Effect of intensive exercise-induced testicular gametogenic and steroidogenic disorders in mature male Wistar strain rats: a correlative approach to oxidative stress

AIMS: In order to investigate the effects of intensive exercise on reproductive dysfunctions in relation to oxidative stress, a total of 12 male rats (age: 3 months, weight: 127 +/- 2.86 g) were randomly divided into: (1) control group (CG, n = 6) and (2) experimental group (Exp. G, n = 6). METHODS: An exercise protocol of 3 h swimming day(-1), 5 days week(-1) was followed for 4 weeks in Exp. G, with no exercise in CG. All the animals were killed; blood, testes and the accessory sex organs were collected for estimation of different parameters. RESULTS: A significant diminution (P < 0.001) was noted in testicular Delta5, 3beta-hydroxy-steroid dehydrogenase (Delta5, 3beta-HSD), 17beta-hydroxy steroid dehydrogenase (17beta-HSD); plasma levels of testosterone, luteinizing hormone (LH); preleptotine spermatocytes (pLSc), midpachytene spermatocytes (mPSc) and stage 7 spermatids (7Sd); with no significant alteration in follicle stimulating hormone (FSH) and spermatogoia A (Asg) after intensive exercise. A significant elevation (P < 0.001) in malondialdehyde (MDA) and conjugated dienes (CD) along with significant reduction (P < 0.001) in glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST) and peroxidase were found in testes of Exp. G. Moreover, the somatic index of testes and accessory sex organs were also decreased significantly (P < 0.001) after exercise. High correlations have been found in 17 beta-HSD with CAT (r = 0.90, P < 0.05) and peroxidase (r = 0.83, P < 0.05), epididymal somatic index with CD (r = -0.91; P < 0.05) and GSH (r = 0.84, P < 0.05). CONCLUSION: The present study focused an chronic intensive exercise-induced oxidative stress that may cause dysfunctions in male reproductive system including steroidogenesis and spermatogenesis.     

Dysfunctional beliefs and attitudes about sleep in children

The objective of the study was to determine whether associations between dysfunctional beliefs and attitudes about sleep and sleep disturbance are evident in children. Cross‐sectional data were collected from 123 children aged 8–10 years (49% boys). The participants came from ethnically diverse backgrounds from two inner‐city schools in London, UK. Children completed the Sleep Self‐Report (SSR) and the Dysfunctional Beliefs and Attitudes about Sleep (DBAS) questionnaire (which was adapted for use with children). Parents completed the Child Sleep Habits Questionnaire (CSHQ). The total DBAS score was associated with sleep disturbances defined as total SSR score (β = 0.40, P < 0.001, r² = 0.15), the SSR insomnia items (β = 0.29, P < 0.01, r² = 0.08) and the total CSHQ score (β = 0.22, P < 0.05, r² = 0.04). Some dysfunctional beliefs about sleep predicted sleep disturbance to a greater extent than others. For example, when controlling for the other DBAS subscales, the ‘control and predictability of sleep’ subscale, but not the ‘sleep requirements expectations’ subscale, predicted total SSR score and SSR insomnia items. Given this preliminary evidence that dysfunctional beliefs and attitudes about sleep appear to be associated with sleep difficulties in children, future work is needed to further developmentally adapt a version of the DBAS appropriate for use with children.     

Gene expression profiling of exercise‐induced cardiac hypertrophy in rats

Aims: Exercise training causes physiological cardiac hypertrophy, which acts to enhance cardiac function during exercise. However, the underlying molecular mechanisms are unclear. We investigated gene expression profile of exercise training‐induced cardiac hypertrophy using left ventricle (LV) excised from exercise‐trained and sedentary control rats (12‐week old). Method: Rats in the training group exercised on a treadmill for 8‐week. Results: Left ventricular mass index and wall thickness in the exercise‐trained group were significantly greater than that in the control group, indicating that the trained rats developed cardiac hypertrophy. Of the 3800 genes analysed in the microarray analyses, a total of 75 relevant genes (upregulation of 33 genes and downregulation of 42 genes) displayed alterations with exercise training. Among these genes, we focused on glycogen synthase kinase (GSK)‐3β, calcineurin‐inhibitor (Cain), and endothelin (ET)‐1 for their implicated roles in pathological cardiac hypertrophy, and confirmed the results of microarray analysis at mRNA and protein/peptide levels using quantitative PCR, Western blot, and EIA analyses. The gene expression of GSK‐3β decreased significantly and those of Cain and ET‐1 increased significantly with exercise training. Furthermore, LV mass index was significantly correlated with GSK‐3β protein activity (r = ?0.70, P < 0.01) and tissue ET‐1 concentration (r = 0.52, P < 0.05). There were no changes in gene expressions in brain natriuretic peptide (BNP), angiotensin‐correcting enzyme (ACE), interleukin‐6, and vascular cell adhesion molecule (VCAM)‐1. Conclusion: These findings suggest that physiological and pathological LV hypertrophy may share some of the same molecular mechanisms in inducing LV hypertrophy (e.g. GSK‐3β, Cain, and ET‐1) and that other genes (e.g. BNP, ACE) may differentiate physiological from pathological LV hypertrophy.     

Enzyme activities in the tibialis anterior muscle of young moderately active men and women: relationship with body composition,muscle cross‐sectional area and fibre type composition

The aims of this study were (i) to assess the differences between men and women in maximal activities of selected enzymes of aerobic and anaerobic pathways involved in skeletal muscle energy production, and (ii) to assess the relationships between maximal enzyme activities, body composition, muscle cross‐sectional area (CSA) and fibre type composition. Muscle biopsies were obtained from the tibialis anterior (TA) muscle of 15 men and 15 women (age 20–31 years) with comparable physical activity levels. The muscle CSA was determined by magnetic resonance imaging (MRI). Maximal activities of lactate dehydrogenase (LDH), phosphofructokinase (PFK), β‐hydroxyacyl‐coenzyme A dehydrogenase (HAD), succinate dehydrogenase (SDH) and citrate synthase (CS), were assayed spectrophotometrically. The proportion, mean area and relative area (proportion × area) of type 1 and type 2 fibres were determined from muscle biopsies prepared for enzyme histochemistry [myofibrillar adenosine triphosphatase (mATPase)]. The men were significantly taller (+6.6%; P < 0.001) and heavier (+19.1%; P < 0.001), had significantly larger muscle CSA (+19.0%; P < 0.001) and significantly larger areas and relative areas of both type 1 and type 2 fibres (+20.5–31.4%; P = 0.007 to P < 0.001). The men had significantly higher maximal enzyme activities than women for LDH (+27.6%; P = 0.007) and PFK (+25.5%; P = 0.003). There were no significant differences between the men and the women in the activities of HAD (+3.6%; ns), CS (+21.1%; P = 0.084) and SDH (+7.6%; ns). There were significant relationships between height and LDH (r = 0.41; P = 0.023), height and PFK (r = 0.41; P = 0.025), weight and LDH (r = 0.45; P = 0.013), and weight and PFK (r = 0.39; P = 0.032). The relationships were significant between the muscle CSA and the activities of LDH (r = 0.61; P < 0.001) and PFK (r = 0.56; P = 0.001), and between the relative area of type 2 fibres and the activities of LDH (r = 0.49; P = 0.006) and PFK (r = 0.42; P = 0.023). There were no significant relationships between HAD, CS and SDH, and height, weight, muscle CSA and fibre type composition, respectively. These data indicate that the higher maximal activities of LDH and PFK in men are related to the height, weight, muscle CSA and the relative area of type 2 fibres, which are all significantly larger in men than women.     

Striated muscle calcium-stimulated cysteine protease (calpain-like) activity promotes myeloperoxidase activity with exercise

 An inflammatory response triggered by neutrophil accumulation into muscle tissue is thought to occur with exercise-induced muscle damage. To investigate the relationship between Ca²⁺-stimulated proteolysis (calpain-like activity) and neutrophil accumulation [myeloperoxidase (MPO) activity], cardiac and plantaris muscles from rats (n = 10) completing 1 h exercise (25 m/min) were investigated. Exercise promoted increases (P<0.05) in both calpain-like and MPO activities; ranging from 2.79 to 58.9 U/g wet weight (ww) and 0.03 to 4.88 U/g ww respectively. Pearson’s correlational analysis (r) on calpain-like and MPO activities for cardiac and plantaris muscle data were 0.97 (P<0.001) and 0.68 (P<0.05) respectively, with a combined r of 0.83 (P<0.001) for both muscles across all conditions. To investigate further the extent to which calpain-like activity may promote neutrophil accumulation, another exercise group (n = 5) was pre-injected with the cysteine protease inhibitor, E64c, 1 h before exercise. Administration of E64c lowered calpain-like and MPO activities by 66% and 56% respectively (average from both muscles). From these results it is concluded that a relationship exists between Ca²⁺-stimulated proteolysis and neutrophil accumulation into striated muscle with exercise, and that the calpain system is involved in localizing the neutrophilic response with exercise. Received: 3 February 1997 / Received after revision: 18 August 1997 / Accepted: 2 December 1997     

Stroke assessment with intravoxel incoherent motion diffusion‐weighted MRI

Intravoxel incoherent motion (IVIM) diffusion‐weighted MRI can simultaneously measure diffusion and perfusion characteristics in a non‐invasive way. This study aimed to determine the potential utility of IVIM in characterizing brain diffusion and perfusion properties for clinical stroke. The multi‐b‐value diffusion‐weighted images of 101 patients diagnosed with acute/subacute ischemic stroke were retrospectively evaluated. The diffusion coefficient D, representing the water apparent diffusivity, was obtained by fitting the diffusion data with increasing high b‐values to a simple mono‐exponential model. The IVIM‐derived perfusion parameters, pseudodiffusion coefficient D*, vascular volume fraction f and blood flow‐related parameter fD*, were calculated with the bi‐exponential model. Additionally, the apparent diffusion coefficient (ADC) was fitted according to the mono‐exponential model using all b‐values. The diffusion parameters for the ischemic lesion and normal contralateral region were measured in each patient. Statistical analysis was performed using the paired Student t‐test and Pearson correlation test. Diffusion data in both the ischemic lesion and normal contralateral region followed the IVIM bi‐exponential behavior, and the IVIM model showed better goodness of fit than the mono‐exponential model with lower Akaike information criterion values. The paired Student t‐test revealed significant differences for all diffusion parameters (all P < 0.001) except D* (P = 0.218) between ischemic and normal areas. For all patients in both ischemic and normal regions, ADC was significantly positively correlated with D (both r = 1, both P < 0.001) and f (r = 0.541, P < 0.001; r = 0.262, P = 0.008); significant correlation was also found between ADC and fD* in the ischemic region (r = 0.254, P = 0.010). For all pixels within the region of interest from a representative subject in both ischemic and normal regions, ADC was significantly positively correlated with D (both r = 1, both P < 0.001), f (r = 0.823, P < 0.001; r = 0.652, P < 0.001) and fD* (r = 0.294, P < 0.001; r = 0.340, P < 0.001). These findings may have clinical implications for the use of IVIM imaging in the assessment and management of acute/subacute stroke patients. Copyright © 2016 John Wiley & Sons, Ltd.     

Oral creatine supplementation decreases plasma markers of adenine nucleotide degradation during a 1‐h cycle test

We investigated the effect of oral creatine supplementation (20 g d^?1 for 7 days) on metabolism during a 1‐h cycling performance trial. Twenty endurance‐trained cyclists participated in this double‐blind placebo controlled study. Five days after familiarization with the exercise test, the subjects underwent a baseline muscle biopsy. Thereafter, a cannula was inserted into a forearm vein before performing the baseline maximal 1‐h cycle (test 1 (T1)). Blood samples were drawn at regular intervals during exercise and recovery. After creatine (Cr) loading, the muscle biopsy, 1‐h cycling test (test 2 (T2)) and blood sampling were repeated. Resting muscle total creatine (TCr), measured by high performance liquid chromatography, was increased (P < 0.001) in the creatine group from 123.0 ± 3.8 ? 159.8 ± 7.9 mmol kg^?1 dry wt, but was unchanged in the placebo group (126.7 ± 4.7 ? 127.5 ± 3.6 mmol kg^?1 dry wt). The extent of Cr loading was unrelated to baseline Cr levels (r=0.33, not significant). Supplementation did not significantly improve exercise performance (Cr group: 39.1 ± 0.9 vs. 39.8 ± 0.8 km and placebo group: 39.3 ± 0.8 vs. 39.2 ± 1.1 km) or change plasma lactate concentrations. Plasma concentrations of ammonia (NH₃) (P < 0.05) and hypoxanthine (Hx) (P < 0.01) were lower in the Cr group from T1 to T2. Our results indicate that Cr supplementation alters the metabolic response during sustained high‐intensity submaximal exercise. Plasma data suggest that nett intramuscular adenine nucleotide degradation may be decreased in the presence of enhanced intramuscular TCr concentration even during submaximal exercise.     

Physically active patients with coronary artery disease: A longitudinal investigation of the processes of exercise behaviour change

Objectives. Although regular exercise is important for patients with coronary artery disease (CAD), most CAD patients are not sufficiently active. The transtheoretical model offers a framework for the process of exercise behaviour change. But until today, it is not clear which processes of exercise behaviour change (POC) support CAD patients in maintaining exercise after discharge. Design. A longitudinal study with baseline measure and 6‐month follow‐up has been conducted. German CAD patients were mailed at home after discharge. POC and exercise were self‐reported. Methods. A total of 204 CAD patients were selected from five rehabilitation centres. A total of 108 CAD patients, which were in the post‐action stages, provided data at baseline and follow‐up. Two different analyses were carried out. Firstly, structural equation modelling with baseline data (N =147) was used to test the hierarchical order of the POC in experiential and behavioural processes. Secondly, cross‐lagged panel analysis was used to investigate whether POC lead to exercise or vice versa and which POC support CAD patients in maintaining exercise. Results. Comparative analysis indicates that the two hierarchical‐factor model fits the data significantly better than the one hierarchical‐factor model (χ²diff ₍₁₎=19.04, p <.001), even though experiential and behavioural processes are highly correlated (r =.98, p <.001). Standardized effects of the antecedent cross‐lags are significant for consciousness raising (β=0.27), reinforcement management (β=0.28), self‐liberation (β=0.28), and stimulus control (β=0.33) indicating that these POC are predictive for CAD patients maintaining exercise. Conclusion. Although some POC support the exercise behaviour change process and the hierarchical structure is apparent, it may be beneficial to adapt the POC to give a more precise understanding of the change processes.     

Similar cardiac vagal withdrawal at the onset of arm and leg dynamic exercise

Electrocardiogram RR intervals duration reduce rapidly in the first seconds of dynamic exercise mainly due to a cardiac vagal withdrawal. However, it remains unclear if this response varies between exercises performed with different body segments (i.e. arm vs. leg). Our aim was to compare the vagal withdrawal at the onset of arm and leg dynamic exercise. Cardiac vagal withdrawal was assessed by the 4-s exercise test (4sET), a pharmacologically validated and highly reliable procedure. Initially, 60 healthy subjects performed the 4sET using arms (ARM 4sET) and legs (LEG 4sET), in a random order. Later, 20 of them repeated the testing, controlling for cycling rate and time of exercise onset within a RR interval, potential intervenient variables. Similar results were found for ARM and LEG 4sET considering the RR interval duration obtained immediately before the onset of exercise (RRB) (mean ± SEM; 852 ± 23 vs. 857 ± 23 ms; P = 0.55), the shortest RR interval duration during exercise (RRC) (570 ± 10 vs. 563 ± 10 ms; P = 0.22) and the cardiac vagal index (CVI), which is the ratio between RRB and RRC (1.49 ± 0.03 vs. 1.52 ± 0.03; P = 0.10). Furthermore, high intraclass correlation coefficients were found (RRB r _i = 0.94, P < 0.001; RRC r _i = 0.85, P < 0.001; CVI r _i = 0.81, P < 0.001). We conclude that similar cardiac vagal withdrawal was induced by 4-s fast unloaded cycling exercise performed with arms or legs.     

Effect of low glycogen on glycogen synthase in human muscle during and after exercise

Subjects cycled at a work load calculated to elicit 75% of maximal oxygen uptake on two occasions: the first to fatigue (34.5 ± 5.3 min; mean ± SE), and the second at the same workload and for the same duration as the first. Biopsies were obtained from the quadriceps femoris muscle before and immediately after exercise, and 5 min post-exercise. Before the first experiment, muscle glycogen was lowered by a combination of exercise and diet, and before the second, experiment muscle glycogen was elevated. In the low glycogen condition (LG), muscle glycogen decreased from 169 ± 15 mmol glucosyl units kg^-1dry wt at to rest to 13 ± 6 after exercise. In the high glycogen condition (HG) glycogen decreased from 706 ± 52 at rest to 405 ± 68 after exercise. Glycogen synthase fractional activity (GSF) was always higher during the LG treatment. During exercise in the HG condition, those subjects who cycled for < 35 min (n= 3) had GSF values in muscle which were lower than at rest, whereas those subjects who cycled for > 35 min (n= 4) had values which were similar to or higher than at rest. Thus the change in GSF in muscle during HG was positively related to the exercise duration (r= 0.94; y = 254–17x + 0.3x²; P < 0.001) and negatively related to the glycogen content at the end of exercise (r=–0.82; y= 516–2x + 0.001x²; P < 0.05). During LG exercise GSF remained constant. GSF increased markedly after 5 min post-exercise in both HG and LG conditions. cAMP dependent protein kinase activity increased similarly during both LG and HG exercise and reverted to the preexercise values 5 min post-exercise. It is concluded that muscle contraction decreases GSF, but low glycogen levels can attenuate or abolish the decrease in GSF. The rapid increase of GSF during recovery from exercise does not require glycogen depletion during the exercise.     

Role of perfusate hydrogen ion activity in kallikrein release from isolated rat kidneys

The present experiments were performed to investigate whether renal kallikrein release by isolated perfused rat kidneys correlates with acid-base-related parameters. Kallikrein excretion per millilitre of glomerular filtrate was inversely correlated with perfusate pH (r = −0.49, P < 0.001) and HCO₃ ⁻ concentration (r = −0.46, P < 0.005). A direct relationship between kallikrein excretion per millilitre of glomerular filtrate and urinary Na⁺/K⁺ ratio was found (r = 0.59, P < 0.001). Some 86% of the variability (F ratio 110, P < 0.00001) of urinary kallikrein activity was attributable to the perfusate pH and the urinary cation ratio. Therefore, urinary kallikrein activity was highly correlated with perfusate H⁺ activity corrected by the urinary Na⁺/K⁺ ratio (r = 0.92, P < 0.0001). Kallikrein secretion into the distal tubular fluid appears to be regulated by blood H⁺ activity, and modulated by factors that affect the distal Na⁺ and K⁺ handling. The HCO3 ⁻ excretion rate was inversely correlated with the urinary kallikrein activity (r = −0.62, P < 0.001). This finding confirms previous data from the author’s laboratory showing a kallikrein involvement in the regulation of HCO₃ ⁻ secretion in rats and rabbits. Kallikrein probably transduces the sensing of interstitial fluid H⁺ activity by the connecting tubule cells into an appropriate translocation of HCO₃ ⁻ or H⁺ to the tubular lumen by the intercalated cells. Received: 24 April 1995/Received after revision: 23 November 1995/Accepted: 8 January 1996     

Live high:train low increases muscle buffer capacity and submaximal cycling efficiency

This study investigated whether hypoxic exposure increased muscle buffer capacity (βm) and mechanical efficiency during exercise in male athletes. A control (CON, n=7) and a live high:train low group (LHTL, n=6) trained at near sea level (600 m), with the LHTL group sleeping for 23 nights in simulated moderate altitude (3000 m). Whole body oxygen consumption (V˙O ₂) was measured under normoxia before, during and after 23 nights of sleeping in hypoxia, during cycle ergometry comprising 4×4‐min submaximal stages, 2‐min at 5.6 ± 0.4 W kg^–1, and 2‐min ‘all‐out’ to determine total work and V˙O _2peak. A vastus lateralis muscle biopsy was taken at rest and after a standardized 2‐min 5.6 ± 0.4 W kg^–1 bout, before and after LHTL, and analysed for βm and metabolites. After LHTL, βm was increased (18%, P < 0.05). Although work was maintained, V˙O _2peak fell after LHTL (7%, P < 0.05). Submaximal V˙O ₂ was reduced (4.4%, P < 0.05) and efficiency improved (0.8%, P < 0.05) after LHTL probably because of a shift in fuel utilization. This is the first study to show that hypoxic exposure, per se, increases muscle buffer capacity. Further, reduced V˙O ₂ during normoxic exercise after LHTL suggests that improved exercise efficiency is a fundamental adaptation to LHTL.     

Serrated Flippers and Directional Asymmetry in the Appendicular Skeleton of the Commerson's Dolphin (Cephalorhynchus commersonii)

Presence of saw‐toothed structures (serrations) on the leading edge of the flippers in the Commerson's dolphin and their relation with directional asymmetry in the appendicular skeleton were investigated in individuals from the Tierra del Fuego population, Argentina. Serrations were more frequent in the left flipper than in the right (P < 0.001) and in males than in females (P < 0.001). Serration length was significantly longer in the left flipper than in the right (P = 0.023), in males than in females (P = 0.004), and in older individuals than young (P < 0.001). The length of the radius (P = 0.028) and the length (P = 0.004), width (P < 0.001) and weight (P = 0.006) of the scapula showed significant directional asymmetry favoring the right side, whereas the length (P < 0.001) and width (P < 0.001) of the second digit favored the left side. The asymmetry appears to be innate in the species but is likely to be enhanced by differential mechanical stress between flippers as a result of lateralized behavior. We propose that the left flipper would be more flexible and preferably used in sensory or tactile activities that involve the serrations, whereas the right flipper would be more responsible for actions requiring a larger muscular exercise, possibly related to the maintenance of stability during swimming. Anat Rec, 2010. © 2010 Wiley‐Liss, Inc.     

Greater growth hormone and insulin response in women than in men during repeated bouts of sprint exercise

Aim: In a previous study, sprint training has been shown to increase muscle cross‐sectional area in women but not in men [Eur J Appl Physiol Occup Physiol 74 (1996) 375]. We hypothesized that sprint exercise induces a different hormonal response in women than in men. Such a difference may contribute to explaining the observed gender difference in training response. Method: Metabolic and hormonal response to three 30‐s sprints with 20‐min rest between the sprints was studied in 18 physically active men and women. Results: Accumulation of blood lactate [interaction term gender (g) × time (t): P = 0.022], and plasma ammonia (g × t: P < 0.001) after sprint exercise was greater in men. Serum insulin increased after sprint exercise more so in women than in men (g × t: P = 0.020), while plasma glucose increased in men, but not in women (g × t: P < 0.001). Serum growth hormone (GH) increased in both women and men reaching similar peak levels, but with different time courses. In women the peak serum GH level was observed after sprint 1, whereas in men the peak was observed after sprint 3 (g × t; P < 0.001). Serum testosterone tended to decrease in men and increase in women (g × t: P = 0.065). Serum cortisol increased approx. 10–15% after sprint exercise, independent of gender (time: P = 0.005). Conclusion: Women elicited a greater response of serum GH and insulin to sprint exercise. This may contribute to explaining the earlier observed muscle hypertrophy in women in response to sprint training.     

Quality of life in patients with an idiopathic rapid eye movement sleep behaviour disorder in Korea

There have been few quality of life studies in patients with idiopathic rapid eye movement sleep behaviour disorder. We compared the quality of life in idiopathic rapid eye movement sleep behaviour disorder patients to healthy controls, patients with hypertension, type 2 diabetes mellitus without complication and idiopathic restless legs syndrome. Sixty patients with idiopathic rapid eye movement sleep behaviour disorder (24 female; mean age: 61.43 ± 8.99) were enrolled retrospectively. The diagnosis was established based on sleep history, overnight polysomnography, neurological examination and Mini‐Mental State Examination to exclude secondary rapid eye movement sleep behavior disorder. All subjects completed questionnaires, including the Short Form 36‐item Health Survey for quality of life. The total quality of life score in idiopathic rapid eye movement sleep behaviour disorder (70.63 ± 20.83) was lower than in the healthy control group (83.38 ± 7.96) but higher than in the hypertension (60.55 ± 24.82), diabetes mellitus (62.42 ± 19.37) and restless legs syndrome (61.77 ± 19.25) groups. The total score of idiopathic rapid eye movement sleep behaviour disorder patients had a negative correlation with the Pittsburg Sleep Quality Index (r = −0.498, P < 0.001), Insomnia Severity Index (r = −0.645, P < 0.001) and the Beck Depression Inventory‐2 (r = −0.694, P < 0.001). Multiple regression showed a negative correlation between the Short Form 36‐item Health Survey score and the Insomnia Severity Index (β = −1.100, P = 0.001) and Beck Depression Inventory‐2 (β = −1.038, P < 0.001). idiopathic rapid eye movement sleep behaviour disorder had a significant negative impact on quality of life, although this effect was less than that of other chronic disorders. This negative effect might be related to a depressive mood associated with the disease.     

Role of adenosine in exercise‐induced human skeletal muscle vasodilatation

The role of adenosine in exercise‐induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline‐induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one‐legged, knee‐extensor exercise at ～48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (F_aBF) by ～20%, i.e. from 3.6 ± 0.5 to 2.9 ± 0.5 L min^?1, and leg vascular conductance (VC) from 33.4 ± 9.1 to 27.7 ± 8.5 mL min^?1 mmHg^?1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) F_aBF from 0.3 ± 0.03 L min^?1 to a 15‐fold peak elevation (P < 0.05) at 4.1 ± 0.5 L min^?1. Continuous infusion of adenosine at rest and during one‐legged exercise at ～62% of peak power output increased (P < 0.05) F_aBF dose‐dependently to level off (P = ns) at 8.3 ± 1.0 and 8.2 ± 1.4 L min^?1, respectively. One‐legged exercise alone increased (P < 0.05) F_aBF to 4.7 ± 1.7 L min^?1. Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least ～20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

The effect of physical activity and physical fitness on plasma adiponectin in adults with predisposition to metabolic syndrome

The purpose of this study was to measure changes in plasma adiponectin (ApN) over 24 months of exercise intervention in middle age adults with a predisposition to metabolic syndrome and to determine if changes in ApN were more affected by physical activity or physical fitness. Thirty-six subjects completed a 24 months home-based exercise program (cycling ≥ three times per week, ≥ 45 min/session at 50–65% of VO_2peak). Body composition, blood samples, and physical fitness were studied at baseline and after 12 and 24 months of participation in the study. The prescribed physical activity was monitored via self-reported exercise diary to determine MET levels, hours, and exercise compliance. Two-tailed repeated measures ANOVA and Spearman Rank Correlation Coefficients were used to detect significant differences and associations between the variables. ApN increased significantly (P < 0.05) after 12 months in males (n = 17; 5.3 ± 1.9–7.0 ± 3.0 μg ml⁻¹) but not in females (n = 9; 8.6 ± 3.8–11.5 ± 4.0 μg ml⁻¹). The net change in ApN over 24 months was significantly correlated to the net change in VO_2peak (physical fitness) (r = 0.66; P < 0.001), whereas exercise intensity was negatively correlated to ΔApN over 12 months (r = −0.4; P ≤ 0.04) and 24 months (r = −0.45; P ≤ 0.02). Based on our results, an improvement in cardiorespiratory fitness of 15% increased plasma ApN concentration. Our findings suggest that moderate physical activity performed over many months induces positive changes in the plasma ApN concentration in adults with a predisposition to metabolic syndrome.