腾讯tm2007,csgo是否抄袭了穿越火线?
从最早的半条命到CS1.5 CS1.6 然后又到零点行动,起源!再到后来的CSOL1和2,最后再到CSGO,这么多经典版本的延伸,腾讯一个到处抄袭游戏的公司,出了一个穿越火线[大笑][大笑]!你们觉得是谁抄袭谁呢?[打脸][打脸][打脸]
您是如何面对一个人生活的?
说下自己真实现状吧。我今年53岁,69年的早上打鸣的鸡。现在离异13年了。如今独自从城里搬到乡下租住,已经三年了。
平时不怕孤单寂寞,就是过年过节,太冷清。
平时没生病都好说,就是病了,缺个端水端饭的。这个最让我郁闷了!
我由于这几年出苦力,把身子累垮了。大毛病没有,就是小病不断,胳膊和手腕疼,腿半月板疼。
腰容易闪,牙掉的不少。所以吃饭也就简单。我一个人过,生活很邋遢。
吃饭一天两顿饭。有时出去吃,有时自己做点。我自己有个山上果园,也能种菜,但今年上半年,天旱,荒废了。
每天就是遛狗兼着锻炼,半月板不好,也溜达少了。
遛狗回来就是看书,看盘,然后写作一天写最少一篇问答或者一个头条。
一天到晚基本就这些事。简单而平凡。
我母亲去世有六年了,还有一个老父亲,有保姆伺候,老爸喜欢清静,不习惯人打扰。
和60-70年代大多家庭一样,我就就弟兄两个,我是老大。弟弟接班老爸,在央企工作,干得不错,现在是中层干部。
我有一个女儿跟前妻。北京理工大硕士毕业,学的计算机编程。女儿学习一直是我的骄傲。
如今,大概是嫌弃我没本事,负能量多,在2019年中秋节,我们父女俩吃饭,谈话不愉快,依然丢下我,独自离去。
从此没有了音讯,因为电话微信都拉黑了我。
我也死要面子活受罪,没去她妈那认错。如今就是多了无尽的思念。
呆呆地看着女儿走,就心碎如刀割。我独自喝着闷酒。真是后悔不已。
也许是我没子女缘。当初是老婆怀了她,才结婚的,也许当时我就做错了。
我一直觉得打掉自己孩子,是罪恶无耻的。好不容易说服她妈留下她。然后说服我岳父母同意结婚。
没离婚的时候,我常常对了女儿说,“老爸我给你两次命”。可能我自大了吧,也许女儿觉得生中道在破落的原生家庭是苦难。
对不起女儿,我错了!没有给你一个完整的家。你抱怨我,没错。
都是我的错!怪自己无能呀!
我错在没有把好机会,自己一手好牌打得稀巴烂。把家整散了。
我年轻的时候,赶上好时候,首先进入外企,接着做蔬菜加工生意,做股票,期货。借着经济起飞,赶上机会挣到资产千万。
现在的话。好风口,猪也能飞上天。
那时候,2005年以前,我36岁的时候,人生达到巅峰。也是最幸福的时候,美满的妻子,聪明的女儿。
那时候我是众人羡慕的对象,也是父母,岳父母的骄傲。
就是小姨子找对象,岳父母不同意,也拿我说话,当初你们不同意,现在姐夫多么厉害呀!
听闻妻子传来这话,我很是自豪,真的!家人就是我的一切,何况我是宠妻狂魔。
一直以为这样幸福安稳的日子,能到永久。夫唱妇随,天荒地老,最幸福就是陪心爱的人一起慢慢变老。
人生的就是一出戏,也不知道谁导演的。反正我从2005年生意破产,期货穿仓,我就开始独角戏。
离婚后,我也想不开过,自杀没死成,也让我明白很多事,仿佛真的长大成熟了。
我用了16年时间还完大部分外债,2016年,从在义乌回来,送走患病老母亲最后一程。
如今剩一个老父亲,我也不想再去远方了。好好尽孝,就是我心愿。
现实最能有说服力,磨难困苦点醒了我,一切靠实力说话,自己不能挣钱是本事不够。
未来不管自己怎么老,争取翻身。真的,我就不服输。
不管未来如何,反正我会认真生活,争取翻身,即使不能翻身,也死而无憾了。
我生活在乡下,最大好处,可以节约生活费用。也离父亲不远,平时有事可以多去照顾他。
如今我有五条狗陪我,一只大橘猫,大猫残疾,三脚猫,但是特通人情。它们陪我一起生活,也不是很寂寞了。
五条狗真的有点多,拉布拉多和边牧,是疫情时候别人不想养便宜卖给我的。
三条小狗是流浪狗,算捡了两条,一条表弟行善捡来的,让我照顾,他出钱。唉,他经常忘给钱。
我也是开玩笑要钱。我表弟是唯一不嫌弃我落魄,一直帮我的亲戚。
我现在每天就是写作和交易挣钱养活自己。
头条写作基本每月2000-3000块钱。交易也开始稳定下来。
我要按计划一步一步来,淡定从容,不急不躁。
在我最难熬的时候,我弟,表弟,还有发小薛弟。网上嘉伟弟,七哥。一直鼓励我,并且资助过我!
期待翻身后,好好报答他们。
生活都是眼泪炼成的,一个人一个命。今天的日子,是昨天自己选择的路。无论如何,自己也得好好走下去不是吗?不管未来日子艰苦,我也要好好活着。活出自我,不枉此生来人世间一回!你看过哪些超级恐怖的电影?
小编看过很多恐怖好看的电影,下面为大家介绍几部个人觉得最好看的,没看过的伙伴们可以搜来看一下。
1《黑暗侵袭一》
2《黑暗侵袭二》
3《死神来了》系列
4《贞子》系列
5《我是传奇》
6《山村老尸》
7《死亡之雪》
8《地面之下》
9《恶魔的艺术》
10《鬼影》
1《黑暗侵袭一》
影片简介:一次意外的车祸,莎拉的丈夫保罗和女儿杰西被一辆货车上飞射过来的尖锐钢管刺穿死去。虽然莎拉侥幸活下来,但自己却从此一蹶不振。一年后,为了让莎拉重返生活正轨,她的5位都刚20岁出头的喜欢户外冒险的朋友们,决定邀她参加一年一度的户外冒险,这次的目的地,是位于美国阿巴拉契亚山脉的查图嘎国家公园的博莱翰岩洞群。她们进入了洞穴,莎拉在一次进入狭窄洞穴的时候被卡住,随后发生了岩洞崩塌,堵住了回路。她们只好向前走,而朱诺也向大家坦白了这里并非是博莱翰岩洞群,而是一个无人发现新的岩洞。她们继续向前走,却发现这里到处都是动物的尸骨,而远处也能听见奇怪的声音。荷莉在寻找出口的时候,意外地摔断了腿。她被大家扶起继续前进。而此时那些隐藏在洞穴里面的远古类人怪物出现了,他们一下子就把荷莉的脑袋拧断。在尖叫声中,其余的五人慌忙逃窜。朱诺表现得非常的勇敢,她和那些怪物进行搏斗。后来贝丝回来打算帮助朱诺,但她却由于精神过度紧张而失手重伤了自己的同伴贝丝。她没有管被刺伤脖子的贝丝,而是继续寻找队伍。朱诺找到了丽贝卡和珊姆。其实,她们本可以逃出去的,因为朱诺发现了洞穴出去的标记。但是,朱诺执意要找到莎拉再走。而莎拉却在洞穴中发现了奄奄一息的贝丝。贝丝在临死前告诉莎拉,朱诺曾和保罗有染而且她自己也是被朱诺害死的。新仇旧恨交织在一起令莎拉很是恼火。随后,莎拉找到了朱诺,但是丽贝卡和珊姆却被那些怪物杀死了。当莎拉和朱诺与那群怪物搏斗后,莎拉刺伤了朱诺的一条腿,莎拉将朱诺留给了其余的怪物。而她自己却在慌乱中跌下深坑。当莎拉醒来后,发现有一条堆满白骨的斜坡通道,通道可以看到阳光,她疯狂地爬上去,逃离洞穴,开车一路下山,看到运木材的货柜车,而后惊见朱诺的鬼魂。原来这仅仅是莎拉的梦而已,莎拉没有获救而是仍然在那座岩洞里。莎拉的心灵堕落于黑暗的洞穴中,幻想中见到死去的女儿和生日蛋糕,她会心一笑,忘记了恐惧,沉浸在和女儿的快乐回忆中,无数饥饿的怪物正从四面八方向她爬来,吼叫声不绝于耳。
2《黑暗侵袭二》
影片简介:《黑暗侵襲2》的故事接著上一集的逃生者莎拉·卡特(肖娜·麥克唐納德飾)。渾身鮮血、精神恍惚的她被人救起,卻對發生過的故事百口莫辯。為了調查真相,一隊專家攜莎拉重返洞穴。莎拉雖然恐懼,但是她必須勇敢面對著噩夢般的經歷才可得到心靈上的救贖……
3《死神来了》共有五部
影片简介:五部故事都是主要讲述主角预知了将要发生的灾难。解救了某些人,让他们避免了死亡。接着,死神找到他们,让这些在灾难中未死去的人按一定顺序一个个猎杀她们,让她们离奇死去。而且死得很惨,很蹊跷。接着发现规律的人们会想方设法的避免灾难发生,与死神较量。有人侥幸躲过来,也是提心吊胆,然而人怎么能跟鬼神斗呢,它叫你三更死你就不能活到五更。
4《贞子》系列,共4部分别为
《午夜凶铃》
《凶铃再现》
《贞子缠身》
《贞相大白》
5《我是传奇》
影片简介:2012年,人类被不知名病毒感染,纽约成为一座空城。威尔史密斯是为军方服务的科学家,也是对病毒有免疫力的幸存者。白天,他带着狗Sam在街道上寻找食物,用广播寻找幸存者,在实验室里研究治愈病毒的方法;晚上,他只能躲在屋子里,因为那些感染病毒而没有死亡的人们,成为了“夜魔”只能夜晚出来活动,丧失理智,会攻击所有的人。某天,Sam也感染病毒死去,威尔史密斯陷入了前所未有的孤独。当他准备和“夜魔”们同归于尽的时候,另外一个幸存者Anna救了他。Anna相信山上的隔离区还有幸存者,但是固执的威尔史密斯却坚持守在纽约。又一个晚上,“夜魔”攻击了威尔史密斯的住所,此时他的研究已经获得成功,但是只有坚持到天亮,人类才能得以延存。
6《乡村老尸》
影片简介:小明与同伴出外游玩,同伴们竟玩起了“招魂游戏”,小明生就阴阳眼,能看到鬼魂,因觉得不妥而拒绝参加这次游戏。结果游戏出现意外,一人当场心脏病发死亡,另三个游戏者也无缘无故地离奇死于非命。小明凭直觉感到事有蹊跷,遂求助于当记者的姐姐Cessy,Cessy也想获得独家新闻,于是介绍对灵学深有研究而且暗恋自己的好友发毛帮助小明。发毛与小明赴事发地点黄山村调查,发现该村在近百年前曾发生离奇。
7《死亡之雪》
影片简介:话说一群挪威少年来山上滑雪,不想却触动了埋伏在这里的一群纳粹僵尸(挪威人一定对二战时被德军占领的历史难以释怀)。为了保命少年们拿起电锯、斧子、机枪等等一切武器,在《欢乐颂》高亢歌声的伴随下,开始和僵尸决一死..年轻人们对此当然嗤之以鼻,但随着一盒财宝的出现,埋藏在雪中的纳粹僵尸开始一一复活,准备夺回一曾属于他们的财宝……
8《地面之下》
影片简介:某座美军废弃的地下工业基地,数年前因一系列恐怖事件而关闭。而今,无所畏惧的时尚男女在这里开启狂欢派对,纵情享乐之际全然不知危险将近。马特、米拉、艾瑞克、詹娜、伊芙和斯托姆等六名好友在派对高潮和另一伙人发生矛盾,冲突过后,他们仓皇躲入一座地下设施内,结果却被对方反锁在里面。少顷曲终人散,马特他们遇见另外两个在此欢爱的男女。他们结伴寻找逃出去的路,谁知竟遭遇了恐怖嗜血的可怕生物。黑暗寒冷的地下,魔鬼的盛宴拉开序幕……
9《恶魔的艺术》
影片简介:一个百万富翁全家人被神秘而诡异的地杀害。没有丝毫线索,无法找到可以指证的凶手。神秘而恐怖的死亡令所有人为之困惑。一位罪案报道记者参与进此案的调查,发现一个美貌的女人有可疑。他该如何向所有人证明她就是那个一直隐藏着的、并且擅长“魔鬼的艺术”的情妇。
10《鬼影》
影片简介:年轻的自由摄影师Thun这日携女友Jane与大学同窗聚会完毕开车归家,途中Jane将一名飘忽而至的女子撞倒在地。Jane欲下车查看女子伤势,被Thun劝阻,两人匆忙逃离肇事现场。Jane开始终日坐立不安,并指责Thun冷血,Thun只叫她放宽心莫多虑。Jane的担心并非多余,一连串怪事紧接将他们找上:Thun所拍的许多照片上多出一个模糊的女影、颈部莫名疼痛起来、那日聚会的同窗先后跳楼死去……两人更在暗室多次突然陷入恐怖氛围中。为了摆脱噩梦,Jane决定展开深入调查,与Thun有关的一个女子的悲惨经历慢慢浮出水面。
恐怖电影给人的感觉是又觉得恐怖,但是又想看,看后又害怕睡不着。伙伴们,你们有这样的感觉吗?
我的世界和迷你世界到底是谁抄袭谁?
这还要说吗,我也不说废话了!不过,为了让我的世界的玩家消消气,我就发一些吃饭物看会笑喷的图片吧!
流的汗水对减肥有效吗?
高温对减脂存在很多不利,出汗只是体温调节行为,主要是失去水分,跟减脂没啥直接关系。
一、高温阻碍脂肪氧化『脂肪燃烧』用正规一点的话来说叫做『脂肪氧化』,大家再看到这几个字的时候不要觉得疑惑和陌生,氧化和燃烧的含义比较类似。提升脂肪氧化水平的因素很多,比如运动。运动强度是影响脂肪氧化的主要因素之一[1]:中等强度(最大摄氧量的40%至60%)时通常会获得最大脂肪氧化速率[2]。其他因素,如运动持续时间、运动前进食[3]、咖啡因[4]和其他一些物质[5]的使用,甚至性别[6],也都能一定程度改变运动期间的脂肪氧化。还有个影响脂肪氧化的重要因素很少被人关注,那就是温度——较高的环境温度下进行有氧和耐力运动,会削弱预期的减脂效果。第一个典型研究是Febbraio等人1994年的[7]。Febbraio等人对具有耐力训练经验的男性研究发现,进行70%最大摄氧量的40分钟自行车运动,在高温下进行,相对低温下进行来说,脂肪氧化减少25%,糖类氧化增加31%;对于减脂来说,这就比较糟糕了。在该研究中,他们用的是一种叫呼吸交换率(RER)的技术进行测量:RER=VCO2/VO2,也就是呼出的二氧化碳和消耗氧气的之比。因为动物同时氧化脂肪和碳水来供能[8][9][10],并且根据体内氧化脂肪和碳水的比例不同,所吸入的氧气和呼出的二氧化碳的比例也不同[11][12][13]。如果只氧化脂肪供能,二氧化碳与氧气消耗之比为0.7;如果只氧化碳水供能,二氧化碳与氧气消耗之比为1。因此,呼吸交换率低,氧化脂肪供能多,氧气的消耗也相对多。从文献原文的截图可见,20°C运动的呼吸交换率平均值是0.88,40°C运动的呼吸交换率则是0.91,升高的呼吸交换率意味着在高温下运动,人体碳水供能增加,脂肪氧化减少[7]。注意0.91后面的星号(*)表示有显著差异第二个典型研究是Gagnon等人2013年的[13]。Gagnon等人招募了10个健康、经常活动的受试者,让他们穿着单薄的衣服,分别在0或者22°C下,进行50%或者70%最大摄氧量的有氧活动。结果并不出人意外,受试者们的呼吸交换率,在低温下更低——也就是说,低温下做有氧,脂肪氧化占比更大,对糖类的利用相对少些。RQ从实际消耗的脂肪和碳水来看,脂肪消耗绝对值最大的是低温跑步(因为低温增加了脂肪氧化,且跑步消耗的总能量高于步行);脂肪消耗的相对比例最大的是低温步行(因为跑步的强度高于步行,更高强度活动对脂肪供能的占比更低)。四种不同运动方式的能量底物消耗比例但不管怎么说,低温的脂肪氧化都更多,这比较明确的向我们强调了减脂运动的思路:低温活动(当然,注意不要感冒了),或者至少是在凉爽的温度下进行;高温环境减脂事倍功半。第三个典型研究是Carlos等人2020年的[14]。Carlos等人研究了12名健康年轻人,让他们分别在两种温度(18.3ºC或36.3ºC)执行多种不同强度的有氧运动(30%—70%最大心率)。根据原文截图,在18.3ºC下,5种强度的有氧运动呼吸交换率平均值从0.78到0.96;在36.3ºC下,5种强度的有氧运动呼吸交换率平均值从0.81到0.99,这说明温度越高,呼吸交换律越高,脂肪氧化占比越少。呼吸交换率注意,炎热环境下运动,身体消耗的总能量也更少,不利于减脂。Carlos等人2021年招募了12名年轻健康的受试者在18.3或者36.3°C下进行坡道自行车测试[15],结果发现相对于凉爽环境,炎热环境导致总热量消耗下降。(1)在50%最大心率的运动中,18.3ºC的凉爽温度下运动时每分钟平均消耗10.47大卡,36.3ºC的炎热温度下运动运动时每分钟平均消耗10.42大卡;(2)在70%最大心率的运动中,18.3ºC的凉爽温度下运动时每分钟平均消耗15.15大卡,36.3ºC的炎热温度下运动运动时每分钟平均消耗14.79大卡。此外,这种规律在动物中也存在。当环境温度从35ºC提高到40ºC,大鼠的肌肉中脂肪酸氧化减少、更偏向使用碳水化合物[16];水温会显著的影响鱼类的长链脂肪酸代谢[17][18][19]和身体脂肪沉淀[20][21][22][23][24]。总之,减脂应该在凉爽的条件下进行,这不仅仅关系到中暑,也关系到脂肪氧化[25],关系到人体能量代谢的改变。二、温度对脂解激素有重要影响脂解激素,顾名思义,就是让脂肪分解的激素。人体内的脂肪主要是甘油三酯[26][27],但它比较大,是一个甘油骨架和三个脂肪酸链组成的[28][29],没法直接运出脂肪细胞,所以人体需要一些激素,激活细胞内的酶[30][31][32],把脂肪酸从甘油骨架上切割下来[33][34][35],再在各类运载蛋白[36][37]的帮助下从血液[38]输送到各器官细胞内的线粒体中氧化[39][40]。这些激活脂肪分解的激素,就是『脂解激素』[41][42],比如肾上腺素[43]和它的衍生物去甲肾上腺素[44]。左-肾上腺髓;右-去甲肾上腺素脂解激素被分泌后,从血液到达脂肪细胞,与脂肪细胞表面的受体结合[45][46][47][48],引发一系列反应[49][50][51][52],让脂肪细胞中的脂肪酸被释放出来[53][54],供肌肉和其他器官使用,这个过程就叫脂解。脂肪的动员温度能影响『脂解激素』:去甲肾上腺素的合成和释放,从而影响脂肪分解和氧化[55];『脂解激素』在相对低的温度下容易被激发释放。1973年,Galbo等人发现,人类在21℃水中游泳1小时,肾上腺素和去甲肾上腺素的水平比27℃的水中游泳时更高[56];2002年,Steven等人通过向健康男性静脉内大量注射4℃冷盐水的方式,使他们的核心温度下降0.7℃,结果他们的血浆去甲肾上腺素增加增加220%;如果进一步注射,受试者们的核心温度进一步降低达到1℃,则受试者血浆去甲肾上腺素浓度增加230%,血浆肾上腺素浓度增加68%[57]。1997年,Frank等人进行了类似的实验,通过向人类静脉注射大量4℃冷盐水的方式降低人类的核心温度,发现当核心温度降低0.7℃时,受试者们的平均血浆去甲肾上腺素浓度增加400%,全身耗氧量增加30%;当核心温度降低1.3摄氏度时,平均去甲肾上腺素浓度增加700%,全身耗氧量增加112%[58]。这些数据都说明,较低的温度可以有利于脂解激素的释放,从而促进脂解和脂肪氧化[59]。注意,Frank等人的研究中[58],受试者们的核心温度下降,脂解激素增加,伴随一个重要现象:『耗氧量增加』。原因是呼吸交换率计算时,氧气是分母,二氧化碳是分子,耗氧量增加意味着更低的呼吸交换率,更多的脂肪氧化和更少的糖酵解。三、高温减少脂肪组织的血流量,从而抑制脂肪分解对于减脂来说,血流量是个极为重要的因素。有大量证据表明,不管是运动、节食,还是运动结合节食,结果都是内脏脂肪优先分解,内脏脂肪的分解明显多于皮下脂肪[60][61][62][63][64][65][66][67][68][69][70][71][72][73][73][74][75][76][77][78][79][80][81][82][83][84][85]。这是因为内脏脂肪的代谢流动性高于皮下脂肪,内脏脂肪对脂解激素更敏感[86][87][88][89]。并且就算这个『局部性』指的不是『内脏脂肪和皮下脂肪的分别』,而是『练哪瘦哪』,也有一些证据支持它成立[90][91][92][93][94][95][96]。注意,『局部减脂』就是建立在血流量基础上的。因为脂肪细胞并不仅仅是能量的容器,它们也是进行积极代谢的细胞,它们非常活跃,富含神经和结缔组织,而且几乎每个脂肪细胞都配有毛细血管[97][98][99],脂肪的运输和代谢受血液流动影响[100][101];运动能减肥,在一定程度上也是因为运动促进全身血管生长的血管生成[102],从而改善脂肪组织的血流量;耐力和有氧运动可以诱导人类[103]和动物[104]皮下脂肪组织中血管生成因子(VEGF)的表达上调[105],从而增加脂肪组织的毛细血管生成,起到预防、对抗肥胖的作用;对健康受试者测试发现,运动腿脂肪组织的血流量显著高于休息腿脂肪组织的血流量[106];权威期刊《应用生理学》表明,在运动期间,运动腿脂肪组织血流量从每100g肌肉1毫升/每分钟,猛增到到最高每100g肌肉4.9毫升/分钟,提高了接近5倍;与此同时,休息腿脂肪组织血流量基本保持不变[107];更重要的是,主要的脂解激素,如肾上腺素和去甲肾上腺素[108][109],是通过血液运输到脂肪细胞[110]的;并且脂解激素也反过来增加脂肪组织的血流量,从而促进脂肪分解。例如,给大鼠注射去甲肾上腺素后,大鼠脂肪组织的血流量从2%增加到15.5%[111]。与此相对的是,肥胖与脂肪组织血流下降、毛细血管稀疏之间存在密切关系:肥胖者的脂肪组织中的毛细血管较为稀疏[112],肥胖者空腹和餐后腹部脂肪组织的血流量较低[113][114][115][116];在肥胖症中,皮下脂肪组织血流量下降、脂肪组织膨胀[117];二型糖尿病患者的皮下脂肪血流量也较低[118];肥胖的小鼠具有较稀疏的毛细血管密度和较低的血管内皮生长因(VEGF)[119][120];肥胖者皮下组织中胎盘生长因子(PlGF)水平较高,抑制脂肪组织毛细血管生成[121][122][123][124][125]。重点:较高的环境温度削减脂肪组织血流量,从而抑制脂肪分解
其实在正常而非炎热的环境下运动时,脂肪组织跟肌肉组织一样,血流量是明显增加的。例如,4小时自行车运动后,皮下脂肪和肾周围脂肪的血流量增加了400%和700%[126];狗在长时间运动后皮下脂肪的血流量增加了2倍,相应导致脂解增加,游离脂肪酸和甘油水平增加[127]。并且, 流向肌肉的血流量,跟流向脂肪组织的血流量之间具有一定程度的同步性,例如伸膝训练使股四头肌的温度增加了2 ℃[128],也导致肌肉附近的脂肪组织的温度和血流量提高[128]。在炎热环境下,脂肪组织的血流量减少,皮肤获得的血流量增加。在33℃的高温环境饲养时,仔猪流向脂肪组织的血流减少42%,流向外皮肤的血流增加44%[129];而在寒冷环境中,1-5日龄的仔猪骨骼肌血流量提升最高达41%,皮肤血流量减少24%[130]。因为皮肤是人和高等动物排汗和调节体温的重要器官,在高温下皮肤会与脂肪组织抢夺血流量。众所周知,皮肤上存在各类感受温度的传感器[131][132],能通过多种路径[133][134][135]感受炎热的外部环境,将『气温太高』的信号传递到神经系统;然后在神经系统信号的调节下[136][137],皮肤的毛细血管舒张[137],血流量增加[138][139][140]来散热,从而调节我们身体的温度 [141]。炎热导致皮肤血流量上升,脂肪组织血流量下降,它们彼此争夺、竞争血流量,从而削减了脂肪组织获得的脂解激素[41][42][43][44]的数量,导致脂肪氧化减少[7][13][14][15][16],减脂效果下降。结 论
减脂,应当选择凉爽的气温环境,夏天温度升高一定要开空调,这样减脂效率更高;闷热/炎热的环境除了不利于脂肪分解,也容易造成脱水、离子损失甚至是中暑,不管对舒适性、运动效果、减脂、安全性都存在负面影响。References1. ^Randell, R. K., Rollo, I., Roberts, T. J., Dalrymple, K. J., Jeukendrup, A. E., & Carter, J. M. (2017). Maximal Fat Oxidation Rates in an Athletic Population. Medicine and Science in Sports and Exercise, 49(1), 133–140.2. ^Achten, J., Gleeson, M., & Jeukendrup, A. E. (2002). Determination of the exercise intensity that elicits maximal fat oxidation. Medicine and Science in Sports and Exercise.3. ^Achten, J., Venables, M. C., & Jeukendrup, A. E. (2003). Fat oxidation rates are higher during running compared with cycling over a wide range of intensities. Metabolism: Clinical and Experimental.4. ^Gutiérrez-Hellín, J., & Del Coso, J. (2018). Effects of p-Synephrine and Caffeine Ingestion on Substrate Oxidation during Exercise. Medicine & Science in Sports & Exercise, 50(9), 1899–1906.5. ^Gutiérrez-Hellín, J., & Del Coso, J. (2016). Acute p-synephrine ingestion increases fat oxidation rate during exercise. British Journal of Clinical Pharmacology.6. ^Venables, M. C., Achten, J., & Jeukendrup, A. E. (2005). Determinants of fat oxidation during exercise in healthy men and women: A cross-sectional study. Journal of Applied Physiology.7. ^abcFebbraio, M. A., Snow, R. J., Stathis, C. G., Hargreaves, M., & Carey, M. F. (1994). Effect of heat stress on muscle energy metabolism during exercise. Journal of Applied Physiology, 77(6), 2827–2831.8. ^Wilson DF. Regulation of cellular metabolism: programming and maintaining metabolic homeostasis. J Appl Physiol. (2013):15:1583–8.9. ^Weekes CE. Controversies in the determination of energy requirements. Proc Nutr Soc. (2007) 66:367–77.10. ^Lowell BB, Spiegelman BM. Towards a molecular understanding of adaptive thermogenesis. Nature (2000) 404:652–60.11. ^Kenny GP, Notley SR, Gagnon D. Direct calorimetry: a brief historical review of its use in the study of human metabolism and thermoregulation. Eur J Appl Physiol. (2017) 117:1765–85.12. ^Poncet S, Dahlberg L. The legacy of henri victor regnault in the arts and sciences. Intl J Arts Sci. (2011) 4:377–400.13. ^abcDominique D. Gagnon,1,* Hannu Rintamäki,2,3 Sheila S. Gagnon,4 Stephen S. Cheung,5 Karl-Heinz Herzig,2,6 Katja Porvari,7 and Heikki Kyröläinen1.Cold exposure enhances fat utilization but not non-esterified fatty acids, glycerol or catecholamines availability during submaximal walking and running.Front Physiol. 2013; 4: 99.14. ^abGagnon, D. D., Perrier, L., Dorman, S. C., Oddson, B., Larivière, C., & Serresse, O. (2020). Ambient temperature influences metabolic substrate oxidation curves during running and cycling in healthy men. European Journal of Sport Science, 20(1), 90–99.15. ^abCarlos Ruíz-Moreno , Jorge Gutiérrez-Hellín , Jaime González-García ,Verónica Giráldez-Costas , Diego Brito de Souza & Juan Del Coso (2020): Effect of ambient temperature on fat oxidation during an incremental cycling exercise test, European Journal of Sport Science,16. ^abPierre-Emmanuel Tardo-Dino 1 2 3, Julianne Touron 1, Stéphane Baugé 1, Stéphanie Bourdon 1, Nathalie Koulmann 1 2 3, Alexandra Malgoyre 1.The effect of a physiological increase in temperature on mitochondrial fatty acid oxidation in rat myofibers.J Appl Physiol (1985). 2019 Aug 1;127(2):312-319.17. ^Calder PC. n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases. The American Journal of Clinical Nutrition. 2006;83(6):S1505–19S.18. ^ocher DR. Fatty acid requirements in ontogeny of marine and freshwater fish. Aquaculture Research. 2010;41(5):717–32.19. ^Hazel JR. Effects of temperature on the structure and metabolism of cell membranes in fish. The American journal of physiology. 1984;246(4 Pt 2):R460–70. Epub20. ^Jobling M, Bendiksen EÅ. Dietary lipids and temperature interact to influence tissue fatty acid compositions of Atlantic salmon, Salmo salar L., parr. Aquaculture Research. 2003;34(15):1423–4121. ^Hazel JR. Influence of thermal acclimation on membrane lipid composition of rainbow trout liver. The American journal of physiology. 1979;236(1):R91–101. Epub22. ^Wodtke E. Lipid adaptation in liver mitochondrial membranes of carp acclimated to different environmental temperatures: phospholipid composition, fatty acid pattern and cholesterol content. Biochimica et biophysica acta. 1978;529(2):280–91. Epub23. ^Bendiksen EÅ, Jobling M. Effects of temperature and feed composition on essential fatty acid (n-3 and n-6) retention in Atlantic salmon (Salmo salar L.) parr. Fish Physiol Biochem. 2003;29(2):133–40.24. ^Arts MT, Palmer ME, Skiftesvik AB, Jokinen IE, Browman HI. UVB radiation variably affects n-3 fatty acids but elevated temperature reduces n-3 fatty acids in juvenile Atlantic Salmon (Salmo salar). Lipids. 2012;47(12):1181–92.25. ^Hurley B., Haymes E. M. (1982). The effects of rest and exercise in the cold on substrate mobilization and utilization. Aviat. Space Environ. Med. 53, 1193–119726. ^Reshef L., Olswang Y., Cassuto H., Blum B., Croniger C.M., Kalhan S.C. Glyceroneogenesis and the triglyceride/fatty acid cycle. Journal of Biological Chemistry. 2003;278(33):30413–30416.27. ^D. Zweytick, K. Athenstaedt, G. Daum, Intracellular lipid particles of eukaryotic cells, BBA-Rev Biomembranes. 1469(2) (2000) 101-120.28. ^aughan, M. J. (1962) J. Biol. Chem. 237, 3354–335829. ^Viecili P.R.N., da Silva B., Hirsch G.E., Porto F.G., Parisi M.M., Castanho A.R. Triglycerides revisited to the serial. Advances in Clinical Chemistry. 2017;80:1–44.30. ^Jocken J.W., Blaak E.E. Catecholamine-induced lipolysis in adipose tissue and skeletal muscle in obesity. Physiol. Behav. 2008;94:219–230.31. ^Holm C., Osterlund T., Laurell H., Contreras J.A. Molecular mechanisms regulating hormone-sensitive lipase and lipolysis. Annu. Rev. Nutr. 2000;20:365–393.32. ^Shen W.J., Patel S., Natu V., Kraemer F.B. Mutational analysis of structural features of rat hormone-sensitive lipase. Biochemistry. 1998;37:8973–8979.33. ^Zechner R, Kienesberger PC, Haemmerle G, Zimmermann R, Lass A 2009. Adipose triglyceride lipase and the lipolytic catabolism of cellular fat stores. J Lipid Res 50: 3–2134. ^Zimmermann R, Strauss JG, Haemmerle G, Schoiswohl G, Birner-Gruenberger R, Riederer M, Lass A, Neuberger G, Eisenhaber F, Hermetter A, et al. 2004. Fat mobilization in adipose tissue is promoted by adipose triglyceride lipase. Science 306: 1383–138635. ^Haemmerle G, Zimmermann R, Hayn M, Theussl C, Waeg G, Wagner E, Sattler W, Magin TM, Wagner EF, Zechner R 2002. Hormone-sensitive lipase deficiency in mice causes diglyceride accumulation in adipose tissue, muscle, and testis. J Biol Chem 277: 4806–481536. ^Ranallo R.F., Rhodes E.C. Lipid metabolism during exercise. Sports Med. 1998;26:29–42.37. ^Campbell J, Martucci AD, Green GR. Plasma albumin as an acceptor of free fatty acids. Biochem J. 1964;93:183–189.38. ^Miller N.E. HDL metabolism and its role in lipid transport. Eur. Heart J. 1990;11:1–3.39. ^Jeukendrup AE. Regulation of fat metabolism in skeletal muscle. Ann N Y Acad Sci. 2002;967:217–235.40. ^Harasim E., Kalinowska A., Chabowski A., Stepek T. The role of fatty-acid transport proteins (FAT/CD36, FABPpm, FATP) in lipid metabolism in skeletal muscles. Postepy Higieny Medycyny Doswiadczalnej. 2008;62:433–441.41. ^abeters S. J., Dyck D. J., Bonen A., Spriet L. L. Effects of epinephrine on lipid metabolism in resting skeletal muscle. The American Journal of Physiology. 1998;275(2 Part 1):E300–E309.42. ^abDyck D. J., Bonen A. Muscle contraction increases palmitate esterification and oxidation and triacylglycerol oxidation. The American Journal of Physiology. 1998;275(5 Part 1):E888–E896.43. ^abLafontan M., Langin D. Lipolysis and lipid mobilization in human adipose tissue. Prog. Lipid Res. 2009;48:275–297.44. ^abJaworski K., Sarkadi-Nagy E., Duncan R.E., Ahmadian M., Sul H.S. Regulation of triglyceride metabolism. IV. Hormonal regulation of lipolysis in adipose tissue. Am. J. Physiol. Gastrointest. Liver Physiol. 2007;293:G1–G4.45. ^ Mi-Jeong Lee,Susan K. Fried.Depot-Specific Biology of Adipose Tissues: Links to Fat Distribution and Metabolic Risk.Book Editor(s):Todd Leff,James G. Granneman.46. ^P Arner 1.Differences in lipolysis between human subcutaneous and omental adipose tissues.Ann Med. 1995 Aug;27(4):435-8.47. ^Peters S. J., Dyck D. J., Bonen A., Spriet L. L. Effects of epinephrine on lipid metabolism in resting skeletal muscle. The American Journal of Physiology. 1998;275(2 Part 1):E300–E309.48. ^Dyck D. J., Bonen A. Muscle contraction increases palmitate esterification and oxidation and triacylglycerol oxidation. The American Journal of Physiology. 1998;275(5 Part 1):E888–E896.49. ^alanian J.L., Tunstall R.J., Watt M.J., Duong M., Perry C.G.R., Steinberg G.R., Kemp B.E., Heigenhauser G.J.F., Spriet L.L. Adrenergic regulation of HSL serine phosphorylation and activity in human skeletal muscle during the onset of exercise. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2006;291:1094–1099.50. ^Zimmermann R., Strauss J.G., Haemmerle G., Schoiswohl G., Birner-Gruenberger R., Riederer M., Lass A., Neuberger G., Eisenhaber F., Hermetter A., et al. Fat mobilization in adipose tissue is promoted by adipose triglyceride lipase. Science. 2004;306:1383–1386.51. ^Villena J.A., Roy S., Sarkadi-Nagy E., Kim K.H., Sul H.S. Desnutrin, an adipocyte gene encoding a novel patatin domain-containing protein, is induced by fasting and glucocorticoids: Ectopic expression of desnutrin increases triglyceride hydrolysis. J. Biol. Chem. 2004;279:47066–47075.52. ^Petridou A., Chatzinikolaou A., Avloniti A., Jamurtas A., Loules G., Papassotiriou I., Fatouros I., Mougios V. Increased triacylglycerol lipase activity in adipose tissue of lean and obese men during endurance exercise. J. Clin. Endocrinol.53. ^Ranallo R.F., Rhodes E.C. Lipid metabolism during exercise. Sports Med. 1998;26:29–42.54. ^Campbell J, Martucci AD, Green GR. Plasma albumin as an acceptor of free fatty acids. Biochem J. 1964;93:183–189.55. ^Arner P., Kriegholm E., Engfeldt P., Bolinder J. (1990). Adrenergic regulation of lipolysis in situ at rest and during exercise. J. Clin. Invest. 85, 893–89856. ^Galbo H., Houston M. E., Christensen N. J., Holst J. J., Nielsen B., Nygaard E., et al. (1979). The effect of water temperature on hormonal response to prolonged swimming. Acta Physiol. Scand. 105, 326–33757. ^Steven M Frank 1, Christine G Cattaneo, Mary Beth Wieneke-Brady, Hossam El-Rahmany, Neeraj Gupta, Joao A C Lima, David S Goldstein.Threshold for adrenomedullary activation and increased cardiac work during mild core hypothermia.Clin Sci (Lond). 2002 Jan;102(1):119-25.58. ^abS M Frank 1, M S Higgins, L A Fleisher, J V Sitzmann, H Raff, M J Breslow.Adrenergic, respiratory, and cardiovascular effects of core cooling in humans.Am J Physiol. 1997 Feb;272(2 Pt 2):R557-62.59. ^Horowitz J. F., Leone T. C., Feng W., Kelly D. P., Klein S. (2000). Effect of endurance training on lipid metabolism in women: a potential role for PPARα in the metabolic response to training. Am. J. Physiol. Endocrinol. Metab. 279, 348–35560. ^Kelley DE, Kuller LH, McKolanis TM, Harper P, Mancino J, Kalhan S. Effects of moderate weight loss and orlistat on insulin resistance, regional adiposity, and fatty acids in type 2 diabetes. Diabetes Care 2004; 27: 33–40.61. ^Ross R, Janssen I, Dawson J, Kungl AM, Kuk JL, Wong SL et al. Exercise-induced reduction in obesity and insulin resistance in women: a randomized controlled trial. Obes Res 2004; 12: 789–798.62. ^Weinsier RL, Hunter GR, Gower BA, Schutz Y, Darnell BE, Zuckerman PA. Body fat distribution in white and black women: different patterns of intraabdominal and subcutaneous abdominal adipose tissue utilization with weight loss. Am J Clin Nutr 2001; 74: 631–636.63. ^ Gower BA, Weinsier RL, Jordan JM, Hunter GR, Desmond R. Effects of weight loss on changes in insulin sensitivity and lipid concentrations in premenopausal African American and White women. Am J Clin Nutr 2002; 76: 923–927.64. ^ Pasquali R, Gambineri A, Biscotti D, Vicennati V, Gagliardi L, Colitta D et al. Effect of long-term treatment with metformin added to hypocaloric diet on body composition, fat distribution, and androgen and insulin levels in abdominally obese women with and without the polycystic ovary syndrome. J Clin Endocrinol Metab 2000; 85: 2767–2774.65. ^Alvarez GE, Davy BM, Ballard TP, Beske SD, Davy KP. Weight loss increases cardiovagal baroreflex function in obese young and older men. Am J Physiol Endocrinol Metab 2005; 289: E665–E669.66. ^Rice B, Janssen I, Hudson R, Ross R. Effects of aerobic or resistance exercise and/or diet on glucose tolerance and plasma insulin levels in obese men. Diabetes Care 1999; 22: 684–691.67. ^Weits T, van der Beek EJ, Wedel M, Hubben MW, Koppeschaar HP. Fat patterning during weight reduction: a multimode investigation. Neth J Med 1989; 35: 174–184.68. ^Okura T, Tanaka K, Nakanishi T, Lee DJ, Nakata Y, Wee SW et al. Effects of obesity phenotype on coronary heart disease risk factors in response to weight loss. Obes Res 2002; 10: 757–76669. ^Fujioka S, Matsuzawa Y, Tokunaga K, Kawamoto T, Kobatake T, Keno Y et al. Improvement of glucose and lipid metabolism associated with selective reduction of intra-abdominal visceral fat in premenopausal women with visceral fat obesity. Int J Obes 1991; 15: 853–859.70. ^Janssen I, Ross R. Effects of sex on the change in visceral, subcutaneous adipose tissue and skeletal muscle in response to weight loss. Int J Obes Relat Metab Disord 1999; 23: 1035–1046.71. ^Tchernof A, Nolan A, Sites CK, Ades PA, Poehlman ET. Weight loss reduces C-reactive protein levels in obese postmenopausal women. Circulation 2002; 105: 564–569.72. ^Thong FS, Hudson R, Ross R, Janssen I, Graham TE. Plasma leptin in moderately obese men: independent effects of weight loss and aerobic exercise. Am J Physiol Endocrinol Metab 2000; 279: E307–E313.73. ^abTiikkainen M, Bergholm R, Vehkavaara S, Rissanen A, Hakkinen AM, Tamminen M et al. Effects of identical weight loss on body composition and features of insulin resistance in obese women with high and low liver fat content. Diabetes 2003; 52: 701–707.74. ^Ross R, Dagnone D, Jones PJ, Smith H, Paddags A, Hudson R et al. Reduction in obesity and related comorbid conditions after dietinduced weight loss or exercise-induced weight loss in men. A randomized, controlled trial. Ann Intern Med 2000; 133: 92–103.75. ^Gambineri A, Pagotto U, Tschop M, Vicennati V, Manicardi E, Carcello A et al. Anti-androgen treatment increases circulating ghrelin levels in obese women with polycystic ovary syndrome. J Endocrinol Invest 2003; 26: 629–634.76. ^Park HS, Sim SJ, Park JY. Effect of weight reduction on metabolic syndrome in Korean obese patients. J Korean Med Sci 2004; 19: 202–208.77. ^Nakamura M, Tanaka M, Kinukawa N, Abe S, Itoh K, Imai K et al. Association between basal serum and leptin levels and changes in abdominal fat distribution during weight loss. J Atheroscler Thromb 2000; 6: 28–32.78. ^ Park HS, Lee K. Greater beneficial effects of visceral fat reduction compared with subcutaneous fat reduction on parameters of the metabolic syndrome: a study of weight reduction programmes in subjects with visceral and subcutaneous obesity. Diabet Med 2005; 22: 266–272.79. ^Okura T, Nakata Y, Lee DJ, Ohkawara K, Tanaka K. Effects of aerobic exercise and obesity phenotype on abdominal fat reduction in response to weight loss. Int J Obes (London) 2005; 29: 1259–1266.80. ^Pare A, Dumont M, Lemieux I, Brochu M, Almeras N, Lemieux S et al. Is the relationship between adipose tissue and waist girth altered by weight loss in obese men? Obes Res 2001; 9: 526–534.81. ^Kelley DE, Kuller LH, McKolanis TM, Harper P, Mancino J, Kalhan S. Effects of moderate weight loss and orlistat on insulin resistance, regional adiposity, and fatty acids in type 2 diabetes. Diabetes Care 2004; 27: 33–40.82. ^ Tiikkainen M, Bergholm R, Rissanen A, Aro A, Salminen I, Tamminen M et al. Effects of equal weight loss with orlistat and placebo on body fat and serum fatty acid composition and insulin resistance in obese women. Am J Clin Nutr 2004; 79: 22–30.83. ^Kim DM, Yoon SJ, Ahn CW, Cha BS, Lim SK, Kim KR et al. Sibutramine improves fat distribution and insulin resistance, and increases serum adiponectin levels in Korean obese nondiabetic premenopausal women. Diabetes Res Clin Pract 2004; 66 (Suppl 1): S139–S144.84. ^Kamel EG, McNeill G, Van Wijk MC. Change in intra-abdominal adipose tissue volume during weight loss in obese men and women: correlation between magnetic resonance imaging and anthropometric measurements. Int J Obes Relat Metab Disord 2000; 24: 607–613.85. ^Yip I, Go VL, Hershman JM, Wang HJ, Elashoff R, DeShields S et al. Insulin–leptin–visceral fat relation during weight loss. Pancreas 2001; 23: 197–203.86. ^Jensen MD. Gender differences in regional fatty acid metabolism before and after meal ingestion. J. Clin. Invest. 1995;96:2297–2303.87. ^Jensen MD, Johnson CM. Contribution of leg and splanchnic free fatty acid (FFA) kinetics to postabsorptive FFA flux in men and women. Metabolism. 1996;45:662–666.88. ^Basu A, et al. Systemic and regional free fatty acid metabolism in type 2 diabetes. Am. J. Physiol. Endocrinol. Metab. 2001;280:E1000–E1006.89. ^Meek S, Nair KS, Jensen MD. Insulin regulation of regional free fatty acid metabolism. Diabetes. 1999;48:10–14.90. ^Swift D.L., McGee J.E., Earnest C.P., Carlisle E., Nygard M., Johannsen N.M. The Effects of Exercise and Physical Activity on Weight Loss and Maintenance. Prog. Cardiovasc. Dis. 2018;61:206–213.91. ^Cureton T. The Effect of Gymnastics upon Boys. College Coaches Gymnastic Clinic; Sarasota, FL, USA: 1954. Unpublished Paper.92. ^Kireilis R.W., Cureton T.K. The relationships of external fat to physical education activities and fitness tests. Res. Q. Am. Assoc. Healthphys. Educ. Recreat. 1947;18:123–134.93. ^Yuhasz M.S. The Effects of Sports Training on Body Fat in Man with Predictions of Optimal Body Weight. University of Illinois at Urbana-Champaign; Champaign, IL, USA: 1962.94. ^Mohr D.R. Changes in Waistline and Abdominal Girth and Subcutaneous Fat Following Isometric Exercises. Res. Q. 1965;36:168–173.95. ^Noland M., Kearney J.T. Anthropometric and densitometric responses of women to specific and general exercise. Res. Q. 1978;49:322–328.96. ^Olson A.L., Edelstein E. Spot reduction of subcutaneous adipose tissue. Res. Q. 1968;39:647–652.97. ^Bartness TJ, Vaughan CH, Song CK. Sympathetic and sensory innervation of brown adipose tissue. Int J Obes (Lond) 2010b;34(Suppl 1):S36–42.98. ^Cao Y. Adipose tissue angiogenesis as a therapeutic target for obesity and metabolic diseases. Nat Rev Drug Discov. 2010;9:107–115.99. ^Rupnick MA, et al. Adipose tissue mass can be regulated through the vasculature. Proc Natl Acad Sci USA. 2002;99:10730–10735.100. ^Coppack SW, Fisher RM, Gibbons GF, Humphreys SM, McDonough MJ, Potts JL, et al. Postprandial substrate deposition in human forearm and adipose tissues in vivo. Clin Sci. 1990101. ^Frayn KN, Karpe F. Regulation of human subcutaneous adipose tissue blood flow. Int J Obes. 2014102. ^Wilhelm EN, González-Alonso J, Parris C, Rakobowchuk M. Exercise intensity modulates the appearance of circulating microvesicles with proangiogenic potential upon endothelial cells. Am J Physiol Heart Circ Physiol. 2016;311:H1297–310.103. ^Van Pelt DW, Guth LM, Horowitz JF. Aerobic exercise elevates markers of angiogenesis and macrophage IL-6 gene expression in the subcutaneous adipose tissue of overweight-to-obese adults. J Appl Physiol (1985) 2017;123:1150–9.104. ^Ludzki AC, Pataky MW, Cartee GD, Horowitz JF. Acute endurance exercise increases Vegfa mRNA expression in adipose tissue of rats during the early stages of weight gain. Appl Physiol Nutr Metab. 2018;43:751–4.105. ^Lee HJ. Exercise training regulates angiogenic gene expression in white adipose tissue. J Exerc Rehabil. 2018;14:16–23.106. ^Bente Stallknecht 1, Flemming Dela, Jørn Wulff Helge.Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions in adjacent muscles in humans?.Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E394-9.107. ^Ilkka Heinonen 1, Marco Bucci, Jukka Kemppainen, Juhani Knuuti, Pirjo Nuutila, Robert Boushel, Kari K Kalliokoski.Regulation of subcutaneous adipose tissue blood flow during exercise in humans.J Appl Physiol (1985). 2012 Mar;112(6):1059-63.108. ^Kurpad A, Khan K, Macdonald I, Elia M. Haemodynamic responses in muscle and adipose tissue and whole body metabolic responses during norepinephrine infusions in man. J Auton Nerv Syst 54: 163–170, 1995.109. ^Stallknecht B, Lorentsen J, Enevoldsen LH, Bülow J, Biering-Sørensen F, Galbo H, Kjær M. Role of the sympathoadrenergic system in adipose tissue metabolism during exercise in humans. J Physiol Lond 536: 283–294, 2001.110. ^Bartness TJ, Vaughan CH, Song CK. Sympathetic and sensory innervation of brown adipose tissue. Int J Obes (Lond) 2010b;34(Suppl 1):S36–42.111. ^N J Rothwell, M J Stock.Influence of noradrenaline on blood flow to brown adipose tissue in rats exhibiting diet-induced thermogenesis.Pflugers Arch. 1981 Mar;389(3):237-42.112. ^Pasarica M, Sereda OR, Redman LM, Albarado DC, Hymel DT, Roan LE, et al. Reduced adipose tissue oxygenation in human obesity evidence for rarefaction, macrophage chemotaxis, and inflammation without an angiogenic response. Diabetes. 2009113. ^Stefania Camastracorresponding author1 and Ele Ferrannini2.Role of anatomical location, cellular phenotype and perfusion of adipose tissue in intermediary metabolism: A narrative review.Rev Endocr Metab Disord. 2022; 23(1): 43–50.114. ^Coppack SW, Fisher RM, Gibbons GF, Humphreys SM, McDonough MJ, Potts JL, Frayn KN. Postprandial substrate deposition in human forearm and adipose tissues in vivo. Clin Sci (Lond) 79: 339–348, 1990.115. ^Summers LKM, Samra JS, Humphreys SM, Morris RJ, Frayn KN. Subcutaneous abdominal adipose tissue blood now: Variation within and between subjects and relationship to obesity. Clin Sci. 1996116. ^Jansson PA, Larsson A, Smith U, Lonnroth P: Glycerol production in subcutaneous adipose tissue in lean and obese humans. J Clin Invest 89: 1610–1617, 1992117. ^Andersson J, Karpe F, Sjöström LG, Riklund K, Söderberg S, Olsson T. Association of adipose tissue blood flow with fat depot sizes and adipokines in women. Int J Obes 36: 783–789, 2012.118. ^Jansson PA, Larsson A, Lönnroth PN. Relationship between blood pressure, metabolic variables and blood flow in obese subjects with or without non-insulin-dependent diabetes mellitus. Eur J Clin Invest 28: 813–818, 1998.119. ^Gastaldelli A, Cusi K, Pettiti M, Hardies J, Miyazaki Y, Berria R, et al. Relationship Between Hepatic/Visceral Fat and Hepatic Insulin Resistance in Nondiabetic and Type 2 Diabetic Subjects. Gastroenterology. 2007120. ^Begovatz P, Koliaki C, Weber K, Strassburger K, Nowotny B, Nowotny P, et al. Pancreatic adipose tissue infiltration, parenchymal steatosis and beta cell function in humans. Diabetologia. 2015121. ^Voros G., et al. Modulation of angiogenesis during adipose tissue development in murine models of obesity. Endocrinology. 2005;146:4545–4554.122. ^Eriksson A., et al. Placenta growth factor-1 antagonizes VEGF-induced angiogenesis and tumor growth by the formation of functionally inactive PlGF-1/VEGF heterodimers. Cancer Cell. 2002;1:99–108.123. ^Inuzuka H., et al. Differential regulation of immediate early gene expression in preadipocyte cells through multiple signaling pathways. Biochem. Biophys. Res. Commun. 1999;265:664–668.124. ^Seida A., et al. Serum bFGF levels are reduced in Japanese overweight men and restored by a 6-month exercise education. Int. J. Obes. Relat. Metab. Disord. 2003;27:1325–1331.125. ^Shang C.A., Thompson B.J., Teasdale R., Brown R.J., Waters M.J. Genes induced by growth hormone in a model of adipogenic differentiation. Mol. Cell. Endocrinol. 2002;189:213–219.126. ^J Bülow, J Madsen.Human adipose tissue blood flow during prolonged exercise II.Pflugers Arch. 1978 Aug 25;376(1):41-5.127. ^J Bülow.Subcutaneous adipose tissue blood flow and triacylglycerol-mobilization during prolonged exercise in dogs.Pflugers Arch. 1982 Jan;392(3):230-4.128. ^abFerguson RA, Ball D, Krustrup P, Aagaard P, Kjaer M, Sargeant AJ, Hellsten Y, Bangsbo J. Muscle oxygen uptake and energy turnover during dynamic exercise at different contraction frequencies in humans. J Physiol 536: 261–271, 2001.129. ^A Collin 1, Y Lebreton, M Fillaut, A Vincent, F Thomas, P Herpin.Effects of exposure to high temperature and feeding level on regional blood flow and oxidative capacity of tissues in piglets.Exp Physiol. 2001 Jan;86(1):83-91.130. ^Lossec 1, C Duchamp, Y Lebreton, P Herpin.Postnatal changes in regional blood flow during cold-induced shivering in sow-reared piglets.Can J Physiol Pharmacol. 1999 Jun;77(6):414-21.131. ^Naoto Fujii 1, Tatsuro Amano 2, Glen P Kenny 3, Yasushi Honda 1, Narihiko Kondo 4, Takeshi Nishiyasu 1.Nicotinic receptors modulate skin perfusion during normothermia, and have a limited role in skin vasodilatation and sweating during hyperthermia.Exp Physiol. 2019 Dec;104(12):1808-1818.132. ^ Naoto Fujii 1, Brendan D McNeely 1, Sarah Y Zhang 1, Yasmine C Abdellaoui 1, Mercy O Danquah 1, Glen P Kenny 1.Activation of protease-activated receptor 2 mediates cutaneous vasodilatation but not sweating: roles of nitric oxide synthase and cyclo-oxygenase.Exp Physiol. 2017 Feb 1;102(2):265-272.133. ^Crandall CG, Etzel RA & Johnson JM (1997). Evidence of functional β‐adrenoceptors in the cutaneous vasculature. Am J Physiol 273, H1038–1043.134. ^Medow MS, Taneja I & Stewart JM (2007). Cyclooxygenase and nitric oxide synthase dependence of cutaneous reactive hyperemia in humans. Am J Physiol Heart Circ Physiol 293, H425–432.135. ^Hodges GJ, Kellogg DL & Johnson JM (2015). Effect of skin temperature on cutaneous vasodilator response to the β‐adrenergic agonist isoproterenol. J Appl Physiol 118, 898–903.136. ^Fujii, N., Louie, J. C., McNeely, B. D., Amano, T., Nishiyasu, T., & Kenny, G. P. (2017a). Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: Roles for KCa, KATP, and KV channels, nitric oxide, and prostanoids. Applied Physiology, Nutrition and Metabolism, 42, 470–478.137. ^abIzumi, H., & Karita, K. (1992). Axon reflex flare evoked by nicotine in human skin. Japanese Journal of Physiology, 42, 721–730.138. ^Johnson, J. M., Minson, C. T., & Kellogg, D. L., Jr. (2014). Cutaneous vasodilator and vasoconstrictor mechanisms in temperature regulation. Comprehensive Physiology, 4, 33–89.139. ^Smith, C. J., & Johnson, J. M. (2016). Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans. Autonomic Neuroscience, 196, 25–36.140. ^Wong, B. J., & Hollowed, C. G. (2017). Current concepts of active vasodilation in human skin. Temperature, 4, 41–59.141. ^Caroline J Smith 1, John M Johnson 2.Responses to hyperthermia. Optimizing heat dissipation by convection and evaporation: Neural control of skin blood flow and sweating in humans.Auton Neurosci. 2016 Apr;196:25-36.