Proceedings of The Physiological Society
Trinity College Dublin (2003) J Physiol 551P, PC40
Blood pressure responses to external compression of the human lower leg during calf muscle chemoreflex stimulation of varying intensity
Michael J. White and Martin P.D. Bell
School of Sport and Exercise Sciences, University of Birmingham, Birmingham B15 2TT, UK
The cardiovascular response to isometric exercise and its control depends to a variable extent upon the afferent information transduced from metabolic and mechanical stimuli generated within the exercising muscle (Kaufman & Rybiki, 1987). During a phase of post-exercise circulatory occlusion (PECO) blood pressure remains elevated above baseline due to continued activation of the muscle chemoreflex (Alam & Smirk, 1937). Application of external compression to the muscle at this time can further increase blood pressure (White et al. 1998). This could result because of activation of muscle mechanoreceptive afferents or sensitisation of active muscle chemoreceptive afferents. The present study was designed to investigate further these two possibilities. If a standardised external compression stimulus applied during PECO increased blood pressure independent of the level of muscle chemoreflex activation then a constant mechanoreceptive reflex stimulation would be suggested. However if the level of response to compression varied with increasing muscle chemoreflex activation then sensitisation, or even saturation, of the reflex response could be inferred.
With local ethics committee approval eight male subjects (mean ± S.E.M. age, 26.3 ± 2.2 years, height, 177.2 ± 1.6 cm, weight, 74.6 ± 2.8 kg) gave written informed consent to perform five trials randomly assigned over two visits separated by a rest period of at least 20 min. Using previously published techniques (Bull et al. 1989) subjects sustained in random order either 30 %, 40 %, 50 %, 60 % or 70 % of maximal voluntary contractile (MVC) force of the calf muscles for 90 s in a dynamometer. Circulation through the lower leg was occluded throughout exercise and for the following 3 min by inflation of a thigh cuff. After 1 min of PECO a second cuff, placed around the calf muscles, was rapidly inflated to 300 mmHg (Hokansen) and was deflated 1 min later. Blood pressure was measured throughout the protocol (Finapres) and heart rate was recorded from ECG. Data were sampled at 1000 Hz by an A-D converter (CED 1401plus) and PC.
Exercise at 30, 40, 50, 60 and 70 % MVC progressively increased mean arterial blood pressure (MAP) during PECO (P < 0.001) by a mean (± S.E.M.) of 3.9 ± 1.4, 9.5 ± 3.4 and 16.2 ± 5.7 mmHg, respectively, above resting levels (MANOVA). External compression caused MAP to rise further with each condition (MANOVA, P < 0.001) reaching 9.2 ± 1.9, 8.6 ± 1.9, 15.9 ± 2.4, 21.9 ± 1.7 and 24.9 ± 2.8 mmHg respectively, above resting values. During compression the mean increases in MAP above those in PECO were 2.4 ± 1.6, 4.7 ± 1.2, 6.4 ± 0.9, 5.6 ± 1.1 and 5.1 ± 2.0 after 30, 40, 50, 60 and 70 % MVC, respectively, and were not significantly related to the preceding exercise intensity. Heart rates were not significantly altered from baseline levels during PECO or compression and were not influenced by preceding exercise intensity. These data show that muscle chemoreflex activation during PECO is influenced by the intensity of preceding exercise and that blood pressure is further elevated by forceful external compression applied at this time.
On the basis of these preliminary data it could be concluded that 300 mmHg external compression activates a population of mechanoreceptive afferents, independent of the level of muscle chemoreflex activation. However study of a wider range of data is required before this can be said with certainty.
Where applicable, experiments conform with Society ethical requirements