Responses to dynamic leg exercise in man as influenced by changes in muscle perfusion pressure.

The influences of induced alterations in muscle perfusion pressure on the physiological responses to rhythmic exercise in man were investigated. The experiments were carried out in healthy subjects performing leg exercise on a cycle ergometer at light to exhaustive work intensities. Increased muscle perfusion pressure was brought about by exposing the working legs of the supine subject to a subatmospheric pressure of -50 mm Hg (Lower Body Negative Pressure, LBNP), decreased perfusion pressure by instead applying a supraatmospheric pressure of 50 mm Hg (Leg Positive Pressure, LPP). In this way, the perfusion pressure in dynamically exercising large muscle groups could be altered in a controlled fashion. The influences of such manipulation of the perfusion pressure on the physiological adjustments to incremental-load exercise were studied and analysed. The main results and conclusions were as follows: (1) Exercise-induced increases in cardiac output were attenuated by LBNP, an effect caused by curtailment of stroke volume secondary to suction-induced sequestration of blood volume in capacitance vessels not affected by the action of the leg muscle pump. This situation resembles that of dynamic leg exercise in the upright body position. Thus, supine exercise with LBNP at -50 mm Hg seems to be a valid model of upright leg exercise, not only in that it increases perfusion pressure in working muscles but also by causing similar changes in the central circulation as a shift from supine to upright leg exercise. (2) Exercise-induced increases in systolic arterial pressure were markedly exaggerated by LPP, an effect attributable to increased exercise responses in both cardiac output and total peripheral resistance. The exaggerated pressor response supports the notion of a muscle chemoreflex drive in response to flow-restricted exercise tending to reduce the existing flow error. (3) Exercise-induced increases in O2 uptake and blood lactate concentration were both attenuated by LBNP and exaggerated by LPP. The changes in blood lactate levels are attributable to perfusion-pressure dependent variations in muscle blood flow, resulting in opposite changes in the share contributed by anaerobic metabolism to the energy release. Possible explanations for the fact that impaired muscle perfusion was associated with increased O2 uptake at given external work loads are discussed. (4) Exercise-induced responses of the pulmonary ventilation were attenuated by LBNP and markedly exaggerated by LPP.(ABSTRACT TRUNCATED AT 400 WORDS)