Growth hormone and prolactin responses during partial and whole body warm‐water immersions

Aim: To elucidate the role of core and skin thermoreceptors in the release of growth hormone (GH) and prolactin (PRL), a sequence of two experiments using whole‐body (head‐out) and partial (one forearm) hot water immersions was performed. Methods: Experiment 1: Nine healthy men were exposed to head‐out and partial water immersions (25 min, 38–39 °C). Results: Head‐out immersion increased the core temperature (38.0 ± 0.1 vs. 36.7 ± 0.1 °C, P < 0.001) and plasma concentration of the hormones (GH, 16.1 ± 4.5 vs. 1.2 ± 0.4 ng mL^?1, P < 0.01; PRL, 9.1 ± 1.0 vs. 6.4 ± 0.4 ng mL^?1, P < 0.05). During the partial immersion the core temperature was slightly elevated (36.8 ± 0.1 vs. 36.6 ± 0.1, P < 0.001), the concentration of GH increased (4.8 ± 1.7 vs. 0.6 ± 0.3, P < 0.05), while plasma PRL decreased (7.6 ± 0.8, 6.0 ± 0.6, 5.2 ± 0.6, P < 0.01). Experiment 2: Seven volunteers immersed one forearm once in 39 °C and once in 38 °C water. The measurements were performed in 5‐min intervals. The GH concentration increased gradually from the beginning of the immersions (min 10; 39 °C: 1.9 ± 1.0 vs. 0.6 ± 0.3 ng mL^?1, P < 0.01; 38 °C: 0.19 ± 0.03 vs. 0.14 ± 0.03, P < 0.05) and peaked after their completion (39 °C: +10 min, 3.7 ± 2.0, P < 0.001; 38 °C: +15 min, 0.86 ± 0.61, P < 0.01). The core temperature was unchanged until min 15 of the 39 °C bath. Thereafter, it increased about 0.15 °C above the baseline (P < 0.01). Immersion in 38 °C water did not induce core temperature changes. Conclusions: Peripheral thermoreceptors are involved in GH release when the body is exposed to elevated environmental temperature while a substantial elevation of core temperature is a precondition of PRL release.     

Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease

Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Exposure to ambient air particulate matter with aerodynamic diameters?<?2.5?μm (PM_2.5) is a risk factor for arteriosclerosis and lung disease, but its effect on NAFLD is unknown. PM_2.5 induces pulmonary dysfunction via Toll-like receptor (TLR) activation on alveolar macrophages. TLR activation of Kupffer cells, resident hepatic macrophages, and subsequent pro-inflammatory cytokine production have been shown to play a key role in NAFLD progression. We hypothesized that PM_2.5 exposure is a significant risk factor for the progression of NAFLD. Thus, following exposure of male C57BL/6 mice fed high fat chow (HFC) to concentrated air particulate matter (CAPs) or filtered air for 6 weeks, progression of NAFLD was evaluated by standardized histological assessment of hepatic inflammation and fibrosis. In mice fed HFC, the hepatic inflammatory grade (3.00?±?0.00 vs. 1.50?±?0.71, P?<?0.001) and fibrosis stage (1.00?±?0.00 vs. 0.60?±?0.52, P?=?0.023) were both significantly higher in mice exposed to CAPs versus filtered air, respectively. Increased numbers of Kupffer cells contained PM in CAPs-exposed mice scores of (2.00?±?0.94 vs. 0.20?±?0.42, respectively, P?<?0.001). PM exposure increased IL-6 secretion up to seven-fold in a dose-dependent manner by isolated wild-type but not TLR4^?/? Kupffer cells (P?<?0.050). In conclusion, ambient PM_2.5 exposure may be a significant risk factor for NAFLD progression.     

Effects of Celebrex and Zyflo on liver metastasis and lipidperoxidation in pancreatic cancer in Syrian hamsters

Selective inhibition of eicosanoid synthesis is thought to have effects on carcinogenesis in lung and colon cancer. However, it is still unknown whether pancreatic cancer might also be influenced. Therefore we evaluated the impact of selective cyclooxygenase-2 inhibitor Celebrex and selective 5-lipoxygenase inhibitor Zyflo on liver metastasis in a solid model of pancreatic adenocarcinoma in Syrian hamster. In week 33, the animals were sacrified and incidence of pancreatic carcinomas and number and size of liver metastases were determined. Activities of antioxidative enzymes (GSHPX/SOD) and concentrations of products of lipidperoxidation were measured in liver metastases and non-metastatic hepatic tissue. The incidence (54.5 vs. 100%), number (3.17±0.98 vs. 6.75±0.71) and size (2.67±1.97 vs. 11.75±1.98 mm²) of liver metastases were decreased by combined therapy of Zyflo and Celebrex (P<0.05). Furthermore, activities of GSHPX ([73.77±5.67]^*10⁵ vs. [15.49±4.02]^*10⁵ U/mg prot.; P<0.05) and SOD (474.92±108.8 vs. 127.89±38.75 U/mg prot.; P<0.05) were increased, while lipidperoxidation (0.31±0.08 nmol/mg prot. vs. 1.54±0.55 nmol/mg prot.; P<0.05) was decreased by combination therapy, in non-metastatic hepatic tissue. Moreover, combined therapy increased lipidperoxidation in liver metastases (0.47±0.09 vs. 1.95±0.12 nmol/mg prot.; P<0.05). Thus, a combination of Celebrex and Zyflo might be a new concept to decrease tumour growth in liver metastases in advanced pancreatic cancer. This revised version was published online in July 2006 with corrections to the Cover Date.     

Physical activity patterns assessed by accelerometry in older people

Research into daily physical activity (PA) patterns of older adults (≥70 years) has primarily relied on self-report. This study used accelerometry, an objective measure of minute-by-minute movement, to assess PA volume and intensity performed by older adults recruited to the Better Ageing project. Results were used to estimate the degree to which current health recommendations for PA were met. Participants [91 older females (OF) aged 76.0 ± 4.0 years (mean ± SD), 70 older males (OM) 76.3 ± 3.9 years, 23 young females (YF) 26.8 ± 4.1 years and 22 young males (YM) 27.0 ± 4.2 years] wore an MTI actigraph model 7164 recording activity in 1-min epochs for 7 days. Only those with at least 5 days, and 10 h of actigraph data per day, were included in the analysis, using Caloric.Bas (CSA Inc. 1999) software and a tailored Microsoft Access 2000 macro. Mean counts min^-1 day^-1 were 37% lower for older adults than for young adults [OF 236.1 ± 84.4 vs. YF 370.0 ± 81.1 counts min^-1 day^-1 t(114) = −6.86, P < 0.001; OM 255.1 ± 103.0 vs. YM 404.3 ± 134.0 ct min^-1 day^-1, t(91) = −5.55, P < 0.001]. Older adults were more restricted in activity intensity range performing significantly fewer minutes of moderate to vigorous (MV) PA day^-1 than young adults [OF 16.7 ± 12.2 vs. YF 38.4 ± 18.4 MVPA min day^-1, t(114) = −6.90, P < 0.001; OM 23.8 ± 20.0 vs. YM 40.4 ± 19.2 MVPA min day^-1, t(91) = −3.47, P = 0.001]. Nearly half of older adults did not perform any sustained 10-min MVPA bouts (OF 48.4% vs. YF 13.0%, χ² = 8.10, P = 0.004; OM 44.3% vs. YM 4.5%, χ ² = 9.97, P = 0.002), and none met current PA recommendations for health. This study is the first to provide objective data on a large sample of adults aged 70 years and over and indicates low levels of daily movement that are likely to be inadequate for optimal health benefit.     

Mechanically versus electro-magnetically braked cycle ergometer: performance and energy cost of the Wingate Anaerobic Test

Performance and metabolic profiles of the Wingate Anaerobic Test (WAnT) were compared between a mechanically resisted (ME) and an electro-magnetically braked (EE) cycle ergometer. Fifteen healthy subjects (24.0±3.5 years, 180.5±6.1 cm, 75.4±11.9 kg) performed a WAnT on ME, and EE 3 days apart. Performance was measured as peak power (PP), minimum power (MP), mean power (AP), time to PP (TTPP), fatigue rate (FR), and maximum cadence (RPM_MAX). Lactic (W _LAC) and alactic (W _PCR) anaerobic energy were calculated from net lactate appearance and the fast component of post-exercise oxygen uptake. Aerobic metabolism (W _AER) was calculated from oxygen uptake during the WAnT. Total energy cost (W _TOT) was calculated as the sum of W _LAC, W _PCR, and W _AER. There was no difference between ME and EE in PP (873±159 vs. 931±193 W) or AP (633±89 vs. 630±89 W). In the EE condition TTPP (2.3±0.7 vs. 4.3±0.7 s) was longer (P<0.001), MP (464±78 vs. 388±57 W) was lower (P<0.001), FR (15.2±5.2 vs. 20.5±6.8%) was higher (P<0.005), and RPM_MAX (168±18 vs. 128±15 rpm) was slower (P<0.001). There was no difference in W _TOT (1,331±182 vs. 1,373±120 J kg⁻¹), W _AER (292±76 vs. 309±72 J kg⁻¹), W _PCR (495±153 vs. 515±111 J kg⁻¹) or W _LAC (545±132 vs. 549±141 J kg⁻¹) between ME and EE devices. The EE produces distinctly different performance measures but valid metabolic WAnT results that may be used to evaluate anaerobic fitness.     

Immunomodulation by 8‐week voluntary exercise in mice

This study was designed to evaluate the effects of voluntary exercise on macrophage and lymphocyte functions in mice. Male A/He inbred mice aged 19 weeks were divided into two groups: a group given voluntary exercise and a control group (n = 10 in each group). Exercise consisted of spontaneous running in wheels for 8 weeks (3 days week^–1). Glucose consumption of peritoneal macrophages in the exercise group during incubation up to 72 h was significantly higher than that in the control group (70 and 13%, respectively). Also, activities of acid phosphatase (APH) (10.75 ± 0.37 IU), β‐glucuronidase (GLU) (1.55 ± 0.07 IU) and lactate dehydrogenase (LDH) (43.3 ± 0.7 IU) in the peritoneal macrophages in the exercise group was significantly increased (P < 0.01). Compared with the control group, the exercise group had a significant increase of about twofold in macrophage production of nitric oxide (NO₂^–) stimulated by lipopolysaccharide (LPS) (11.1 ± 0.1 vs. 5.9 ± 0.1 μM mL^–1 in exercise and control groups, respectively; P < 0.01). Stimulation indices both by concanavalin A (Con A) and phytohaemagglutinin were also significantly higher in the exercise group (P < 0.01). A significant increase in the splenocyte production of interleukin‐2 (IL‐2) stimulated by Con A was noticed in the exercise group (354.1 ± 28.8 vs. 218.9 ± 23.5 pg mL^–1 in exercise and control groups, respectively; P < 0.01). These findings suggest that voluntary exercise enhances not only macrophage function but also lymphocyte responsiveness in mice. In the studies of voluntary exercise, evaluation of NO₂^– production, as an indicator of macrophage function, is recommended.     

Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle mass

We tested the hypothesis that pharmacological reduction of the increase in cardiac output during dynamic exercise with a large muscle mass would influence the cerebral blood velocity/perfusion. We studied the relationship between changes in cerebral blood velocity (transcranial Doppler), rectus femoris blood oxygenation (near-infrared spectroscopy) and systemic blood flow (cardiac output from model flow analysis of the arterial pressure wave) as induced by dynamic exercise of large (cycling) vs. small muscle groups (rhythmic handgrip) before and after cardioselective β₁ adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.). During rhythmic handgrip, the increments in systemic haemodynamic variables as in middle cerebral artery mean blood velocity were not influenced significantly by metoprolol. In contrast, during cycling (e.g. 113 W), metoprolol reduced the increase in cardiac output (222 ± 13 vs. 260 ± 16%), heart rate (114 ± 3 vs. 135 ± 7 beats min^?1) and mean arterial pressure (103 ± 3 vs.112 ± 4 mmHg), and the increase in cerebral artery mean blood velocity also became lower (from 59 ± 3 to 66 ± 3 vs. 60 ± 2 to 72 ± 3 cm s^?1; P < 0.05). Likewise, during cycling with metoprolol, oxyhaemoglobin in the rectus femoris muscle became reduced (compared to rest; ?4.8 ± 1.8 vs. 1.2 ± 1.7 μmol L^?1, P < 0.05). Neither during rhythmic handgrip nor during cycling was the arterial carbon dioxide tension affected significantly by metoprolol. The results suggest that as for the muscle blood flow, the cerebral circulation is also affected by a reduced cardiac output during exercise with a large muscle mass.     

Skeletal muscle buffering capacity is higher in the superficial vastus than in the soleus of spontaneously running rats

Skeletal muscle buffering capacity (βm_titr) was determined in soleus (type I) and superficial vastus (type II) muscles of 16 Long–Evans rats with differing levels of spontaneous activity and in 11 sedentary control rats. βm_titr was 24% higher (P<0.001) in superficial vastus muscle than in soleus muscle (268±50 vs. 216±30 μmol H⁺ g muscle dry wt^-1 pH unit^-1) (mean±SD). There was no relationship between βm_titr and mean weekly running distance amongst spontaneously running rats, nor was βm_titr any greater in these rats than in a group of sedentary control rats. Protein to wet wt ratio was 31% higher (P<0.0001) in the superficial vastus muscle when compared with soleus muscle (22.04±3.74 vs. 16.77±3.00 mg protein, 100 mg wet wt muscle^-1), but there was no relationship between protein to wet wt ratio and running distance. Initial muscle homogenate pH (pH_i) was lower in superficial vastus muscle compared with soleus muscle (6.36±0.25 vs. 6.63±0.16). Running rats had a significantly lower pH_i in both soleus and superficial vastus than sedentary controls. There was an exponential relationship between weekly running distance and pH_i in both the superficial vastus muscle (r=-0.86, P<0.001) and the soleus muscle (r=-0.73, P<0.01). Citrate synthase activity correlated with weekly running distance in superficial vastus muscle (r=0.66, P<0.01) but not in soleus muscle. The results confirm a higher βm_titr in the type II superficial vastus muscle when compared with the predominantly type I soleus muscle. We suggest that this may be partly the result of a higher protein concentration in type II muscle. Future studies measuring βm_titr in mixed muscle (e.g. human vastus lateralis) should report fibre type composition.     

Non‐invasive diagnosis and metabolic consequences of congenital portosystemic shunts in C57BL/6 J mice

This study demonstrates the suitability of magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) for the imaging of congenital portosystemic shunts (PSS) in mice, a vascular abnormality in which mesenteric blood bypasses the liver and is instead drained directly to the systemic circulation. The non‐invasive diagnosis performed in tandem with other experimental assessments permits further characterization of liver, whole‐body and brain metabolic defects associated with PSS. Magnetic resonance measurements were performed in a 26‐cm, horizontal‐bore, 14.1‐T magnet. MRA was obtained with a three‐dimensional gradient echo sequence (GRE; in‐plane resolution, 234 × 250 × 234 μm³) using a birdcage coil. Two‐dimensional GRE MRI with high spatial resolution (in‐plane resolution, 100 × 130 μm²; slices, 30 × 0.3 mm) was performed using a surface coil. Brain‐ (dorsal hippocampus) and liver‐localized ¹H magnetic resonance spectroscopy (MRS) was also performed with the surface coil. Whole‐body metabolic status was evaluated with an oral glucose tolerance test (OGTT). Both MRA and anatomical MRI allowed the identification of hepatic vessels and the diagnosis of PSS in mice. The incidence of PSS was about 10%. Hepatic lipid content was higher in PSS than in control mice (5.1 ± 2.8% versus 1.8 ± 0.6%, p = 0.02). PSS mice had higher brain glutamine concentration than controls (7.3 ± 1.0 μmol/g versus 2.7 ± 0.6 μmol/g, p < 0.0001) and, conversely, lower myo‐inositol (4.2 ± 0.6 μmol/g versus 6.0 ± 0.4 μmol/g, p < 0.0001), taurine (9.7 ± 1.2 μmol/g versus 11.0 ± 0.4 μmol/g, p < 0.01) and total choline (0.9 ± 0.1 μmol/g versus 1.2 ± 0.1 μmol/g, p < 0.001) concentrations. Fasting blood glucose and plasma insulin were lower in PSS than in control mice (4.7 ± 0.5mM versus 8.8 ± 0.6mM, p < 0.0001; and 0.04 ± 0.03 μg/L versus 0.3 ± 0.2 μg/L, p = 0.02, respectively). Glucose clearance during OGTT was delayed and less efficient in PSS mice than in controls. Thus, given the non‐negligible incidence of PSS in inbred mice, the undiagnosed presence of PSS will, importantly, have an impact on experimental outcomes, notably in studies addressing brain, liver or whole‐body metabolism.     

Altering the blood-brain barrier in the rat by intracarotid infusion of polycations: a comparison between protamine,poly-L-lysine and poly-L-arginine

To evaluate the role of surface charge for the blood-brain barrier permeability, the albumin content was determined in the cerebrospinal fluid and in the brain 1 h after intracarotid infusion of protamine sulphate, a natural polycationic protein with a high content of arginine (mol. wt 4000–4400), poly-L-arginine (mol. wt 11600) or poly-L-lysine (mol. wt 10200). Five milligrams (4 ± 10^-4 mmol) poly-L-arginine increased the albumin content in the brain IS times more than S mg (5 ± 10^-4 mmol) poly-L-lysine (P < 0.001) and 3.5 times more than 5 mg (1 times 10^-3 mmol) protamine (P < 0.001); the difference between protamine and poly-L-lysine was also significant (P < 0.05). After 0.5 mg (4 ± 10^-4 mmol) poly-L-arginine the albumin extravasation was still higher than after 5 mg protamine (P < 0.01) and 5 mg poly-L-lysine (P < 0.001). Cisternal albumin increased from control values 0.08 mg ml^-1 to 0.30, 0.46 and 1.21 mg ml^-1 in rats given 5 mg poly-L-lysine, protamine and poly-L-arginine, respectively (P < 0.01 for difference between arginine and the other two substances). The higher mol. wt and positive charge of poly-L-arginine may at least in part explain the more pronounced albumin leakage after arginine than after protamine. However, the difference between poly-L-arginine and poly-L-lysine suggests that other factors, possibly related to the guanidino groups, contribute to the blood-brain barrier opening by poly-L-arginine.     

DNA damage in Pakistani agricultural workers exposed to mixture of pesticides

A cross‐sectional study was designed to determine whether occupational exposure to a complex mixture of pesticides results in a significant increase of DNA damage in farmers chronically exposed to pesticides in open fields. Leukocytes from 47 agriculture workers exposed to pesticides and 50 controls were evaluated with comet assay. Workers recruitment was based on their exposure to pesticides during the spraying season on cotton crop. Serum from these individuals was also analyzed for pesticides presence using high performance liquid chromatography. Statistically significant difference (P < 0.001) in DNA damage of exposed individuals (mean ± S.D 14.80 ± 3.04 μm) was observed when compared with control group (6.54 ± 1.73 μm) as studied on the basis of comet tail length. Smokers had significantly higher mean comet tail length than nonsmokers and ex‐smokers in both workers (20.26 ± 3.53 vs. 14.19 ± 4.25, P < 0.001) and controls (7.86 ± 1.09 vs. 5.80 ± 1.59, P < 0.001), whereas age had a minimal effect on DNA damage (P < 0.05). The length of pesticide exposure is positively associated with DNA damage in exposed individuals (P < 0.001). Our study shows that chronic exposure to pesticides produces DNA damage in pesticide sprayers and suggests that this type of monitoring is recommended in preventive policies for pesticide sprayers. Environ. Mol. Mutagen., 2009. © 2008 Wiley‐Liss, Inc.     

Reduced arterial O2 saturation during supine exercise in highly trained cyclists

Performance of intense dynamic exercise in highly trained athletes is associated with a reduced arterial haemoglobin saturation for O₂ (SaO ₂) and lower arterial PO ₂ (PaO ₂). We hypothesized that compared with upright exercise, supine exercise would be accompanied by a smaller reduction in SaO ₂ because of a lower maximal O₂ uptake (VPO _2max) and/or a more even ventilation–perfusion distribution. Eight elite bicyclists completed progressive cycle ergometry to exhaustion in both positions with concomitant determinations of ventilatory data, arterial blood gases and pH. During upright cycling VPO _2max averaged 75±1.6 mL O₂ min^-1 kg^-1 (±SEM) and it was 10.6±1.7% lower during supine cycling (P<0.001). Also the maximal pulmonary and alveolar ventilation were lower during supine cycling (by 15±2% and 21±3%, respectively; P< 0.001) which related to a 0.8±0.1 L lower tidal volume (P<0.001). In all subjects and independent of work posture PaO ₂ and SaO ₂ decreased from rest to exhaustion (from 99±3 to 82±2 Torr and 98.1±0.2 to 95.2±0.4%, respectively; P<0.001); alveolar–arterial PO ₂ difference increased from 6±2 to 37±3 Torr in both body positions. At exhaustion arterial PCO ₂ was lower in upright than in supine (33.4±0.6 vs. 35.9±0.9 Torr; P<0.01), suggesting a greater relative hyperventilation in upright. Arterial pH was similar in upright and supine at rest (both 7.41±0.01) and at exhaustion (7.31±0.01 vs. 7.32±0.01, respectively). We conclude that despite a lower VPO _2max and supposedly an improved ventilation–perfusion distribution, altering body position from upright to supine does not influence arterial O₂ desaturation during intense exercise.     

Genotypes and titers of hepatitis C virus for predicting response to interferon in patients with chronic hepatitis C

Interferon induces remission in about 50% of patients with chronic hepatitis C, but it is difficult to predict which patients will respond. Host and viral factors were evaluated for correlation with response to interferon in patients with chronic hepatitis C. Recombinant interferon alpha-2b with a total dose of 480-560 million units was given to 136 patients, of whom 74 (54%) responded. Genotypes of hepatitis C virus (HCV) in sera, I, II, III, IV, and V, were determined by poly-merase chain reaction (PCR) with type-specific primers. In 72 patients, pretreatment levels of HCV RNA were titrated by PCR in serial tenfold dilutions of RNA extracted from serum. Response to interferon occurred in 34 (40%) of 85 patients infected with HCV of genotype II, less frequently than in 22 (85%) of 26 with genotype III (P < 0.001) or in 7 (70%) of 10 with genotype IV. Of 51 patients with genotype II HCV, 6 of 8 (75%) with HCV RNA titers <10⁶ responded, more frequently than 4 of 43 (9%) with titers ≥ 10⁶ (P < 0.001). Responders were younger than non-responders (45.7 ± 11.7 vs. 50.3 ± 9.6 yr) and had received transfusions less frequently (26/74 or 35% vs. 37/62 or 60%, P < 0.01). Response to interferon correlated inversely with the severity of liver histopathology. These results indicate that response to interferon is influenced by HCV genotypes and pretreatment levels of HCV RNA in serum. © 1994 Wiley-Liss, Inc.     

The effect of the Ramadan fast on physical performance and dietary habits in adolescent soccer players

The purpose of this study was to examine the effect of the Ramadan fast on performance capacities, dietary habits, and the daily behavioral patterns in adolescent (14–16-year-old) soccer players. Nineteen male players performed a series of fitness tests before and at the end of Ramadan fast. Caloric intake, physical activity pattern and sleep habits were evaluated during the week before the Ramadan fast and during the last week of the Ramadan fast. The fast resulted in a significant reduction in aerobic capacity [3,000 m run time (mean ± SD): 812.8 ± 73.3 s vs. 819.9 ± 73.4 s, P < 0.001], speed endurance (Sum 6 × 40 m run time: 46.36 ± 1.36 s vs. 46.73 ± 1.31 s, P < 0.001, and performance decrement: 9.0 ± 1.5% vs. 9.5 ± 1.7%, P < 0.05), and jumping performance (44.8 ± 4.5 cm vs. 44.0 ± 4.5 cm, P < 0.05), but had no significant effect on sprint performance (7.38 ± 0.25 s vs. 7.40 ± 0.26 s, P = 0.20) or agility (4 × 10 m shuttle run time: 9.53 ± 0.35 s vs. 9.55 ± 0.37 s, P = 0.26). Daily intense physical activity was significantly reduced during Ramadan (6.4 ± 0.2 h/week vs. 4.5 ± 0.1 h/week, P < 0.005). There were no significant differences in total caloric intake (3012 ± 412 kcal/day vs. 3240 ± 348 kcal/day, P = 0.39) or total daily sleeping hours (8.6 ± 0.7 h/day vs. 8.6 ± 0.5 h/day, P = 0.80) between Ramadan and a regular month. The results indicate that Ramadan fasting can lead to a significant decrease in athletic performance capacities. The decrease in performance does not necessarily relate to changes in caloric intake and sleeping hours during the fast.     

Additivity of adrenaline and contractions on hormone‐sensitive lipase,but not on glycogen phosphorylase,in rat muscle

Aim: Hormone‐sensitive lipase (HSL) has been proposed to regulate triacylglycerol (TG) breakdown in skeletal muscle. In muscles with different fibre type compositions the influence on HSL of two major stimuli causing TG mobilization was studied. Methods: Incubated soleus and extensor digitorum longus (EDL) muscles from 70 g rats were stimulated by adrenaline (5.5 μm , 6 min) or contractions (200 ms tetani, 1 Hz, 1 min) in maximally effective doses or by both adrenaline and contractions. Results: Hormone‐sensitive lipase activity was increased significantly by adrenaline as well as contractions, and the highest activity (P < 0.05) was seen with combined stimulation [Soleus: 0.40 ± 0.03 (SE) m‐unit mg protein^?1 (basal), 0.65 ± 0.02 (adrenaline), 0.65 ± 0.03 (contractions), 0.78 ± 0.03 (adrenaline and contractions); EDL: 0.18 ± 0.01, 0.30 ± 0.02, 0.26 ± 0.02, 0.32 ± 0.01]. Glycogen phosphorylase activity was always increased more by adrenaline compared with contractions [Soleus: 60 ± 4 (a/a + b)% vs. 46 ± 3 (P < 0.05); EDL: 60 ± 5 vs. 39 ± 6 (P < 0.05)]. After combined stimulation glycogen phosphorylase activity in soleus [59 ± 3 (a/a + b)%] was identical to and in EDL [45 ± 4 (a/a + b)%] smaller (P < 0.05) than the activity after adrenaline only. Conclusions: In slow‐twitch oxidative as well as in fast‐twitch glycolytic muscle HSL is activated by both adrenaline and contractions. These stimuli are partially additive indicating at least partly different mechanisms of action. Contractions may impair the enhancing effect of adrenaline on glycogen phosphorylase activity in muscle.     

Cardiac autonomic dysfunction in rats chronically treated with anabolic steroid

To date no published data exist regarding the effects of chronic high-dose anabolic-androgenic steroid administration on tonic cardiac autonomic control. The aim of this study was to evaluate, by power spectral analysis of heart rate variability (HRV), the effects of chronic treatment with supraphysiological doses of nandrolone decanoate (DECA) on tonic cardiac autonomic regulation in sedentary rats. Male Wistar rats were treated weekly with 10 mg kg⁻¹ of DECA (n=7) or vehicle (CONTROL, n=7) for 10 weeks. At the 8th week of treatment, electrocardiogram was recorded in the conscious state, for time- and frequency-domain HRV analysis. Parasympathetic indexes were reduced in DECA group: high-frequency power (CONTROL=11.1±3.0 ms2 vs. DECA=3.8±0.6 ms2, P<0.05), RMSSD (CONTROL=5.9±0.9 ms vs. DECA 3.5±0.3 ms; P<0.05) and pNN5 (CONTROL=31.5±7.5 ms vs. DECA=13.2±2.6 ms; P<0.05). The sympathetic index LF/HF tended to be higher in DECA group (CONTROL=0.65±0.15 vs. DECA=1.17±0.26, P=0.0546). In conclusion, chronic treatment with DECA, in rats, impairs tonic cardiac autonomic regulation, which may provide a key mechanism for anabolic steroid-induced arrhythmia and sudden cardiac death.     

Potential association between endogenous leptin and sympatho‐vagal activities in young obese Japanese women

Leptin is an adipocyte‐derived hormone that decreases food intake and increases energy expenditure through the activation of the sympathetic nervous system (SNS). Notwithstanding recent intensive research, the underlying physiological mechanism of leptin as well as the etiology of obesity in humans remains elusive. The present study attempted to investigate the potential association between endogenous circulating leptin and sympatho‐vagal activities in age‐ and height‐matched obese and nonobese healthy young women. Plasma leptin concentrations were measured by radioimmunoassay. The autonomic nervous system activity was assessed during the resting condition by means of a recently devised power spectral analysis of heart rate variability, which serves to identify three separate frequency components, very low (VLO), low (LO), and high (HI). Plasma leptin concentrations were greater in the obese than in the control group (45.7 ± 5.89 vs. 11.2 ± 1.10 ng · ml^?1, P < 0.01). As to the contribution of endogenous leptin to SNS activity, both the ratios of the VLO frequency component reflecting thermoregulatory sympathetic function and the global SNS index [(VLO + LO)/HI] to plasma leptin concentration were markedly reduced in the obese compared to the control group (VLO per leptin: 5.9 ± 1.39 vs. 37.8 ± 8.1 ms² · ml · ng^?1, P < 0.01; SNS index per leptin: 0.04 ± 0.008 vs. 0.33 ± 0.01 ml ?· ng^?1, P < 0.01). Additionally, a nonlinear regression analysis revealed that these ratios exponentially decreased as a function of body fat content (VLO per leptin r² = 0.57, P < 0.01; SNS index per leptin r² = 0.53, P < 0.01). Our data suggest that reduced sympathetic responsiveness to endogenous leptin production, implying peripheral leptin resistance, might be a pathophysiological feature of obesity in otherwise healthy young women. The findings regarding the association of leptin, body fat content, and SNS activity further indicate that the 30% of total body fat, which has been used as a criterion of obesity, might be a critical point at which leptin resistance is induced. Am. J. Hum. Biol. 15:8–15, 2003. © 2002 Wiley‐Liss, Inc.     

Plasma oxytocin,prolactin, insulin and LH after 24 h of fasting and after refeeding in lactating sows

The effects of 24 h of fasting and refeeding on the release of oxytocin, prolactin, insulin and LH in three lactating sows were investigated. The sows were starved, but supplied with water ad libitum, from 09.00 h on day 27 of lactation until 15.00 h on day 28 of lactation, when they were refed. Blood samples were collected continuously, using an automatic collection system, at a rate of 1 ml min^-1 from 09.00 to 21.00 h on day 28 (P1 = 6 h period after the 24 h fast, P2 = 6 h period after refeeding). For both P1 and P2 the mean number of nursings was 7.0 ± 1.0. Plasma insulin and glucose decreased to very low levels during fasting and increased (P < 0.001) after refeeding (insulin, 2.5 ± 0.7 vs. 28.9 ± 0.7 mU 1^-1; glucose, 2.6 ± 0.3 vs. 6.4 ± 0.3 mmol 1^-1). Following fasting, levels of prolactin were low (2.8 ± 0.1 μg 1^-1), and sucking did not induce significant release of prolactin. However, prolactin increased rapidly after refeeding (5.4 ± 0.1 μg 1^-1, P < 0.001). Neither the 24 h fast nor refeeding had a marked effect on basal levels of oxytocin, the percentage of sucklings with an oxytocin peak or the size of oxytocin peak. LH release (average and basal levels and number of pulses/6 h) during fasting was similar to that measured after refeeding. Plasma CCK increased significantly after feeding. The results indicate that the release of prolactin is also regulated by feed intake. Consequently the 24 h fast in lactating sows may alter milk production via an inhibition of prolactin release. Neither a stimulatory effect of insulin nor an inhibitory effect of prolactin on LH release was observed.     

Baseline dietary intake and physical activity of Japanese American men in relation to glucose tolerance at 5-year follow-up

Japanese American men (n = 124), with normal glucose tolerance (NGT, n = 69) or impaired glucose tolerance (IGT, n = 55) at baseline, were studied for effects of baseline dietary intake and physical activity on glucose tolerance at baseline and at 5-year follow-up. At baseline, both NGT and IGT men with positive family history of diabetes (FH) showed high intakes of animal fat and protein, but only the NGT men countered this with high levels of energy expenditure. In the total sample at 5-year follow-up, 2-hour plasma glucose was significantly related to intake of animal fat (AF), partial correlation r = 0.32, P < 0.001, adjusted for total energy intake, age, self-reported health, body mass index, FH, and baseline glucose tolerance category. Energy expenditure (EE) was not related to 5-year 2-hour plasma glucose in the total sample, but displayed a relationship with 5-year 2-hour plasma glucose in those IGT (r = −0.27, P < 0.05), but not in those NGT at baseline, and in those with positive FH (r = −0.33, P < 0.05), but not in those with negative FH. Additionally, AF showed a relationship to 5-year 2-hour plasma glucose only for those in the lowest (r = 0.37, P < 0.05) and middle (r = 0.33, P < 0.05) tertiles, but not in the highest tertile of EE. For baseline IGT men, 5-year 2-hour plasma glucose was related to “high vs. low risk” categories of AF intake and EE, but only in men with a positive FH (AF ≥ 25 vs. < 25 g/day: 180.1 ± 38.6 vs. 143.6 ± 39.7 mg/dl, P = 0.048; EE ≤ 2,000 kcal/week vs. > 2,000 kcal/week, 189.9 ± 39.2 vs. 150.8 ± 37.4 mg/dl, P = 0.028; with risk categories combined, i.e., both high, mixed, both low: 192.0 ± 41.3, 165.4 ± 28.4, 139.4 ± 40.9 mg/dl, P = 0.045, linear trend, P = 0.014). Thus, high AF intake and low EE may have long-range detrimental effects on glucose tolerance, especially for those with IGT and positive FH. © 1996 Wiley-Liss, Inc.     

Iron status in HIV-1 infection: implications in disease pathology

Background

There had been conflicting reports with levels of markers of iron metabolism in HIV infection. This study was therefore aimed at investigating iron status and its possible mediation of severity of HIV- 1 infection and pathogenesis.

Method

Eighty (80) anti-retroviral naive HIV-1 positive and 50 sero-negative controls were recruited for the study. Concentrations of serum total iron, transferrin, total iron binding capacity (TIBC), CD₄⁺ T -lymphocytes, vitamin C, zinc, selenium and transferrin saturation were estimated.

Results

The mean CD₄⁺ T-lymphocyte cell counts, serum iron, TIBC, transferrin saturation for the tests and controls were 319 ± 22, 952 ± 57 cells/μl (P < 0.001), 35 ± 0.8, 11.8 ± 0.9?μmol/l (P < 0.001), 58.5 ± 2.2, 45.2 ± 2.4?μmol/l (P < 0.005) and 68.8 ± 3.3, 27.7 ± 2.2%, (P <0.001), respectively, while mean concentrations of vitamin C, zinc and selenium were 0.03 ± 0.01, 0.3 ± 0.04 (P < 0.001), 0.6 ± 0.05, 11.9 ± 0.26?μmol/l (P < 0.001) and 0.1 ± 0.01, 1.2 ± 0.12?μmol/l (P < 0.001) respectively. Furthermore, CD₄⁺ T-lymphocyte cell count had a positive correlation with levels of vitamin C (r = 0.497, P < 0.001), zinc (r = 0.737, P < 0.001), selenium (r = 0.639, P < 0.001) and a negative correlation with serum iron levels (r = ?0.572, P < 0.001).

Conclusion

It could be inferred that derangement in iron metabolism, in addition to oxidative stress, might have contributed to the depletion of CD₄⁺ T cell population in our subjects and this may result in poor prognosis of the disease.