單次阻力運動後攝取果糖對健康年輕男性尿酸濃度之影響

Abstract

背景：高尿酸血症是一種嘌呤代謝混亂所引發的疾病。目前全球高尿酸血症盛行率和發生率呈上升的趨勢，其所引發的合併症包括心血管疾病、慢性腎臟病、糖尿病等代謝疾病，已造成全球醫療負擔，使得高尿酸血症逐漸成為全球性的公共衛生問題。同時，近年來越來越多流行病學研究顯示，果糖攝取量增加與高尿酸血症有關，主因是果糖未如葡萄糖代謝具有負回饋調節機制，當攝取大量果糖，將會造成三磷酸腺苷 (Adenosine triphosphate, ATP) 被快速消耗，活化腺苷降解程序生成尿酸，增加罹患高尿酸血症的風險。先前研究發現，當進行高強度的運動時，骨骼肌中的 ATP 也會快速消耗，產生嘌呤相關代謝物進入血液，經肝臟作用產生尿酸。綜合上述可知，果糖與劇烈運動均會造成血液中尿酸濃度上升，但過往針對運動的研究多以高強度間歇或連續有氧運動為主，阻力運動研究較少，故需要更進一步探討阻力運動所帶來的反應。目的：探討單次阻力運動後攝取果糖對尿酸濃度的變化。方法：招募健康年輕實驗參與者 12 名，運動處方為進行 4 項阻力運動動作 (硬舉、臥推、深蹲、划船)，強度為 70% 1RM；果糖攝取劑量為給予每公斤體重 0.75 公克的 300 毫升果糖溶液，並以 SPSS 25.0 版使用二因子重複量數變異數分析考驗依變項 (尿酸、乳酸、收縮壓、舒張壓、心率) 在 4 種不同處理 (EF：阻力運動後攝取果糖、EW：阻力運動後攝取水分、CF：靜坐休息後攝取果糖、CW：靜坐休息後攝取水分) 與 8 個時間點 (空腹、運動前、運動後立即、運動半小時、運動後 1 小時、運動後 2 小時、運動後 4 小時、運動後 24 小時) 下是否有顯著差異。顯著水準設定 α = .05。結果：血液尿酸濃度在經過阻力運動後皆會顯著提高，此血液尿酸濃度上升的現象會持續至運動後 24 小時 (EF: 7.02 mg/dL, ↑1.31 mg/dL, 23%; EW: 6.84 mg/dL, ↑1.08 mg/dL, 17%)，而單獨攝取果糖後，血液尿酸濃度會在攝取後半小時 (6.24 mg/dL, ↑0.58 mg/dL, 10%) 和 1 小時 (6.08 mg/dL, ↑0.43 mg/dL, 8%) 顯著上升，但當阻力運動結合果糖處理則會在運動後 1 小時 (9.03 mg/dL, ↑3.59 mg/dL, 63%)、2 小時 (9.04 mg/dL, ↑3.33 mg/dL, 58%) 顯著高於其他三種處理。血液乳酸濃度，在進行阻力運動後皆會顯著上升至運動後 1 小時 (p< .05)，而攝取果糖後亦會在攝取後 1 小時內顯著提高 (p < .05) ，但阻力運動合併果糖處理的血液乳酸濃度在運動後 1 小時高於單獨進行阻力運動處理 (EF: ↑2.38 mg/dL, 179%; EW: ↑1.65 mg/dL, 149%) 且在運動後 2 小時 (↑1.19 mg/dL, 89%) 仍未回到基準值。此外，心率則與血液乳酸濃度變化趨勢相似，當阻力運動結合果糖攝取後，心率在運動後 4 小時的時間點仍顯著高於其他三種處理 (EF: 74.58 bmp; EW: 67.42 bmp; CF:65.68 bmp; CW: 65.83 bmp)。血壓則是在不同處理間無顯著差異 (p > .05)。結論：不論是在單獨進行阻力運動後或是單獨攝取果糖後都會引發血液尿酸濃度上升，當兩者合併處理時會使得尿酸增加的幅度更大；阻力運動結合果糖攝取後並未造成血壓產生明顯的變化，但卻會使乳酸與心率恢復較單次阻力運動後慢。

Background: The incidence and prevalence of hyperuricemia, caused by purine metabolism disorders, have considerably increased. Moreover, patients with hyperuricemia often have multiple comorbidities such as hypertension, chronic renal disease, and other metabolic syndromes. Therefore, hyperuricemia has a negative impact on public health. Epidemiological studies have indicated that excessive fructose intake has strong correlation with hyperuricemia. Fructokinase catalyzes fructose by using adenosine triphosphate (ATP). However, fructokinase has no negative feedback system to prevent excessive phosphorylation, which results in ATP depletion and activation of purine degradation to overproduce uric acid. Strenuous exercise also causes rapid ATP depletion in the skeletal muscles. After purine metabolites are released into the blood, uric acid is synthesized in the liver. Both fructose intake and strenuous exercise can increase blood uric acid levels. Although studies have evaluated the effect of acute high-intensity intermittent exercise or acute continuous aerobic exercise on uric acid levels, few have examined changes in uric acid levels after acute resistance exercise. Purpose: The present study investigated the effect of acute resistance exercise combined with high fructose intake on uric acid levels. Methods: Twelve healthy young men (age: 23.00 ± 2.50) were recruited in this study and were randomized into four trials: resistance exercise + fructose (EF), resistance exercise + water (EW), no exercise + fructose (CF), and no exercise + water (CW). The participants performed 70% 1RM of whole-body resistance exercise (deadlift → bench press → squat → standing row) and then ingested a test drink (containing fructose: 0.75 g/kg). Blood uric acid and lactate levels, heart rate, and blood pressure were measured at fasting; before exercise; and immediately, 0.5 h , 1 h , 2 h, 4 h, and 24 h after exercise. All testing data were analyzed using 4 (trial) × 8 (time) two-way repeated-measures analysis of variance. Result: Blood uric acid levels were significantly increased after resistance exercise and lasted until 24 h after exercise (EF: 7.02 mg/dL, ↑1.31 mg/dL, 23%; EW: 6.84 mg/dL, ↑1.08 mg/dL, 17%). After fructose ingestion, blood uric acid significantly increased at 0.5 h after exercise (6.24 mg/dL, ↑0.58 mg/dL, 10%) and at 1 h after exercise (6.08 mg/dL, ↑0.43 mg/dL, 8%). The combination of resistance exercise and fructose ingestion significantly increased the levels of uric acid more than resistance exercise or fructose ingestion alone at 1 h after exercise (9.03 mg/dL, ↑3.59 mg/dL, 63%) and at 2 h after exercise (9.04 mg/dL, ↑3.33 mg/dL, 58%). Blood lactate levels were significantly increased until 1 h after exercise (p< .05) after resistance exercise. After fructose ingestion, blood lactate was significantly increased in 1 hour (p < .05). Blood lactate was significantly higher with the combination of resistance exercise and fructose ingestion than resistance exercise alone (EF: ↑2.38 mg/dL, 179%; EW: ↑1.65 mg/dL, 149%) and didn’t return to baseline at 2 h after exercise (↑1.19 mg/dL, 89%). The changes in heart rate displayed a similar trend to blood lactate levels. The heart rate was significantly higher in the EF trial than in the other three trials, at 4 h after exercise (EF: 74.58 bmp; EW: 67.42 bmp; CF:65.68 bmp; CW: 65.83 bmp). Blood pressure was not significantly different among trials (p> .05). Conclusion: After acute resistance exercise or fructose ingestion alone, uric acid levels immediately increased, and this increase was even higher with the combination of resistance exercise and fructose ingestion. Moreover, with the combination treatment, blood pressure did not change but blood lactate and heart rate decreased more slowly.