Citrulline malate supplementation does not improve German Volume Training performance or reduce muscle soreness in moderately trained males and females

Background Use of supplements to aid performance is common practice amongst recreationally active individuals, including those without a sufficient evidence base. This investigation sought to assess whether acute supplementation with 8 g of citrulline malate (CM) (1.11: 1 ratio) would improve anaerobic performance. Methods A randomised double blind placebo control trial was employed, using a counterbalanced design. We recruited recreationally active men and women to take part in an isokinetic chair protocol, based on German Volume Training (GVT) whereby participants attempted to perform 10 sets of 10 repetitions against a force representing 70% of their peak concentric force. Results The number of repetitions achieved over the course of the GVT was 94.0 ± 7.9 and 90.9 ± 13.9 for placebo and CM respectively. There was no significant difference between the placebo and CM treatment for number of repetitions (P = 0.33), isometric (P = 0.60), concentric (P = 0.38), or eccentric (P = 0.65) peak force following the GVT. Total muscle soreness was significantly higher in the CM compared to the placebo treatment following the GVT protocol over 72 h (P = 0.01); although this was not accompanied by a greater workload/number of repetitions in the CM group. Conclusions We conclude that an acute dose of CM does not significantly affect anaerobic performance using an isokinetic chair in recreational active participants. Practical implications include precaution in recommending CM supplementation. Coaches and athletes should be aware of the disparity between the chemical analyses of the products reviewed in the present investigation versus the manufacturers’ claims

The CPLEAR detector at CERN

The CPLEAR collaboration has constructed a detector at CERN for an extensive programme of CP-, T- and CPT-symmetry studies using ${\rm K}^0$ and $\bar{\rm K}^0$ produced by the annihilation of $\bar{\rm p}$'s in a hydrogen gas target. The ${\rm K}^0$ and $\bar{\rm K}^0$ are identified by their companion products of the annihilation ${\rm K}^{\pm} \pi^{\mp}$ which are tracked with multiwire proportional chambers, drift chambers and streamer tubes. Particle identification is carried out with a liquid Cherenkov detector for fast separation of pions and kaons and with scintillators which allow the measurement of time of flight and energy loss. Photons are measured with a lead/gas sampling electromagnetic calorimeter. The required antiproton annihilation modes are selected by fast online processors using the tracking chamber and particle identification information. All the detectors are mounted in a 0.44 T uniform field of an axial solenoid of diameter 2 m and length 3.6 m to form a magnetic spectrometer capable of full on-line reconstruction and selection of events. The design, operating parameters and performance of the sub-detectors are described.

Impairment of muscle energy metabolism in patients with sleep apnoea syndrome

AbstractImpairment of muscle energy metabolism has been demonstrated in normal subjects with chronic hypoxaemia (altitude chronic respiratory failure). The purpose of this study was to verify the hypothesis that a comparable condition could develop in patients with sleep apnoea syndrome (SAS), considering that they are exposed to prolonged and repeated hypoxaemia periods. Muscle metabolism was assessed in 11 patients with SAS performing a maximal effort on cycloergometer. In comparison with normal subjects, SAS patients reached lower maximal loads [144 ± 7 vs. 182 ± 10 W (P<0·005)] and lower peak oxygen uptakes [26·4 ± 1·2 vs. 33·2 ± 1·4 ml kg−1 min−1 (P<0·005)]. Abnormal metabolic features were found: maximal blood lactate concentration was significantly lower than in normal subjects [0·034 ± 0·004 vs. 0·044 ± 0·002 mmol 1−1 W−1 (P<0·05)]; and lactate elimination rate, calculated during a 30-min recovery period, was reduced [0·127 ± 0·017 vs. 0·175 ± 0·014 mmol 1−1 min−1 (P<0·025)]. The extent of these anomalies correlated with the severity of SAS. The patients also showed higher maximal diastolic blood pressures than normal subjects [104 ± 5 vs. 92 ± 4 mmHg (P<0·05)].These results can be interpreted as indications of an impairment of muscle energy metabolism in patients with SAS. Decrease in maximum blood lactate concentration suggests an impairment of glycolytic metabolism, while decrease in the rate of lactate elimination indicates a defect in oxidative metabolism. Since no respiratory pathology apart from SAS was found in this group of patients, it seems legitimate to link the genesis of these impairments to repeated bouts of nocturnal hypoxaemia

Opposite effects of urea on hemoglobin-oxygen affinity in anemia of chronic renal failure

Opposite effects of urea on hemoglobin-oxygen affinity in anemia of chronic renal failure. We studied the action of urea on the spin-spin relaxation rate of 2,3-diphosphoglycerate (2,3-DPG) phosphorus atoms in normal and uremic erythrocytes. At concentrations from 10 to 60 mM, urea increased the relaxation rates of 2,3-DPG P-3 phosphorus atoms. This evidenced a stronger binding of 2,3-DPG to hemoglobin (Hb), suggesting that the deoxyform of Hb was stabilized. This hypothesis was confirmed by measurements of the association constant of oxygen to hemoglobin (K) in normal erythrocytes in presence of urea concentrations in the range of those observed in uremic patients (30 mM). Indeed, the observed decrease in K suggests that the T structure of hemoglobin is stabilized. By contrast, with higher urea concentrations (120 mM), measurements of P50 showed an increase in the hemoglobin affinity for oxygen (decrease in P50). Moreover, the relaxation rates of 2,3-DPG P-3 phosphorus atoms were not modified, which is consistent with the simultaneous increase of K. This may be attributed to the formation of carbamylated hemoglobin in presence of urea. These results suggest two opposite effects of urea on Hb-O2 affinity: the first reinforces 2,3-DPG-Hb binding and leads to a decrease in O2 affinity; the second, mediated by carbamylation of Hb, hinders the binding of 2,3-DPG and increases the O2 affinity. These findings are consistent with the fact that, despite the presence of carbamylated hemoglobin, uremic patients do not present increased Hb-O2 affinity