12 research outputs found

    T (2007) Effect of cycling position on oxygen uptake and preferred cadence in trained cyclists during hill climbing at various power outputs

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    Abstract Numerous researchers have studied the physiological responses to seated and standing cycling, but actual field data are sparse. One open issue is the preferred cadence of trained cyclists while hill climbing. The purpose of this study, therefore, was to examine the affect of cycling position on economy and preferred cadence in trained cyclists while they climbed a moderate grade hill at various power outputs. Eight trained cyclists (25.8 ± 7.2 years, _ VO 2 max 68.8 ± 5.0 ml kg -1 min -1 , peak power 407.6 ± 69.0 W) completed a seated and standing hill climb at approximately 50, 65 and 75% of peak power output (PPO) in the order shown, although cycling position was randomized, i.e., half the cyclists stood or remained seat on their first trial at each power output. Cyclists also performed a maximal trial unrestricted by position. Heart rate, power output, and cadence were measured continuously with a power tap; ventilation _ Ve, BF and cadence were significantly higher with seated climbing at all intensities; there were no other physiological differences between the climbing positions. These data support the premise that trained cyclists are equally economical using high or low cadences, but may face a limit to benefits gained with increasing cadence

    Identifying social clusters of endangered main Hawaiian Islands false killer whales

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    The presence of distinct social groups within an animal population can result in heterogeneity in many aspects of its life history and ecology. The ability to accurately assess social group membership increases with the number of times individuals are identified, but obtaining sufficient sightings of rarely encountered species can be difficult. Three social clusters were previously identified for the endangered population of false killer whales Pseudorca crassidens around the main Hawaiian Islands, using modularity among associations within a 12 yr photographic dataset with no restrictions on the number of times seen. In this study, we used photo-identification data over a 23 yr period to reassess the number and membership of social clusters, restricted to individuals seen on at least 5 different days. We compared the robustness of clustering assignments from 6 community detection algorithms using modularity and found that the 3 highest-ranking algorithms all identified the same number (4) and membership of social clusters. Spatial use of clusters varied among the islands, with 3 of the 4 clusters encountered regularly only off 1 or 2 of the 3 main island study areas. Comparison of genetic differentiation among social clusters revealed significant differentiation in nuclear DNA. Furthermore, all individuals in 2 of the clusters possess the same mitochondrial DNA haplotype, while in the other 2 clusters, approximately 40% of animals possess a second haplotype. This level of clustering and associated heterogeneity within the population may have implications for mark-recapture abundance estimation, as well as for mitigating exposure to anthropogenic activities, including interactions with fisheries.HŌ‘ULU‘ULU MANA‘O: Pili nā ‘ano like ‘ole o ka nohona a me ke kālaikaiaola o nā pū‘uo holoholona i ka loa‘a ‘ana o nā pū‘ulu kiko‘ī. Pi‘i a‘e ka hiki ke helu kūpono‘ia ka māhuahua ‘ana o nā heluna o ia mau pū‘ulu i ka helu ‘ana i nā wā e ‘ike ‘ia ai kēlā me kēia holoholona, ‘o ka lawa ‘ana na‘e o ka ‘ike ‘ana i nā lāhulu ‘ane halapohe kekahi ālaina. Hō‘ia ‘ia ‘ekolu pū‘ulu o ke koholā ‘ane halapohe, ‘o ka Pseudorca crassidens, a puni nā mokupuni nui ‘ewalu o Hawai‘i, ma ka ho‘owae‘anona ‘ana i ka pilina i loko o kekahi ‘ikepili ki‘a he ‘umikūmālua makahiki me ke kāohi ‘ole i ka nui o ka ‘ike ‘ia ‘ana. Ma kēia kilo ‘ana, ua ho‘ohana mākou i ka ‘ikepili ma o nā makahiki he iwakāluakūmākolu i mea e hō‘oia hou ai i ka heluna a me nā lālā o nā pū‘ulu launa i loko o kekahi pū‘uo holoholona, a pāpā ‘ia nā kālailaina i nā mea i ‘ike ‘ia ma ‘elima mau lā ‘oko‘a ma ka li‘ili‘i loa. Ho‘ohālikelike mākou i ke ‘ano me ka ikaika o kēia mau pū‘ulu launa ma ka ho‘ohana ‘ana i ka ho‘owae‘anona ‘ana ma ‘eono pū‘ulu ha‘ilula a ‘o ka mea i loa‘a, ‘o ia ho‘i ka ‘ike ‘ana, ma o nā ha‘ilula nui ‘ekolu, i ka heluna a me ka lālā ho‘okahi o nā pū‘ulu launa. Loli ka ho‘ohana ‘ana i ke koana o nā pū‘ulu ma waena o nā mokupuni, ‘ike ‘ia ‘ekolu pū‘ulu ma ho‘okahi a ‘elua paha mokupuni mai loko mai o nā mokupuni nui ‘ekolu e kālailai ‘ia ana. Ma ka ho‘ohālikelike ‘ana aku i nā hi‘ohi‘ona ōewe ‘oko‘a o nā pū‘ulu launa, ‘ike ‘ia ka ‘oko‘a ‘ano nui ma ka piko ōewe o nā pū‘ulu. A no laila, loa‘a i nā mea a pau o ia mau pū‘ulu ‘elua ke ōewe ho‘oilina ho‘okahi, a ma nā pū‘ulu ‘ē a‘e ‘elua, loa‘a he hi‘ohi‘ona ōewe ‘elua i nā holoholona he 40 pākēneka. Hiki nō paha i kēia ‘ano ho‘opū‘ulu ‘ana me kēia ‘ano wae‘anona ōewe ho‘opili ma kekahi pū‘uo ke pili i ke kuhi ‘ana i ka nui ma ka hopu kaha ‘ana, a i ke kāohi a ho‘ēmi ‘ana mai i nā hopena o nā hana kanaka, e la‘a ho‘i me ka hana ma ke kai lawai‘a

    CBP Mediates NF-κB-Dependent Histone Acetylation and Estrogen Receptor Recruitment to an Estrogen Response Element in the BIRC3 Promoter

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    Estrogen receptor (ER) and NF-κB are transcription factors with profound effects on breast cancer cell proliferation and survival. While many studies demonstrate that ER and NF-κB can repress each other, we previously identified a gene signature that is synergistically upregulated by these two factors in more aggressive luminal B breast tumors. Herein, we examine a novel mechanism of cross talk between ER and NF-κB that results in the upregulation of the antiapoptotic gene BIRC3 (also known as cIAP2). We demonstrate that NF-κB, acting through two response elements, is required for ER recruitment to an adjacent estrogen response element (ERE) in the BIRC3 promoter. This effect is accompanied by a major increase in NF-κB-dependent histone acetylation around the ERE. Interestingly, CBP, a histone acetyltransferase previously implicated in repressive interactions between ER and NF-κB, plays a permissive role by promoting histone acetylation and ER recruitment, as well as enhanced expression of BIRC3. These findings suggest a new gene regulatory mechanism by which inflammation and NF-κB activation can influence ER recruitment to inherently inactive ER binding sites. This fine-tuning mechanism may explain how two factors that generally repress each other's activity may work together on certain genes to promote breast cancer cell survival and tumor progression
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