Physiological differences between genders. Implications for sports conditioning

It is commonly accepted that there are physiological and morphological gender differences. These differences become evident in the specific responses or magnitude of response to various training regimens. Very little difference is seen in the response to different modes of progressive resistance strength training. Men and women experience similar relative strength gains when training under the same programme. The evidence on body composition changes that occur with strength training is equivocal at this point. Researchers, however, suggest that there appears to be less muscle hypertrophy with strength improvement in women when compared to men. The data suggest that there are no differences between genders in central or peripheral cardiovascular adaptations to aerobic training. However, women in general have a reduced O2 carrying capacity. Another factor that may be responsible for the sex differences seen in the metabolic responses to exercise may be the greater, essential sex specific fat of women. Sparling and Cureton (1983) have shown that differences in similarly trained male and female distance runners are due largely to percentage body fat, less to cardiorespiratory fitness and least to running economy. Pate et al. (1985) determined that men and women who are capable of similar performances, in this case a 15 mile race, do not differ in body composition, cardiorespiratory response or metabolic response. There appear to be no differences in relative increases in VO2max for men and women when they are trained under the same intensity, frequency and duration. Mode of training also appears to elicit no sex difference. Hormonal factors lead to greater initial levels of high density lipoproteins in women. This appears to cause a smaller change in the total cholesterol-high density lipoprotein ratio than occurs with aerobic training in men. Generally, the menstrual cycle phase makes no difference to performance in women. The special cases of exercise in hot and cold environments present conflicting evidence. When men and women are matched for surface area:mass, VO2max and percentage body fat, the major disadvantages women have in the heat disappear. The question of gender differences in the cold has yet to be fully explored. When the general population is compared, men appear to have an advantage over women.     

IL-6-STAT3 controls intracellular MHC class II alphabeta dimer level through cathepsin S activity in dendritic cells

We found IL-6-STAT3 pathway suppresses MHC class II (MHCII) expression on dendritic cells (DCs) and attenuates T cell activation. Here, we showed that IL-6-STAT3 signaling reduced intracellular MHCII alphabeta dimmer, Ii, and H2-DM levels in DCs. IL-6-mediated STAT3 activation decreased cystatin C level, an endogenous inhibitor of cathepsins, and enhanced cathepsin activities. Importantly, cathepsin S inhibitors blocked reduction of MHCII alphabeta dimer, Ii, and H2-DM in the IL-6-treated DCs. Overexpression of cystatin C suppressed IL-6-STAT3-mediated increase of cathepsin S activity and reduction of MHCII alphabeta dimer, Ii, and H2-DM levels in DCs. Cathepsin S overexpression in DCs decreased intracellular MHCII alphabeta dimer, Ii, and H2-DM levels, LPS-mediated surface expression of MHCII and suppressed CD4(+) T cell activation. IL-6-gp130-STAT3 signaling in vivo decreased cystatin C expression and MHCII alphabeta dimer level in DCs. Thus, IL-6-STAT3-mediated increase of cathepsin S activity reduces the MHCII alphabeta dimer, Ii, and H2-DM levels in DCs, and suppresses CD4(+) T cell-mediated immune responses.     

Physiological responses to high radiant heat exposure

The physiological responses to four levels of radiant heat (R) in combination with two work loads and three ambient humidity levels were studied on seven clothed young men. The globe temperature (t_g) ranged from 40 to 74°C; metabolic work load (M) was either 20 or 50% of maximal aerobic capacity (V?₀₂ max); ambient vapor pressure was either 13 or 23 mm Hg; and dry-bulb temperature (t_db) was 38 or 49°C. The criteria for heat strain were the changes in rectal temperature (T_re), mean skin temperature (T_sk), heart rate (HR), and sweating (Sw). Stress was defined by the calculated heat load requiring dissipation (M + R + C = E_req), the ambient evaporative capacity (E_max), and the skin wettedness (w), defined as the ratio of E_req/E_max. The progressive increase in R resulted in a concomitant rise of T_re and HR reflecting the physiological strain. Similarly the increase in either M or in the humidity resulted in higher T_re and HR. The changes in R or E_max were best defined by the w, thus w and the physiological responses were highly correlated. For practical application a multiple regression of the increments of HR(ΔHR) on t_db above neutral (25°C) and on t_g above t_db was derived as follows:

$\text{△HR}{}_{\mathrm{<mtext>bpm</mtext>}}\text{= 0.96(t}{}_{\mathrm{<mtext>db</mtext>}}\text{? 25°}\text{C}\text{) + 0.81(t}{}_{\mathrm{g}}\text{? t}{}_{\mathrm{db}}\text{) ? 1}$

It was concluded that the calculated skin wettedness is most suitable in the evaluation of heat stress.     

Hemophagocytic lymphohistiocytosis following dengue hemorrhagic fever in Hb H/Hb Constant Spring patient

Infection‐associated hemophagocytic syndrome (IAHS), a secondary form of hemophagocytic lymphohistiocytosis (HLH), has been found following several types of infections and can be fatal. We report herein a case of IAHS following dengue infection in a 14‐year‐old patient with underlying α‐thalassemia syndrome (non‐deletional Hb H/Hb Constant Spring disease). He developed prolonged fever, thrombocytopenia, and progressive splenomegaly. Further investigations indicated hyperferritinemia, and increased reactive histiocytes with hemophagocytic activity in the bone marrow. He responded promptly to dexamethasone and i.v. immune globulin. Physicians should be aware of this condition, especially in countries where both dengue hemorrhagic fever and thalassemia are prevalent. The fatal outcome of IAHS can be prevented with prompt appropriate treatment.     

Increased circulating levels of soluble Fas ligand are correlated with disease activity in patients with fibrosing lung diseases

OBJECTIVE: The Fas-Fas ligand (FasL) pathway is one of the important apoptosis-signalling molecule systems. We previously determined that this pathway may be involved in the pathogenesis of fibrosing lung diseases. In the present study, we evaluated the clinical significance of the levels of soluble forms of Fas (sFas) and FasL (sFasL) in serum from patients with fibrosing lung diseases. METHODOLOGY: We measured sFas, sFasL, KL-6 (a measure of alveolar type II cell damage), surfactant protein D (SP-D), and surfactant protein A (SP-A) levels in serum from 35 patients with idiopathic pulmonary fibrosis (IPF), 17 patients with interstitial pneumonia associated with collagen vascular diseases (CVD-IP), and 13 normal healthy controls using enzyme-linked immunosorbent assays (ELISA). RESULTS: The serum levels of sFasL were significantly increased in patients with active IPF and CVD-IP, compared with those with inactive disease and controls. There was no significant difference in sFasL levels between patients with inactive disease and controls. Serum sFasL levels were significantly correlated with lactate dehydrogenase and KL-6 levels in IPF. The decrease in sFasL levels following corticosteroid therapy was not correlated with the clinical course of IPF. There was no significant difference in serum sFas levels between IPF or CVD-IP patients and controls. CONCLUSIONS: Although further studies need to be performed on a large number of patients with histologically proven IPF or CVD-IP, it would seem that serum sFasL levels may reflect the activity of IPF and CVD-IP.     

Documented subacute stent thrombosis within thirty days after stenting with sirolimus-eluting stent (Cypher) for acute myocardial infarction: a Japanese single center retrospective non-randomized study.

BACKGROUND: The incidence of subacute stent thrombosis (SAT) within 30 days after stenting with a sirolimus-eluting stent (Cypher) for acute myocardial infarction (AMI) was retrospectively compared to that with bare-metal stents (BMS). METHODS AND RESULTS: Among 559 lesions in 558 consecutive AMI from April 2003 to February 2006, the incidence of documented SAT after Cypher implantation (2/276 lesions, 0.72%) was almost the same as for BMS (2 cases, 0.71%). Aspirin (81-100 mg/day) plus ticlopidine (200 mg/day) were administered continuously after admission in all 4 cases. CONCLUSION: Documented SAT did not increase after stenting with Cypher for AMI under aspirin plus ticlopidine.     

A newly developed maneuver,field change conversion (FCC), improved evaluation of the left ventricular volume more accurately on quantitative gated SPECT (QGS) analysis

PURPOSE: To investigate whether a newly developed maneuver that reduces the reconstruction area by a half more accurately evaluates left ventricular (LV) volume on quantitative gated SPECT (QGS) analysis. METHODS: The subjects were 38 patients who underwent left ventricular angiography (LVG) followed by G-SPECT within 2 weeks. Acquisition was performed with a general purpose collimator and a 64 x 64 matrix. On QGS analysis, the field magnification was 34 cm in original image (Original: ORI), and furthermore it was changed from 34 cm to 17 cm to enlarge the re-constructed image (Field Change Conversion: FCC). End-diastolic volume (EDV) and end-systolic volume (ESV) of the left ventricle were also obtained using LVG. RESULTS: EDV was 71 +/- 19 ml, 83 +/- 20 ml and 98 +/- 23 ml for ORI, FCC and LVG, respectively (p < 0.001: ORI versus LVG, p < 0.001: ORI versus FCC, p < 0.001: FCC versus LVG). ESV was 28 +/- 12 ml, 34 +/- 13 ml and 41 +/- 14 ml for ORI, FCC and LVG, respectively (p < 0.001: ORI versus LVG, p < 0.001: ORI versus FCC, p < 0.001: FCC versus LVG). CONCLUSION: FCC was better than ORI for calculating LV volume in clinical cases. Furthermore, FCC is a useful method for accurately measuring the LV volume on QGS analysis.     

A case of anorexia nervosa with severe hyperlipoproteinemia

OBJECTIVE: The complication of severe hyperlipoproteinemia with anorexia nervosa is very rare. We investigated the mechanisms of severe hyperlipoproteinemia in a patient with anorexia nervosa. METHODS: The measurement of plasma levels of lipids, apolipoproteins (Apo), lipoprotein subfractions, free T3, and estrogen, apo (lipoprotein) E phenotyping, and the assay of lymphocyte low-density lipoprotein (LDL)-receptor activity were accomplished in a 40-year-old female patient with anorexia nervosa. RESULTS: Her body mass index was 10.3 kg/m2. Her plasma levels of total cholesterol (C), triglyceride (TG), apoB, apoE, very-low-density lipoprotein (VLDL)-C, and intermediate-density lipoprotein (IDL)-C were 757 mg/dl, 526 mg/dl, 288 mg/dl, 13.6 mg/dl, 133 mg/dl, and 99 mg/dl, respectively. VLDL was cholesterol rich (C/TG ratio = 0.68; normal value = 0.2). The plasma LDL was high and skewed to less dense fractions. Her apoE phenotype was E 3/2. Her lymphocyte LDL-receptor activity was 79% of normal subjects. The plasma level of estradiol was low and that of free T3 was subnormal. DISCUSSION: We concluded that the plasma lipoprotein abnormality of this anorexia nervosa patient was induced by the impaired removal of TG-rich lipoprotein remnants and less dense LDL due to apoE phenotype E 3/2, subnormal LDL-receptor activity, subnormal plasma level of free T3, and diminished secretion of estrogen.