Effects of uninterrupted chest compressions on the rescuer's physical condition.

STUDY OBJECTIVE: Recent guidelines have emphasized the need for uninterrupted chest compressions. The purpose of this study was to evaluate the rescuer's tolerability of uninterrupted chest compressions. METHODS: Twenty-five healthy subjects performed uninterrupted chest compressions for 7 minutes at a rate of 100 compressions per minute using a training manikin. The quality of chest compressions was assessed in terms of the total number and percentage of chest compressions, compression depth, recoil distance, and duty cycle. Correct chest compression was defined as a depth of 38 to 51 mm. Physiological and laboratory parameters were measured before and after the procedure. Fatigue was measured using a numerical rating scale. Data were compared before and after the procedure. RESULTS: The participants were 10 emergency physicians and 15 medical students. The compression rate was nearly 100 compressions per minute. The number and percentage of correct compressions decreased gradually after 3 minutes. The compression depth decreased significantly after 2 minutes. The recoil distance and duty cycle were unchanged over 7 minutes. Systolic blood pressure, pulse rate, respiratory rate, numerical rating scale, serum lactate, adrenalin, and noradrenalin increased significantly after the procedure. Noradrenalin levels measured before the procedure were significantly and negatively correlated with the total number and percentage of correct compressions (r = -0.587, P = .004; r = -0.549, P = .008, respectively). CONCLUSIONS: Performing uninterrupted chest compressions for 7 minutes is an arduous procedure. Higher noradrenalin levels before the procedure might be associated with incorrect chest compressions.

Postmortem diagnosis of gestational psittacosis: A case report.

Background: Gestational psittacosis is one of the causes of unanticipated maternal death but has been difficult to diagnose early in clinical practice. Case Presentation: A 28-year-old woman who was 7 months pregnant experienced flu-like symptoms, which deteriorated. She was brought to our hospital in shock, and the fetus was nonviable. The patient was diagnosed with pneumonia and septic shock and administered meropenem. Despite aggressive resuscitation, she died 7 h after symptom onset. After obtaining consent from the patient's family, the autopsy was done to identify the cause of death. Microscopically, there was intervillous neutrophil accumulation in the placenta. Genetic analysis detected the Chlamydia psittaci gene in several organs, including placenta. Conclusion: Gestational psittacosis should be considered for a pregnant woman with flu-like symptoms. Moreover, unanticipated death of a pregnant woman might warrant a detailed autopsy to reveal the cause of death.

Association between increased nonaerated lung weight and treatment failure in patients with de novo acute respiratory failure: Difference between high-flow nasal oxygen therapy and noninvasive ventilation in a multicentre retrospective study.

PURPOSE: To determine the association between lung collapse and treatment failure in high-flow nasal cannula oxygen therapy (HFNC) or noninvasive ventilation (NIV). METHODS: We performed a quantitative analysis of chest computed tomography in patients with de novo acute respiratory failure who received HFNC (HFNC group) or NIV (NIV group) between January 2012 and December 2017. In the HFNC and NIV group, the nonaerated lung weight were compared between patients in whom respiratory treatment succeeded or failed, respectively. We used logistic regression to examine the association between the nonaerated lung weight and treatment failure. RESULTS: Treatment failed in 70/118 (59%) patients in the HFNC group and 66/101 (65%) patients in the NIV group. The nonaerated lung weight was significantly greater in unsuccessfully treated patients than in successfully treated patients in the HFNC group (p = 0.005), but not in the NIV group (p = 0.535). Logistic regression revealed that greater nonaerated lung weight was associated with increased risk of HFNC failure (adjusted odds ratio 1.30 per 5% increase, 95% confidence interval 1.09-1.55, p = 0.003) but not of NIV failure. CONCLUSIONS: Patients with a greater nonaerated lung weight had a higher risk of HFNC failure, but not of NIV failure.

Comparison of the predictability of neurological outcome by serum procalcitonin and glial fibrillary acidic protein in postcardiac-arrest patients.

BACKGROUND: In past research, procalcitonin (PCT) and glial fibrillary acidic protein (GFAP) have been reported to be useful biomarkers in predicting neurological outcome after the return of spontaneous circulation (ROSC) following out-of-hospital cardiac arrest (CA), although they have only been studied separately. In this study, we compared the usefulness of PCT and GFAP in predicting neurological outcome. METHODS: This study was a retrospective, single-center analysis, conducted in the intensive-care unit of a university hospital. Twenty-one sequential post-CA patients were included. Serum samples were collected from patients at 12 and 24 h after ROSC. Serum PCT and GFAP were measured and compared in patients with favorable and unfavorable neurological outcomes, evaluated at 6 months using the Glasgow-Pittsburgh Cerebral Performance Categories. RESULTS: Serum PCT was significantly higher at 12 and 24 h in patients with unfavorable outcomes (P = 0.004 and 0.002, respectively). Serum GFAP was not significantly higher at 12 and 24 h in patients with unfavorable outcomes (P = 0.118 and 0.079, respectively). The combination of PCT and GFAP showed high predictive value for unfavorable outcomes (86.7% sensitivity and 100% specificity at 12 h; 100% sensitivity and 83.3% specificity at 24 h). CONCLUSION: Serum PCT is a marker of unfavorable neurological outcome in post-CA patients, and is superior to serum GFAP in the early phase.

Comparison of high-flow nasal cannula oxygen therapy and non-invasive ventilation as first-line therapy in respiratory failure: a multicenter retrospective study.

AIM: To identify which subgroups of respiratory failure could benefit more from high-flow nasal cannula oxygen therapy (HFNC) or non-invasive ventilation (NIV). METHODS: We undertook a multicenter retrospective study of patients with acute respiratory failure (ARF) who received HFNC or NIV as first-line respiratory support between January 2012 and December 2017. The adjusted odds ratios (OR) with 95% confidence intervals (CI) for HFNC versus NIV were calculated for treatment failure and 30-day mortality in the overall cohort and in patient subgroups. RESULTS: High-flow nasal cannula oxygen therapy and NIV were used in 200 and 378 patients, and the treatment failure and 30-day mortality rates were 56% and 34% in the HFNC group and 41% and 39% in the NIV group, respectively. The risks of treatment failure and 30-day mortality were not significantly different between the two groups. In subgroup analyses, HFNC was associated with increased risk of treatment failure in patients with cardiogenic pulmonary edema (adjusted OR 6.26; 95% CI, 2.19-17.87; P < 0.01) and hypercapnia (adjusted OR 3.70; 95% CI, 1.34-10.25; P = 0.01), but the 30-day mortality was not significantly different in these subgroups. High-flow nasal cannula oxygen therapy was associated with lower risk of 30-day mortality in patients with pneumonia (adjusted OR 0.43; 95% CI, 0.19-0.94; P = 0.03) and in patients without hypercapnia (adjusted OR 0.51; 95% CI, 0.30-0.88; P = 0.02). CONCLUSION: High-flow nasal cannula oxygen therapy could be more beneficial than NIV in patients with pneumonia or non-hypercapnia, but not in patients with cardiogenic pulmonary edema or hypercapnia.

Serum macrophage migration inhibitory factor reflects adrenal function in the hypothalamo-pituitary-adrenal axis of septic patients: an observational study.

BACKGROUND: The hypothalamo-pituitary-adrenal (HPA) axis modulates the inflammatory response during sepsis. Macrophage migration inhibitory factor (MIF), which counteracts the anti-inflammatory activity of glucocorticoid (GC), is one of the mediators of the development of inflammation. An inflammatory imbalance involving GC and MIF might be the cause or result of adrenal insufficiency. Our objective was to clarify the relationship between serum MIF and adrenal function in the HPA axis of sepsis patients using the adrenocorticotropic hormone (ACTH) stimulation test. METHODS: An observational study was performed in a university intensive care unit over a two-year period. Of 64 consecutive sepsis patients, 41 were enrolled. The enrolled patients underwent an ACTH stimulation test within 24 h of the diagnosis of severe sepsis or septic shock. Clinical and laboratory parameters, including serum MIF and cortisol, were measured. RESULTS: Based on their responses to the ACTH stimulation test, the patients were divided into a normal adrenal response (NAR) group (n = 22) and an adrenal insufficiency (AI) group (n = 19). The AI group had significantly more septic shock patients and higher prothrombin time ratios, serum MIF, and baseline cortisol than did the NAR group (P < 0.05). Serum MIF correlated significantly with the SOFA (Sequential Organ Failure Assessment) score, prothrombin time ratio, and delta max cortisol, which is maximum increment of serum cortisol concentration after ACTH stimulation test (rs = 0.414, 0.355, and -0.49, respectively, P < 0.05). Serum MIF also correlated significantly with the delta max cortisol/albumin ratio (rs = -0.501, P = 0.001). Receiver operating characteristic curve analysis identified the threshold serum MIF concentration (19.5 ng/mL, P = 0.01) that segregated patients into the NAR and AI groups. CONCLUSIONS: The inverse correlation between serum MIF and delta max cortisol or the delta max cortisol/albumin ratio suggests that high serum MIF reflects an insufficient adrenal response in the HPA axis. Serum MIF could be a valuable clinical marker of adrenal insufficiency in sepsis patients.

Successful treatment with hydrocortisone for heat stroke with critical illness-related corticosteroid insufficiency: transitional changes in serum cytokine and cortisol concentrations.

A 37-year-old man was transferred to our emergency center because of heat stroke with circulatory shock. Despite aggressive body cooling, massive intravenous transfusion, and supply of inotropic agents, shock was persistent. To evaluate adrenal function, an adrenocorticotropic hormone stimulation test was conducted and the results indicated that he had critical illness-related corticosteroid insufficiency (CIRCI) as a result of adrenal insufficiency. Continuous hydorocortisone administration was started and he recovered from shock within a few hours. He was discharged on the thirty-seventh hospital day. Serum cortisol and cytokine concentrations were initially high and the cytokines decreased subsequent to hydrocortisone administration. It is speculated that CIRCI is an exacerbating factor in heat stroke, and hydrocortisone may be a potential therapeutic approach in such patients.

Endothelin and the heart in health and diseases.

Endothelin-1 (ET-1), a 21-amino acid peptide, was initially identified in 1988 as a potent vasoconstrictor and pressor substance isolated from the culture supernatant of porcine aortic endothelial cells. From human genomic DNA analysis, two other family peptides, ET-2 and ET-3, were found. They showed different effects and distribution, suggesting that each peptide may play separate roles in different organs. In the heart, ET-1 also causes positive inotropic and chronotropic responses and hypertrophic activity of the cardiomyocytes. ETs act via activation of two receptor subtypes, ETA and ETB receptors, both of which are coupled to various GTP-binding proteins depending on cell types. Endogenous ET-1 may be involved in progression of various cardiovascular diseases. ET antagonists are currently used clinically in the treatment for patients with pulmonary hypertension, and are considered to have further target diseases as heart failure, cardiac hypertrophy and other cardiac diseases, renal diseases, systemic hypertension, and cerebral vasospasm.

Sex differences in steroidogenesis in skeletal muscle following a single bout of exercise in rats.

Sex steroid hormones, such as testosterone and estradiol, play important roles in developing both strength and mass of skeletal muscle. Recently, we demonstrated that skeletal muscle can synthesize sex steroid hormones. Whether there are sex differences in basal steroidogenesis or acute exercise-induced alterations of steroidogenesis in the skeletal muscle is unknown. We examined sex differences in the levels of testosterone, estradiol, and steroidogenesis-related enzymes, such as 17beta-hydroxysteroid dehydrogenase (HSD), 3beta-HSD, and aromatase cytochrome P-450 (P450arom), in the skeletal muscle at rest and after exercise. We studied the gastrocnemius muscles of resting rats (10 wk old) and exercised rats (10 wk old, treadmill running, 30 m/min, 30 min). Basal muscular testosterone levels were higher in males than females, whereas estradiol did not differ between sexes. Additionally, 17beta-HSD, 3beta-HSD, and P450arom transcript and protein expression were greater in females. After acute exercise, testosterone levels and 17beta-HSD expression increased in muscle in both sexes. By comparison, muscular estradiol levels increased in males following exercise but were unchanged in females. Expression of P450arom, which regulates estrogen synthesis, increased after acute exercise in males but decreased after exercise in females. Thus a single bout of exercise can influence the steroidogenic system in skeletal muscle, and these alterations differ between sexes. The acute exercise-induced alteration of steroidogenic enzymes may enhance the local steroidogenesis in the skeletal muscle in both sexes.

Estrogen receptor-alpha genotype affects exercise-related reduction of arterial stiffness.

PURPOSE: Arterial stiffness, an independent risk factor for cardiovascular disease, increases with advancing age. Arterial stiffness is improved by regular exercise, but individual responses to exercise training are variable. Given that estrogen and estrogen receptor-alpha (ER-alpha) can induce vasodilation and can exert an antiatherosclerotic effect in vessels, we hypothesized that gene polymorphisms of ER-alpha might influence the ability of regular exercise to improve arterial stiffness in postmenopausal women. METHODS: One hundred ninety-five healthy postmenopausal women (62 +/- 6 yr, mean +/- SD) participated in our cross-sectional study. We determined the genotype of single-nucleotide polymorphisms (SNP) at -401T/C of intron 1 of the ER-alpha gene. Arterial stiffness was measured by brachial-ankle pulse wave velocity (baPWV), and daily physical activity was estimated by a uniaxial accelerometer. Subjects were divided into active and inactive groups according to the median value (200 kcal.d(-1)) of energy expenditure. RESULTS: baPWV in individuals with the TT variant of -401T/C genotype were significantly higher than for individuals with the TC+CC genotype. No significant differences in mean baPWV values were found between the active group and the inactive group (P = 0.09). A significant reduction of baPWV secondary to increased daily physical activity was observed in individuals with the TC+CC genotype but not in individuals with the TT genotype (TT/active: 1470 +/- 36 cm.s(-1); TT/inactive: 1457 +/- 34 cm.s(-1); TC+CC/active: 1359 +/- 21 cm.s(-1); TC+CC/inactive: 1433 +/- 24 cm.s(-1)). CONCLUSION: These results suggest that ER-alpha polymorphism affects the regular exercise-related reduction in arterial stiffness in healthy postmenopausal women.

Severe Legionella pneumonia successfully treated by independent lung ventilation with intrapulmonary percussive ventilation.

A case of severe Legionella pneumonia was successfully treated by independent lung ventilation (ILV) with intrapulmonary percussive ventilation (IPV). A 57-year-old man with lobar pneumonia was intubated and mechanically ventilated because of his deteriorating respiratory status. The diagnosis of Legionella pneumonia was made on the fourth day after admission and appropriate antibiotic therapy was commenced. On the fifth hospital day, ILV was commenced because the right unaffected lung was over-distended, his haemodynamic state was unstable and his left lung was producing copious amounts of purulent sputum. His right lung was ventilated and his left lung was treated with IPV owing to the existence of massive atelectasis. After treatment with antibiotics and ILV combined with IPV, his respiratory and haemodynamic status gradually improved. On the tenth day after admission, ILV was changed to conventional bilateral ventilation. The patient was extubated on the sixteenth hospital day and discharged from the intensive care unit 30 days after admission. The combination of ILV and IPV was therapeutically effective during the acute phase of unilateral severe Legionella pneumonia.

Relationship between arterial stiffness and athletic training programs in young adult men.

BACKGROUND: We examined the relationships of endurance and strength exercise training and the adolescent duration of training to arterial stiffness in young adult men. We hypothesized that young adults participating in endurance sports would have decreased arterial stiffness, whereas those in strength-based sports would have increased arterial stiffness. In addition, we predicted that these trends would be more pronounced with an increase in the duration of sport participation. METHODS: Subjects were male endurance-trained men with short (current age, 20 years; age at beginning of competitive sport, 15 years; sport careers, 5 years; n = 7, S-ET) and long (current age, 20 years; age at beginning of competitive sport, 12 years; sport careers, 8 years; n = 7, L-ET) competitive sport careers, strength-trained men with short (current age, 20 years; age at beginning of competitive sport, 16 years; sport careers, 4 years; n = 7, S-ST) and long (current age, 22 years; age at beginning of competitive sport, 15 years; sport careers, 7 years; n = 7, L-ST) careers, and sedentary control men (aged, 20 years; n = 7, C). RESULTS: The exercise training was associated with aortic pulse wave velocity (PWV), a traditional index of arterial stiffness, and the associations were statistically independent of blood pressure (BP). Aortic PWV was lower in L-ET than C and ST. Aortic PWV in L-ST was greater than that of C. The associations of exercise training with systemic arterial compliance (SAC), which inversely correlates with arterial stiffness, were also positive and BP independent. The SAC was greater in the ET groups compared with C and ST groups. The SAC in L-ST was lower than in C. CONCLUSIONS: These results suggest that changes in arterial stiffness associated with different training programs appear in young adults as well as in older humans, and these changes may begin in adolescence.

Sex differences in the relationship between estrogen receptor alpha gene polymorphisms and arterial stiffness in older humans.

BACKGROUND: Increased arterial stiffness is an independent risk factor for cardiovascular disease. The estrogen system (estrogen and estrogen receptor-alpha [ER-alpha]) has potent vasodilator and antiatherosclerotic activity in vascular tissue and therefore was implicated in the regulation of arterial stiffness. We hypothesized that the relationship between arterial stiffness and gene polymorphisms in ER-alpha has a sex-specific component in older humans. METHODS: Two hundred healthy older subjects, comprised of 85 men and 115 postmenopausal women (men, 66 +/- 5 years old; women, 64 +/- 7 years old; mean +/- SD) participated in a cross-sectional study. We determined the genotypes of single-nucleotide polymorphisms (SNPs) at -401T/C of intron 1 and at 30T/C of exon 1 of ER-alpha, using a TaqMan-polymerase chain reaction method. Arterial stiffness was estimated by brachial-ankle pulse-wave velocity (baPWV). RESULTS: Polymorphisms of both -401T/C and 30T/C in ER-alpha affected baPWV values in postmenopausal women but did not affect men. The baPWV in women was significantly lower in the CC genotype at both -401T/C and 30T/C than in the TT genotype (both P < .05), and the CC genotype of two SNPs in women was significantly lower than in men. CONCLUSIONS: The present study suggests that the relationship between arterial stiffness and -401T/C or 30T/C polymorphisms in ER-alpha is different between sexes in older humans. These polymorphisms may be important in the health and clinical care of cardiovascular function and disease in older women.

Effect of systemic nitric oxide synthase inhibition on arterial stiffness in humans.

Stiffening of large elastic arteries impairs the buffering function of the arterial system and contributes to cardiovascular disease. The aim of this study was to determine whether endothelium-derived nitric oxide (NO) modulates the stiffness of large elastic arteries in humans. Seven apparently healthy adults (60+/-3 years, 2 males and 5 females) underwent systemic alpha-adrenergic blockade (phentolamine) and systemic NO synthase inhibition using NG-monomethyl-L-arginine (L-NMMA) in sequence. Phentolamine was given first to isolate contribution of NO to arterial stiffness by preventing reflex changes in sympathetic tone that result from systemic NO synthase inhibition, and also to compare arterial stiffness at a similar mean arterial pressure. Mean arterial blood pressure decreased (p<0.05) after phentolamine infusion but returned to baseline levels after L-NMMA infusion. The carotid beta-stiffness index (via simultaneous ultrasound and applanation tonometry on the common carotid artery) did not change after the restraint of systemic alpha-adrenergic nerve activity (9.8+/-1.2 vs. 9.1+/-1.1 U) but increased (p<0.05) after NO synthase inhibition (12.6+/-2.0 U). These results suggest that NO appears to modulate central arterial stiffness in humans.

Antagonism of endothelin action normalizes altered levels of VEGF and its signaling in the brain of stroke-prone spontaneously hypertensive rat.

Stroke-prone spontaneously hypertensive rats (SHRSP) often suffer from spontaneous stroke, in part, due to abnormalities in the cerebrovasculature. Here, we investigate the profile of key angiogenic factors and their basic signaling molecules in the brain of SHRSP during the age-dependent stages of hypertension. The profile of VEGF and its receptor, Flk-1, was dependent on age and stage of hypertension (i.e., down regulated at pre-hypertensive and malignant hypertensive stages, but up regulated at typical hypertensive stage), while that of its downstream components, pAkt and eNOS, were down regulated in a time-dependent manner in the frontal cortex of SHRSP compared to age-matched genetic control, normotensive WKY rats. On the other hand, the expression of endothelin-1 and its type A receptor (endothelin ETA receptor) were up regulated, depending on age and stage of hypertension. In contrast, levels of endothelin type B receptor were down regulated. The regional cerebral blood flow decreased during the development of malignant hypertension. Thus, subsequent experiments were designed to investigate whether endothelin-1 receptor antagonism, using endothelin-A/-B dual receptor antagonist SB209670, could normalize the molecular profile of these factors in SHRSP brain. Interestingly, blockage of endothelin-1 receptor restored to normal, levels of cerebral endothelin-1, endothelin ETA receptor and endothelin ETB receptor; VEGF and Flk-1; endothelial nitric oxide synthase (eNOS) and pAkt, in SHRSP, compared to age-matched WKY. Endothelin receptor blocker might be important to prevent the progression in the defect in VEGF and its angiogenic signaling cascade in the pathogenesis of hypertension-induced vascular remodeling in frontal cortex of SHRSP rats.

Postexercise heart rate recovery accelerates in strength-trained athletes.

UNLABELLED: The left ventricle morphologically adapts to endurance exercise training (eccentric cardiac remodeling) and strength exercise training (concentric remodeling). In addition, the acceleration of vagally mediated heart rate (HR) recovery after exercise is one of the functional adaptations of the heart in endurance-trained humans. However, the effect of strength training on HR recovery is unclear. PURPOSE: The purpose of this study was to investigate whether postexercise HR recovery accelerates in strength-trained athletes. METHODS: Subjects were young strength-trained athletes (ST; N = 12), endurance-trained athletes (ET; N = 12), and age-matched sedentary control men (C; N = 12). HR and oxygen uptake were measured during submaximal exercise (cycling exercise, 40% maximal oxygen uptake for 8 min) and 30 s after the exercise (the postexercise period). RESULTS: Left ventricular end-diastolic dimension was higher in both types of athletes compared with C, but greater in ET than in ST (C, 4.3 +/- 0.1 cm; ET, 5.0 +/- 0.1 cm; ST, 4.8 +/- 0.1 cm). Left ventricular average wall thickness was greater in ST in comparison with ET, although it was higher in both trained men compared with C (C, 0.85 +/- 0.02 cm; ET, 0.90 +/- 0.02 cm; ST, 1.00 +/- 0.02 cm). The time constant of postexercise HR decay, an index of vagally mediated postexercise HR recovery, was lower in ST and ET compared with C (C, 94.4 +/- 9.2 s; ET, 65.9 +/- 4.3 s; ST, 69.1 +/- 4.0 s). Oxygen pulse was greater in ST and ET than in C (C, 9.4 +/- 0.6 mL per beat; ET, 13.0 +/- 0.9 mL per beat; ST, 12.8 +/- 0.4 mL per beat), and it results in increased oxygen debt for both types of athletes (C, 0.257 +/- 0.024 L; ET, 0.343 +/- 0.030 L; ST, 0.331 +/- 0.017 L). We did not find significant differences in these indices between ST and ET. CONCLUSIONS: These results suggest that the HR recovery immediately after exercise is accelerated in both strength- and endurance-trained athletes.

The number of microvascular complications is associated with an increased risk for severity of periodontitis in type 2 diabetes patients: Results of a multicenter hospital-based cross-sectional study.

AIMS/INTRODUCTION: To explore the relationships between periodontitis and microvascular complications as well as glycemic control in type 2 diabetes patients. MATERIALS AND METHODS: This multicenter, hospital-based, cross-sectional study included 620 patients with type 2 diabetes. We compared the prevalence and severity of periodontitis between patients with ≥1 microvascular complication and those without microvascular complications. We also compared the prevalence and severity of periodontitis among patients with different degrees of glycemic control. RESULTS: After adjusting for confounding factors, multiple logistic regression analysis showed that the severity of periodontitis was significantly associated with the number of microvascular complications (odds ratio 1.3, 95% confidence interval 1.1-1.6), glycated hemoglobin ≥8.0% (64 mmol/mol; odds ratio 1.6; 95% confidence interval 1.1-2.3), and older age (≥50 years; odds ratio 1.7; 95% confidence interval 1.1-2.6). However, the prevalence of periodontitis was not significantly associated with the number of microvascular complications, but was associated with male sex, high glycated hemoglobin (≥8.0% [64 mmol/mol]), older age (≥40 years), longer duration of diabetes (≥15 years) and fewer teeth (≤25). Furthermore, propensity score matching for age, sex, diabetes duration and glycated hemoglobin showed that the incidence of severe periodontitis was significantly higher among patients with microvascular complications than among those without microvascular complications (P < 0.05). CONCLUSIONS: The number of microvascular complications is a risk factor for more severe periodontitis in patients with type 2 diabetes, whereas poor glycemic control is a risk factor for increased prevalence and severity of periodontitis.

Activation pattern of MAPK signaling in the hearts of trained and untrained rats following a single bout of exercise.

Since exercise training causes cardiac hypertrophy and a single bout induces mechanical stress to the heart, the present study aimed to characterize the activation patterns of multiple MAPK signaling pathways in the heart after a single bout of exercise or chronic exercises. The hearts of untrained rats received 5, 15, and 30 min of treadmill running exercise (Ex5 to Ex30) and rested for 0.5, 1, 3, 6, 12, and 24 h (PostEx0.5 to PostEx24) before subjecting them to the following different experiments. Activation of MAPKs (ERK, JNK, and p38) and MAPKKs (MEK1/2, SEK, and MKK3/6) increased immediately after acute exercise in a time-dependent manner, with ERK, JNK, and p38 peaking at Ex15, Ex15, and Ex30, respectively. Expression of immediate early genes (c-fos, c-jun, and c-myc) was augmented and activator protein-1 DNA binding activity was enhanced in untrained rats immediately after a single bout of exercise. The elevated levels of MAPKs declined to the resting levels within 24 h after exercise. In another set of experiments, following 4, 8, and 12 wk of exercise training, the rats exhibited significant cardiac hypertrophy by week 12. Activation of MAPKs in the 4-wk-trained rats increased after a 30-min single bout of exercise but decreased in the 8-wk group. Finally, the activity of MAPKs signaling in the 12-wk-trained rats exposed to an acute bout of exercise was unaltered. We conclude that exercise induces the activation of multiple MAPK (ERK, JNK, and p38) pathways in the heart, an effect that gradually declines with the development of exercise-induced cardiac hypertrophy.

Age-related reduction of systemic arterial compliance relates to decreased aerobic capacity during sub-maximal exercise.

A decrease in systemic arterial compliance (SAC) increases left ventricular load along with the demand for excessive myocardial oxygen consumption when the age-related reduction of SAC reaches a marked level, and consequently may depress left ventricular pump function. Reduced left ventricular pump function decreases aerobic capacity, and some study groups have shown that SAC and/or central arterial distensibility is correlated with maximal aerobic capacity in humans. We thus hypothesize that, once the age-related reduction of SAC reaches a marked level, the participation of SAC in aerobic capacity will be significant even during sub-maximal exercise. Thirty young humans and 46 elderly humans participated in this study. SAC, oxygen uptake at the ventilatory threshold (VO2VT), and the ratio of increase in oxygen uptake, in cardiac output, and in effective arterial elastance to increase in work rate (deltaVO2/deltaWR, deltaCO/deltaWR and deltaEa/deltaWR) were measured. SAC was significantly higher in young subjects compared with elderly subjects, and was significantly related to VO2VT in elderly subjects. SAC also significantly correlated with deltaVO2/deltaWR, deltaCO/deltaWR and deltaEa/deltaWR in elderly subjects. When total subjects were divided by the value of SAC into 6 groups, the VO2VT values in the 3 groups with lower SAC were significantly lower than those in the 3 groups with higher SAC, and gradually decreased with the reduction of SAC. There were no changes in VO2VT among the 3 groups with higher SAC. These results suggest that the participation of SAC in aerobic capacity is significant even during sub-maximal exercise in individuals who show a pronounced age-related reduction of SAC.

Age-related reduction of systemic arterial compliance induces excessive myocardial oxygen consumption during sub-maximal exercise.

Reduction of systemic arterial compliance (SAC) with aging increases left ventricular afterload. The present study was designed to examine whether age-related reduction of SAC is related to excessive myocardial oxygen consumption during sub-maximal aerobic exercise. We studied elderly (60-69 years; n = 25) and senior (70-82 years; n = 25) subjects. We measured SAC immediately before the start of the ramp-fashion exercise (i.e., at the end of the 20 W warm-up exercise) and the double product (DP: systolic blood pressure x heart rate) during the ramp-fashion exercise (20-50 W). SAC was significantly lower in senior subjects (0.76 +/- 0.25 ml mmHg(-1) m(-2)) compared with elderly subjects (0.95 +/- 0.22 ml mmHg(-1) m(-2)). DP was higher in senior subjects (20 W: 14.3 +/- 3.1; 30 W: 15.9 +/- 4.2; 40 W: 17.7 +/- 4.9; 50 W: 20.6 +/- 5.6 [x 10(3) mmHg bpm]) than in elderly subjects (12.8 +/- 3.0, 14.0 +/- 3.5, 15.1 +/- 4.0, 17.1 +/- 4.3 [x 10(3) mmHg bpm]). In total subjects, SAC correlated significantly with DP (r = -0.64, r = -0.64, r = -0.64, r = -0.64). In senior subjects, SAC was related significantly to DP (r = -0.83, r = -0.78, r = -0.76, r = -0.74). In elderly subjects, SAC tended to correlate with DP although its relationships were not statistically significant (r = -0.34, r = -0.36, r = -0.33, r = -0.31). Correlation coefficients at each respective exercise intensity were significantly higher in senior subjects compared with elderly subjects. These results suggest that the age-related reduction of SAC is related to excessive myocardial oxygen consumption during sub-maximal aerobic exercise in older humans, but this relation does not become significant until the SAC reduction becomes pronounced.