文化大學機構典藏 CCUR:Item 987654321/28072
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    Please use this identifier to cite or link to this item: https://irlib.pccu.edu.tw/handle/987654321/28072


    Title: 高強度游泳間歇訓練對內皮前驅細胞及血管內皮生長因子之立即影響
    The Acute Effects of High Intensity Interval Training on Circulating EPCs and VEGF in Trained Swimmers
    Authors: 李凌純
    Lee, Ling-Chun
    Contributors: 體育學系運動教練碩博士班
    Keywords: 臨界速度
    血循內皮細胞
    免疫反應
    細胞激素
    critical velocity
    circulating endothelial cells
    immune response
    cytokine
    Date: 2014-06
    Issue Date: 2014-09-05 14:50:23 (UTC+8)
    Abstract: 內皮前驅細胞(endothelial progenitor cells, EPCs)源自骨髓,具有增生、遷徙以及分化成內皮細胞的能力,能修復受損的血管內皮,且具有增生新血管之功能,在維持健康心血管功能上扮演重要角色。運動刺激能增加循環血液中EPCs的數量;且運動似乎有驅動EPCs的效果,能增進增生新血管的能力。高強度間歇訓練(high intensity interval training, HIIT)已被證實能快速有效提升運動表現,然而激烈運動訓練卻也可能具潛在性傷害;完好的內皮細胞功能可能取決於內皮細胞的傷害程度及修復的能力而定,在過去,探討運動員因從事高強度間歇運動而引發內皮細胞傷害及驅動EPCs修復影響的研究不多,且多數以跑步及騎腳踏車等陸上運動為主。游泳運動訓練多數以大量高強度間歇模式進行,因此,本研究計畫目的為:(1) 探討單次高強度間歇游泳訓練對內皮前驅細胞EPCs、血循內皮細胞 (Circulating Endothelial Cells, CECs)、凋零的血循內皮細胞(poptotic CECs)、血管內皮生長因子VEGF、IL-6、Creatinine、TNF-α、ALT之立即影響;(2) 探討各項生理檢測參數,與免疫檢測參數的關連性。15名健康受過訓練游泳選手進行單次以105%臨界速度游100公尺二十趟,作業期與休息期為3:1之高強度間歇游泳訓練,分別於運動前及運動後0分鐘、30分鐘採集靜脈血,量測上述變項。統計分析:以重複量數單因子變異數分析(repeated measure one way ANOVA)或無母數Friedman檢定分析,檢定上述免疫檢測參數。以Pearson積差相關或Spearman等級相關探討各項生理檢測參數,與免疫檢測參數的關聯性。研究結果發現,單次高強度臨界速度游泳間歇運動能驅動EPCs,顯著增加血循EPCs的數量(Friedman test: 運動前為5、運動後立即為4以及運動後30分鐘 11 counts/100000cells, χ2(2) = 25.200, P < 0.001).。運動後30分鐘時平均數量顯著提升約為運動前之2.65倍。被視為內皮傷害標的物的CECs於運動後顯著上升(Friedman test:運動前為45、運動後立即為31以及運動後30分鐘為66 counts/100000cells, χ2(2) = 20.933, P < 0.001)。CECs數量於運動後30分鐘時平均顯著提升為運動前之1.854倍。運動前凋零的CECs之中位數為3.8251% ; 運動後立即為3.3639%; 運動後30分鐘為4.7382%。凋零的CECs比例於運動後30分鐘與運動後立即間差異達顯著,顯示高強度臨界速度間歇運動對血管內皮產生傷害。血管內皮生長因子VEGF似乎是驅動EPC由骨髓釋出之影響因子;運動使VEGF濃度上升(運動前44.65 ±11.76、運動後立即 61.38±13.83以及運動後30分鐘47.32 ±10.37 pg/ml, F(2) = 11.214, P < 0.001),且EPC數量與VEGF濃度呈現正相關r=0.756(P<0.01)。血清肌酸酐Creatinine與丙氨酸轉胺ALT皆於運動刺激後顯著升高,但其範圍仍未超出一般正常值,可見高強度間歇訓練對腎臟及肝臟組織的損傷似乎不大。IL6 引發的反應與多數研究類似,在運動後顯著上升且呈指數型態上升,運動後30分鐘後為運動前之6.75倍 (Friedman test: 運動前.37、運動後立即1.69 以及運動後30分鐘2.64 pg/ml, χ2(2) =30.000, P < 0.001)。TNFα 在運動後上升且在運動後30分鐘後仍高於運動前 (運動前.94 ±.15、運動後立即1.29±.13以及運動後30分鐘1.09 ±.14 pg/ml, F(2) = 60.266, P < 0.001),顯示運動引發輕微免疫促發炎反應。值得注意的是,運動刺激後CECs上升的數量遠超過EPCs上升的數量,似乎代表著傷害大於修復程度,然而,本研究僅採集運動後30分鐘之血液分析,有其他研究指出EPCs數量於運動刺激後24~48小時達到高峰,故高強度游泳間歇運動所引發之傷害是否大於修復程度,未來可延後觀察時間進一步探討EPCs與CECs數目之比值以探討HIIT對維持血管內皮健康之影響;並可針對不同運動強度與模式,研究探討EPCs驅動程度之差異,找出傷害較小而且有效的訓練模式。

    Endothelial progenitor cells (EPCs), originated from bone marrow, have the ability to proliferate, mobilize, and differentiate into endothelial cells. EPCs can repair damaged endothelium and have angiogenic and vasculogenic potential; therefore, they play an important role in maintaining vascular health. Exercise has been shown to increase EPCs numbers and to induce mobilization of EPCs from the bone marrow as well as increase their angiogenic capacity. High intensity interval training (HIIT) has been proven to be fast and effectively improves athletic performance; however, it may also have some adverse effects. The homeostasis of healthy endothelial function may depend on the balance between the rate of damage and the ability to repair in endothelial cells. In the past, limited researches had examined the effects of exercise on EPCs in trained athletes, and mostly on land exercise. Swimming is a sport that utilized vast amount of interval training, the effect of interval training on EPCs has never been investigated. Due to lack of available data, this study aims at investigate (1) the effect of single bout of high intensity interval swimming exercise on acute immune responses in well-trained swimmer (EPCs, CECs, apoptotic CECs, VEGF, IL-6, TNF-α, Creatinine, ALT) (2)the relationship among the above immune parameters in high intensity interval swimming exercise. 15 well- trained competitive swimmers participated in this study. Subjects swan 20 repeats of 100m freestyle at 105% critical velocity with work/rest ratio equaled to 3:1. Blood were drawn before and immediately at 0mins, 30mins after exercise, and the following immune responses were assessed: EPCs, CECs, apoptotic CECs, VEGF, IL-6, TNF-α, Creatinine and ALT. Statistical analysis: one-way repeated measures ANOVA for the within subject comparisons or nonparametric Friedman test were used if appropriate. Also, Pearson’s correlation or Spearman's rank correlation was used to exam the relationships among above parameters when appropriate.
    The results of this study show that a single bout of HIIT swimming exercise can significantly increase EPCs numbers (Friedman test: before exercise 5, 0mins after exercise 4, and 30mins after exercise 11 counts/100000 cells, χ2(2) = 25.200, P < 0.001). EPCs at 30mins after exercise increased almost 2.65 folds than that of before exercise. The CECs considered being a marker of endothelial damage increased 30mins after exercise (Friedman test: before exercise 45, 0mins after exercise 31, and 30mins after exercise 66 counts/100000cells, χ2(2) = 20.933, P < 0.001).; the increment was about 1.854 folds than that of before exercise. VEGF seems to be the factor to mobilized EPCs, VEGF increased immediately after exercise (before exercise 44.65 ±11.76, 0mins after exercise 61.38±13.83, and 30mins after exercise 47.32 ±10.37 pg/ml, F(2) = 11.214, P < 0.001) and was positively correlated with the number of EPCs at 30mins after exercise(r=0.756, P<0.01). Serum ALT significantly increased at the peak immediately after exercise then recovered after 30mins (Friedman test: before exercise 12, 0mins after exercise 19, and 30mins after exercise 14 U/L, χ2(2) = 21.926, P < 0.001). Serum Creatinine significantly increased at the peak immediately after exercise and maintain elevated 30mins after exercise (Friedman test: before exercise 0.8, 0mins after exercise 1.2, and 30mins after exercise 1.0 mg/dl, χ2(2) =27.193, P < 0.001). Although Creatinine and ALT elevated after exercise, but the magnitude had not exceed normal range indicated that no serious damage cause by exercise. Similar to the results of previous researches, the IL6 escalated in an exponential fashion and reached 6.75 folds at 30mins after exercise (Friedman test: before exercise .37, 0mins after exercise 1.69, and 30mins after exercise 2.64 pg/ml, χ2(2) =30.000, P < 0.001). The TNFα increased after exercise and maintain elevated 30mins after exercise(before exercise .94 ±.15, 0mins after exercise 1.29±.13, and 30mins after exercise 1.09 ±.14 pg/ml, F(2) = 60.266, P < 0.001), which indicated exercise cause slight pro-inflammatory immune response. The CECs outnumbered EPCs after exercise which indicated a single bout of high intensity interval swimming exercise induce damage exceed repair capacity, which may have adverse effects on endothelium. However, other researches results show EPCs numbers peaked at 24~48hrs after exercise; therefore, future study can extend duration of observation and compare ratio between EPCs/CECs in different mode of HIIT for finding an effective training mode that without the adverse effects.
    Appears in Collections:[Graduate Institute of Sport Coaching Science ] thesis

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