Kenny Glen P, Jay Ollie, Zaleski Wytek M, Reardon Mark L, Sigal Ronald J, Journeay W Shane, Reardon Francis D
Faculty of Health Sciences, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada.
Am J Physiol Regul Integr Comp Physiol. 2006 Sep;291(3):R580-8. doi: 10.1152/ajpregu.00918.2005.
We examined the effect of two levels of exercise-induced hypotension on esophageal (Tes) and active and nonactive muscle temperatures during and following exercise. Seven males performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their peak oxygen consumption during bilateral knee extensions (VO2sp). This was followed on separate days by 15-min of isolated bilateral knee extensions at moderate (60% VO2sp) (MEI) and high (80% VO2sp) (HEI) exercise intensities, followed by 90 min of recovery. Muscle temperature was measured with an intramuscular probe inserted in the left vastus medialis (Tvm) and triceps brachii (Ttb) muscles under ultrasound guidance. The deepest sensor (tip) was located approximately 10 mm from the femur and deep femoral artery and from the superior ulnar collateral artery and humerus for the Tvm and Ttb, respectively. Additional sensors were located 15 and 30 mm from the tip with an additional sensor located at 45 mm for the Tvm measurements only. Following exercise, mean arterial pressure (MAP) remained significantly below preexercise rest for the initial 60 min of recovery after MEI and for the duration of the postexercise recovery period after HEI (P< or =0.05). After HEI, significantly greater elevations from preexercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP compared with MEI (P< or =0.05). By the end of 90-min postexercise recovery, MAP, Tes, and all muscle temperatures remained significantly greater after HEI than MEI. Furthermore, a significantly shallower muscle temperature profile across Tvm, relative to preexercise rest, was observed at the end of exercise for both HEI and MEI (P< or=0.05), and for 30 min of recovery for MEI and throughout 90 min of recovery for HEI. No significant differences in muscle temperature profile were observed for Ttb. Thus we conclude that the increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude and recovery time of the postexercise esophageal and active muscle temperatures.
我们研究了两种程度的运动诱发低血压对运动期间及运动后食管温度（Tes）、活动肌肉和非活动肌肉温度的影响。七名男性在Kin-Com等动装置上进行了递增等张测试，以确定他们在双侧膝关节伸展过程中的峰值耗氧量（VO2sp）。随后在不同日期，以中等强度（60%VO2sp）（MEI）和高强度（80%VO2sp）（HEI）进行15分钟的双侧膝关节伸展分离运动，然后进行90分钟的恢复。在超声引导下，将肌内探头插入左侧股内侧肌（Tvm）和肱三头肌（Ttb）测量肌肉温度。对于Tvm和Ttb，最深的传感器（尖端）分别距离股骨和股深动脉以及尺侧上副动脉和肱骨约10毫米。额外的传感器分别位于距尖端15毫米和30毫米处，仅在测量Tvm时有一个额外的传感器位于45毫米处。运动后，MEI恢复的最初60分钟内以及HEI运动后恢复期内，平均动脉压（MAP）显著低于运动前休息时的水平（P≤0.05）。与MEI相比，HEI后，Tes和所有肌肉温度相对于运动前休息时的显著升高与MAP的更大下降平行（P≤0.05）。运动后90分钟恢复结束时，HEI后的MAP、Tes和所有肌肉温度仍显著高于MEI。此外，在运动结束时，HEI和MEI的Tvm肌肉温度相对于运动前休息时均观察到明显较浅的温度曲线（P≤0.05），MEI恢复30分钟时以及HEI恢复90分钟全程均如此。Ttb的肌肉温度曲线未观察到显著差异。因此，我们得出结论，随着运动强度增加诱发的运动后低血压反应增强，运动后食管和活动肌肉温度的升高幅度及恢复时间也相应增加。
