BIRTLES, D. B., M. P. RAYSON, A. CASEY, D. A. JONES, and D. J. NEWHAM. Venous Obstruction in Healthy Limbs: A Model for Chronic Compartment Syndrome? Med. Sci. Sports Exerc., Vol. 35, No. 10, pp. 1638–1644, 2003.
Purpose: Chronic exertional compartment syndrome (CECS) in the anterior tibial (AT) compartment is generally believed to be the result of reduced venous blood flow caused by restrictive compartments and increased intramuscular pressures. If this is so, then restricting venous flow in the muscles of healthy subjects during exercise should mimic CECS.
Methods: This hypothesis was tested in 10 control subjects (aged 19–41 yr, five males) with and without external venous occlusion induced by a sphygmomanometer cuff fitted just below the knee and inflated to 80 mm Hg. Twenty CECS patients (20-39 yr, 16 males) were studied without external occlusion. Subjects performed intermittent, isometric maximal voluntary contractions (MVC) of the AT for 20 min (1.6-s contractions, 0.5 duty cycle). MVC, tetanic force (2 s at 50 Hz), muscle thickness (ultrasound imaging), and pain were measured during exercise and 10 min of recovery.
Results: Venous occlusion in the controls induced greater pain, fatigue, and increase in muscle thickness (P < 0.01). Initially the patients fatigued more slowly than the occluded controls, but at the end of exercise, the fatigue and pain were similar in these two groups. The controls showed a greater increase in muscle size (P = 0.01). Recovery was similar in all three groups, although the size of the patients’ muscles recovered rather more slowly.
Conclusion: External venous occlusion of the AT muscles in control subjects induces changes very similar to those of CECS patients, although the different time courses indicate that different processes are involved. The AT compartment of CECS patients is capable of distension.
Chronic exertional compartment syndrome (CECS) is a common cause of exercise-induced lower-leg pain, which most often affects the anterior and deep posterior compartments (1,13,20).
It is a transient and reversible condition triggered by activity and relieved by rest. CECS patients can experience considerable pain and temporary neurological deficit (10), and in many cases, the pain is severe enough to restrict exercise and potentially affect career prospects, e.g., in service personnel and competitive athletes.
Although not a universal finding, several authors (5,12,13,18,19,20) have demonstrated abnormally elevated intramuscular pressures during exercise in CECS patients, and these also are associated with reduced muscle blood flow (2,19,21,23,25).
Turnipseed et al. (25) investigated the effects of increased compartment pressure on anterior tibial arteriovenous flow patterns and reported normal arterial flow but impaired tibial vein drainage in CECS patients. No venous occlusions or anatomical abnormalities were found, so reduced flow was attributed to the increased venous pressure. The fascia of the affected compartment in the patients was also found to be significantly thicker and stiffer than that taken from unaffected compartments and from control subjects. During exercise, it is normal for muscle volume to increase by up to 20% via increased capillary perfusion, blood volume, and interstitial edema and muscle fiber swelling (10). It is possible that in an abnormally inextensible compartment, the tissue swelling that is a normal consequence of metabolic activity during exercise leads to an increase in pressure sufficient to compromise tissue perfusion (5,8,10,12,13).
Although widely accepted, there is little direct evidence for these suggestions of the cause of CECS, specifically the mechanisms whereby the circulatory impairment occurs, i.e., some direct changes in the venous circulation or an indirect effect through increased tissue pressures. If the former were the cause, then the expectation would be that the syndrome could be simulated in healthy people by external occlusion of venous flow to exercising muscle. Therefore, we have compared the response to exercise in terms of muscle function, thickness, and pain in CECS patients with normal controls. The latter performed two bouts of exercise, one with a free circulation and the other with partial occlusion.
1Applied Biomedical Research Centre, GKT School of Biomedical Sciences, King’s College London, UNITED KINGDOM;
2Optimal Performance Ltd., Farnham, Surrey, UNITED KINGDOM;
3QinetiQ Centre for Human Sciences, Farnborough, Hampshire, UNITED KINGDOM; and
4School of Sport and Exercise Science, University of Birmingham, Birmingham, UNITED KINGDOM
Address for correspondence: Prof. D. J. Newham, Applied Biomedical Research Centre, GKT School of Biomedical Sciences, King’s College, London, Shepherd’s House, Guy’s Campus, London SE1 1UL, United Kingdom; E-mail: firstname.lastname@example.org.
Submitted for publication November 2002.
Accepted for publication June 2003.