Effects of oral creatine-pyruvate supplementation in cycling performance

A double-blind study was performed to evaluate the effects of oral creatine-pyruvate administration on exercise performance in well-trained cyclists. Endurance and intermittent sprint performance were evaluated before (pretest) and after (posttest) one week of creatine-pyruvate intake (Cr(pyr), 2 x 3.5 g x d-1, n = 7) or placebo (PL, n = 7). Subjects first performed a 1-hour time trial during which the workload could be adjusted at 5-min intervals. Immediately they did five 10-sec sprints interspersed by 2-min rest intervals. Tests were performed on an individual race bicycle that was mounted on an ergometer. Steady-state power production on average was about 235-245 W, which corresponded to blood lactate concentrations of 4-5 mmol x l -1 and heart rate in the range of 160-170 beats x min -1. Power outputs as well as blood lactate levels and heart rates were similar between Cr(pyr) and PL at all times. Total work performed during the 1-h trial was 872 +/- 44 KJ in PL versus 891 +/- 51 KJ in CR pyr. During the intermittent sprint test power peaked at about 800-1000 watt within 2-3 sec, decreasing by 15-20 % towards the end of each sprint. Peak and mean power outputs were similar between groups at all times. Peak lactate concentrations after the final sprint were approximately 11 mmol x l -1 in both groups during both the pretest and the posttest. It is concluded that one week of creatine-pyruvate supplementation at a rate of 7 g x d -1 does not beneficially impact on either endurance capacity or intermittent sprint performance in cyclists.     

Effects of calcium antagonism on the resting and exercise-stimulated renin-aldosterone axis

The effect of short-term calcium antagonism with felodipine on blood pressure and on some biochemical plasma variables such as catecholamines, renin and aldosterone was studied in 10 normal volunteers at rest and during incremental bicycle exercise. At rest, diastolic blood pressure was slightly decreased during felodipine, whereas systolic pressure and heart rate were not significantly changed. The plasma noradrenaline concentration and plasma renin activity were increased during felodipine treatment; the plasma adrenaline and aldosterone concentrations on the contrary, were not significantly changed. The rises in plasma renin activity, plasma aldosterone and plasma adrenaline and noradrenaline concentrations produced by exercise were not significantly affected by felodipine. The plasma calcium concentration was significantly higher during felodipine treatment than during placebo and this was accompanied by an increased urinary calcium excretion. It is concluded that the rise in plasma renin activity during calcium antagonism with felodipine is not accompanied by a significant increase in plasma aldosterone. Furthermore, the present data suggest that, at least during exercise, calcium antagonism does not interfere with the mechanisms underlying the exercise-induced activation of renin and aldosterone release.     

Changes in erythrocyte sodium and plasma lipids associated with physical training

The intracellular concentrations and transmembrane fluxes of Na+ and K+ in erythrocytes, and plasma lipids were investigated in 30 middle-aged volunteers, before and after physical training. During the first 4 months of the study, half of the subjects (group A) were subjected to a training programme (3 h/week), while the others (group B) served as controls. At the end of the control period the group B subjects also underwent a period of training. At the end of the training, in both experimental groups, the intra-erythrocyte Na+ concentration was decreased (P less than 0.001); the magnitude of this decrease was related to the increase achieved in physical working capacity (r = -0.44; P less than 0.05). After training the activity of the erythrocyte Na+-Li+ counter-transport system was decreased (P less than 0.001) in both groups, whereas Na+,K+ cotransport activity was increased (P less than 0.001). The training intervention did not affect erythrocyte ouabain-sensitive 86Rb uptake, or the calculated rate constant for ouabain-sensitive Na+ efflux. Furthermore, the plasma concentrations of high density lipoproteins (HDL)2- and HDL3-cholesterol (P less than 0.001) markedly increased in both groups during the training period. However, these changes were not significantly correlated with the observed training-induced changes in erythrocyte transmembrane cationic fluxes. It is concluded that physical training decreases intra-erythrocyte Na+ concentration. No significant associations between training-induced changes in plasma lipids and erythrocyte sodium balance could be demonstrated.     

Effect of exercise-induced dehydration on lactate parameters during incremental exercise

Cyclists often use heart rate limits or power output zones, obtained from lactate parameters during incremental exercise testing, to control training intensity. However, the relationship between heart rate or power output, and blood lactate can be changed by several factors including dehydration. Therefore, in the current study we investigated the impact of exercise-induced dehydration on lactate parameters during graded exercise. Nine triathletes completed two test sessions in random order, with a 1-week interval. Each session consisted of 2 graded cycling tests to exhaustion (pretest, posttest), interspersed by a 2-h endurance exercise bout. In one session the cyclists received adequate fluid replacement (EH, 1350 ml . h (-1)) whilst in the other session dehydration was not prevented (DH, 225 ml . h (-1)). Subjects received equal amounts of carbohydrates (150 g) during either condition. The 4-mmol lactate threshold (OBLA) and the d (max) lactate threshold (TH-Dm) were calculated from the power : lactate curves. Weight loss was 0.5 +/- 0.3 kg in EH versus 2.5 +/- 0.2 kg in DH (p < 0.05). Heart rate (HR) at TH-Dm remained unchanged in all test occasions. Conversely, HR at OBLA increased by approximately 10 beats . min (-1) from the pretest to the posttest (p < 0.05), in both EH and DH. Compared to the pretest, in the posttest power output at TH-Dm was reduced (minus approximately 12 %, p < 0.05) in DH, but not in EH. Gross mechanical efficiency at TH-Dm was 20.7 +/- 1 % in the pretest in EH and was not different from the pretest value in DH (21.4 +/- 0.7 %, n.s.). Gross efficiency decreased in the posttest in DH (18.4 +/- 0.6 %, p < 0.05), but not in EH (20.2 +/- 0.8 %, n.s.). It is concluded that heart rate rather than power output should be used to monitor training load in cyclists exercising in environmental conditions predisposing to dehydration. Furthermore, in the latter condition, adequate rehydration is essential to preserve optimal mechanical efficiency.     

Training in the fasted state facilitates re-activation of eEF2 activity during recovery from endurance exercise

Nutrition is an important co-factor in exercise-induced training adaptations in muscle. We compared the effect of 6 weeks endurance training (3 days/week, 1–2 h at 75% VO_2peak) in either the fasted state (F; n = 10) or in the high carbohydrate state (CHO, n = 10), on Ca²⁺-dependent intramyocellular signalling in young male volunteers. Subjects in CHO received a carbohydrate-rich breakfast before each training session, as well as ingested carbohydrates during exercise. Before (pretest) and after (posttest) the training period, subjects performed a 2 h constant-load exercise bout (~70% of pretest VO_2peak) while ingesting carbohydrates (1 g/kg h⁻¹). A muscle biopsy was taken from m. vastus lateralis immediately before and after the test, and after 4 h of recovery. Compared with pretest, in the posttest basal eukaryotic elongation factor 2 (eEF2) phosphorylation was elevated in CHO (P < 0.05), but not in F. In the pretest, exercise increased the degree of eEF2 phosphorylation about twofold (P < 0.05), and values returned to baseline within the 4 h recovery period in each group. However, in the posttest dephosphorylation of eEF2 was negated after recovery in CHO, but not in F. Independent of the dietary condition training enhanced the basal phosphorylation status of Phospholamban at Thr¹⁷, 5′-AMP-activated protein kinase α (AMPKα), and Acetyl CoA carboxylase β (ACCβ), and abolished the exercise-induced increase of AMPKα and ACCβ (P < 0.05). In conclusion, training in the fasted state, compared with identical training with ample carbohydrate intake, facilitates post-exercise dephosphorylation of eEF2. This may contribute to rapid re-activation of muscle protein translation following endurance exercise.     

Effects of training on erythrocyte 2,3-diphosphoglycerate in normal men

Summary The erythrocyte 2,3-diphosphoglycerate concentration (2,3-DPG) and the activity of red cell hexokinase, pyruvate kinase, glucose-6 phosphate dehydrogenase and gluthatione reductase were studied in 27 normal volunteers before and after 2 and 4 months of physical endurance training. The 4 months of training increased maximal oxygen uptake and physical working capacity (PWC₁₃₀) by 16% (p<0.001) and 29% (p<0.001) respectively. Resting heart rate was decreased (p<0.001) by 11 beats·min^–1. With 2 months of training the erythrocyte 2,3-DPG concentration increased by 9% (p<0.001); with 4 months training the increase was only 4% (p<0.05). The training-induced increase in red cell 2,3-DPG was not accompanied by enhanced activity of erythrocyte hexokinase, pyruvate kinase, glucose-6 phosphate dehydrogenase or glutathione reductase. It is concluded that the rise in red cell 2,3-DPG induced by physical endurance training is not due to activation of red cell glycolytic enzymes or the enzymes involved in the pentose-phosphate cycle     

The cardiomyopathy of idiopathic hemochromatosis]

A retrospective study of the case histories of 216 patients with idiopathic haemochromatosis has highlighted the frequency of cardiac involvement in this condition (53%). Two forms can be distinguished: a latent one (65%), in which the changes are predominantly electrocardiographic, and a clinical form (35%) with the features of congestive cardiomyopathy, notable for the rapidity of onset after right heart failure, the degree of cardiomegaly, the constant finding of abnormalities of ventricular repolarisation, the relative frequency of latent disorders of supra-His atrio-ventricular conduction, and the finding of elongation of the isovolumic contraction time on the phonomechanocardiogram. A haemodynamic profile is the same as for non-obstructive hypotonic cardiomyopathies, and is usually associated with a slow rise in left ventricular pressure. The cardiomyopathy, which is the most frequent cause of death, determines the prognosis in this condition. It may be found in association with diabetes and gonad failure. The finding of cardiomyopathy indicates basic treatment by veresection, which may be the only means of establishing a favourable outcome.     

Acute systemic insulin intolerance does not alter the response of the Akt/GSK-3 pathway to environmental hypoxia in human skeletal muscle

Purpose

To investigate how acute environmental hypoxia regulates blood glucose and downstream intramuscular insulin signaling after a meal in healthy humans.

Methods

Fifteen subjects were exposed for 4 h to normoxia (NOR) or to normobaric hypoxia (HYP, F_iO₂ = 0.11) in a randomized order 40 min after consumption of a high glycemic meal. A muscle biopsy from m. vastus lateralis and a blood sample were taken before (T0), after 1 h (T60) and 4 h (T240) in NOR or HYP and blood glucose levels were measured before exposure and every 30 min.

Results

In HYP, blood glucose was reduced 100 min (110.1 ± 5.4 in NOR vs 89.5 ± 4.7 mg dl^?1 in HYP) and 130 min (98.7 ± 3.8 in NOR vs 85.6 ± 4.9 mg dl^?1 in HYP) after completion of a meal, which resulted in an 83 % lower AUC in HYP compared to NOR (p = 0.006). This coincided with 40 % lower GLUT4 protein in the cytosolic fraction (p = 0.013) and a tendency to increase in the crude membrane fraction (p = 0.070) in HYP compared to NOR. At T240, blood glucose concentration was similar between HYP and NOR, whereas plasma insulin as well as phosphorylation of muscle Akt and GSK-3 was ~2-fold higher in HYP compared to NOR (p < 0.05). In contrast, Rac1 protein was less abundant in the membrane fraction in HYP compared to NOR (p = 0.003), reflecting lower activation.

Conclusion

Acute environmental hypoxia initially reduced blood glucose response to a meal, possibly via an increase in GLUT4 abundance at the sarcolemmal membrane. Later on, whole body insulin intolerance developed independently of defects in conventional insulin signaling in skeletal muscle.