There is now strong evidence that exercise has an acute effect on the urge to smoke and the accompanying withdrawal symptoms. However, the perceptions by heavy smokers of exercise and its relationship to the urge to s...There is now strong evidence that exercise has an acute effect on the urge to smoke and the accompanying withdrawal symptoms. However, the perceptions by heavy smokers of exercise and its relationship to the urge to smoke have not been well documented. The aim of the present study is to understand the experiences of heavy smokers with regard to exercise and its effect on their urge to smoke. Five physically inactive, heavy smokers are asked to abstain from smoking the night before exercising on a cycle ergometer under two conditions (one at medium and one at vigorous intensity done a week apart). Semi-structured, in-depth interviews are conducted after the second exercise session. Thematic analysis reveals six themes describing the participants’ experience of exercise, urge to smoke, exercise preferences, exercise and smoking relationship, exercise as an aid to quit smoking, and the effects of the experimental procedure. Overall, the participants’ experiences support the existing literature, which has posited affective, biological, and cognitive mechanisms contributing to a delay in the urge to smoke after exercise. The main findings pertain to: (1) the “feel-good” effect after exercise as a relief from the “feel-bad” effect during exercise;(2) the decreased urge to smoke after exercise, stated by all participants regardless of reported positive and negative feelings;and (3) exercise as a “clearing the mind” mechanism rather than an attention-distracting mechanism.展开更多
Recent evidence has suggested the neuroprotective effects of physical exercise on cerebral ischemic injury. However, the role of physical exercise in cerebral ischemia-induced hippocampal damage remains controversial....Recent evidence has suggested the neuroprotective effects of physical exercise on cerebral ischemic injury. However, the role of physical exercise in cerebral ischemia-induced hippocampal damage remains controversial. The aim of the present study was to evaluate the effects of pre-ischemia treadmill training on hippocampal CA1 neuronal damage after cerebral ischemia. Male adult rats were randomly divided into control, ischemia and exercise ＋ ischemia groups. In the exercise ＋ ischemia group, rats were subjected to running on a treadmill in a designated time schedule（5 days per week for 4 weeks）. Then rats underwent cerebral ischemia induction th rough occlusion of common carotids followed by reperfusion. At 4 days after cerebral ischemia, rat learning and memory abilities were evaluated using passive avoidance memory test and rat hippocampal neuronal damage was detected using Nissl and TUNEL staining. Pre-ischemic exercise significantly reduced the number of TUNEL-positive cells and necrotic cell death in the hippocampal CA1 region as compared to the ischemia group. Moreover, pre-ischemic exercise significantly prevented ischemia-induced memory dysfunction. Pre-ischemic exercise mighct prevent memory deficits after cerebral ischemia through rescuing hippocampal CA1 neurons from ischemia-induced degeneration.展开更多
文摘There is now strong evidence that exercise has an acute effect on the urge to smoke and the accompanying withdrawal symptoms. However, the perceptions by heavy smokers of exercise and its relationship to the urge to smoke have not been well documented. The aim of the present study is to understand the experiences of heavy smokers with regard to exercise and its effect on their urge to smoke. Five physically inactive, heavy smokers are asked to abstain from smoking the night before exercising on a cycle ergometer under two conditions (one at medium and one at vigorous intensity done a week apart). Semi-structured, in-depth interviews are conducted after the second exercise session. Thematic analysis reveals six themes describing the participants’ experience of exercise, urge to smoke, exercise preferences, exercise and smoking relationship, exercise as an aid to quit smoking, and the effects of the experimental procedure. Overall, the participants’ experiences support the existing literature, which has posited affective, biological, and cognitive mechanisms contributing to a delay in the urge to smoke after exercise. The main findings pertain to: (1) the “feel-good” effect after exercise as a relief from the “feel-bad” effect during exercise;(2) the decreased urge to smoke after exercise, stated by all participants regardless of reported positive and negative feelings;and (3) exercise as a “clearing the mind” mechanism rather than an attention-distracting mechanism.
基金supported by a grant(under the contract number 91052159)sponsored by the Iran National Science Foundation(INSF)
文摘Recent evidence has suggested the neuroprotective effects of physical exercise on cerebral ischemic injury. However, the role of physical exercise in cerebral ischemia-induced hippocampal damage remains controversial. The aim of the present study was to evaluate the effects of pre-ischemia treadmill training on hippocampal CA1 neuronal damage after cerebral ischemia. Male adult rats were randomly divided into control, ischemia and exercise ＋ ischemia groups. In the exercise ＋ ischemia group, rats were subjected to running on a treadmill in a designated time schedule（5 days per week for 4 weeks）. Then rats underwent cerebral ischemia induction th rough occlusion of common carotids followed by reperfusion. At 4 days after cerebral ischemia, rat learning and memory abilities were evaluated using passive avoidance memory test and rat hippocampal neuronal damage was detected using Nissl and TUNEL staining. Pre-ischemic exercise significantly reduced the number of TUNEL-positive cells and necrotic cell death in the hippocampal CA1 region as compared to the ischemia group. Moreover, pre-ischemic exercise significantly prevented ischemia-induced memory dysfunction. Pre-ischemic exercise mighct prevent memory deficits after cerebral ischemia through rescuing hippocampal CA1 neurons from ischemia-induced degeneration.
