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PERSPECTIVES |
1 Medical College of Wisconsin and VA Medical Center, Milwaukee, WI 53295, USA
2 Pepperdine University, Malibu, CA 90263,USA
Email: pcliff{at}mcw.edu
The influence of muscular compression on the blood flow in skeletal muscle has been pondered for many years. Anrep & von Saalfeld (1935) first showed that arterial inflow is reduced during contraction due to compression of the intramuscular vessels, an effect later confirmed by Wesche (1986) in humans. Compression of the veins aids venous return to the heart (Guyton et al. 1962) and has been postulated to increase skeletal muscle perfusion by reducing the downstream venous pressure during relaxation, i.e. the muscle pump effect. Evidence in support of this notion is scanty, but the absence of contraction-induced hyperaemia when vascular smooth muscle relaxation is impaired implies that immediate increases in blood flow are attributable to rapid vasodilatation rather than a muscle pump effect (Hamann et al. 2004). Indeed, there is definitive evidence of rapid vasodilation at the onset of contractions in the rat spinotrapezius muscle (Marshall & Tandon, 1984), hamster cremaster muscle (Mihok & Murrant, 2004), and the hamster retractor muscle (VanTeeffelen & Segal, 2006).
An additional way that compression could influence blood flow is through activation of a myogenic-like response. This idea was first put to the test by Mohrman & Sparks (1974) who showed that inflation of a cuff placed around isolated canine gastrocnemius muscle could cause vasodilatation. In addition, they observed that changes in vascular conductance following contraction were related to intramuscular pressure. More recent data demonstrated that brief periods of mechanical compression elicit dilatation in isolated soleus feed arteries (Clifford et al. 2006). The time course of the vasodilatation was remarkably similar to that for the change in blood flow after a brief muscle contraction. In addition, multiple pressure pulses evoked a greater magnitude of dilatation than a singe pressure pulse. On the basis of these results it was suggested that compression of the intramuscular vasculature could provide a mechanism for rapid vasodilatation following contraction.
The study by Kirby et al. (2007) in this issue of The Journal of Physiology represents another important landmark in this story. The clever manipulations employed by this group are a superb example of how to study integrative human physiology. Moreover, the results show quite clearly that mechanical compression can elicit hyperaemia in the human forearm. The existence of a dose–response relationship over a range of cuff pressures between 25 and 100 mmHg provides the potential to produce graded vasodilatation in response to graded compression of the vasculature. Importantly, the observation of a temporal dissociation between the peak response to compression and that elicited by contractions argues that mechanical influences do not completely explain contraction-induced vasodilatation. In considering these results, one must keep in mind that it cannot be determined whether the forearm cuff faithfully mimics the compression elicited by forceful muscular contraction.
One issue that remains to be resolved is whether this mechanism is operative in all types of muscle under all conditions. Berg et al. (1997) and vanTeeffelen & Segal (2006) maintain that vessel compression is not a factor in thin muscle in situ preparations. However, it must be emphasized that complete collapse of the vessel is not required to evoke this response. In fact, subjects in the study of Kirby et al. with a mean arterial pressure of 89 mmHg exhibited significant dilatation when external pressure was applied at only 50 mmHg. In the in vitro model (Clifford et al. 2006), high extravascular pressures were employed to simulate intramuscular pressures during maximal contraction. More recent experiments (unpublished observations Clifford & Jasperse) reveal that compression-induced dilatation can occur with little discernible reduction in vessel diameter. Substantial dilatation was observed when a brief pressure pulse matching intraluminal pressure was applied to the outside of the vessel. We speculate that contraction of muscle fibres may evoke sufficient vascular compression to elicit dilatation in the in situ muscle preparations.
There has been considerable discussion of redundant factors being involved in complex physiological responses such as exercise hyperaemia. The present findings suggest a scenario where there may be temporally distinct phases of vasodilatation. Mechanically induced feed forward vasodilatation could occur with the initial contraction. Vasodilatation could then continue as potassium rapidly accumulates in the interstitium. After sufficient time to allow production and diffusion of metabolites from skeletal muscle, the blood flow could be adjusted by feedback mechanisms to match blood flow with oxygen consumption. A critical challenge for physiologists interested in this topic will be to begin teasing out the time course over which each of these overlapping mechanisms may act. The paper by Kirby et al. (2007) makes a key contribution by demonstrating that mechanically induced vasodilatation is most important in the very initial phase of hyperaemia.
Until recently, little consideration has been given to a mechanical mechanism to explain vasodilatation during exercise. Kirby and colleagues have provided the impetus for further study of this mechanism. It seems clear that the influence of mechanical factors must be incorporated into our models for the overall picture of exercise hyperaemia.
References
Anrep GV & von Saalfeld E (1935). J Physiol 85, 375–399.
Berg BR, Cohen KD & Sarelius IH (1997). Am J Physiol Heart Circ Physiol 272, H2693–H2700.
Clifford PS, Kluess HA, Hamann JJ, Buckwalter JB & Jasperse JL (2006). J Physiol 572, 561–567.
Guyton AC, Douglas BH, Langston JB & Richardson TQ (1962). Circ Res 11, 431–441.
Hamann JJ, Buckwalter JB & Clifford PS (2004). J Physiol 557, 1013–1020.
Kirby BS, Carlson RE, Markwald RR, Voyles WF & Dinenno FA (2007). J Physiol 583, 861–874.
Marshall JM & Tandon HC (1984). J Physiol 350, 447–459.
Mihok ML & Murrant CL (2004). Can J Physiol Pharmacol 82, 282–287.[CrossRef][Medline]
Mohrman DE & Sparks HV (1974). Am J Physiol 227, 531–535.
VanTeeffelen JW & Segal SS (2006). Am J Physiol Heart Circ Physiol 290, H119–H127.
Wesche J (1986). J Physiol 377, 445–462.
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