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Before Automated Database Searches: Let’s Not Forget the Classics!!

Joyner, Michael J.

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Exercise and Sport Sciences Reviews: April 2003 - Volume 31 - Issue 2 - p 59-60
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Since the late 1960s automated (computerized) searches of the medical and scientific literature have become increasingly available, practical, and user friendly. As these systems have developed, more information is contained in them and the ease of complex searches has increased. For recent publications, the scientific community has the output of almost every major journal “at their fingertips” irrespective of language of publication and country of origin. Medline and related products have also vastly augmented the capabilities of smaller libraries that do not possess extensive collections of journals. This trend has been reinforced by the ability to download many recent key articles in various formats.

However, one key limitation of electronic databases, searches, and article retrieval is the general absence of papers published before the late 1960s, before the advent of the early electronic cataloging and retrieval systems. This is especially true in areas related to physiology in general, and exercise physiology in specific. Data from a variety of sources that track publication trends indicate that many integrative (i.e., exercise) physiology articles have cited a half-life of >10 yrs. This means that the relevance of key findings can remain high for decades. In this context, in this Exercise and Sport Sciences Reviews News Brief, four classic papers from the pre–electronic-database era will be used to demonstrate the continuing relevance of papers that might be seen by some as historical and to show how these classic papers continue to shape the debate about a variety of topics in exercise and integrative physiology.

There are continuing interest and controversy about the many factors that govern the autonomic nervous system during exercise in conscious humans. In the late 1930s, Alam and Smirk (1,2) published two papers on this topic. These papers demonstrated that a powerful blood-pressure–raising reflex existed in skeletal muscle and suggested that skeletal muscle afferents that were sensitive to muscle metabolites could cause profound increases in arterial pressure during exercise. They also suggested that skeletal muscle afferents affected blood pressure and not heart rate. The second study also contained a key “experiment in nature” that was conducted on a patient with a sensory deficit (but normal motor function) in one leg; this patient showed in the normal leg a sustained rise in blood pressure during postexercise ischemia that was absent in the insensitive leg. Although there were many key observations made before World War II on the autonomic control of the circulation during exercise in both animals and humans, the mechanisms highlighted in these papers continue to be explored at a variety of levels in various animal and human models. The second paper also demonstrates the power of “experiments in nature” that can be conducted in selected human patients and can provide unique insight into various physiological mechanisms.

By the late 1950s and early 1960s, several classic studies were performed that attempted to understand better the interaction of sympathetic vasoconstriction and metabolic vasodilation in contracting skeletal muscles. In a series of observations in patients with autonomic dysfunction for a variety of reasons, Marshall, Schirger, and Shepherd (3) showed that supine or head-down cycle ergometry was associated with a fall in blood pressure in these patients whose sympathetic nerves could not “restrain” blood flow to active skeletal muscle. One observation was particularly startling. It was made in a middle-aged male who had undergone bilateral thoracolumbar sympathectomies. In this era, there was limited pharmacologic therapy for high blood pressure, and when blood pressure could not be controlled and reached life-threatening levels, surgical sympathectomies were occasionally used as a last resort. This individual’s blood pressure fell during supine exercise, and when he was placed in a 15° head-down tilt (to maximize venous return and, hopefully, cardiac output) blood pressure still fell during exercise. Again, these observations frame the ongoing discussion and debate about functional sympatholysis and again demonstrate the power of straightforward and elegant observations in unique patients.

The fourth study highlighted also concerns how the autonomic nervous system functions during exercise, and focuses on the competition between sympathetic vasoconstriction and metabolic vasodilation in contracting muscle. In this study, Remensnyder, Mitchell, and Sarnoff (4) stimulated sympathetic vasoconstrictor nerves to the hind limbs of anesthetized dogs. Rather than using electrical stimulation, they activated the sympathetic vasoconstrictor nerves by occlusion of the carotid artery and engagement of baroreflex pathways. They used perfusion of the hind limb at various rates and demonstrated that, for any given level of hind limb flow, blood pressure was higher at rest when the sympathetic nerves were active. This clearly demonstrated that the resting skeletal muscles were in fact vasoconstricted by activation of the sympathetic nerves. Next, they repeated the same protocol during exercise while they measured arterial pressure before and during sympathetic activation. In contrast to the data at rest, carotid occlusion during exercise did not change the relationship between blood flow and perfusion pressure, demonstrating that the sympathetic nerves were unable to evoke vasoconstriction in contracting skeletal muscle. This paper remains one of the fundamental observations in support of functional sympatholysis and is one of the intellectual foundations of the whole discussion regarding how skeletal muscle blood flow is or is not regulated by the sympathetic nerves during exercise in humans and animals. Although this is an animal study, it shares several key features with the human studies noted above, most notably that the experimental design was simple and straightforward, as were the techniques used.


In summary, how the autonomic nervous system is regulated during exercise is an area of continuing interest to those in exercise science. Individuals focused on physiology are interested in this topic because the autonomic nervous system is a key regulator of homeostasis. In normal subjects, when the autonomic nervous system functions correctly, homeostasis is maintained during exercise. In athletes, the adaptations to training frequently permit homeostasis to be maintained in spite of high workloads or challenging environmental conditions. However, in diseases such as congestive heart failure, autonomic dysfunction can contribute to exercise limitation. The papers noted above form the intellectual cornerstones of how the autonomic nervous system operates during exercise. Similar examples can be found in other key areas of exercise science. Together, the brilliance and continued relevance of these papers highlight the depth of our intellectual foundations and remind us to look beyond automated databases to understand and appreciate these older studies.


1. Alam, M. and F.H. Smirk. Observation in man upon a blood pressure raising reflex arising from the voluntary muscle. J. Physiol. 89: 372–383, 1937.
2. Alam, M. and F.H. Smirk. Unilateral loss of a blood pressure raising, pulse accelerating, reflex from voluntary muscle due to a lesion of the spinal cord. Clin. Science. 3: 247–252, 1938.
3. Marshall, R.J A. Schirger, and J.T. Shepherd. Blood pressure during supine exercise in idiopathic orthostatic hypotension. Circulation. 24: 76–81, 1961.
4. Remensnyder, J.P. J.H. Mitchell, and S.J. Sarnoff. Functional sympatholysis during muscular activity. Circ. Res. 11: 370–380, 1962.
©2003 The American College of Sports Medicine