根據美國心臟協會的資料，一般人的靜息心率每分鐘約跳60到100下，而長跑運動員可低至每分鐘40下。然而，長期運動訓練是如何降低靜息心率的機制仍不清楚，目前的證據顯示與靜息時自主神經系統中之副交感神經活性增加有關。副交感神經系統在大腦的調節中心位於下視丘旁室核 (hypothalamic paraventricular nucleus)。已知，旁室核中的催產素神經元會投射到背側迷走神經複合體 (dorsal vagal complex)，此一副交感神經路徑可透過迷走神經纖維調控心臟、肺臟和胃腸道的收縮。據此，我假設長期運動可透過調控旁室核中的催產素神經元，進而影響迷走神經的活性，導致靜息心率降低。為了檢驗這一假設，我們以小鼠為研究模型，分析運動訓練對小鼠的靜息心率和心率變異性(heart rate variability)的影響，作為評估自主神經系統活性的指標。我們讓八週齡的雄性小鼠進行為期六週或八週的自主滾輪跑步運動，或是不同強度(輕度或中度)的跑步機運動訓練。結果發現，只有中等強度跑步機運動訓練八週後的小鼠，在運動結束2天後才會顯現較低的靜息心率；同時，其副交感神經活性亦顯著增強。免疫螢光染色顯示，這些小鼠旁室核尾部區域的催產素細胞數目、共表達c-Fos的催產素細胞數目，以及背側迷走神經複合體中之背側迷走運動核 (dorsal vagal motor nucleus) 和孤束核 (nucleus tractus solitarius)的催產素纖維訊號量都有增加。把逆行追蹤劑FluoroGold注射入背側迷走運動核7天後，可在旁室核尾部區域內的細胞發現FluoroGold訊號，但是在旁室核頭部區域則無。在這些FluoroGold細胞中，我發現共表達催產素的數目，以及共表達c-Fos與催產素的數目會因八週中等強度跑步機運動訓練而增加。這些結果顯示長期中等強度跑步運動可增強旁室核尾部區域內的催產素神經元活性，進而增強副交感神經的活性。為了確立旁室核中催產素神經元與運動活化副交感神經活性的因果關係，我使用體內嗎啉基寡核苷 (Vivo-Morpholinos) 抑制旁室核中催產素蛋白質的轉譯，或是在以hM4Di-DREADDs (designer receptor exclusively activated by designer drugs)的方法在Oxytocin Ires Cre小鼠中抑制旁室核催產素神經元的活性。結果顯示，此二方法均能逆轉運動訓練所引起的靜息心率下降和副交感神經活性增強的反應。總結來說，本研究表明，長期中等強度跑步運動可增加旁室核尾部區域中催產素神經元的數目和活性，進而通過激活副交感神經活性，降低靜息心率。

According to the American Heart Association, the resting heart rate (RHR) of an average person typically ranges from 60 to 100 beats per minute, while long-distance runners may have a RHR as low as 40 beats per minute. However, the mechanism underlying long-term exercise-induced reductions in RHR remains unclear. Current evidence suggests it may involve increased parasympathetic nervous system (PNS) activity in the resting state. The regulatory center of the PNS is located in the hypothalamic paraventricular nucleus (PVN). It has been shown that oxytocin neurons in the PVN project to the dorsal vagal complex, an efferent component of the PNS that regulates the heart, lungs, and gastrointestinal functions via the vagus nerve. Accordingly, I hypothesized that long-term exercise affects PVN oxytocin neuron activity, which in turn mediates vagus nerve activity, leading to reductions in RHR. To test this hypothesis, I used mice as an animal model to analyze the effects of long-term exercise on their RHR and heart rate variability, indicators of autonomic nervous system activity. Eight-week-old male mice were subjected to either six or eight weeks of voluntary wheel running exercise or treadmill exercise at two different intensities (mild or moderate). The results showed that only mice subjected to moderate-intensity treadmill exercise for eight weeks exhibited a lower RHR two days after the exercise, along with enhanced PNS activity. In these mice, immunofluorescence staining revealed an increased number of oxytocin cells in the caudal PVN, as well as a higher number of oxytocin cells co-expressing c-Fos in the same region. Additionally, oxytocin fiber signals were elevated in the dorsal vagal complex, specifically in the dorsal motor nucleus (DMV) and nucleus tractus solitarius. After injecting retrograde tracer FluoroGold into the DMV for 7 days, FluoroGold signals were detected in the cells of the caudal PVN, but not in the rostral PVN. Among these FluoroGold-positive cells, the number of cells co-expressing oxytocin, as well as those co-expressing both c-Fos and oxytocin, increased following eight-week moderate-intensity treadmill exercise. These results suggest that long-term moderate-intensity treadmill exercise enhanced the activity of oxytocin neurons in the caudal PVN, thereby increasing PNS activity. To verify the causal relationship between PVN oxytocin neurons and exercise-induced activation of PNS activity, I employed Vivo-Morpholinos to inhibit oxytocin protein translation in the PVN and used hM4Di-DREADDs (designer receptor exclusively activated by designer drugs) approach to inhibit the activity of PVN oxytocin neurons in Oxytocin-Ires-Cre mice. The results showed that both methods reversed the long-term exercise-induced reductions in RHR and enhanced PNS activity. In conclusion, this study demonstrates that long-term moderate-intensity treadmill running can increase the number and activity of oxytocin neurons in the caudal PVN, leading to enhanced PNS activity and consequently reducing RHR.

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