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POINT-COUNTERPOINT COMMENTS
Human Vascular Control Laboratory
School of Physical and Health Education and Department of Physiology
Queen's University
Kingston, Ontario, Canada
e-mail: mt29{at}post.queensu.ca
The following letters are in response to the Point:Counterpoint series "The muscle metaboreflex does/does not restore blood flow to contracting muscles" that appeared in the January issue (vol. 100: 357–361, 2006; http://jap.physiology.org/content/vol100/issue1).
To the Editor: This letter addresses the Point:Counterpoint debate concerning the statement "The muscle metaboreflex does/does not restore blood flow to contracting muscles" (3). It highlights the need to consider the purpose (teleological implications) of physiological control systems and frames the issue in terms of sympathetic restraint vs. sympatholysis. Finally, it suggests that the flow-restorative capacity of this reflex may be dependent on the amount of exercising muscle that is metabolically stressed and therefore the amount of total vascular conductance represented by the metabolically stressed muscle vascular bed.
Muscle metaboreflex: it "senses" metabolic stress in the muscle and evokes a pressor response. Functional or futile? Joyner's argument suggests the reflex is self-defeating because it evokes dominant sympathetic vasoconstriction in the very muscle bed from which the feedback signal originates. Consideration of sympathetic restraint vs. sympatholysis, and the body of evidence in the literature concerning this in humans (2, 4–6) provides a critical frame of reference. The ultimate "outcome" of the pressor response depends on the relative magnitude of pressure elevation vs. effectiveness of local vasoconstriction. Joyner's citation of Tschakovsky et al. (6) to support domination of muscle vasoconstriction is a misrepresentation of data that actually demonstrates severe blunting of sympathetic vasoconstriction in exercising muscle. I would direct Joyner, O'Leary, and readers to the study by Tschakovsky and Hughson (5) that demonstrated that in an exercising forearm, blood flow goes up in proportion to the blood pressure increase evoked by muscle metaboreflex stimulation in the calf (i.e., an exercising muscle bed subject to metaboreflex evoked sympathetic vasoconstriction demonstrates a dominance of sympatholysis, not sympathetic, restraint, and benefits from the pressor response). Joyner's argument may apply when the metabolically stressed muscle evoking the pressor response represents virtually all of the available vascular conductance for pressure elevation. Augustyniak et al. (1) cited by O'Leary might support this. I see this debate directing us to ask "What are the exercise conditions that determine how the pressor response and local muscle vasoconstriction responses interact to determine the net "flow-restorative" effect of the muscle metaboreflex?"
REFERENCES
1- and 2-adrenergic vasoconstriction is blunted in contracting human muscle. J Physiol 547: 971–976, 2003.
School of Kinesiology
University of Western Ontario
London, Ontario, Canada
e-mail: kshoemak{at}uwo.ca
To the Editor: In this Point:Counterpoint discussion (2), I propose that we do not get too side-tracked by the issue of whether cardiac output is maximal at the point of decision but that we are clear on whether we are discussing muscle perfusion (blood flow) or its vascular conductance. In addition, the evidence of constriction in exercising muscle should be balanced against other human data, based on direct measures of limb blood flow, that challenge the idea of metaboreflex-induced sympathetic constriction in inactive or active muscle (4, 5). If this latter scenario is accurate, then a critical question is "how was BP elevated in these studies"? As identified in O'Leary's rebuttal, an increase in cardiac output with metaboreflex activation has been reported in humans, but whether it changes enough to account for concurrent pressor responses has not been addressed adequately. Indirect evidence may help. During knee extensor (3) or forearm (1) exercise to fatigue, there is a linear increase in limb blood flow with incremental work in concert with a pressor response. These data indicate that vascular conductance must be plateauing in the heavier contractions. That is, the dilation was constrained but the continued increase in blood pressure facilitated a linear increase in limb perfusion. Therefore, a testable hypothesis is that the change in cardiac output can account for the pressor response to fatiguing exercise and contribute to the linear increase in limb perfusion with work rate despite (sympathetically mediated?) constraint on muscle vasodilation.
REFERENCES
Department of Kinesiology and Physical Education
Wilfrid Laurier University
Waterloo, Ontario, Canada
e-mail: mbabcock{at}wlu.ca
To the Editor: Contrary to Dr. O'Leary's statement in his Point article (3), I would direct him to some data in the literature that have examined the functioning of the skeletal metaboreflex in human muscle. Our report that showed that increasing the work of the inspiratory muscle during maximal whole body exercise caused a decrease in the blood flow to the active leg muscles. This was a clear indication that the skeletal muscle metaboreflex was operating in the inspiratory muscles (specifically the diaphragm) in humans, granted the study was done at maximal exercise (2). Subsequent studies have provided evidence that the metaboreflex fails to restore blood flow to ischemic respiratory muscle tissue by simply increasing the cardiac output. In each of the studies, a common protocol was used that was known to produce fatigue in the respiratory muscles as shown by task failure. St. Croix et al. (5) reported that the muscle sympathetic nerve activity (MSNA) increased in an inactive leg as the subjects performed the inspiratory muscle fatiguing trial. Furthermore, it has been shown that leg blood flow decreased and leg vascular resistance increased during a similar fatiguing trial (4). Similar changes in MSNA, leg blood flow, and leg vascular resistance have been reported in expiratory muscles of humans under the same fatiguing conditions reported above (1). In all studies, non-fatiguing increases in respiratory efforts had no effect on MSNA, leg blood flow, or leg vascular resistance. These findings suggest that the skeletal metaboreflex in human respiratory muscle may be involved in blood flow distribution during whole body exercise, exactly how remains to be determined.
REFERENCES
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