These results indicate that calcification of the aorta is independently associated with aortic stiffness and serum 25(OH)D level in patients with PAD and in healthy subjects. Aortic stiffness and abnormal vitamin D level may contribute to vascular calcification and are related to higher severity grade of atherosclerotic disease.

This study assessed the effects of dietary sodium citrate supplementation during a 16 h recovery from 5% rapid body mass loss (RBML) on physiological functions, affective state, and performance in trained wrestlers. Sixteen wrestlers performed an upper body intermittent sprint performance (UBISP) test under three conditions: before RBML, after RBML, and after a 16 h recovery from RBML. During recovery, the subjects ate a prescribed diet supplemented with sodium citrate (600 mg·kg(-1); CIT group, N = 8) or placebo (PLC group, N = 8) and drank water ad libitum. RBML reduced (p < 0.05) UBISP mean power and increased urine specific gravity (USG). Reduction in mean power was associated with changes in plasma volume (PV) (r = 0.649, p = 0.006) and USG (r = -0.553, p = 0.026). During the 16 h recovery, increases in body mass (BM) and PV were greater (p < 0.05) in the CIT group than in the PLC group. BM gain was associated with water retention in the CIT group (r = 0.899, p = 0.002) but not in the PLC group (r = 0.335, p = 0.417). Blood pH, HCO(3)(-) concentration, and base excess increased (p < 0.05) only in the CIT group. Changes in UBISP, general negative affect, and general positive affect did not differ in the two groups. In conclusion, ingestion of sodium citrate increases blood buffering capacity and PV and stimulates BM regain during a 16 h recovery from RBML in trained wrestlers. However, sodium citrate does not improve UBISP nor does it have an impact on the affective state.

The importance of elevated homocysteine (Hcy) as a risk marker for cardiovascular disease is continuously under debate. Lifestyle factors may increase the total Hcy (tHcy) level of the plasma, but there are no consistent findings relating to Hcy, physical activity, and cardiorespiratory fitness. Cross-sectional measurement from an ongoing follow-up study was performed on 77 former male athletes and 33 sedentary controls (age range 35-62 years). Lifestyle parameters (current physical activity patterns, smoking, etc.), anthropometric and blood pressure data, and data about tHcy, reduced, and oxidized glutathione (GSH, GSSG, respectively) in blood, lipoproteins, and maximal oxygen consumption (VO(2max)) were collected. Our study results showed that the subgroup of physically active ex-athletes (n=52) had a significantly lower tHcy level and glutathione redox ratio (GSSG:GSH) in comparison with the subgroup of sedentary ex-athletes (n=25). tHcy level was inversely related to cardiorespiratory fitness (VO(2max)/kg). Dietary and smoking habits were not significantly associated with the tHcy level in our study group. In conclusion, the research findings indicate that both current physical activity and cardiorespiratory fitness are significantly inversely associated with an elevated homocysteine level in middle-aged former athletes.

The independent association between OPG and aPWV in patients with PAD and in controls suggests that the calcification inhibitor OPG may influence aortic stiffening in atherosclerosis and in clinically healthy subjects.

The adaptogen Rhodiola rosea (RR) may mitigate stress responses and have beneficial effects on endurance capacity (EC) and mental performance. Heat acclimation (HA) improves EC in the heat, but the potential impact of RR on the HA process is unknown. Therefore, our intent was to determine if RR has a positive impact on HA. Twenty male subjects (age, 22.5 ± 3.0 years) completed 2 EC tests involving walking (6 km·h) until volitional exhaustion in a climate chamber (air temperature, 42 °C; relative humidity, 18%) before (H1) and after (H2) an 8-day HA period. One group (SHR; n = 10) ingested standardised extract SHR-5 of RR (a single daily dose of 432 mg), while a second group (PLC; n = 10) administered a placebo prior to each HA session. Efficacy of HA was evaluated on the basis of changes that occurred from H1 to H2 in the time to exhaustion (TTE), exercise heart rate (HR), core and skin temperatures (T, T), stress hormones, ratings of perceived exertion (RPE) and fatigue (RPF), and thermal sensation (TS). HA significantly increased TTE (133.1 ± 44.1 min in H1; 233.4 ± 59.8 min in H2; p < 0.0001) and decreased (p < 0.0001) HR, T, T, stress hormones as well as RPE, RPF, and TS. However, the magnitude of all these changes was similar (p > 0.05) in the SHR and PLC groups. These results suggest that the use of RR during HA has no beneficial performance, physiological, or perceptual effects in young healthy males.

We examined the effect of heat acclimation (HA) on endurance capacity and blood prolactin (PRL) response to moderate intensity exercise in the heat in young male subjects (n = 21). Three exercise tests (ET) were completed on a treadmill: H1 (walk at 60% VO(2)peak until exhaustion at 42°C), N (walk at 22°C; duration equal to H1) and H2 (walk until exhaustion at 42°C after a 10-day HA program). Heart rate (HR), skin (T (sk)) and core (T (c)) temperatures and body heat storage (HS) were measured. Blood samples were taken immediately before, during and immediately after each ET. HA resulted in lower HR, T (sk), T (c) and HS rate (P < 0.05) during ET, whereas endurance capacity increased from 88.6 ± 27.5 min in H1 to 162.0 ± 47.8 min in H2 (P < 0.001). Blood PRL concentration was lower (P < 0.05) during exercise in H2 compared to H1 but the peak PRL level observed at the time of exhaustion did not differ in the two trials. Blood PRL concentration at 60 min of exercise in H1 correlated with time to exhaustion in H1 (r = -0.497, P = 0.020) and H2 (r = -0.528, P = 0.014). In conclusion, HA slows down the increase in blood PRL concentration but does not reduce the peak PRL level occurring at the end of exhausting endurance exercise in the heat. Blood PRL response to exercise in the heat in non-heat-acclimated subjects is associated with their endurance capacity in the heat in a heat-acclimated state.

The purpose of this study was to assess the impact of sodium citrate (CIT) ingestion (600 mg·kg) during recovery from dehydrating cycling exercise (DE) on subsequent 40-km cycling performance in a warm environment (32 °C). Twenty male nonheat-acclimated endurance athletes exercised in the heat until 4% body mass (BM) loss occurred. After 16 h recovery with consumption of water ad libitum and prescribed diet (evening meal 20 kcal·kg, breakfast 12 kcal·kg) supplemented in a double-blind, randomized, crossover manner with CIT or placebo (PLC), they performed 40-km time-trial (TT) on a cycle ergometer in a warm environment. During recovery greater increases in BM and plasma volume (PV) concomitant with greater water intake and retention occurred in the CIT trial compared with the PLC trial (p < 0.0001). During TT there was greater water intake and smaller BM loss in the CIT trial than in the PLC trial (p < 0.05) with no between-trial differences (p > 0.05) in sweat loss, PV decrement, ratings of perceived exertion, or TT time (CIT 68.10 ± 3.28 min, PLC 68.11 ± 2.87 min). At the end of TT blood lactate concentration was higher (7.58 ± 2.44 mmol·L vs 5.58 ± 1.32 mmol·L; p = 0.0002) and rectal temperature lower (39.54 ± 0.50 °C vs 39.65 ± 0.52 °C; p = 0.033) in the CIT trial than in the PLC trial. Compared with pre-DE time point, PV had decreased to a lower level in the PLC trial than in the CIT trial (p = 0.0001). In conclusion, CIT enhances rehydration after exercise-induced dehydration but has no impact on subsequent 40-km cycling TT performance in a warm uncompensable environment.

Arterial stiffness is a prominent feature of vascular ageing and strongly predicts cardiovascular and total mortality. The β2-microglobulin, (β2M) a newly identified biomarker of peripheral arterial disease (PAD), is related to renal insufficiency, inflammatory and neoplastic diseases, but may also play a role in vascular dysfunction. However, the relationship between arterial stiffness and β2M has not been previously studied in patients with atherosclerosis. In the present study we examined a possible association between β2M and arterial stiffness in patients with PAD and in healthy subjects. Plasma β2M levels and parameters of arterial stiffness such as aortic pulse wave velocity (aPWV) and augmentation index (AIx) were measured in 66 patients with PAD and in 66 apparently healthy subjects. Plasma levels of β2M, aPWV and AIx were significantly increased in patients with PAD compared with controls (1858.1 ± 472.8 vs 1554.5 ± 277.9 μg/L, p < 0.001; 9.9 ± 2.2 m/s vs 7.6 ± 1.6 m/s, p < 0.001; 28 ± 8 vs 14 ± 11%, p < 0.001; respectively). There existed significant correlation between aPWV and β2M for the patient group (R = 0.47; p < 0.001), but not for the controls (R = 0.14; p = 0.26). In multivariate analysis, β2M remained independently associated with aPWV, fetuin-A, age and glomerular filtration rate in patients (R(2) = 0.5, p < 0.001). We found no relationship between β2M and AIx in either group. We demonstrated that among patients with PAD elevated plasma β2M levels were associated with higher aortic stiffness irrespective of cardiovascular disease risk factors. These data suggest that β2M may influence the pathogenesis of aortic stiffness in atherosclerosis.