Cardiac function and arteriovenous oxygen difference during exercise in obese adults

The purpose of this study was to assess cardiac function and arteriovenous oxygen difference (a-vO₂ difference) at rest and during exercise in young, normal-weight (n = 20), and obese (n = 12) men and women who were matched for age and fitness level. Participants were assessed for body composition, peak oxygen consumption (VO_2peak), and cardiac variables (thoracic bioimpedance)—cardiac index (CI), cardiac output (Q), stroke volume (SV), heart rate (HR), and ejection fraction (EF)—at rest and during cycling exercise at 65% of VO_2peak. Differences between groups were assessed with multivariate ANOVA and mixed-model ANOVA with repeated measures controlling for sex. Absolute VO_2peak and VO_2peak relative to fat-free mass (FFM) were similar between normal-weight and obese groups (Mean ± SEE 2.7 ± 0.2 vs. 3.3 ± 0.3 l min⁻¹, p = 0.084 and 52.4 ± 1.5 vs. 50.9 ± 2.3 ml kg FFM⁻¹ min⁻¹, p = 0.583, respectively). In the obese group, resting Q and SV were higher (6.7 ± 0.4 vs. 4.9 ± 0.1 l min⁻¹, p < 0.001 and 86.8 ± 4.3 vs. 65.8 ± 1.9 ml min⁻¹, p < 0.001, respectively) and EF lower (56.4 ± 2.2 vs. 65.5 ± 2.2%, p = 0.003, respectively) when compared with the normal-weight group. During submaximal exercise, the obese group demonstrated higher mean CI (8.8 ± 0.3 vs. 7.7 ± 0.2 l min⁻¹ m⁻², p = 0.007, respectively), Q (19.2 ± 0.9 vs. 13.1 ± 0.3 l min⁻¹, p < 0.001, respectively), and SV (123.0 ± 5.6 vs. 88.9 ± 4.1 ml min⁻¹, p < 0.001, respectively) and a lower a-vO₂ difference (10.4 ± 1.0 vs. 14.0 ± 0.7 ml l00 ml⁻¹, p = 0.002, respectively) compared with controls. Our study suggests that the ability to extract oxygen during exercise may be impaired in obese individuals.     

Influences of a dietary supplement in combination with an exercise and diet regimen on adipocytokines and adiposity in women who are overweight

The influence of a proprietary blend of modified cellulose and cetylated fatty acids (Trisynex™, Imagenetix, Inc., San Diego, CA 92127, USA) on adipocytokine and regional body composition responses to a weight loss program was examined. Twenty-two women (Supplement group (S) (n = 11): age = 36.8 ± 7.2 years; weight = 87.1 ± 6.2 kg; % body fat = 43.4 ± 4.1; Placebo group (P) (n = 11): age = 38.3 ± 6.8 years; weight = 86.9 ± 4.7 kg; % body fat = 44.3 ± 2.0) completed an 8-week placebo-controlled, double-blind study consisting of a caloric restricted diet and cardiovascular exercise. Body composition and serum insulin, leptin, and adiponectin were assessed at pre-, mid-, and post-intervention. From pre- to post-intervention, significant decreases (P < 0.05) were observed for body weight (S: 87.1 ± 6.2–77.9 ± 5.1 kg; P: 86.9 ± 4.7–82.7 ± 3.8 kg) (P < 0.05 S vs. P), % body fat (S: 43.4 ± 4.1–36.1 ± 3.6; P: 44.3 ± 2.0–40.6 ± 1.2) (P < 0.05 S vs. P), leptin (S: 28.3 ± 3.5–16.2 ± 2.6 ng ml⁻¹; P: 29.4 ± 3.2–19.9 ± 1.1 ng ml⁻¹) (P < 0.05 S vs. P), and insulin (S: 7.3 ± 0.8–5.1 ± 0.2 mU l⁻¹; P: 7.7 ± 0.9–5.1 ± 0.3 mU l⁻¹). Serum adiponectin increased (P < 0.05) (S: 12.2 ± 2.4–26.3 ± 3.0 μg ml⁻¹: 12.6 ± 2.0–21.8 ± 3.1 μg ml⁻¹) (P < 0.05 for S vs. P). Supplementation with a proprietary blend of modified cellulose and cetylated fatty acids during an 8-week weight loss program exhibited favorable effects on adipocytokines and regional body composition.     

Electrocardiogram Signals to Assess Zebrafih Heart Regeneration: Implication of Long QT Intervals

Zebrafish is an emerging model system for cardiac conduction and regeneration. Zebrafish heart regenerates after 20% ventricular resection within 60 days. Whether cardiac conduction phenotype correlated with cardiomyocyte regeneration remained undefined. Longitudinal monitoring of the adult zebrafish heart (n = 12) was performed in terms of atrial contraction (PR intervals), ventricular depolarization (QRS complex) and repolarization (heart rated corrected QTc interval). Baseline electrocardiogram (ECG) signals were recorded one day prior to resection and twice per week over 59 days. Immunostaining for gap junctions with anti-Connexin-43 antibody was compared between the sham (n = 5) and ventricular resection at 60 days post-resection (dpr) (n = 7). Heart rate variability, QTc prolongation and J-point depression developed in the resected group but not in the sham. Despite a trend toward heart rate variability in response to ventricular resection, the differences between the resected and sham fish were, by and large, statistically insignificant. At 10 dpr, J-point depression was statistically significant (sham: −0.179 ± 0.061 mV vs. ventricular resection: −0.353 ± 0.105 mV, p < 0.01, n = 7). At 60 days, histology revealed either cardiomyocyte regeneration (n = 4) or scar tissues (n = 3). J-point depression was no longer statistically significant at 59 dpr (sham: −0.114 ± 0.085 mV; scar tissue: −0.268 ± 0.178 mV, p > 0.05, n = 3; regeneration: −0.209 ± 0.119 mV, p > 0.05, n = 4). Despite positive Connexin-43 staining in the regeneration group, QTc intervals remained prolonged (sham: 325 ± 42 ms, n = 5; scar tissues: 534 ± 51 ms, p < 0.01, n = 3; regeneration: 496 ± 31 ms, p < 0.01, n = 4). Thus, we observed delayed electric repolarization in either the regenerated hearts or scar tissues. Moreover, early regenerated cardiomyocytes lacked the conduction phenotypes of the sham fish.     

Physiological fitness and health adaptations from purposeful training using off-road vehicles

The purpose of this study was to evaluate fitness and health adaptations from a training program riding all-terrain vehicles (ATV) and off-road motorcycles (ORM) as the exercise stimulus. Participants (n = 58) were randomized to a control group (n = 12) or one of four experimental groups; 2 days/week ATV (n = 11), 2 days/week ORM (n = 12), 4 days/week ATV (n = 11), or 4 days/week ORM (n = 12). Aerobic fitness, musculoskeletal fitness, body composition, clinical health, and quality of life (QOL) were compared at baseline and following 6 weeks of training. In all riding groups, there were improvements in blood pressure (SBP = 9.4 ± 10.1, DBP = 5.8 ± 6.2 mmHg), fasting glucose (0.5 ± 0.7 mmol/l), subcutaneous adiposity (0.9 ± 1.1%), body mass (0.7 ± 2.7 kg), waist circumference (1.3 ± 2.5 cm), and isometric leg endurance (26 ± 44 s). All changes were of moderate to large magnitude (Cohen’s d 0.52–0.94) with the exception of a small loss of body mass (Cohen’s d = 0.27). Although changes occurred in the riding groups for aerobic power (2.9 ± 4.6 ml kg⁻¹ min⁻¹), leg power (172 ± 486 w), and curl-ups (13.2 ± 22.7), these changes were not significantly different from the control group. No significant alterations occurred in resting heart rate, trunk flexibility, back endurance, hand grip strength, long jump, pull/push strength, or push-up ability as a result of training. Physical domain QOL increased in all 2 days/week riders but mental domain QOL increased in all ORM, but not ATV riders regardless of volume. Ambient carbon monoxide levels while riding (<30 ppm) were within safe exposure guidelines. Positive adaptations can be gained from a training program using off-road vehicle riding as the exercise stimulus.     

Hormonal response to Taekwondo fighting simulation in elite adolescent athletes

Exercise training efficiency depends on the training load, as well as on the athlete’s ability to tolerate it. The aim of the present study was to evaluate the effect of fighting simulation (3 fights, 6 min each, 30 min rest between fights) on anabolic (IGF-I, LH, FSH, estradiol, and testosterone) and catabolic hormones (cortisol) in elite, male (n = 10) and female (n = 10) adolescent (12–17 years) Taekwondo fighters. Blood samples were collected before the first and immediately after the third fight. The fighting simulation practice led to significant (p < 0.05) decreases in IGF-I (males −27.1 ± 25.6, females −22.4 ± 36.3 ng/ml), LH (males −0.7 ± 1.2, females −2.3 ± 3.3 U/L), and FSH (males −0.9 ± 0.5, females −1.5 ± 1.1 U/L), and to a significant increase (p < 0.05) in cortisol (males 141.9 ± 30.1, females 64.1 ± 30.6 mcg/dL) in both genders. Fighting simulation decreases in testosterone (males −1.9 ± 1.6, females −0.02 ± 0.06 ng/mL), and free androgen index (males −20.1 ± 21.5, females −0.3 ± 0.5) were significant (p < 0.05) only in male fighters. Exercise had no significant effect on estradiol, sex-hormone-binding globulins or thyroid function tests. Our data demonstrate that the physiologic and psychologic strain of a Taekwondo fighting simulation day led to a catabolic-type circulating hormonal response.     

Influence of group training frequency on arterial stiffness in elderly women

We evaluated the effects of different training frequencies on arterial stiffness. 77 elderly women (mean 68.8 years and 7.0 SD) were divided into two training (1DW and 2DW) and a CONTROL group (n = 23). 1DW (n = 29) participated in 90-min group training once a week for 12 weeks, while 2DW (n = 25) attended twice a week. Each training program included recreational activities, six to eight resistance exercises for circuit training, and leg exercises for chair-based exercise. Brachial systolic and diastolic blood pressures and the brachial-to-ankle pulse-wave velocity (baPWV) were obtained in the supine position. Muscle strength and ventilatory threshold were also measured. After the training program, a reduction (P < 0.01) in baPWV was observed in 2DW (−7.8 ± 7.0%) but not in 1DW (−1.5 ± 7.5%) and CONTROL (−0.4 ± 7.5%) without any changes in other measurements. The results suggest that, in order to improve arterial stiffness, an exercise frequency of at least twice a week is to be recommended for elderly.     

Glycemic control influences lung membrane diffusion and oxygen saturation in exercise-trained subjects with type 1 diabetes: alveolar-capillary membrane conductance in type 1 diabetes

Lung diffusing capacity (DLCO) is influenced by alveolar-capillary membrane conductance (D _M) and pulmonary capillary blood volume (V _C), both of which can be impaired in sedentary type 1 diabetes mellitus (T1DM) subjects due to hyperglycemia. We sought to determine if T1DM, and glycemic control, affected DLNO, DLCO, D _M, V _C and SaO₂ during maximal exercise in aerobically fit T1DM subjects. We recruited 12 T1DM subjects and 18 non-diabetic subjects measuring DLNO, DLCO, D _M, and V _C along with SaO₂ and cardiac output (Q) at peak exercise. The T1DM subjects had significantly lower DLCO/Q and D _M/Q with no difference in Q, DLNO, DLCO, D _M, or V _C (DLCO/Q = 2.1 ± 0.4 vs. 1.7 ± 0.3, D _M/Q = 2.8 ± 0.6 vs. 2.4 ± 0.5, non-diabetic and T1DM, p < 0.05). In addition, when considering all subjects there was a relationship between DLCO/Q and SaO₂ at peak exercise (r = 0.46, p = 0.01). Within the T1DM group, the optimal glycemic control group (HbA1c <7%, n = 6) had higher DLNO, DLCO, and D _M/Q than the poor glycemic control subjects (HbA1c ≥7%, n = 6) at peak exercise (DLCO = 38.3 ± 8.0 vs. 28.5 ± 6.9 ml/min/mmHg, DLNO = 120.3 ± 24.3 vs. 89.1 ± 21.0 ml/min/mmHg, D _M/Q = 3.8 ± 0.8 vs. 2.7 ± 0.2, optimal vs. poor control, p < 0.05). There was a negative correlation between HbA1c with DLCO, D _M and D _M/Q at peak exercise (DLCO: r = −0.70, p = 0.01; D _M: r = −0.70, p = 0.01; D _M/Q: r = −0.68, p = 0.02). These results demonstrate that there is a reduction in lung diffusing capacity in aerobically fit athletes with T1DM at peak exercise, but suggests that maintaining near-normoglycemia potentially averts lung diffusion impairments.     

Exercise-induced muscle damage and the repeated bout effect: evidence for cross transfer

We examined whether a prior bout of eccentric exercise in the elbow flexors provided protection against exercise-induced muscle damage in the contralateral arm. Fifteen males (age 22.7 ± 2.1 years; height 178.6 ± 6.8 cm, mass 75.8 ± 9.3 kg) were randomly assigned to two groups who performed two bouts of 60 eccentric contractions (30°/s) separated by 2 weeks: ipsilateral (n = 7, both bouts performed in the same arm), contralateral (n = 8, one bout performed in each arm). Strength, muscle soreness and resting arm angle (RAA) were measured at baseline and at 1, 24 and 48 h post exercise. Surface electromyography was recorded during both bouts of exercise. The degree of strength loss was attenuated (p < 0.05) in the ipsilateral group after the second bout of eccentric exercise (−22 cf. −3% for bout 1 and 2 at 24 h, respectively). Strength loss following eccentric exercise was also attenuated (p < 0.05) at 24 h in the contralateral group (−30 cf. 13% for bout 1 and 2, respectively). Muscle soreness (≈34 cf 19 mm) and change in RAA (≈5 cf. 3%) were also lower following the second bout of eccentric exercise (p < 0.05), although there was no difference in the overall change in these values between groups. Median frequency (MF) was decreased by 31% between bouts, with no difference between groups. Data support observations that the repeated bout effect transfers to the opposite (untrained) limb. The similar reduction in MF between bouts for the two groups provides evidence for a centrally mediated, neural adaptation.     

Skin microvascular reactivity in trained adolescents

Whilst endothelial dysfunction is associated with a sedentary lifestyle, enhanced endothelial function has been documented in the skin of trained individuals. The purpose of this study was to investigate whether highly trained adolescent males possess enhanced skin microvascular endothelial function compared to their untrained peers. Seventeen highly and predominantly soccer trained boys ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 55 ± 6 mL kg⁻¹ min⁻¹) and nine age- and maturation-matched untrained controls ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 43 ± 5 mL kg⁻¹ min⁻¹) aged 13–15 years had skin microvascular endothelial function assessed using laser Doppler flowmetry. Baseline and maximal thermally stimulated skin blood flow (SkBF) responses were higher in forearms of trained subjects compared to untrained participants [baseline SkBF: 11 ± 4 vs. 9 ± 3 perfusion units (PU), p < 0.05; SkBF_max: 282 ± 120 vs. 204 ± 68 PU, p < 0.05]. Similarly, cutaneous vascular conductance (CVC) during local heating was superior in the forearm skin of trained versus untrained individuals (CVC_max: 3 ± 1 vs. 2 ± 1 PU mmHg⁻¹, p < 0.05). Peak hyperaemia following arterial occlusion and area under the reactive hyperaemia curve were also greater in forearm skin of the trained group (peak hyperaemia: 51 ± 21 vs. 35 ± 15 PU, p < 0.05; area under curve: 1596 ± 739 vs. 962 ± 796 PUs, p < 0.05). These results suggest that chronic exercise training in adolescents is associated with enhanced microvascular endothelial vasodilation in non-glabrous skin.     

Ultra short-term heart rate recovery after maximal exercise in continuous versus intermittent endurance athletes

This study tested the hypothesis that athletes participating in intermittent sports would exhibit a faster heart rate recovery (HRR) during the initial phase (<30 s) following maximal exercise than athletes participating in continuous endurance sports. Forty-six male athletes were allocated into continuous (CNT, n = 24) or intermittent groups (INT, n = 22), matched for age and aerobic fitness. Athletes performed maximal exercise on a treadmill using the ramp protocol. Immediately upon exercise cessation, subjects were placed supine with continuous measurement of HR during the first minute of recovery. Data were analyzed in 10-s intervals and compared between the groups. Repeated measures ANOVA showed a group × time interaction effects (p ≤ 0.01) for HRR expressed in both beats min⁻¹ and in percentage of peak post-exercise HR (% HR_peak). The INT group had lower HR than CNT group at 10 s (189 vs. 192 beats min⁻¹, p = 0.04; and 96.3 vs. 97.9% HR_peak, p = 0.009) and 20 s (184 vs. 188 beats min⁻¹, p = 0.049; and 93.6 vs. 95.7% HR_peak, p = 0.021) intervals of recovery. The results suggest that athletes engaged in intermittent sports are likely to have faster HRR during the first 20 s after maximal exercise than their counterparts trained for continuous performance.     

Induction and decay of short-term heat acclimation

The purpose of this work was to investigate adaptation and decay from short-term (5-day) heat acclimation (STHA). Ten moderately trained males (mean ± SD age 28 ± 7 years; body mass 74.6 ± 4.4 kg; [(V)\dot]_{\textO 2\textpeak} \dot{V}_{{{\text{O}}_{ 2{\text{peak}}} }} 4.26 ± 0.37 l min⁻¹) underwent heat acclimation (Acc) for 90-min on 5-days consecutively (T _a = 39.5°C, 60% RH), under controlled hyperthermia (rectal temperature 38.5°C). Participants completed a heat stress test (HST) 1 week before acclimation (Acc), then on the 2nd and 8th day (1 week) following Acc (T _a = 35°C, 60% RH). Seven participants completed HSTs 2 and 3 weeks after Acc. HST consisted of 90-min cycling at 40% peak power output before an incremental performance test. Rectal temperature at rest (37.1 ± 0.4°C) was not lowered by Acc (95% CI −0.3 to 0.2°C), after 90-min exercise (38.6 ± 0.5°C) it reduced 0.3°C (−0.5 to −0.1°C) and remained at this level 1 week later (−0.5 to −0.1°C), but not two (0.1°C −0.4 to 0.5°C; n = 7) or 3 weeks. Similarly, heart rate after 90-min exercise (146 ± 21 b min⁻¹) was reduced (−13: −6 to −20 b min⁻¹) and remained at this level after 1 week (−13: −6 to −20 b min⁻¹) but not two (−9: 6 to −23 b min⁻¹; n = 7) or 3 weeks. Performance (746 s) increased 106 s: 59 to 152 s after Acc and remained higher after one (76 s: 31 to 122) but not two (15 s: −88 to 142 s; n = 7) or 3 weeks. Therefore, STHA (5-day) induced adaptations permitting increased heat loss and this persisted 1 week but not 2 weeks following Acc.     

Post-concurrent exercise hemodynamics and cardiac autonomic modulation

Concurrent training is recommended for health improvement, but its acute effects on cardiovascular function are not well established. This study analyzed hemodynamics and autonomic modulation after a single session of aerobic (A), resistance (R), and concurrent (A + R) exercises. Twenty healthy subjects randomly underwent four sessions: control (C:30 min of rest), aerobic (A:30 min, cycle ergometer, 75% of VO₂ peak), resistance (R:6 exercises, 3 sets, 20 repetitions, 50% of 1 RM), and concurrent (AR: A + R). Before and after the interventions, blood pressure (BP), heart rate (HR), cardiac output (CO), and HR variability were measured. Systolic BP decreased after all the exercises, and the greatest decreases were observed after the A and AR sessions (−13 ± 1 and −11 ± 1 mmHg, respectively, P < 0.05). Diastolic BP decreased similarly after all the exercises, and this decrease lasted longer after the A session. CO also decreased similarly after the exercises, while systemic vascular resistance increased after the R and AR sessions in the recovery period (+4.0 ± 1.7 and +6.3 ± 1.9 U, respectively, P < 0.05). Stroke volume decreased, while HR increased after the exercises, and the greatest responses were observed after the AR session (SV, A = −14.6 ± 3.6, R = −22.4 ± 3.5 and AR = −23.4 ± 2.4 ml; HR, A =+13 ± 2, R =+15 ± 2 vs. AR =+20 ± 2 bpm, P < 0.05). Cardiac sympathovagal balance increased after the exercises, and the greatest increase was observed after the AR session (A = +0.7 ± 0.8, R = +1.0 ± 0.8 vs. AR = +1.2 ± 0.8, P < 0.05). In conclusion, the association of aerobic and resistance exercises in the same training session did not potentiate post-exercise hypotension, and increased cardiac sympathetic activation during the recovery period.     

Modulation of the transient outward K+ current by inhibition of endothelin-A receptors in normal and hypertrophied rat hearts

Inhibition of endothelin-A (ET_A) receptors has been shown to reduce ventricular electrical abnormalities associated with cardiac failure. In this study, we investigate the effect of ET_A-receptor inhibition on the development of regional alterations of the transient outward K⁺ current (I _to) in the setting of pressure-induced left ventricular (LV) hypertrophy. Cardiac hypertrophy was induced in female Sprague–Dawley rats by stenosis of the ascending aorta (AS) for 7 days. Treatment with the selective ET_A-receptor antagonist darusentan (LU135252, 35 mg [kg body weight]⁻¹ day⁻¹) was started 1 day before the surgery. AS induced a 46% increase in the relative LV weight (p < 0.001) and caused a significant reduction in I _to (at +40 mV) in epicardial myocytes (19.5 ± 1.2 pA pF⁻¹, n = 32 vs 23.2 ± 1.2 pA pF⁻¹, n = 35, p < 0.05). Darusentan further reduced I _to in AS (15.4 ± 1.3 pA pF⁻¹, n = 37, p < 0.05) and sham-operated animals (19.8 ± 1.6 pA pF⁻¹, n = 48, ns.). The effects of AS and darusentan on I _to were significant and independent as tested by two-way analysis of variance. I _to was not affected in endocardial myocytes. These results indicate that endothelin-1 may exert a tonic effect on the magnitude of I _to in the epicardial region of the left ventricle but that ET_A-receptor activation is not necessary for the development of electrical alterations associated with pressure-induced hypertrophy.     

Oxidative stress, inflammation and recovery of muscle function after damaging exercise: effect of 6-week mixed antioxidant supplementation

There is no consensus regarding the effects of mixed antioxidant vitamin C and/or vitamin E supplementation on oxidative stress responses to exercise and restoration of muscle function. Thirty-eight men were randomly assigned to receive either placebo group (n = 18) or mixed antioxidant (primarily vitamin C & E) supplements (n = 20) in a double-blind manner. After 6 weeks, participants performed 90 min of intermittent shuttle-running. Peak isometric torque of the knee flexors/extensors and range of motion at this joint were determined before and after exercise, with recovery of these variables tracked for up to 168 h post-exercise. Antioxidant supplementation elevated pre-exercise plasma vitamin C (93 ± 8 μmol l⁻¹) and vitamin E (11 ± 3 μmol l⁻¹) concentrations relative to baseline (P < 0.001) and the placebo group (P ≤ 0.02). Exercise reduced peak isometric torque (i.e. 9–19% relative to baseline; P ≤ 0.001), which persisted for the first 48 h of recovery with no difference between treatment groups. In contrast, changes in the urine concentration of F₂-isoprostanes responded differently to each treatment (P = 0.04), with a tendency for higher concentrations after 48 h of recovery in the supplemented group (6.2 ± 6.1 vs. 3.7 ± 3.4 ng ml⁻¹). Vitamin C & E supplementation also affected serum cortisol concentrations, with an attenuated increase from baseline to the peak values reached after 1 h of recovery compared with the placebo group (P = 0.02) and serum interleukin-6 concentrations were higher after 1 h of recovery in the antioxidant group (11.3 ± 3.4 pg ml⁻¹) than the placebo group (6.2 ± 3.8 pg ml⁻¹; P = 0.05). Combined vitamin C & E supplementation neither reduced markers of oxidative stress or inflammation nor did it facilitate recovery of muscle function after exercise-induced muscle damage.     

The intraocular pressure response to dehydration: a pilot study

The aim of this study was to determine the intraocular pressure response to differing levels of dehydration. Seven males participated in 90 min of treadmill walking (5 km h⁻¹ and 1% grade) in both temperate (22°C) and hot (43°C) conditions. At baseline and 30 min intervals intraocular pressure, nude body mass, body temperature and heart rate were recorded. Statistically significant interactions (p < 0.05) were observed for intraocular pressure (hot condition: baseline 17.0 ± 2.9, 30 min 15.6 ± 3.5, 60 min 14.5 ± 3.7 and 90 min 13.6 ± 2.9 mmHg; temperate condition: baseline 16.8 ± 2.7, 30 min 16.5 ± 2.6, 60 min 15.8 ± 2.5 and 90 min 15.7 ± 1.8 mmHg) and body mass loss (hot condition: 30 min −1.07 ± 0.35, 60 min −2.17 ± 0.55 and 90 min −3.13 ± 0.74%; temperate condition: 30 min −0.15 ± 0.11, 60 min −0.47 ± 0.18 and 90 min −0.78 ± 0.25%). Significant linear regressions (p < 0.05) were observed for intraocular pressure and body mass loss (adjusted r ² = 0.24) and intraocular pressure change and body mass loss (adjusted r ² = 0.51). In conclusion, intraocular pressure was progressively reduced during a period of exercise causing dehydration, but remained relatively stable when hydration was maintained. The present study revealed a moderate relationship between dehydration (body mass loss) and intraocular pressure change.     

Comparison of muscle buffer capacity and repeated-sprint ability of untrained, endurance-trained and team-sport athletes

We measured the muscle buffer capacity (βm) and repeated-sprint ability (RSA) of young females, who were either team-sport athletes (n=7), endurance trained (n=6) or untrained but physically active (n=8). All subjects performed a graded exercise test to determine followed 2 days later by a cycle test of RSA (5×6 s, every 30 s). Resting muscle samples (Vastus lateralis) were taken to determine βm. The team-sport group had a significantly higher βm than either the endurance-trained or the untrained groups (181±27 vs. 148±11 vs. 122±32 μmol H⁺ g dm⁻¹ pH⁻¹ respectively; P<0.05). The team-sport group also completed significantly more relative total work (299±27 vs. 263±31 vs. 223±21 J kg⁻¹, respectively; P<0.05) and absolute total work (18.2±1.6 vs. 14.6±2.4 vs. 13.0±1.9 kJ, respectively; P<0.05) than the endurance-trained or untrained groups during the RSA test. The team-sport group also had a greater post-exercise blood lactate concentration, but not blood pH. There was a significant correlation between βm and RSA (r = 0.67; P<0.05). Our findings show that young females competing in team sports have a larger βm than either endurance-trained or untrained females. This may be the result of the intermittent, high-intensity activity during training and the match play of team-sport athletes. The team-sport athletes also had a greater RSA than either the endurance-trained or untrained subjects. The greater total work by team-sport athletes was predominantly due to a better performance during the early sprints of the repeated-sprint bout.     

Afferent arteriolopathy and glomerular collapse but not segmental sclerosis induce tubular atrophy in old spontaneously hypertensive rats

In chronic renal disease, the temporal and spatial relationship between vascular, glomerular and tubular changes is still unclear. Hypertension, an important cause of chronic renal failure, leads to afferent arteriolopathy, segmental glomerulosclerosis and tubular atrophy in the juxtamedullary cortex. We investigated the pathological changes of hypertensive renal disease in aged spontaneously hypertensive rats using a large number of serial sections, where we traced and analyzed afferent arteriole, glomerulus and proximal tubule of single nephrons. Our major finding was that both afferent arteriolopathy and glomerular capillary collapse were linked to tubular atrophy. Only nephrons with glomerular collapse (n = 13) showed tubules with reduced diameter indicating atrophy [21.66 ± 2.56 μm vs. tubules in normotensive Wistar Kyoto rats (WKY) 38.56 ± 0.56 μm, p < 0.05], as well as afferent arteriolar wall hypertrophy (diameter 32.74 ± 4.72 μm vs. afferent arterioles in WKY 19.24 ± 0.98 μm, p < 0.05). Nephrons with segmental sclerosis (n = 10) did not show tubular atrophy and tubular diameters were unchanged (35.60 ± 1.43 μm). Afferent arteriolar diameter negatively correlated with glomerular capillary volume fraction (r = −0.36) and proximal tubular diameter (r = −0.46) implying reduced glomerular and tubular flow. In line with this, chronically damaged tubules showed reduced staining for the ciliary protein inversin indicating changed ciliary signalling due to reduced urinary flow. This is the first morphological study on hypertensive renal disease making correlations between vascular, glomerular and tubular components of individual nephron units. Our data suggest that afferent arteriolopathy leads to glomerular collapse and reduced urinary flow with subsequent tubular atrophy.     

Individual differences in the responses to endurance and resistance training

Large individual differences in the responsiveness of cardiorespiratory fitness (VO_2peak) to endurance training have been observed in healthy subjects. We tested the hypothesis that subjects with a poor responsiveness to endurance training might benefit from resistance training in terms of aerobic fitness. The study population consisted of sedentary healthy male and female subjects (n=91, 42±5 year) assigned to either a training (n=73) or a control group (n=18). The randomized cross-over study design included a 2-week laboratory-controlled endurance or resistance training period with a 2-month detraining period between the interventions. Large individual differences were observed in the changes of VO_2peak (ΔVO_2peak) after both the endurance (average 8±6 %, P<0.001, range −5 to +22%) and resistance training (average 4±5%, P<0.001, range −8 to +16%). The average increase in ΔVO_2peak between genders was similar after both the endurance (8±6% for both genders, P=ns) and resistance training (3±5% for males and 5±6% for females, P=ns). There was no linear relationship between the changes in VO_2peak after each training intervention (r=−.09, P=ns). On the contrary, when the study group was divided into quartiles according to the endurance training response (1±3, 6±1, 9±1, and 16±3% increase in VO_2peak), the group with the lowest response to endurance training increased VO_2peak after the resistance training intervention (ΔVO_2peak 7±5%, P<0.001). The individual responsiveness of VO_2peak to exercise training is related to the mode of training. The healthy males and females whose training response is low after endurance training seem to result in a marked improvement in their cardiorespiratory fitness by resistance training.     

Increased Extracellular Survivin in the Synovial Fluid of Rheumatoid Arthritis Patients: Fibroblast-like Synoviocytes as a Potential Source of Extracellular Survivin

Survivin belongs to the family of inhibitor of apoptosis proteins and plays an important role in the hyperplastic growth of tissues and tumors. In this study, we assessed the expression of survivin in rheumatoid synovial fluids (SF) and synovial tissues (ST) of rheumatoid arthritis (RA) patients in order to investigate the role of extracellular survivin in the pathogenesis of RA. The survivin level from SF was significantly higher in RA patients (n = 38) than in osteoarthritis patients (n = 18; 10.68 ± 2.76 vs. 1.0 ± 0.56 pg/ml, p = 0.02). In addition, SF survivin level was higher in erosive RA patients (n = 23) than in non-erosive RA patients (n = 15; 15.26 ± 4.26 vs. 4.47 ± 1.12 pg/ml, p = 0.05). SF survivin level in RA was positively correlated with disease activity score 28, but did not reach statistical significance (r = 0.309, p = 0.07). RA SF survivin level was also positively correlated with peripheral blood leukocyte counts (r = 0.443, p = 0.005). The immunohistochemical staining and Western blot analysis revealed survivin expression in the ST and fibroblast-like synoviocytes of RA patients, respectively. These findings suggest that extracellular survivin may be produced from rheumatoid FLS and may play an important role in the destructive RA process.