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Maximum anaerobic performance of childhood-onset GH-deficient adults
No full textTo date, physical capacity of adults with GH deficiency (GHD) has been studied in terms of muscle strength, contractile properties and aerobic performance. As a result, scanty data are available regarding the maximum anaerobic performance of these patients with reference to healthy controls. Therefore, the objective of this study was to evaluate maximum anaerobic power of adults with GHD and of age-matched controls by two methods, one testing lactacid power (W(c)) through a 15-s-maximal bout on a bicycle ergometer, the other testing alactic power (W(j)) through a vertical jump on a force platform. Absolute W(c) and W(j) values were both found to be 35% lower(P<0.04) in GHD patients than in controls. Similarly, peak pedalling velocity (V(peak)) was 21% lower (P<0.04) in patients. When W(c) and W(j) were respectively normalized for thigh and lower limb muscle plus bone volumes and V(peak) for muscle length, differences between patients and controls were no longer significant. Furthermore, the rate of power loss during the cycling bout was ~35% in both groups. This observation was in line with similar delta (peak minus baseline) lactate capillary blood concentrations, being 6.3 mM/l in patients and 7.5 mM/l in controls (NS). Lactacid capacity, which represents the energy extracted from lactate metabolism, normalized for body mass was similar in the two groups. In conclusion, the maximum anaerobic power that can be developed by short-statured childhood-onset GHD adults is significantly lower in terms of absolute values, but not different from that of controls once appropriately normalized. Therefore, the changes in maximum anaerobic power of GH deficient patients seem to be a consequence of their smaller muscle mass
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise
Full text linkPatients:6 healthy subjects mean age 25.5 years were studied.TypeofStudy:This study determined the effects of selective beta-adrenergic blockade with Lopresor on the oxygen flow in arterial blood (Q̇aO2) and oxygen flow in mixed venous blood (oxygen return, Q̇v̄O2) in humans exercising in normoxia and in acute normobaric hypoxia.DosageDuration:Initially 7.5 mg iv bolus; additional doses up to 30-40 mg until a quasi-complete receptor blockade was achieved.Results:Without Lopresor, PaO2 and PaCO2 were lower in hypoxia than in normoxia. In both hypoxia and normoxia conditions, Lopresor did not induce significant differences in PaO2 and PaCO2 with respect to control condition. Arterialized blood pH was higher in hypoxia than in normoxia and was unaffected by Lopresor. [La]b was higher in hypoxia than in normoxia and was unaffected by Lopresor. The highest [La]b values were observed at 150 W in hypoxia. Without Lopresor the fH, SV, Q̇ and Q̇aO2 increased significantly at exercise in both normoxia and in hypoxia. fH was systematically and significantly higher in hypoxia than in normoxia at each workload. SaO2 and CaO2 were lower in hypoxia than in normoxia. In hypoxia, they also decreased with increasing workload. As a result of this, and despite the lower arterial-venous O2 differences in hypoxia, the O2 extraction coefficient was greater in hypoxia than in normoxia. In normoxia the difference between Q̇aO2 and V̇02 (=Q̇V̄O2) did not change with increasing workload. In hypoxia, Q̇V̄O2 decreased as a function of workload. The resting Q̇v̄O2 value in normoxia was significantly lower than the corresponding invariant values at exercise. In hypoxia the resting Q̇V̄O2 value did not differ significantly from the corresponding value in normoxia. However, the Q̇V̄O2 values at 100 and 150 power (W) in C were significantly lower than the corresponding values in normoxia. With Lopresor, the fH, SV, Q̇, and Q̇aO2 increased significantly during exercised in both normoxia and hypoxia conditions. At rest and at each workload, Lopresor systematically and significantly decreased fH, both in normoxia and in hypoxia. The lower fH at any given V̇O2 implied a significant increase in the oxygen pulse with Lopresor. Q̇ values were found significantly higher at each fH level under Lopresor in hypoxia than in normoxia as a consequence of increased SV. SV values were significantly higher under Lopresor than in control condition in both normoxia and hypoxia. In normoxia, Q̇ was significantly decreased by Lopresor at 100 power (W) exercise and above, and in hypoxia at rest and at 50 W. As in control condition, SaO2 and CaO2 were lower in hypoxia than in normoxia. In hypoxia they also decreased with increasing workload. In both conditions the values observed under Lopresor were not significantly different from those found in control condition. The Q̇v̄O2 decrease as a function of workload in hypoxia paralleled an analogous decrease in SaO2.AdverseEffects:No adverse events were mentionedAuthorsConclusions:The results of the present study are in agreement with the tested hypothesis, as this study showed that selective blockade of beta1-adrenergic receptors decreased Q̇aO2 and Q̇v̄O2 significantly during exercise in normoxia as well as during rest and light exercise in hypoxia.FreeText:Experiments were performed in normoxia and in acute normobaric hypoxia. In both conditions the subjects performed two incremental exercise tests, one without Lopresor and one after having induced quasi-complete beta-adrenergic blockade with Lopresor. Tests: oxygen consumption (V̇O2), carbon dioxide output (V̇CO2), expired ventilation (V̇E), heart rate (fH, electrocardiography), SaO2 (oximetry), hemoglobin (Hb), blood lactate concentration ([La]b), cardiac output (Q̇), stroke volume (SV), arterialized blood carbon dioxide partial pressure (PaCO2), and arterialized blood oxygen partial pressure (PaO2)
The effects of b1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise.
No full textThe role of anthropometric changes due to aging on human walking: Mechanical work, pendulum and efficiency
No full textThe aging process modifies body composition and the inertial properties of body limbs might change accordingly. Pendular energy exchange, mechanical work and locomotion efficiency should be affected by these changes. To check this hypothesis, seven elderly subjects were asked to walk on a treadmill at five speeds ranging from 0.55 to 1.66 m·s-1. The internal work is indeed reduced when calculated by using specific anthropometric tables for the elderly. The pendular recovery and external work are not affected by the anthropometric profile. Our results suggest that the mass-specific mechanical work based on anthropometric tables consistently decreases with age and consequently the greater metabolic cost is counterbalanced, in part, by decreased mechanical work, resulting in a similar locomotion efficiency
NT-proBNP concentrations in mountain marathoners.
No full textThe 76 amino acid N-terminal proB-type natriuretic peptide (NT-proBNP) is proposed for evaluating and monitoring heart pathologies characterized by myocardial wall stress. Strenuous exercise might generate transitory ischemia, myocardial stress, and diastolic left ventricular dysfunction, possibly inducing an increase of some biochemical parameter concentrations. An alert has been claimed owing to biochemical and instrumental signs of heart dysfunction in recreational athletes during marathon races. We studied the behaviour of NT-proBNP in 15 mountain marathoners before and after a race. The concentrations of the parameter were lower than that observed in controls at rest and were similar to that observed in professional soccer and rugby players. The concentrations significantly increased after the race. NT-proBNP is low at rest in professional athletes, and the increase after physical exercise is physiological. The marathoners, even when performing races in a high-altitude environment, show NT-proBNP concentrations similar to those of athletes from other sports disciplines, characterized by low levels of effort and by a mix of aerobic and anaerobic metabolism. The increase of NT-proBNP is linked to strenuous physical exercise and to heavy heart effort, testified also by an increase of troponin I. However, the role of the NT-proBNP could be important to screen recreational and professional marathoners to avoid possible heart problems and sudden cardiac death in subjects with occult heart disease. The results of the present study are relevant to the design and evaluation of training programs for improving strength and function of professional marathoners
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