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題名：高強度間歇訓練中不同氧氣濃度恢復對壓力與耐力指標的影響
作者：王錠堯
作者(外文)：Ting-Yao Wang
校院名稱：國立體育大學
系所名稱：教練研究所
指導教授：詹貴惠
學位類別：博士
出版日期：2012
主題關鍵詞：氧氣濃度；硫酸巴比妥酸反應物；細胞凋亡；皮質醇；肌酸激酶；oxygen concentration；thiobarbituric acid reactive substances；apoptosis；cortisol；creatine kinase
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目的：探討高強度間歇訓練 (high-intensity interval training, HIT) 的恢復期以常氧 (20.9%)、低氧 (16%) 或高氧 (60%) 進行恢復時對於：一、HIT中之訓練強度指標心跳率、血乳酸與血糖，以及HIT後血液之氧化壓力生物指標硫酸巴比妥酸反應物 (thiobarbituric acid reactive substances, TBARS)、淋巴球粒線體膜電位下降(mitochondrial transmembrane potential decline, MTP decline)、細胞凋亡與壞死、代謝壓力生物指標皮質醇及機械壓力生物指標肌酸激酶 (creatine kinase, CK) 的影響。二、5次HIT後對HIT中之訓練強度指標及HIT後各項壓力生物指標的適應情形。三、兩週共6次的HIT後對VO2max、換氣閾值、跑步經濟性、最大攝氧量速度及力竭時間等耐力指標的影響。方法：以24名健康男性 (年齡：22.1±2.5 歲；身高：173.5±6.5 公分；體重：73.9±9.6 公斤) 為受試者，隨機將受試者分配至不同氧氣濃度恢復的組別。訓練前、後，受試者各進行一次漸增強度跑步測試至力竭，以測量受試者的VO2max、換氣閾值、跑步經濟性、最大攝氧量速度及力竭時間，並計最大攝氧量速度。之後進行為期兩週共6次強度為90% VO2max、運動期4 min、恢復期2 min、共7回合的HIT，訓練中的恢復期受試者依組別以60% (Hyper組) 或20.9% (Nor組) 或16% (Hypo組) 的氧氣濃度進行恢復。第1、6次HIT在訓練前與訓練之第1、4、7回合後 (1x、4x、7x) 立即測量心跳率，並測量血乳酸與血糖；訓練前、後立即與訓練後1、2、48小時 (1 h、2 h、48 h) 亦由採集血液以測量皮質醇、TBARS、CK以及淋巴球MTP decline、細胞凋亡與壞死的狀況。所得結果以重複量數單因子ANOVA比較單次HIT組內各時間點訓練強度與壓力指標的差異；以單因子ANCOVA比較單次HIT組間各時間點訓練強度與壓力指標的差異及兩週訓練後耐力指標的差異；另以相依樣本t檢定比較第1、6次HIT相同時間點的訓練強度與壓力指標差異，顯著水準訂為α = .05。結果：一、HIT中使用不同氧氣濃度恢復不影響HIT中運動期的訓練強度指標。Hypo組HIT後2 h的CK活性與1 h的TBARS濃度即與訓練前無差異，且在1 h時的細胞凋亡顯著低於Hyper組 (15.16% ± 5.22% vs. 22.70% ± 8.18%, p < .05)；Hyper組在HIT後不會造成皮質醇上升，且在1 h時顯著低於Hypo組 (249.8 ± 107.0 nmol/L vs. 362.7 ± 158.2 nmol/L, p < .05)。二、5次HIT適應後，三組訓練中的心跳率都顯著下降，Hypo組訓練前、後與1 h時的TBARS亦都顯著下降 (p < .05)。三、Hypo組訓練後可以有效增進VO2max、換氣閾值與力竭時間 (p < .05)，Hyper組則無改變。結論：HIT中以16%低氧恢復可降低氧化壓力及機械壓力，經過適應後可降低訓練所產生的氧化壓力，且可增進耐力指標，因此高強度間歇訓練的恢復期採用低氧恢復可降低訓練產生的傷害及提升有氧能力。
Purpose: To investigate the effects of recovery with normoxia (20.9%), hypoxia (16%) or hyperoxia (60%) during high-intensity interval training (HIT) on: 1. The training intensity markers (heart rate, blood lactate acid and glucose), as well as biomarkers of oxidative stress [thiobarbituric acid reactive substances (TBARS), lymphocyte mitochondrial transmembrane potential decline (MTP decline), apoptosis and necrosis], metabolic stress (cortisol) and mechanical stress (creatine kinase, CK) after one single bout of HIT. 2. The adaption of training intensity, oxidative stress, metabolic stress and mechanical stress markers after 5 times HIT. 3. The effects of endurance determinants (VO2max, VT, RE, vVO2max and time to fatigue) after 6 times HIT in two weeks. Methods: Twenty four healthy males (age: 22.1±2.5 yrs, height: 173.5±6.5 cm, weight: 73.9±9.6 kg) randomly assigned to hypoxia (16%, Hypo), normoxia (20.9%, Nor) or hyperoxia (60%, Hyper) groups. Participants were asked to perform an incremental running test to fatigue before and after the experiment intervention to measure VO2max, VT, RE and time to fatigue and calculate vVO2max. After the pre-test, participant performed 6 times HIT (7 reptitions, 4-min interval at 90% VO2max, 2-min rest between intervals) with different oxygen concentration provided in rest intervals. In the 1st and 6th HIT, the heart rate, La and Glu were measured before and after the 1st, 4th and 7th reptition during HIT. Blood sample were also collected to measure cortisol, TBARS, CK, lymphocyte MTP decline, apoptosis and necrosis before and immediately, 1 h, 2 h and 48 h after HIT. Training intensity and exercise induced stress biomarkers in single bout of HIT within group were compared by one way ANOVA with repeated measurment. Training intensity, exercise induced stress biomarkers in single bout HIT and endurance determinants after 2 weeks training between groups were compared by one way ANCOVA. Paired t-test was used to compare training intensity and exercise induced stress biomarkers between 1st and 6th HIT. The significant level was set as α = .05. Results: 1. The training intensity markers during HIT were not affected by different oxygen concentration recovery. The CK activity of 2 h and TBARS concentration of 1 h after HIT were no significant difference to before training in Hypo group. The apoptosis of 1 h after HIT in Hypo group was significantly lower than in Hyper group (15.16%±5.22% vs. 22.70%±8.18%, p < .05). In Hyper group, the cortisol concentration did not elevate after HIT. The cortisol of 1 h after HIT in Hyper group significantly lower than in Hypo group (249.8±107.0 nmol/L vs. 362.7±158.2 nmol/L, p < .05). 2. After 5 times adaption of HIT, the heart rate during training in three groups were significantly decreased. The TBARS concentrations of before and immediately, 1 h after HIT in Hypo group were significantly decreased (p < .05). 3. The VO2max、VT and time to fatigue in Hypo group were significantly improved after traing (p < .05), but there was no change in Hyper group. Conclusion: Recovery by 16% hypoxia during HIT could decrease oxidative and mechanical stress as well as decrease the oxidative stress from HIT after adaption. It can also improve endurance determinants. Using hypoxia recovery during HIT may reduce exercise induced damage and increase aerobic capacity.
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