glucose uptake in that tissue. NEW & NOTEWORTHY The cellular mechanism by which disuse rapidly induces muscle insulin resistance for glucose uptake remains to be identified. Using a rat hindlimb immobilization model, our findings suggest the possibility that transcriptional upregulation of thioredoxin-interacting protein is associated with the immobilization-induced rapid development of insulin resistance in skeletal muscle.

Aerobic exercise training enhances cerebrovascular pulsatility response to acute aerobic exercise in older adults.

The brain's low resistance ensures a robust blood flow throughout systole and diastole and is susceptible to flow pulsatility. Increased cerebral pulsatility contributes to the progression of cerebrovascular disease. Although aerobic exercise affects vascular function, little is known about the effect of exercise on the cerebral pulsatility index in older adults. The aim of this study was to investigate the effect of exercise training on the post-exercise cerebral pulsatility response in older adults. Ten healthy older adults participated in a 12-week exercise training intervention. Before and after the intervention, we measured the pulsatility index of the middle cerebral artery by means of transcranial Doppler method at baseline and following a cycling exercise bout performed at an intensity corresponding to the ventilatory threshold. Before exercise training, there was no significant change in the cerebral pulsatility response to an acute bout of cycling exercise. However, after the intervention, cerebral pulsatility decreased significantly following 30 min of an acute cycling exercise (P < 0.05). This study demonstrated that cerebral pulsatility index did not change following an acute bout of cycling exercise at an intensity corresponding to ventilatory threshold, but that, after 12 weeks of exercise training, cerebral pulsatility index was reduced at 30 min after a single bout of cycling exercise. These results suggest that long-term aerobic exercise training may enhance the post-exercise reduction in pulsatility index in older adults.

Resistance training-induced decrease in central arterial compliance is associated with decreased subendocardial viability ratio in healthy young men.

High-intensity resistance training decreases central arterial compliance (CAC). Subendocardial viability ratio (SEVR) is a useful tool that reflects the balance between coronary perfusion and left ventricular afterload. Animal studies have demonstrated that decreased CAC is associated with SEVR deterioration. Therefore, resistance training-induced decrease in CAC may be associated with changes in SEVR. The objective of the present study was to investigate the association between SEVR and CAC using both cross-sectional and longitudinal (i.e., resistance training) study designs. To achieve this, we first conducted a cross-sectional study to investigate the association between SEVR and CAC in 89 young men. Thereafter, a longitudinal study was performed to examine the effects of resistance training on SEVR and CAC in young men. A total of 28 young men were divided into 2 groups: control (n = 13) and training (n = 15). In the training group, subjects underwent supervised resistance training for 4 weeks (5 sets of 10 repetitions at 75% of 1-repetition maximum, 3 times/week). CAC and SEVR were then measured in all subjects. In the cross-sectional study, SEVR was significantly positively correlated with CAC, whereas resistance training significantly decreased both SEVR and CAC. Moreover, training-induced changes in CAC were significantly correlated with changes in SEVR. Thus, these results suggest that resistance training-induced decrease in CAC is associated with decreased SEVR in young men.

Effect of BCAA supplement timing on exercise-induced muscle soreness and damage: a pilot placebo-controlled double-blind study.

BACKGROUND: The aim of the present study was to compare the effects of branched-chain amino acid (BCAA) supplementation taken before or after exercise on delayed onset muscle soreness (DOMS) and exercise-induced muscle damage (EIMD). METHODS: Fifteen young men (aged 21.5±0.4 years) were given either BCAA (9.6 g·day-1) or placebo before and after exercise (and for 3 days prior to and following the exercise day) in three independent groups: the control group (placebo before and after exercise), the PRE group (BCAA before exercise and placebo after exercise), and the POST group (placebo before exercise and BCAA after exercise). Participants performed 30 repetitions of eccentric exercise with the non-dominant arm. DOMS, upper arm circumference (CIR), elbow range of motion (ROM), serum creatine kinase (CK), lactate dehydrogenase (LDH), and aldolase, BCAA, and ß-hydroxy-ß-methylbutyrate (3HMB) were measured immediately before and after the exercise and on the following 4 days. RESULTS: Serum BCAA and 3HMB concentrations increased significantly in the PRE group immediately after the exercise, recovering to baseline over the following days. In the days following the exercise day, DOMS, CIR, and ROM were significantly improved in the PRE group compared to the control group, with weaker effects in the POST group. Serum activities of CK, LDH, and aldolase in the days following the exercise day were significantly suppressed in the PRE group compared to control group. CONCLUSIONS: The present study confirmed that repeated BCAA supplementation before exercise had a more beneficial effect in attenuating DOMS and EIMD induced by eccentric exercise than repeated supplementation after exercise.

Lactotripeptides Supplementations Alleviate the Decrease in Maximal Isometric Force After High-Intensity Eccentric Exercise: A Randomized, Placebo-Controlled, Double-Blind Clinical Trial.

OBJECTIVE: The aim of the study was to investigate whether lactotripeptides supplementations alleviate the decrease in the maximal isometric force, an indirect marker of muscle damage, after eccentric exercise (ECC). DESIGN: Twenty-two young men performed 50 ECC of the elbow flexors using an isokinetic dynamometer. The subjects were randomly assigned to either the placebo or lactotripeptides group and were each given a 4.5 mg/d placebo or lactotripeptides thrice on the exercise day and the day after. Maximal isometric force and brachial arterial diameter were assessed before and 2 days after the ECC. RESULTS: The interaction of time and group on maximal isometric force was significant (P < 0.05); maximal isometric force was significantly decreased in both groups after ECC (P < 0.005). The interaction of brachial arterial diameter was significant (P < 0.05); brachial arterial diameter was significantly increased in only the lactotripeptides group (P < 0.005). In addition, the change in maximal isometric force was significantly related to the change in brachial arterial diameter after adjusting for body weight and change in range of motion (P < 0.05). CONCLUSIONS: The present results suggest that lactotripeptides supplementation alleviates the decrease in the maximal isometric force via an increase in brachial arterial diameter after ECC.