Paull Gabrielle, Dervis Sheila, McGinn Ryan, Haqani Baies, Flouris Andreas D, Kondo Narihiko, Kenny Glen P
Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada;
Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada; FAME Laboratory, Department of Exercise Science, University of Thessaly, Trikala, Greece; and.
Am J Physiol Regul Integr Comp Physiol. 2015 Dec 1;309(11):R1415-24. doi: 10.1152/ajpregu.00287.2015. Epub 2015 Sep 16.
We examined whether sustained changes in baroreceptor loading status during prolonged postexercise recovery can alter the metaboreceptors' influence on heat loss. Thirteen young males performed a 1-min isometric handgrip exercise (IHG) at 60% maximal voluntary contraction followed by 2 min of forearm ischemia (to activate metaboreceptors) before and 15, 30, 45, and 60 min after a 15-min intense treadmill running exercise (>90% maximal heart rate) in the heat (35°C). This was repeated on three separate days with continuous lower body positive (LBPP, +40 mmHg), negative (LBNP, -20 mmHg), or no pressure (Control) from 13- to 65-min postexercise. Sweat rate (ventilated capsule; forearm, chest, upper back) and cutaneous vascular conductance (CVC; forearm, upper back) were measured. Relative to pre-IHG levels, sweating at all sites increased during IHG and remained elevated during ischemia at baseline and similarly at 30, 45, and 60 min postexercise (site average sweat rate increase during ischemia: Control, 0.13 ± 0.02; LBPP, 0.12 ± 0.02; LBNP, 0.15 ± 0.02 mg·min(-1)·cm(-2); all P < 0.01), but not at 15 min (all P > 0.10). LBPP and LBNP did not modulate the pattern of sweating to IHG and ischemia (all P > 0.05). At 15-min postexercise, forearm CVC was reduced from pre-IHG levels during both IHG and ischemia under LBNP only (ischemia: 3.9 ± 0.8% CVCmax; P < 0.02). Therefore, we show metaboreceptors increase postexercise sweating in the middle to late stages of recovery (30-60 min), independent of baroreceptor loading status and similarly between skin sites. In contrast, metaboreflex modulation of forearm but not upper back CVC occurs only in the early stages of recovery (15 min) and is dependent upon baroreceptor unloading.
我们研究了长时间运动后恢复过程中压力感受器负荷状态的持续变化是否会改变代谢感受器对热量散失的影响。13名年轻男性在热环境(35°C)中进行了15分钟的高强度跑步机跑步运动(>90%最大心率),运动前、运动后15、30、45和60分钟时,先进行1分钟的等长握力运动(IHG),运动强度为最大自主收缩的60%,随后进行2分钟的前臂缺血(以激活代谢感受器)。在运动后13至65分钟期间,分三天分别重复进行持续的下体正压(LBPP,+40 mmHg)、负压(LBNP,-20 mmHg)或无压力(对照)实验。测量了出汗率(通气胶囊;前臂、胸部、上背部)和皮肤血管传导率(CVC;前臂、上背部)。相对于IHG前水平,所有部位在IHG期间出汗增加,在基线缺血期间以及运动后30、45和60分钟时同样保持升高(缺血期间部位平均出汗率增加:对照,0.13±0.02;LBPP,0.12±0.02;LBNP,0.15±0.02 mg·min⁻¹·cm⁻²;所有P<0.01),但在15分钟时没有增加(所有P>0.10)。LBPP和LBNP并未调节对IHG和缺血的出汗模式(所有P>0.05)。在运动后15分钟时,仅在LBNP条件下,前臂CVC在IHG和缺血期间均从IHG前水平降低(缺血时:3.9±0.8% CVCmax;P<0.02)。因此,我们发现代谢感受器在恢复的中晚期(30 - 60分钟)增加运动后出汗,与压力感受器负荷状态无关,且在不同皮肤部位之间情况相似。相比之下,前臂而非上背部CVC的代谢反射调节仅发生在恢复的早期(15分钟),并且依赖于压力感受器卸载。