Behavioral activities and cardiovascular functions. II. Effects of sustained static work in squirrel monkeys

Mean arterial blood pressure (MABP) and heart rate (HR) were measured in unanesthetized squirrel monkeys trained to sustain for 20 seconds a forceful downward pull on an inverted T-bar. The MABP change during the strong static contraction of skeletal muscles involved in the pull was polyphasic, consisting of a brief initial rise and fall followed by a rise to a level above resting values which was sustained. At the end of the pull, the pressure fell transiently below the resting level. HR was elevated throughout the pull, returning towards the resting value in the minute following the pull. After hexamethonium, which reduced the resting MABP from about 120 mm Hg to about 80 mm Hg, the fall in MABP following the initial rise was enhanced, the level sustained through the pull was less than the resting level, and MABP fell still lower following the end of the pull. Phentolamine caused similar changes. Hexamethonium reduced the resting HR and abolished the HR changes during pulling. Raising the MABP after hexamethonium with phenylephrine further enhanced the falls in pressure during and following the pull. It is concluded that the polyphasic MABP changes to pulling involve direct mechanical effects of contracting skeletal muscle (responsible for the initial rise and contributing to the sustained rise), sympathetic vasoconstrictor discharge (contributing to the sustained rise and opposing the falls in MABP during and after the pull) and vasodilatation in active skeletal muscle (opposing the sustained rise during the pull and causing the fall after the pull). Although the participation of these factors in cardiovascular responses to exercise are generally well recognized, comparison of the patterns of response in rhesus and squirrel monkeys reveals large quantitative differences in the contributions of different factors and emphasizes again the caution that should be exercised in inferring direct environmental, emotional or conditioning effects on cardiovascular function.