| 摘要: | 背景：低通氣在游泳項目是不可避免，而過多低通氣下伴隨而來的可能是高二氧化碳產生的呼吸渴望、血液酸中毒、降低血氧濃度、提高氧化壓力等影響，低通氣可能成為一種類似高地訓練的方法，因此本研究探究陸上自主低通氣訓練是否能成為一項高二氧化碳及低血氧濃度的替代性訓練。目的：探討自主低通氣訓練對於游泳測功儀運動表現之立即影響。方法：招募14名文化大學游泳選手，每位受試者皆進行2次游泳測功儀的自由式划手運動，一次為正常呼吸，一次為自主低通氣，每次運動進行3組2分鐘划手，組間休息1分鐘，划頻設定為每分鐘50下。受試者以能獲得最大輸出之風扇阻力為個人游泳測功儀阻力設定。觀察血乳酸、心率變異度、心跳率、排出二氧化碳、呼吸頻率、攝氧量、運動自覺疲勞、呼吸感知困難、血氧濃度以及每划輸出功率之變化差異。動脈血二氧化碳分壓PaCO2推估值以排出二氧化碳量進行推估。結果：正常呼吸PaCO2推估值第一趟平均為34.1 ±3.8 mmHg；正常呼吸PaCO2推估值第二趟平均為29.9 ±3.7 mmHg；正常呼吸PaCO2推估值第三趟平均為27.6 ±4.2 mmHg。自主低通氣PaCO2推估值第一趟平均為43.9 ±8.0 mmHg；自主低通氣PaCO2推估值第二趟平均為37.4 ±5.8 mmHg；自主低通氣PaCO2推估值第三趟平均為34.1 ±6.3 mmHg。正常呼吸血氧濃度第一趟平均為91.3 ±5.5 %；正常呼吸血氧濃度第二趟平均為93.4 ±4.5 %；正常呼吸血氧濃度第三趟平均為94.1 ±4.4 %。自主低通氣血氧濃度第一趟平均為89.5 ±5.3 %；自主低通氣血氧濃度第二趟平均為90.8 ±5.4 %；自主低通氣血氧濃度第三趟平均為94.5 ±3.8 %。不同呼吸方式之間PaCO2推估值達顯著差異，雖未達高二氧化碳標準但平均PaCO2推估值在第一趟已接近高碳標準，呼吸頻率亦達顯著差異。在心跳率、乳酸、血氧濃度、輸出功率、心率變異度高頻功率及低頻功率、運動自覺疲勞以及呼吸感知困難等在兩種情況下皆未達顯著差異。結論：自主低通氣與正常呼吸之心跳率、輸出功率、運動自覺疲勞未達顯著差異，表示自主低通氣在不會增加受試者負擔，僅需做一趟約最大心跳率65%的2分鐘游泳測功儀運動，即可達到接近高碳低氧狀態。且自主性控制呼吸能產生較高的二氧化碳狀態，對於需要高二氧化碳耐受之各種運動項目，自主低通氣方式應可被運用於訓練中，至於長期訓練效果是否能增進無氧能力及作用肌群之緩衝能力，則可進一步研究探討。
Background: Restricted breathing is inevitable in swimming, and excessively restricted breathing may induce hypercapnia, blood acidosis, hypoxia, and increased oxidative stress. As stated above, breathing restriction may become a training method that induces a similar hypoxic condition that equivalent to altitude training. Therefore, this study investigated whether voluntary hypoventilation training can induce hypercapnia and hypoxia in swimmers. Purpose: To investigate the acute effects of voluntary hypoventilation training on swim ergometer performance. Method: 14 swimmers recruited from the Chinese Cultural University. Each subject performed two dry-land front crawl stroke workouts on the swimming ergometer, one under normal breathing and one under voluntary hypoventilation condition. Each session performed three sets of 2 minutes of simulated swimming and took 1-minute rest between sets. During exercise, the resistance of the swim ergometer was set at the level that allowed the subject to produce maximum peak power, and the stroke frequency was set at 50 strokes per minute with a metronome; a full stroke cycle means the subject completed the left- hand and the right-hand stroke. Blood lactate was measured before and 1,3,5 mins after exercise. HR, VCO2, oxygen uptake, blood oxygen concentration, output power per stroke, RPE, and RPD were measured before and during exercise. Also, HRV was collected before, during, and 5 mins after exercise. PaCO2 was estimated by VCO2. Results: The mean estimated PaCO2 in normal breathing condition for the three simulated 2 minutes swimming were 34.1 ±3.8 mmHg,29.9 ±3.7 mmHg and 27.6 ±4.2 mmHg, respectively. And for the hypoventilation condition, the mean estimated PaCO2 of the three simulated 2 minutes swimming were 43.9 ±8.0 mmHg, 37.4 ±5.8 mmHg, 34.1 ±6.3 mmHg, respectively. PaCO2 estimated value was significantly different between the two conditions but barely reached the hypercapnia standard at the first 2 minutes simulated swimming. The mean spo2 in normal breathing condition for the three exercise repeats were 91.3 ±5.5 %, 93.4 ±4.5 %, and 94.1 ±4.4 %, respectively. And for the hypoventilation condition, the mean SpO2 were 89.5 ±5.3 %, 90.8 ±5.4 %, and 94.5 ±3.8 %, respectively. Moreover, BF, HR, lactate, SpO2, average output power, and HF power and LF Power of HRV had not reached significant differences between the two sessions. conclusion: A single bout of two minutes voluntary hypoventilation workout at near 65% HRmax is strenuous enough to induce a hypercapnic hypoxia condition. Further investigation is needed about the differences in duration, intensity, and work/rest ratio to ensure that voluntary hypoventilation training can enhance anaerobic capacity and the working muscles' buffer capacity. |
