Effects of yoga exercise on salivary beta-defensin 2

Purpose

Yoga stretching can be done comfortably and easily by beginners and older adults to compensate for lack of exercise or poor health maintenance. The aim of this study was to determine the effect of yoga stretching on mucosal immune functions, primarily human β-defensin 2 (HBD-2) in saliva.

Methods

Fifteen healthy adults (age, 60.4 ± 8.0 years) participated in the study. Participants rested for 90 min on the first day and performed yoga for 90 min on the second day. Measurements were carried out before and after rest or yoga. Saliva samples were collected by chewing a sterile cotton at a frequency of 60 cycles per min. Salivary HBD-2 concentration was measured using an enzyme-linked immunosorbent assay.

Results

HBD-2 concentration after yoga stretching (165.4 ± 127.1 pg/mL) was significantly higher than that before yoga stretching (84.1 ± 63.4 pg/mL; p < 0.01). HBD-2 expression rate after yoga stretching (232.8 ± 192.9 pg/min) was significantly higher than that before yoga stretching (110.7 ± 96.8 pg/min; p < 0.01). HBD-2 concentration (p < 0.05) and HBD-2 expression rate (p < 0.01) at post on the second day (yoga) was significantly higher than that on the first day (rest). POMS score of anger-hostility was lower after yoga than before.

Conclusions

Yoga stretching for 90 min can increase salivary HBD-2 expression in older adults. Therefore, yoga stretching might be useful for older adults and athletes to maintain their health.     

The effects of short-term fish oil supplementation on pulmonary function and airway inflammation following a high-fat meal

Introduction

Many environmental and dietary influences can cause immune cells to produce biological mediators that increase airway inflammation. A high-fat meal (HFM) is one stimulus that increases airway inflammation in healthy individuals. Supplementation with omega-3 fatty acids can reduce inflammation systemically and may be beneficial to the airways.

Purpose

To determine if omega-3 fatty acid supplementation via fish oil would mitigate the airway inflammatory response induced by a single HFM.

Methods

Seventeen non-asthmatic men (22 ± 2 years.) were supplemented with 3,000 mg × day^?1 fish oil or a placebo for 3 weeks. Fractional exhaled nitric oxide (FE_NO; a marker of airway inflammation), impulse oscillometry (a measure of respiratory impedance), pulmonary function, and triglycerides were measured prior to and 2 h following a HFM.

Results

Following a HFM, triglycerides increased in both fish oil and placebo groups compared to pre-HFM (~59 and ~49 %, respectively, p < 0.05). The percent increase in FE_NO was greater in the placebo group compared to the fish oil group (25.7 ± 16.7 vs. ?1.99 ± 10.5 %, respectively, p < 0.05). A significant correlation was observed between blood triglycerides and FE_NO in the placebo group (r = 0.61; p < 0.05), but not the fish oil group (p = 0.21).

Conclusion

A single HFM increases airway inflammation and omega-3 fatty acid supplementation via fish oil protects against HFM associated changes in airway health.     

Trends in Underweight and Overweight/Obesity Prevalence in Chinese Youth, 2004–2009

Background

There is a paucity of recent data on Chinese childhood overweight and underweight prevalence especially since 2004.

Purpose

The purpose of this study was to examine trends in underweight and overweight/obesity (“overweight” hereafter) prevalence and energy balance-related behaviors of Chinese youth from 2004 to 2009.

Methods

Data from the China Health and Nutrition Survey, 2004–2009 (N?=?4,061 students aged 6–18 years), were analyzed. Trained health workers took anthropometric measures at the participant’s house or at a local clinic following a reference protocol recommended by the World Health Organization. The international age- and sex-specific body mass index reference standard proposed by the International Obesity Task Force was used to define underweight and overweight children in this study.

Results

Among 6- to 11-year-old boys, underweight prevalence increased from 14.5 % (2004) to 20.1 % (2009, p?=?0.068). Among 12- to 18-year-old boys, however, overweight prevalence increased from 7.5 to 12.6 % (p?=?0.034). From 2004 to 2009, after-school sedentary behavior increased from 2.3 to 3.4 h/day for 6- to 11-year-olds (p?<?0.001) and from 2.2 to 3.1 h/day for 12- to 18-year-olds (p?<?0.01). Meanwhile, the total energy intake decreased 7 % for 6- to 11-year-olds (p?<?0.05) and 10 % for 12- to 18-year-olds (p?<?0.01).

Conclusions

Both underweight and overweight Chinese students are increasing, with underweight increases more pronounced in 6- to 11-year-olds and overweight increases more pronounced in 12- to 18-year-olds. Nationwide efficacious interventions are needed that improve the diet, decrease sedentary behavior, and encourage a healthy and realistic body image in Chinese youth.     

Human cytomegalovirus-encoded miR-UL112 contributes to HCMV-mediated vascular diseases by inducing vascular endothelial cell dysfunction

Human cytomegalovirus (HCMV) infection has been linked to the pathogenesis of vasculopathy by inducing dysfunction of vascular cells such as endothelial cells. Hcmv-miR-UL112 is the most well-characterized HCMV-encoded microRNA occurring in the plasma of patients with cardiovascular diseases such as hypertension, while the specific underlying pathophysiological mechanisms are yet to be defined. The current study investigated the effect of hcmv-miR-UL112 on the growth and proliferation of human umbilical vascular endothelial cells (HUVECs); it might also be associated with signaling pathways. An adenovirus vector was designed and synthesized to stably express hcmv-miR-UL112 in HUVECs. Cell Counting Kit-8 results showed that ectopically expressed hcmv-miR-UL112 can significantly increase the proliferation of HUVECs (p < 0.05). Flow cytometry revealed that the S-phase fraction in the cell cycle analysis was raised significantly after overexpression of hcmv-miR-UL112 (p < 0.05). Gene expression profile analysis, using the microarray technology, revealed 303 up-regulated and 62 down-regulated genes in HUVECs by comparing the AD-hcmv-miR-UL112-infected and control groups (p < 0.05 and > 2 fold change). Kyoto Encyclopedia of Genes and Genomes and Reactome Pathway, chosen as the functional annotation categories, were affected by hcmv-miR-UL112 adenovirus vector. The significantly altered pathways mainly include the mitogen-activated protein kinase signaling pathway, cell adhesion molecules, chemokine signaling pathway, cytokine–cytokine receptor interaction, circadian rhythm-mammal, mineral absorption, protein processing in the endoplasmic reticulum, proximal tubule bicarbonate reclamation, vasopressin-regulated water reabsorption, and arachidonic acid metabolism. In conclusion, hcmv-miR-UL112 could serve as a potential biomarker, and the miRNA-mediated regulation of signaling pathways might play significant roles in the physiological effects of hcmv-associated diseases.     

Lung inflammation is induced by renal ischemia and reperfusion injury as part of the systemic inflammatory syndrome

Introduction

Ischemia and reperfusion injury (IRI) are mainly caused by leukocyte activation, endothelial dysfunction and production of reactive oxygen species. Moreover, IRI can lead to a systemic response affecting distant organs, such as the lungs.

Aim

The objective was to study the pulmonary inflammatory systemic response after renal IRI.

Methods

Male C57Bl/6 mice were subjected to 45 min of bilateral renal ischemia, followed by 4, 6, 12, 24 and 48 h of reperfusion. Blood was collected to measure serum creatinine and cytokine concentrations. Bronchoalveolar lavage fluid (BALF) was collected to determine the number of cells and PGE₂ concentration. Expressions of iNOS and COX-2 in lung were determined by Western blot. Gene analyses were quantified by real time PCR.

Results

Serum creatinine increased in the IRI group compared to sham mainly at 24 h after IRI (2.57 ± 0.16 vs. 0.43 ± 0.07, p < 0.01). The total number of cells in BAL fluid was higher in the IRI group in comparison with sham, 12 h (100 × 10⁴ ± 15.63 vs. 18.1×10⁴ ± 10.5, p < 0.05) 24 h (124 × 10⁴ ± 8.94 vs. 23.2×10⁴ ± 3.5, p < 0.05) and 48 h (79 × 10⁴ ± 15.72 vs. 22.2 × 10⁴ ± 4.2, p < 0.05), mainly by mononuclear cells and neutrophils. Pulmonary COX-2 and iNOS were up-regulated in the IRI group. TNF-α, IL-1β, MCP-1, KC and IL-6 mRNA expression were up-regulated in kidney and lungs 24 h after renal IRI. ICAM-1 mRNA was up-regulated in lungs 24 h after renal IRI. Serum TNF-α, IL-1β and MCP-1 and BALF PGE₂ concentrations were increased 24 h after renal IRI.

Conclusion

Renal IRI induces an increase of cellular infiltration, up-regulation of COX-2, iNOS and ICAM-1, enhanced chemokine expression and a Th1 cytokine profile in lung demonstrating that the inflammatory response is indeed systemic, possibly leading to an amplification of renal injury.     

Association of Psychiatric History and Type D Personality with Symptoms of Anxiety, Depression, and Health Status Prior to ICD Implantation

Background

Personality factors and psychiatric history may help explain individual differences in risk of psychological morbidity and poor health outcomes in patients with an implantable cardioverter defibrillator (ICD).

Purpose

We examined associations between previous anxiety and depressive disorder, type D personality, anxiety or depressive symptoms, and health status in ICD patients prior to ICD implantation.

Method

Patients (N?=?278; 83 % men; mean age?=?62.2 years ±11) receiving a first ICD from September 2007 through April 2010 at the Medisch Spectrum Twente, The Netherlands completed validated questionnaires before implantation assessing type D personality (14-item Type D Scale), anxiety and depressive symptoms (Hospital Anxiety and Depression Scale), and health status (36-item Short Form Health Survey). History of anxiety or depressive disorder was assessed with the Mini International Neuropsychiatric Interview structural interview.

Results

Previous anxiety or depressive disorder was prevalent in 8 and 19 % of patients, respectively. Type D personality was present in 21 %, depressive symptoms in 15 %, and anxiety in 24 %. In adjusted analyses, type D personality was a dominant correlate of previous depressive disorder (odds ratio (OR) 6.2, p?<?0.001) and previous anxiety disorder (OR 3.9, p?=?0.004). Type D personality (OR 4.0, p?<?0.001), age (OR 1.03, p?=?0.043), and gender (OR 2.5, p?=?0.013) were associated with anxiety symptoms at baseline. Type D personality (OR 5.9. p?<?0.001) was also associated with increased depressive symptoms at baseline. Heart failure and type D personality were related to poorer health status.

Conclusion

In ICD patients, prior to ICD implantation, a previous anxiety or depressive disorder, type D personality, and anxiety and depressive symptoms were associated with poorer health status. Type D personality was also independently associated with increased anxiety and depression symptoms.     

Influence of exercise intensity on respiratory muscle fatigue and brachial artery blood flow during cycling exercise

Purpose

During high intensity exercise, both respiratory muscle fatigue and cardiovascular reflexes occur; however, it is not known how inactive limb blood flow is influenced. The purpose of this study was to determine the influence of moderate and high exercise intensity on respiratory muscle fatigue and inactive limb muscle and cutaneous blood flow during exercise.

Methods

Twelve men cycled at 70 and 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) for 20 min. Subjects also performed a second 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) test after ingesting 1,800 mg of N-acetylcysteine (NAC), which has been shown to reduce respiratory muscle fatigue (RMF). Maximum inspiratory pressures (P _Imax), brachial artery blood flow (BABF), cutaneous vascular conductance (CVC), and mean arterial pressure were measured at rest and during exercise.

Results

Significant RMF occurred with 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) (P _Imax, ?12.8 ± 9.8 %), but not with 70 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) (P _Imax, ?5.0 ± 5.9 %). BABF and BA vascular conductance were significantly lower at end exercise of the 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) test compared to the 70 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) test. CVC during exercise was not different (p > 0.05) between trials. With NAC, RMF was reduced (p < 0.05) and BABF was significantly higher (~30 %) compared to 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) (p < 0.05).

Conclusions

These data suggest that heavy whole-body exercise at 85 % \(\dot{V}{\text{O}}_{{ 2_{ {\rm max} } }}\) leads to RMF, decreases in inactive arm blood flow, and vascular conductance, but not cutaneous blood flow.     

Role of nitric oxide in muscle regeneration following eccentric muscle contractions in rat skeletal muscle

We examined the role of nitric oxide (NO) in muscle repair and regeneration following repetitive eccentric contractions (ECC). A standardized exercise protocol was used to create eccentric contraction-induced injury to the left tibialis anterior muscle of 48 male Wistar rats (body wt 250–350 g), using a customized isokinetic test device and a bout of 40 ECCs under electrical stimulation. A nitric oxide synthase inhibitor, N(G)-nitro-l-arginine-methyl ester (l-NAME; 35 mg kg^?1 day^?1), was included in the diet for half the animals (n = 24) beginning 3 days prior to the ECC and continuing throughout the experiment, whereas the other half (n = 24) received a control diet. ECC/+l-NAME and ECC/?l-NAME were killed after the ECC protocol at 0, 1, 3 and 7 days (n = 6 on each day). An unexercised contralateral limb with and without l-NAME infusion served as a respective control muscle at each time point. Muscle NO content, skeletal muscle damage, leukocyte infiltration, calpain activity, and MyoD and myogenin expression were assessed. NO has both pro-inflammatory and anti-inflammatory properties, and several possible roles for NO in skeletal muscle damage have been postulated. NO content was greater in the ECC/?l-NAME group at all time points (p < 0.05) compared to ECC/+l-NAME. Additionally, significant differences in NO content were observed on day 0 (p < 0.05), and day 3 (p < 0.05), ECC/+l-NAME versus ECC/?l-NAME. One day following the bout of ECC, and NO levels were increased in the ECC/?l-NAME group. Three days following ECC, there was greater myofiber damage (measured by β-glucuronidase activity) and leukocyte invasion in the ECC/?l-NAME group as compared to the ECC/+l-NAME group. One day after ECC, calpain activity was significantly increased in ECC/?l-NAME compared with control muscles (p < 0.05). On days 3 and 7, Myo-D and myogenin gene expression was increased in both groups; however, the degree of regeneration was less in the ECC/+l-NAME-treated animals. These data suggest that NO dynamics have important implications in the regulation of various factors during skeletal muscle regeneration following damaging eccentric muscle contractions.     

Faster \dot{V}{\text{O}}_{ 2} kinetics after eccentric contractions is explained by better matching of O2 delivery to O2 utilization

Purpose

This study examined the impact of eccentric exercise-induced muscle damage on the rate of adjustment in muscle deoxygenation and pulmonary O₂ uptake ( \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) kinetics during moderate exercise.

Methods

Fourteen males (25 ± 3 year; mean ± SD) completed three step transitions to 90 % θ_L before (Pre), 24 h (Post24) and 48 h after (Post48) eccentric exercise (100 eccentric leg-press repetitions with a load corresponding to 110 % of the participant’s concentric 1RM). Participants were separated into two groups: phase II \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) time constant (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) ≤ 25 s (fast group; n = 7) or τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\)  > 25 s (slow group; n = 7). \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) and [HHb] responses were modeled as a mono-exponential.

Results

In both groups, isometric peak torque (0°/s) at Post24 was decreased compared to Pre (p < 0.05) and remained depressed at Post48 (p < 0.05). τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) was designed to be different (p < 0.05) at Pre between the Fast (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ; 19 ± 4 s) and Slow (32 ± 6 s) groups. There were no differences among time points (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) : Pre, 19 ± 4 s; Post24, 22 ± 3 s; Post48, 20 ± 4 s) in the Fast group. In Slow, there was a speeding (p < 0.05) from the Pre (32 ± 6 s) to the Post24 (25 ± 6) but not Post48 (31 ± 6), resulting in no difference (p > 0.05) between groups at Post24. This reduction of τ \(\dot{V}{\text{O}}_{{2{\text{p}}}} \,\) was concomitant with the abolishment (p < 0.05) of an overshoot in the [HHb]/ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ratio.

Conclusion

We propose that the sped \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) kinetics observed in the Slow group coupled with an improved [HHb]/ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ratio suggest a better matching of local muscle O₂ delivery to O₂ utilization following eccentric contractions.     

Immunoglobulin Dosage and Switch from Intravenous to Subcutaneous Immunoglobulin Replacement Therapy in Patients with Primary Hypogammaglobulinemia: Decreasing Dosage Does Not Alter Serum IgG Levels

Objective

The impact of reducing immunoglobulin dosage while switching from intravenous to subcutaneous replacement therapy was evaluated.

Methods

Sixty-five patients with primary hypogammaglobulinemia on stable intravenous replacement therapy were included in a monocentric longitudinal trial. IgG trough levels were measured at baseline and during 1 year following the switch to the subcutaneous route.

Results

Mean IgG trough level after 12 months of subcutaneous therapy was increased by 5.4% (8.37–8.82 g/l, p?=?0.3), while immunoglobulin dosage had been reduced by 28.3% (151–108 mg/kg/week, p?<?0.0001). For the patients with the lowest serum IgG level upon intravenous infusions, serum IgG level rose by 37% (5.33–7.33 g/l, p?=?0.003), while mean immunoglobulin dosage was reduced by 36% (170–109 mg/kg/week, p?=?0.04).

Conclusion

The present study shows that sustained serum IgG levels can be achieved after switching towards subcutaneous replacement despite using reduced immunoglobulin doses.     

Can a combination of handgrip exercise and prolonged forearm occlusion elicit a maximal brachial artery FMD response?

Introduction

The upper limit of brachial artery (BA) flow-mediated dilation (FMD) has not been thoroughly interrogated, and long duration occlusion + handgrip exercise may create larger shear stress stimuli than previous manipulations.

Purpose

To determine whether novel combinations of occlusion + handgrip exercise can extend the range of FMD stimulus–response relationship characterization and permit identification of a BA-FMD response ceiling.

Methods

Ten healthy subjects performed eight reactive hyperemia (RH) FMD trials: 5, 10, and 15 min of occlusion (5RH, 10RH, 15RH); 5, 10 and 15 min of occlusion + 3-min ischemic exercise (IE) (5IE, 10IE, 15IE); 10 and 15 min of occlusion + 3-min IE + 4-min post-occlusion exercise (PE) (10IEPE, 15IEPE). Shear stress was estimated as shear rate (SR = blood velocity/BA diameter; (ultrasound assessment)) (SR stimulus = area under the curve (AUC) until peak diameter). Data are mean ± SE.

Results

There were no differences in SR-AUC among IE and IEPE trials (p > 0.70), however, IE consistently increased the SR-AUC (IE + IEPE trial average 17,845.1 ± 2,023.3 a.u.) vs. the 5RH and 10RH trials (4,943.0 ± 428.4 a.u., 6,800.6 ± 805.9 a.u.) (p < 0.05). The %FMD ranged from 7.3 ± 0.8 % (5RH) to 19.1 ± 2.0 % (15IEPE) (p < 0.001) with no differences among IE and IEPE trials (p > 0.16). FMD increased with increasing SR-AUC (all subjects, all trials: r ² 0.36, p < 0.001)

Conclusions

The stimulus created by brief (5 min) occlusion + ischemic exercise was not significantly enhanced by prolonging occlusion or continuing to exercise post-occlusion. The FMD response did not clearly plateau with increasing stimulus magnitude; however, the FMD capacity was shown to be more than double the FMD magnitude that was elicited with a standard 5-min occlusion test.     

Maximal strength,power, and aerobic endurance adaptations to concurrent strength and sprint interval training

Purpose

This study was designed to examine whether concurrent sprint interval and strength training (CT) would result in compromised strength development when compared to strength training (ST) alone. In addition, maximal oxygen consumption (VO₂max) and time to exhaustion (TTE) were measured to determine if sprint interval training (SIT) would augment aerobic performance.

Methods

Fourteen recreationally active men completed the study. ST (n = 7) was performed 2 days/week and CT (n = 7) was performed 4 days/week for 12 weeks. CT was separated by 24 h to reduce the influence of acute fatigue. Body composition was analyzed pre- and post-intervention. Anaerobic power, one-repetition maximum (1RM) lower- and upper-body strength, VO₂max and TTE were analyzed pre-, mid-, and post-training. Training intensity for ST was set at 85 % 1RM and SIT trained using a modified Wingate protocol, adjusted to 20 s.

Results

Upper- and lower-body strength improved significantly after training (p < 0.001) with no difference between the groups (p > 0.05). VO₂max increased 40.9 ± 8.4 to 42.3 ± 7.1 ml/kg/min (p < 0.05) for CT, whereas ST remained unchanged. A significant difference in VO₂max (p < 0.05) was observed between groups post-intervention (CT: 42.3 ± 7.1 vs. ST: 36.0 ± 3.0 ml/kg/min). A main effect for time and group was observed in TTE (p < 0.05). A significant main effect for time was observed in average power (p < 0.05).

Conclusion

Preliminary findings suggest that performing concurrent sprint interval and strength training does not attenuate the strength response when compared to ST alone, while also improves aerobic performance measures, such as VO₂max at the same time.     

Atrial functional and geometrical remodeling in highly trained male athletes: for better or worse?

Purpose

Highly trained athletes have an increased risk of atrial arrhythmias. Atrial geometrical and functional remodeling may be the underlying substrate. We analyze and relate atrial size, deformation and performance in professional handball players compared with non-sportive subjects.

Methods

24 Professional handball players and 20 non-sportive males were compared. All subjects underwent an echocardiographic study with evaluation of left (LA), right atrial (RA) dimensions and deformation by strain (Sa) and strain rate (SRa). Atrial performance was assessed from the atrial stroke volume (SV). With computational geometrical models, we studied the relation between atrial volumes, strains and SV and compared atrial working conditions. We estimated the functional reserve and a resulting average wall stress.

Results

LA and RA volumes were larger in athletes than in controls (35.2 ± 8.8 vs. 24.8 ± 4.3 ml/m², p < 0.01 and 29.0 ± 8.4 vs. 19.0 ± 5.1 ml/m², p < 0.01 respectively). LASa and RASa during active atrial contraction were decreased in athletes (?12.2 ± 2.0 vs. ?14.5 ± 2.1 %, p < 0.01 and ?12.1 ± 1.8 vs. ?14.2 ± 1.5 %, p < 0.01 respectively). LASV was similar between groups (6.6 ± 1.4 vs. 7.3 ± 1.1 ml, p = 0.19) and RASV was lower in athletes (6.2 ± 1.3 vs. 7.2 ± 1.1 ml, p < 0.01). Computational models showed that this different operational mode potentially increases performance reserve, but at the cost of higher atrial wall stress.

Conclusion

A proportion of athletes with enlarged LA and RA showed different atrial contractile performance, likely resulting in atria working at higher wall stress.     

Heart rate recovery normality data recorded in response to a maximal exercise test in physically active men

Background

Despite a growing clinical interest in determining the heart rate recovery (HRR) response to exercise, the limits of a normal HRR have not yet been well established.

Purpose

This study was designed to examine HRR following a controlled maximal exercise test in healthy, physically active adult men.

Methods

The subjects recruited (n = 789) performed a maximal stress test on a treadmill. HRR indices were calculated by subtracting the first and third minute heart rates (HRs) during recovery from the maximal HR obtained during stress testing and designated these as HRR-1 and HRR-3, respectively. The relative change in HRR was determined as the decrease in HR produced at the time points 1 and 3 min after exercise as a percentage of the peak HR (%HRR-1/HR_peak and %HRR-3/HR_peak, respectively). Percentile values of HRR-1 and HRR-3 were generated for the study population.

Results

Mean HHR-1 and HHR-3 were 15.24 ± 8.36 and 64.58 ± 12.17 bpm, respectively, and %HRR-1/HR_peak and %HRR-3/HR_peak were 8.60 ± 4.70 and 36.35 ± 6.79 %, respectively. Significant correlation was detected between Peak VO₂ and HRR-3 (r = 0.36; p < 0.001) or %HRR-3/HR_peak (r = 0.23; p < 0.001).

Conclusions

Our study provides normality data for HRR following a maximal Ergometry test obtained in a large population of physically active men.     

The order effect of combined endurance and strength loadings on force and hormone responses: effects of prolonged training

Purpose

To examine acute responses and recovery of force and serum hormones to combined endurance and strength loadings utilizing different orders of exercises before and after training.

Methods

Physically active men were matched to an order sequence of endurance followed by strength (E + S, n = 12) or strength followed by endurance (S + E, n = 17). The subjects performed one experimental loading consisting of steady-state cycling and a leg press protocol before and after 24 weeks of order-specific combined training.

Results

No between-group difference in acute reductions of force was observed at week 0 (E + S ?23 %, p < 0.001; S + E ?22 %, p < 0.01) and 24 (E + S ?25 %, p < 0.001; S + E ?27 %, p < 0.001) and recovery in force was completed after 24 h in both groups at week 0 and 24. Concentrations of growth hormone (22-kDa) increased post-acute loading at week 0 (E + S, +57 fold, p < 0.05; S + E, +300 fold, p < 0.001; between-groups p < 0.001) and 24 (E + S, +80 fold, p < 0.01; S + E, +340 fold, p < 0.05; between-groups p < 0.05). No significant acute responses in concentrations of testosterone were observed at week 0 or 24. However, at week 0 testosterone was reduced during recovery following the E + S loading only (24 h ?23 %, p < 0.01; 48 h ?21 %, p < 0.001; between-groups at 24 and 48 h, p < 0.05), but was no longer observed after training. 1RM strength improved similarly in E + S (13 %, p < 0.001) and S + E (17 %, p < 0.001).

Conclusions

This study showed an order effect (E + S vs. S + E) in concentrations of testosterone during 2 days of recovery at week 0, which was diminished after 24 weeks of training. The initial difference in testosterone concentrations during recovery did not seem to be associated with strength development.     

The validity of the Moxus Modular metabolic system during incremental exercise tests: impacts on detection of small changes in oxygen consumption

Purpose

We investigated the accuracy of the Moxus Modular Metabolic System (MOXUS) against the Douglas Bag Method (DBM) during high-intensity exercise, and whether the two methods agreed when detecting small changes in $\dot{V}{\text{O}}_{2}$ between two consecutive workloads ( $\Delta {\dot{{V}}\text{O}}_{ 2}$ ).

Methods

Twelve trained male runners performed two maximal incremental running tests while gas exchange was analyzed simultaneously by the two systems using a serial setup for four consecutive intervals of 30 s on each test. Comparisons between methods were performed for $\dot{V}{\text{O}}_{2}$ , ${\dot{{V}}}_{\text{E}}$ , fractions of expired O₂ (FeO₂) and CO₂ (FeCO₂) and $\Delta {\dot{{V}}\text{O}}_{ 2}$ .

Results

The MOXUS produced significant higher (mean ± SD, n = 54) readings for $\dot{V}{\text{O}}_{2}$ (80 ± 200 mL min^?1, p = 0.005) and ${\dot{{V}}}_{\text{E}}$ (2.9 ± 4.2 L min^?1, p < 0.0001), but not FeO₂ (?0.01 ± 0.09). Log-transformed 95 % limits of agreement for readings between methods were 94–110 % for $\dot{V}{\text{O}}_{2}$ , 97–108 % for $\dot{V}_{\text{E}}$ and 99–101 % for FeO₂. $\Delta \dot{V}{\text{O}}_{2}$ for two consecutive measurements was not different between systems (120 ± 110 vs. 90 ± 190 mL min^?1 for MOXUS and DBM, respectively, p = 0.26), but agreement between methods was very low (r = 0.25, p = 0.12).

Discussion

Although it was tested during high-intensity exercise and short sampling intervals, the MOXUS performed within the acceptable range of accuracy reported for automated analyzers. Most of the differences between equipments were due to differences in $\dot{V}_{\text{E}}$ . Detecting small changes in $\dot{V}{\text{O}}_{2}$ during an incremental test with small changes in workload, however, might be beyond the equipment’s accuracy.     

Simvastatin inhibits cytokines in a dose response in patients with rheumatoid arthritis

Objective and design

To evaluate the effects of simvastatin in peripheral blood mononuclear cell (PBMC) cytokines profiles and correlate with the disease state of rheumatoid arthritis (RA) patients.

Methods

The PBMC from 22 RA patients were purified and stimulated or not stimulated with phorbol myristate acetate/ionomycin and were treated with simvastatin in different doses. Cytokine levels were quantified by ELISA and patients were assessed for clinical and laboratory variables. This assessment included disease activity measures [Clinical Disease Activity Index (CDAI), Disease Activity Score for 28 joints (DAS28)] and a Health Assessment Questionnaire.

Results

The IL-17A, IL-6, IL-22 and IFN-γ were significantly reduced in a dose response after simvastatin treatment (50 μM, p = 0.0005; p < 0.0001; p < 0.02; p = 0.0005, respectively). The IL-17A and IL-6 cytokines were also significantly reduced in lower concentrations of simvastatin (10 μM) compared to controls (p = 0.018; p = 0.04) and compared to the standard drug (p = 0.007; p = 0.0001). The results also showed that only RA patients with severe disease (DAS28 >5.1 and CDAI >22) had poor response to simvastatin in reducing cytokines levels, mainly for IL-17A and IL-22 cytokines (p = 0.03; p = 0.039, respectively).

Conclusion

The RA patients in clinical remission, mild or moderate had lower levels of all cytokines analyzed after simvastatin treatment, showing that these patients have better response to treatment. Our findings suggest that the simvastatin therapy modulates different cytokines in a dose dependent manner and its effect is associated with stratification of patients according to disease activity.     

Kidney-synthesized erythropoietin is the main source for the hypoxia-induced increase in plasma erythropoietin in adult humans

Purpose

Erythropoietin (EPO) is mainly synthesized within renal peritubular fibroblasts, and also other tissues such as the liver possess the ability. However, to what extent non-kidney produced EPO contributes to the hypoxia-induced increase in circulating EPO in adult humans remains unclear.

Methods

We aimed to quantify this by assessing the distribution of EPO glycoforms which are characterized by posttranslational glycosylation patterns specific to the synthesizing cell. The analysis was performed on samples obtained in seven healthy volunteers before, during and after 1 month of sojourn at 3,454 m altitude.

Results

Umbilical cord (UC) plasma served as control. As expected a peak (p < 0.05) in urine (2.3 ± 0.5-fold) and plasma (3.3 ± 0.5-fold) EPO was observed on day 1 of high-altitude exposure, and thereafter the concentration decreased for the urine sample obtained after 26 days at altitude, but remained elevated (p < 0.05) by 1.5 ± 0.2-fold above the initial sea level value for the plasma sample. The EPO glycoform heterogeneity, in the urine samples collected at altitude, did not differ from values at sea level, but were markedly lower (p < 0.05) than the mean percent migrated isoform (PMI) for the umbilical cord samples.

Conclusion

Our studies demonstrate (1) UC samples express a different glycoform distribution as compared to adult humans and hence illustrates the ability to synthesis EPO in non-kidney cells during fetal development (2) as expected hypoxia augments circulating EPO in adults and the predominant source here for remains being kidney derived.     

Mild to moderate hypohydration reduces boys’ high-intensity cycling performance in the heat

Purpose

To evaluate the effect of 1 and 2 % hypohydration on high-intensity cycling performance of 10- to 12-year-old boys in the heat.

Methods

In a counterbalanced order, nine boys attended three sessions in which they cycled intermittently (6 × 10-min bouts at 40–45 % $\dot{V}{\text{O}}_{2\hbox{max} }$ ) in a climate chamber. During each session, environmental conditions and water intake were individually adjusted to achieve a target hypohydration level of 0, 1 or 2 %, based on change in body weight (BW). Following 45 min of rest in thermoneutral conditions when the target hypohydration was maintained, each boy re-entered the climate chamber (35 °C and 50–55 % RH) to perform the cycling performance test at 90 % $\dot{V}{\text{O}}_{2\hbox{max} }$ until exhaustion. Heart rate (HR) and rectal temperature (T _re) were recorded continuously throughout each session. Total mechanical work (TMW) was taken as a measure of cycling performance.

Results

Actual hypohydration level at the start of the cycling performance test in each session was: 0.1 ± 0.0 %, 1.1 ± 0.1 % and 2.0 ± 0.1 %. With 2 % hypohydration, TMW (35.5 ± 6.8 kJ) was significantly (p < 0.05) lower than with 0 % hypohydration (49.3 ± 9.8 kJ). When expressed as a percentage of TMW with 0 % hypohydration, TMW was reduced by 15.5 and 23.3 % with 1 and 2 % hypohydration, respectively (p < 0.05 for both). At the start of the cycling performance test, HR was 13 and 15 bpm higher, and T _re was 0.3 °C higher (p < 0.05 for all) with 1 and 2 % hypohydration, respectively, compared with 0 % hypohydration.

Conclusion

Mild (~1 %) to moderate (~2 %) hypohydration reduces high-intensity cycling performance of healthy young boys in the heat.