invited editorial Closer to the edge ? Contractions , pressures , waterfalls and blood flow to contracting skeletal muscle

THE MECHANICAL EFFECTS OF muscle contraction on blood flow to the muscle tissue are interesting, complex, and, we believe, important. It is clear that forceful muscle contractions can stop arterial inflow and propel blood rapidly from the veins. Although there is no controversy about vigorous contractions stopping arterial inflow, controversy continues about the relative importance of the “muscle pump effect” facilitating muscle perfusion during rhythmic contractile activity. Many physiologists believe this controversy is not cutting edge or that the muscle pump makes a minor contribution to venous return but no contribution to muscle blood flow. However, recent evidence demonstrating high muscle blood flow during exercise in conscious animals (including humans) and discussions about exercise hyperemia at the onset of exercise have brought renewed interest to this controversy. Two manuscripts contained in this issue of the Journal of Applied Physiology focus attention on these issues [Hamann et al. (5) and Dobson and Gladden (1)]. The muscle pump hypothesis emerged from observations on the interaction of gravity and walking on venous pressures in human limbs (10). Folkow and colleagues (3) demonstrated that blood flow to contracting human calf muscles was greater when the limbs were in the dependent position (upright posture) than when the limbs were at heart level (supine). Since these fundamental observations, there have been a number of studies examining the relative importance of the muscle pump in providing muscle blood flow (6, 7), and the main conclusion seems to be “it depends.” Rhythmic muscle contraction can interfere with blood flow under a number of conditions (1, 5, 7), and rhythmic contraction can be responsible for 30–60% of the driving force for skeletal muscle blood flow (11, 12). The study of Hamann et al. (5) employed an elegantly instrumented animal model of treadmill exercise to determine whether the muscle pump increases blood flow in skeletal muscle vasculature that is already vasodilated. Hamann et al. infused adenosine into the femoral artery at a rate that increased blood flow more than the blood flow measured when the dog walked at 3 miles/h on the treadmill. At the initiation of treadmill (3 miles/h), exercise blood flow decreased in the leg vasodilated with adenosine, whereas a normal hyperemic response was observed in the contralateral leg. Thus, not only was no muscle pump effect observed, blood flow decreased with imposition of locomotory exercise. As indicated below, this result may be related to the lack of a significant hydrostatic column in these subjects. The study of Dobson and Gladden (1) also examined the effects of rhythmic muscle contractions on peak skeletal muscle blood flow in dog skeletal muscle. The gastrocnemius muscle preparation was perfused spontaneously, and the muscle was stimulated to contract with tetanic contractions (200-ms duration, 50 Hz), at one per second. This is a powerful preparation that can be used to determine the effects of contraction on blood flow with tight control of the experimental conditions. The results indicate that muscle contraction, during maximal vasodilation, decreased blood flow, and the authors correctly conclude that their experiment provides no evidence of a muscle pump effect. These results may also be influenced by lack of a hydrostatic column in the preparations. In addition, there is concern that the venous flow probe-cannulation system used may have modified the compliance characteristics of the venous system sufficiently to interfere with the muscle pump effect inasmuch as muscle contraction increased venous pressures from 4–5 to 8–10 mmHg (8). Have these two new papers finally “solved” all outstanding issues related to the muscle pump and the mechanical interactions of contractions and perfusion in active muscle? The simple answer is no. The observations of Hamann et al. (5) and Dobson and Gladden (1) demonstrate that during drug-induced vasodilation no muscle pumping effect is apparent in isolated, conAddress for reprint requests and other correspondence: M. H. Laughlin, E102, Vet. Med. Bldg., Univ. of Missouri, Columbia, MO 65211 (E-mail: [email protected]). J Appl Physiol 94: 3–15, 2003; 10.1152/japplphysiol.00829.2002.