RESUMO
Speed climbing is an Olympic discipline within the combined sport climbing event in 2020 for the first time. Speed climbing is a high-speed and anaerobic exercise against gravity over a few seconds with extreme psychological pressure. Although there is some literature on heart rate (HR) when lead climbing, there is no literature on the behavior of the HR when speed climbing. The HR of seven near-elite participants was measured with a Polar HR monitor while climbing a 10- and 15-m wall, respectively, three times each, with pauses of 5 min between the first and last three climbs and a 20-min pause between the third and fourth climb. The average climbing times on the 10- and 15-m walls were 9.16 ± 3.06 s and 14.95 ± 3.14 s, respectively (data pooled between climbing heights). The peak HR on the 10- and 15-m walls were 164.57 ± 7.45 bpm and 176.43 ± 8.09 bpm. The rates of change in HR were as follows: average HR acceleration before peak HR, 2.53 ± 0.80 bpm/s; peak HR acceleration before peak HR, 4.16 ± 1.08 bpm/s; and average HR deceleration after peak HR, -0.98 ± 0.30 bpm/s. The average HR during the pauses ranged from 105.80 to 117.89 bpm. From the results, in comparison to the literature, we conclude that athletes, trained for sustaining high physical exertion and psychological pressure, have a far smaller HR acceleration than untrained people during light and unstressful exercises. Furthermore, the current rule that athletes shall have a minimum resting time of 5 min between climbing attempts during a speed climbing competition seems justified as sufficient time for HR recovery.
RESUMO
Renal osteodystrophy affects the majority of patients with advanced chronic kidney disease (CKD) and is characterized by progressive bone loss. This study evaluated the effects of sclerostin knockout on bone in a murine model of severe, surgically induced CKD in both sclerostin knockout and wild-type mice. Mice of both genotypes with normal kidney function served as controls. Tibiae were analyzed using micro-computed tomography, and lumbar vertebrae were analyzed by histomorphometry. Results were tested for statistical significance by 2-way ANOVA to investigate whether bone of the knockout mice reacted differently to CKD compared with bone of wild-type mice. In the tibiae, there was no difference after creation of CKD between wild-type and knockout animals for cortical thickness or cross-sectional moment of inertia. Increases in cortical porosity induced by CKD differed significantly between genotypes in the tibial metaphysis but not in the diaphysis. In the trabecular compartment, no difference in reaction to CKD between genotypes was found for bone volume, trabecular number, trabecular thickness, and trabecular separation. In the lumbar vertebrae, significant differences in response to CKD between wild-type and knockout mice were seen for both bone volume and trabecular thickness. Osteoblast parameters did not differ significantly, whereas osteoclast numbers significantly increased in the wild-type but significantly decreased in knockout mice with CKD. No differences in response to CKD between genotypes were found for bone formation rate or mineral apposition rate. Thus, complete absence of sclerostin has only minor effects on CKD-induced bone loss in mice.
