Point Prevalence of the Biomechanical Dimension of Dysfunctional Breathing Patterns Among Competitive Athletes.

ABSTRACT: Shimozawa, Y, Kurihara, T, Kusagawa, Y, Hori, M, Numasawa, S, Sugiyama, T, Tanaka, T, Suga, T, Terada, RS, Isaka, T, and Terada, M. Point prevalence of the biomechanical dimension of dysfunctional breathing patterns among competitive athletes. J Strength Cond Res 37(2): 270-276, 2023-There is growing evidence of associations between altered biomechanical breathing patterns and numerous musculoskeletal and psychological conditions. The prevalence of dysfunctional and diaphragmatic breathing patterns is unknown among athletic populations. The purpose of this study was to examine the prevalence of dysfunctional and diaphragmatic breathing patterns among athletic populations with a clinical measure to assess the biomechanical dimension of breathing patterns. Using a cross-sectional design, 1,933 athletes across multiple sports and ages were screened from 2017 to 2020. Breathing patterns were assessed using the Hi-Lo test in the standing position. Scores of the Hi-Lo test were determined based on the presence or absence of abdominal excursion, anterior-posterior chest expansion, superior rib cage migration, and shoulder elevation. The Hi-Lo test scores were used to categorize observational breathing mechanics as dysfunctional and diaphragmatic breathing patterns. The prevalence of athletes with dysfunctional breathing patterns was 90.6% (1,751 of 1,933). Athletes with diaphragmatic breathing patterns accounted for 9.4% of all athletes in our sample (182 of 1,933). There were no differences in the proportion of breathing patterns between male and female athletes ( p = 0.424). Breathing patterns observations were associated with sport-setting categories ( p = 0.002). The highest percentages of dysfunctional breathers were in middle school student athletes (93.7%), followed by elementary school student athletes (91.2%), high school student athletes (90.6%), professional/semiprofessional athletes (87.5%), and collegiate athletes (84.8%). The current study observed that dysfunctional breathing patterns (90.6%) in the biomechanical dimension were more prevalent than diaphragmatic breathing pattern (9.4%) among competitive athletes. These results suggest that clinicians may need to consider screening breathing patterns and implementing intervention programs aimed to improve the efficiency of biomechanical dimensions of breathing patterns in athletic populations. This study may help raise awareness of impacts of dysfunctional breathing patterns on athletes' health and performance.

Altered gut microbiota richness in individuals with a history of lateral ankle sprain.

This study aimed to examine differences in the intestinal microbiota diversity in individuals with and without a history of a lateral ankle sprain (LAS). Fifty male college student athletes with (n=32) and without (n=18) a LAS history participated in this study. Faecal samples were collected in the morning after awakening during an off-season, and faecal microbiota were characterized via bacteria 16S rRNA amplicon sequencing. Alpha-diversity metrics and ß-diversity indices were calculated to assess the gut microbiota diversity. The LAS-history group significantly had lower Chao1 (p=0.020) and abundance-based coverage estimators (p=0.035) indices compared to the control group. Gut microbiota composition was not significantly different between athletes with a LAS history and controls (R2 =0.01, p 0.414). Athletes with a history of LASs had significantly higher proportions of Bacteroides Fragilis (p=0.024) and Ruminococcus Gnavus (p=0.021) compared with controls. The gut microbiota of athletes with a LAS history had less richness compared to controls, indicating potential associations between a LAS and the gut microbiota. This study highlights the potential link of a LAS to global health. This study may help raise awareness of strategies to prevent long-term health-related negative consequences in people suffering from LASs.

Relationship Between Body Segment Mass and Running Performance in Well-Trained Endurance Runners.

This study examined the relationship between body segment mass and running performance in endurance runners. The total (muscle, fat, and bone masses), lean (muscle mass), and fat masses of the leg, arm, and trunk segments in 37 well-trained endurance runners were measured using dual-energy X-ray absorptiometer. The relative segment mass was calculated by normalizing the absolute mass to body mass. There were no significant correlations between absolute total, lean, and fat masses of all 3 segments and personal best 5000-m race time. No significant correlations were also observed between all 3 relative masses of the arm segment and personal best 5000-m race time. In contrast, medium positive correlations were observed between the relative total and lean masses of the leg segment and personal best 5000-m race time (r = .387 and .335, respectively, both P ≤ .031). Furthermore, large negative correlations were observed between the relative total and lean masses of the trunk segment and personal best 5000-m race time (r = -.500 and -.548, respectively, both P ≤ .002). These findings suggest that a mass distribution with smaller leg mass and greater trunk mass may be advantageous for achieving better running performance in endurance runners.

Achilles Tendon Length Is Not Related to 100-m Sprint Time in Sprinters.

This study examined the relationship between Achilles tendon (AT) length and 100-m sprint time in sprinters. The AT lengths at 3 different portions of the triceps surae muscle in 48 well-trained sprinters were measured using magnetic resonance imaging. The 3 AT lengths were calculated as the distance from the calcaneal tuberosity to the muscle-tendon junction of the soleus, gastrocnemius medialis, and gastrocnemius lateralis, respectively. The absolute 3 AT lengths did not correlate significantly with personal best 100-m sprint time (r = -.023 to .064, all Ps > .05). Furthermore, to minimize the differences in the leg length among participants, the 3 AT lengths were normalized to the shank length, and the relative 3 AT lengths did not correlate significantly with personal best 100-m sprint time (r = .023 to .102, all Ps > .05). Additionally, no significant correlations were observed between the absolute and relative (normalized to body mass) cross-sectional areas of the AT and personal best 100-m sprint time (r = .012 and .084, respectively, both Ps > .05). These findings suggest that the AT morphological variables, including the length, may not be related to superior 100-m sprint time in sprinters.

Muscle denervation reduces mitochondrial biogenesis and mitochondrial translation factor expression in mice.

The mitochondrial translation process, in which mitochondrial DNA (mtDNA)-encoded genes are translated into their corresponding proteins, is crucial for mitochondrial function, biogenesis, and integrity. This process is divided into four phases-initiation, elongation, termination, and mitoribosome recycling-which are regulated by specific translation factors, including mitochondrial initiation factor 2 and 3 (mtIF2 and mtIF3), mitochondrial elongation factor Tu, Ts, and G1 (mtEFTu, mtEFTs, and mtEFG1), mitochondrial translational release factor 1-like (mtRF1L), and mitochondrial recycling factor 1 and 2 (mtRRF1 and mtRRF2). Muscle denervation downregulates mitochondrial biomass and induces skeletal muscle atrophy. However, it is unknown whether denervation affects the expression of mitochondrial translation factors in skeletal muscle. In this study, we hypothesized that denervation decreases the expression of mitochondrial translation factors. Therefore, we investigated the effect of muscle denervation on mitochondrial protein and mitochondrial translation factor expression in soleus muscle after surgery. Denervation induced muscle atrophy and activated the ubiquitin-proteasome pathway in soleus muscle. Additionally, muscle denervation decreased the expression of mitochondrial translation factors as well as nuclear DNA and mtDNA-encoded mitochondrial proteins in soleus muscle. Further, a correlation was found between the expression of mitochondrial translation factors and mtDNA-encoded proteins three and seven days after denervation. Taken together, these results demonstrated that the denervation-induced decrease in mitochondrial biogenesis corresponded with changes in mitochondrial translation factors in murine skeletal muscle, providing novel molecular-level insight into the effects of muscle denervation on the mitochondrial translation process.

Exercise training increases CISD family protein expression in murine skeletal muscle and white adipose tissue.

Mitochondrial function in skeletal muscle and white adipose tissue (WAT) declines with aging and the progression of type 2 diabetes and insulin resistance. Although exercise increases mitochondrial biogenesis and function in both tissues, the molecular mechanisms are not fully understood. CDGSH iron sulfur domain-containing proteins (CISDs) are a novel family of proteins that regulate mitochondrial activity and biogenesis. However, the relationship between exercise and CISD expression is unclear. We addressed this in the present study by examining changes in the expression of CISDs and mitochondrial proteins in skeletal muscle and WAT of mice subjected to chronic exercise training. Mice were randomly assigned to either the sedentary or exercise group and were housed for 4 weeks in a standard cage without or with a running wheel, respectively. CISD and mitochondrial protein levels in the plantaris and soleus muscles and epididymal WAT were evaluated by western blotting. Chronic exercise increased CISD1 and CISD2 as well as mitochondrial protein expression in plantaris muscle and WAT but not soleus muscle. Moreover, this exercise-induced adaptation was strongly correlated with mitochondrial protein expression. Thus, mitochondrial biogenesis induced by chronic exercise coincides with the expression of CISDs in specific tissues, which may be critical for the maintenance of mitochondrial integrity.

Relationship between Achilles tendon length and running performance in well-trained male endurance runners.

This study aimed to determine the relationship between Achilles tendon (AT) length and running performance, including running economy, in well-trained endurance runners. We also examined the reasonable portion of the AT related to running performance among AT lengths measured in three different portions. The AT lengths at three portions and cross-sectional area (CSA) of 30 endurance runners were measured using magnetic resonance imaging. Each AT length was calculated as the distance from the calcaneal tuberosity to the muscle-tendon junction of the soleus, gastrocnemius medialis (GMAT ), and gastrocnemius lateralis, respectively. These AT lengths were normalized with shank length. The AT CSA was calculated as the average of 10, 20, and 30 mm above the distal insertion of the AT and normalized with body mass. Running economy was evaluated by measuring energy cost during three 4-minutes submaximal treadmill running trials at 14, 16, and 18 km/h, respectively. Among three AT lengths, only a GMAT correlated significantly with personal best 5000-m race time (r=-.376, P=.046). Furthermore, GMAT correlated significantly with energy cost during submaximal treadmill running trials at 14 km/h and 18 km/h (r=-.446 and -.429, respectively, P<.05 for both), and a trend toward such significance was observed at 16 km/h (r=-.360, P=.050). In contrast, there was no correlation between AT CSA and running performance. These findings suggest that longer AT, especially GMAT , may be advantageous to achieve superior running performance, with better running economy, in endurance runners.

Potential Relationship between Passive Plantar Flexor Stiffness and Running Performance.

The present study aimed to determine the relationship between passive stiffness of the plantar flexors and running performance in endurance runners. Forty-eight well-trained male endurance runners and 24 untrained male control subjects participated in this study. Plantar flexor stiffness during passive dorsiflexion was calculated from the slope of the linear portion of the torque-angle curve. Of the endurance runners included in the present study, running economy in 28 endurance runners was evaluated by measuring energy cost during three 4-min trials (14, 16, and 18 km/h) of submaximal treadmill running. Passive stiffness of the plantar flexors was significantly higher in endurance runners than in untrained subjects. Moreover, passive plantar flexor stiffness in endurance runners was significantly correlated with a personal best 5000-m race time. Furthermore, passive plantar flexor stiffness in endurance runners was significantly correlated with energy cost during submaximal running at 16 km/h and 18 km/h, and a trend towards such significance was observed at 14 km/h. The present findings suggest that stiffer plantar flexors may help achieve better running performance, with greater running economy, in endurance runners. Therefore, in the clinical setting, passive stiffness of the plantar flexors may be a potential parameter for assessing running performance.

Association between Forefoot Bone Length and Performance in Male Endurance Runners.

Recently, we reported that the forefoot bones were longer in sprinters than in non-sprinters, and that longer forefoot bones correlated with higher sprint performance in sprinters. To further understand the superiority of long forefoot bones in athletic performance, we examined whether forefoot bone length was associated with running performance in endurance runners. The length of the forefoot bones of the big and second toes were measured using magnetic resonance imaging in 45 male well-trained endurance runners and 45 male untrained subjects. After normalization with the foot length, it was found that the forefoot bones of the big and second toes were significantly longer in endurance runners than in untrained subjects (P<0.05 for both). Furthermore, longer forefoot bones of the big toe, but not of the second toe, correlated significantly with better personal best 5000-m race time in endurance runners (r=-0.322, P=0.031). The present findings demonstrated that forefoot bones were longer in endurance runners than in untrained subjects. These findings were similar to our findings for sprinters. In addition, we found that longer forefoot bones may be advantageous for achieving higher running performance in endurance runners.

Hip Flexor and Knee Extensor Muscularity Are Associated With Sprint Performance in Sprint-Trained Preadolescent Boys.

PURPOSE: We attempted to determine the relationships between the cross-sectional area (CSA) of the trunk and lower limb muscles and sprint performance in male preadolescent sprinters. METHODS: Fifteen sprint-trained preadolescent boys (age 11.6 ± 0.4 y) participated in this study. The CSAs of the participants' trunk and lower limb muscles were measured using magnetic resonance imaging, and these muscles were normalized with free-fat mass. To assess participants' sprint performance, sprint time and variables during the 50-m sprint test were measured. The sprint variables were expressed as their indices by normalizing with body height. RESULTS: The relative CSAs of psoas major, adductors, and quadriceps femoris were significantly correlated with sprint time (r = -.802, -.643, and -.639). Moreover, the relative CSAs of these muscles were significantly correlated with indices of sprint velocity (r = .694, .612, and .630) and step frequency (r = .687, .740, and .590) but not with that of step length. CONCLUSIONS: These findings suggest that greater hip flexor and knee extensor muscularity in male preadolescent sprinters may help achieve superior sprint performance by potentially enhancing their moments, which may be induced by increased step frequency rather than step length during sprinting.

The knee extensor moment arm is associated with performance in male sprinters.

PURPOSE: Although large knee extensor torque contributes to superior sprint performance, previous findings have indicated that the quadriceps cross-sectional area (CSA), a pivotal morphological regulator of knee extensor torque, is not correlated with performance in sprinters. We hypothesized that the knee extensor moment arm (MA), another main morphological regulator of knee extensor torque, may affect sprint performance. To test this hypothesis, we examined the relationship between knee extensor MA and sprint performance. METHODS: The quadriceps CSA and knee extensor MA in 32 well-trained male sprinters and 32 male non-sprinters were measured using magnetic resonance imaging. RESULTS: Knee extensor MA, but not quadriceps CSA, was greater in sprinters than in non-sprinters (P = 0.013). Moreover, knee extensor MA, but not the quadriceps CSA, was correlated with the personal best time in a 100-m race in sprinters (r = -0.614, P < 0.001). Furthermore, among 24 sprinters who participated in the 60-m sprint test, knee extensor MA was correlated with sprinting velocities in the acceleration (r = 0.717, P < 0.001) and maximum speed (r = 0.697, P < 0.001) phases. CONCLUSION: The present study demonstrates that the knee extensor MA is greater in sprinters than in non-sprinters, and this morphological structure in sprinters is associated with sprint performance. Therefore, for the first time, we provided evidence that a greater knee extensor MA in sprinters may be an advantageous for achieving superior sprint performance.

Association between hand muscle thickness and whole-body skeletal muscle mass in healthy adults: a pilot study.

[Purpose] Handgrip strength is a surrogate indicator for assessing disease-related and age-related skeletal muscle loss. Clinical utility as such a surrogate can be at least partially explained by the close relationship between handgrip strength and whole-body skeletal muscle mass. The handgrip strength is related to hand muscle size. Thus, the present study examined whether hand muscle thickness is associated with whole-body skeletal muscle mass. [Subjects and Methods] Thirty healthy male adults participated in this study. All subjects were right-hand dominant. Two muscle thicknesses (lumbrical and interosseous muscles) in the right hand were measured using ultrasonography. Whole-body and appendicular skeletal muscle masses were assessed using dual-energy X-ray absorptiometry. [Results] Although lumbrical muscle thickness was not correlated with whole-body skeletal muscle mass, there was a significant correlation with appendicular skeletal muscle mass. Furthermore, interosseous muscle thickness was significantly correlated with both whole-body and appendicular skeletal muscle masses. [Conclusion] The present findings suggest that two muscle thicknesses in the hand are related to whole-body and/or appendicular skeletal muscle mass in healthy adults. Therefore, we propose that despite being smaller than other limb muscles, hand muscle thickness may be useful as surrogate indicator for assessing disease-related and age-related skeletal muscle loss.

Applicability of ultrasonography for evaluating trunk muscle size: a pilot study.

[Purpose] Ultrasonography (US) is widely applied to measure the muscle size in the limbs, as it has relatively high portability and is associated with low costs compared with large clinical devices such as magnetic resonance imaging (MRI). However, the applicability of US for evaluating trunk muscle size is poorly understood. This study aimed to examine whether US-measured muscle thickness (MT) in the trunk abdominal and back muscles correlated with MT and muscle cross-sectional area (MCSA) measured by MRI. [Subjects and Methods] Twenty-four healthy young males participated in this study. The MT and MCSA in the subjects were measured by US and MRI in a total of 10 sites, including the bilateral sides of the rectus abdominis (upper, central, and lower parts), abdominal wall, and multifidus lumborum. [Results] The interclass correlation coefficients of US-measured MT on the total 10 sites showed excellent values (n=12, 0.919 to 0.970). The US-measured MT significantly correlated with the MRI-measured MT (r=0.753 to 0.963) and MCSA (r=0.634 to 0.821). [Conclusion] US-measured MT could represent a surrogate for muscle size measured by MRI. The application of US for evaluating trunk muscle size may be a useful tool in the clinical setting.

Applicability of ultrasonography for evaluating trunk muscles size in athletes: a study focused on baseball batters.

[Purpose] Recently, we demonstrated that the thicknesses of trunk muscles measured using ultrasonography were correlated strongly with the cross-sectional areas measured using magnetic resonance imaging in untrained subjects. To further explore the applicability of ultrasonography in the clinical setting, the present study examined the correlation between ultrasonography-measured thicknesses and magnetic resonance imaging-measured cross-sectional areas of trunk muscles in athletes with trained trunk muscles. [Subjects and Methods] The thicknesses and cross-sectional areas at total 10 sites of the bilateral sides of the upper, central, and lower parts of the rectus abdominis, abdominal wall, and multifidus lumborum in 30 male baseball batters were measured. [Results] Overall thicknesses and cross-sectional areas of the trunk muscles in baseball batters were higher than those in untrained subjects who participated in our previous study. The ultrasonography-measured thicknesses at all 10 sites of the trunk muscles correlated highly with the magnetic resonance imaging-measured cross-sectional areas in baseball batters. [Conclusion] These results suggest that the thicknesses of the trunk muscles measured using ultrasonography can be used as a surrogate marker for the cross-sectional area measured using magnetic resonance imaging, in athletes who have larger trunk muscles than that of untrained subjects.

(Pro)renin receptor in skeletal muscle is involved in the development of insulin resistance associated with postinfarct heart failure in mice.

We previously reported that insulin resistance was induced by the impairment of insulin signaling in the skeletal muscle from heart failure (HF) via NAD(P)H oxidase-dependent oxidative stress. (Pro)renin receptor [(P)RR] is involved in the activation of local renin-angiotensin system and subsequent oxidative stress. We thus examined whether (P)RR inhibitor, handle region peptide (HRP), could ameliorate insulin resistance in HF after myocardial infarction (MI) by improving oxidative stress and insulin signaling in the skeletal muscle. C57BL6J mice were divided into four groups: sham operated (Sham, n = 10), Sham treated with HRP (Sham+HRP, 0.1 mg·kg(-1)·day(-1), n = 10), MI operated (MI, n = 10), and MI treated with HRP (MI+HRP, 0.1 mg/kg/day, n = 10). After 4 wk, MI mice showed left ventricular dysfunction, which was not affected by HRP. (P)RR was upregulated in the skeletal muscle after MI (149% of sham, P < 0.05). The decrease in plasma glucose after insulin load was smaller in MI than in Sham (21 ± 2 vs. 44 ± 3%, P < 0.05), and was greater in MI+HRP (38 ± 2%, P < 0.05) than in MI. Insulin-stimulated serine phosphorylation of Akt and glucose transporter 4 translocation were decreased in the skeletal muscle from MI by 48 and 49% of Sham, both of which were ameliorated in MI+HRP. Superoxide production and NAD(P)H oxidase activities were increased in MI, which was inhibited in MI+HRP. HRP ameliorated insulin resistance associated with HF by improving insulin signaling via the inhibition of NAD(P)H oxidase-induced superoxide production in the skeletal muscle. The (P)RR pathway is involved in the development of insulin resistance, at least in part, via the impairment of insulin signaling in the skeletal muscle from HF.

Activation of natural killer T cells ameliorates postinfarct cardiac remodeling and failure in mice.

RATIONALE: Chronic inflammation in the myocardium is involved in the development of left ventricular (LV) remodeling and failure after myocardial infarction (MI). Invariant natural killer T (iNKT) cells have been shown to produce inflammatory cytokines and orchestrate tissue inflammation. However, no previous studies have determined the pathophysiological role of iNKT cells in post-MI LV remodeling. OBJECTIVE: The purpose of this study was to examine whether the activation of iNKT cells might affect the development of LV remodeling and failure. METHODS AND RESULTS: After creation of MI, mice received the injection of either α-galactosylceramide (αGC; n=27), the activator of iNKT cells, or phosphate-buffered saline (n=31) 1 and 4 days after surgery, and were followed during 28 days. Survival rate was significantly higher in MI+αGC than MI+PBS (59% versus 32%, P<0.05). LV cavity dilatation and dysfunction were significantly attenuated in MI+αGC, despite comparable infarct size, accompanied by a decrease in myocyte hypertrophy, interstitial fibrosis, and apoptosis. The infiltration of iNKT cells were increased during early phase in noninfarcted LV from MI and αGC further enhanced them. It also enhanced LV interleukin (IL)-10 gene expression at 7 days, which persisted until 28 days. AntienIL-10 receptor antibody abrogated these protective effects of αGC on MI remodeling. The administration of αGC into iNKT cell-deficient Jα18(-/-) mice had no such effects, suggesting that αGC was a specific activator of iNKT cells. CONCLUSIONS: iNKT cells play a protective role against post-MI LV remodeling and failure through the enhanced expression of cardioprotective cytokines such as IL-10.

Circulating Plasma Oxytocin Level Is Elevated by High-Intensity Interval Exercise in Men.

PURPOSE: We evaluated whether repeated high-intensity interval exercise (HIIE) influences plasma oxytocin (OT) concentration in healthy men, and, given that OT is mainly synthesized in the hypothalamus, we assessed the concentration difference between the arterial (OT ART ) versus the internal jugular venous OT concentration (OT IJV ). Additionally, we hypothesized that an increase in cerebral OT release and the circulating concentration would be augmented by repeated HIIE. METHODS: Fourteen healthy men (age = 24 ± 2 yr; mean ± SD) performed two identical bouts of HIIE. These HIIE bouts included a warm-up at 50%-60% maximal workload ( Wmax ) for 5 min followed by four bouts of exercise at 80%-90% Wmax for 4 min interspersed by exercise at 50%-60% Wmax for 3 min. The HIIE bouts were separated by 60 min of rest. OT was evaluated in blood through radial artery and internal jugular vein catheterization. RESULTS: Both HIIE bouts increased both OT ART (median [IQR], from 3.9 [3.4-5.4] to 5.3 [4.4-6.3] ng·mL -1 in the first HIIE, P < 0.01) and OT IJV (from 4.6 [3.4-4.8] to 5.9 [4.3-8.2] ng·mL -1 , P < 0.01), but OT ART-IJV was unaffected (from -0.24 [-1.16 to 1.08] to 0.04 [-0.88 to 0.78] ng·mL -1 , P = 1.00). The increased OT levels were similar in the first and second HIIE bouts (OT ARTP = 0.25, OT IJVP = 0.36). CONCLUSIONS: Despite no change in the cerebral OT release via the internal jugular vein, circulating OT increases during HIIE regardless of the accumulated exercise volume, indicating that OT may play role as one of the exerkines.

Activation of invariant natural killer T cells by α-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice.

Invariant natural killer T (iNKT) cells orchestrate tissue inflammation via regulating various cytokine productions. However the role of iNKT cells has not been determined in myocardial ischemia/reperfusion (I/R) injury. The purpose of this study was to examine whether the activation of iNKT cells by α-galactosylceramide (α-GC), which specifically activates iNKT cells, could affect myocardial I/R injury. I/R or sham operation was performed in male C57BL/6J mice. I/R mice received the injection of either αGC (I/R+αGC, n=48) or vehicle (I/R+vehicle, n=49) 30 min before reperfusion. After 24h, infarct size/area at risk was smaller in I/R+αGC than in I/R+vehicle (37.8 ± 2.7% vs. 47.1 ± 2.5%, P<0.05), with no significant changes in area at risk. The numbers of infiltrating myeloperoxidase- and CD3-positive cells were lower in I/R+αGC. Apoptosis evaluated by TUNEL staining and caspase-3 protein was also attenuated in I/R+αGC. Myocardial gene expression of tumor necrosis factor-α and interleukin (IL)-1ß in I/R+αGC was lower to 46% and 80% of that in I/R+vehicle, respectively, whereas IL-10, IL-4, and interferon (IFN)-γ were higher in I/R+αGC than I/R+vehicle by 2.0, 4.1, and 9.6 folds, respectively. The administration of anti-IL-10 receptor antibody into I/R+αGC abolished the protective effects of αGC on I/R injury (infarct size/area at risk: 53.1 ± 5.2% vs. 37.4 ± 3.5%, P<0.05). In contrast, anti-IL-4 and anti-IFN-γ antibodies did not exert such effects. In conclusion, activated iNKT cells by αGC play a protective role against myocardial I/R injury through the enhanced expression of IL-10. Therapies designed to activate iNKT cells might be beneficial to protect the heart from I/R injury.

The effect of attending rehabilitation after traumatic knee joint injury on femoral articular cartilage morphology in collegiate rugby players with a history of intracapsular knee joint injury during two-year consecutive rugby seasons.

Introduction: This present study aimed to compare ultrasonographic measures of femoral articular cartilage during two-year seasons between collegiate rugby players who have attended supervised rehabilitation following intracapsular knee joint injury and those without a history of knee injury. Methods: Using a prospective observational study design, 12 male collegiate rugby players with a previous history of intracapsular knee joint injury who have received and completed supervised rehabilitation following their injury and 44 players without knee joint injury participated in this study. Ultrasonographic images were used to verify changes in femoral articular cartilage thickness and cross-sectional area (CSA) with or without a previous history of knee joint injury over two consecutive rugby seasons. Results: Significant time main effects were observed for the lateral condylar thickness (p < 0.001), the intercondylar thickness (p = 0.001), the medial condylar thickness (p < 0.001), and CSA (p < 0.001). No significant interactions nor group main effects were identified for all femoral articular cartilage (p < 0.05). Conclusions: Collegiate rugby players demonstrated a decrease in femoral articular cartilage thickness and CSA over two-year consecutive rugby seasons. These findings indicate that engaging in collegiate rugby induces alterations in femoral articular cartilage structure. Furthermore, there were no differences in all femoral cartilage outcome measures between rugby players with and without a previous history of traumatic knee joint injury. Therefore, attending supervised rehabilitation at the time of their knee joint injury appeared to reduce the impact of a previous history of intracapsular knee joint injury on the change in femoral articular cartilage thickness and CSA among active rugby players.

The lactate response to a second bout of exercise is not reduced in a concurrent lower-limb exercise program.

We aimed to evaluate the blood lactate level in response to two bouts of exercise. First, we hypothesized that blood lactate elevation in response to moderate-intensity aerobic exercise (MIAE) would be lower at the end of the second bout of MIAE than the first bout of MIAE. In this context, we also hypothesized that lactate accumulation at the end of resistance exercise (RE) would be reduced if MIAE is performed before RE (i.e., concurrent exercise; CE). If so, we hypothesized that the order of the CE (i.e., RE + MIAE vs. MIAE + RE) influences blood lactate kinetics. To test the hypotheses, forty-three healthy men participated in three studies. In study 1, 20 men (age 21 ± 2 years) performed two bouts of a 20-min MIAE separated by a 20-min rest interval. In study 2, 11 men (age 22 ± 1 years) performed RE only and CE (MIAE + RE; ARCE) with a 20-min rest interval in a crossover design. In study 3, 12 men (age 21 ± 2 years) performed both CEs, which were ARCE and RE + MIAE (RACE), with a 20-min rest interval in a crossover design. We measured blood lactate before and at the end of each exercise session. In study 1, the blood lactate response to the second bout of MIAE was lower than that of the first bout (P < 0.001, r = 0.68). However, the blood lactate response to the ARCE trial was not lower than the response to the RE trial in study 2 (P = 0.475, r = 0.22). The results of study 3 showed that the RACE and ARCE trials induced a similar lactate response (MIAE P = 0.423, r = 0.28; RE P = 0.766, d = 0.03). These observations indicate that whereas lactate accumulation might be diminished by a second bout of MIAE, a different type of exercise (i.e., aerobic/resistance) did not result in a diminished lactate accumulation in response to a second bout of exercise.