Why the study?
Does central command or muscle afferent activation drive the exercise-induced increase in anterior cerebral artery blood velocity in humans?
Does central command or muscle afferent activation drive the exercise-induced increase in anterior cerebral artery blood velocity in humans?
Increases in anterior cerebral artery blood velocity during calf exercise are dependent on central command rather than skeletal muscle afferent activation.
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Central command may drive ACA velocity increases during voluntary exercise; leaves open afferent roles in other settings or vascular beds.
The purpose of the present study was to determine the relative importance of peripheral feedback from mechanically (mechanoreflex) and metabolically (metaboreflex) sensitive muscle afferents and central signals arising from higher centers (central command) to the exercise-induced increases in regional cerebral perfusion. To accomplish this, anterior cerebral artery (ACA) mean blood velocity (V(mean)) responses were assessed during sustained and rhythmic passive calf muscle stretch (mechanoreflex), volitional calf exercise (mechanoreflex, metaboreflex, and central command), and electrically stimulated calf exercise (mechanoreflex and metaboreflex but no central command) at 35% of maximum voluntary contraction (n = 16). In addition, a period of postexercise muscle ischemia (PEMI) was used to isolate the metaboreflex. Blood pressure, cardiac output, and the end-tidal partial pressure of carbon dioxide (Pet(CO2)) were also measured. ACA V(mean) was unchanged from rest during either sustained or rhythmic calf muscle stretch (P > 0.05). However, ACA V(mean) was increased from rest during both isometric (+15 +/- 1%) and rhythmic (+15 +/- 2%, voluntary exercise P < 0.05) but remained unchanged during stimulated exercise (P > 0.05). Isometric and rhythmic exercise-induced increases in blood pressure and cardiac output were similar during voluntary and stimulated exercise (P > 0.05 between conditions). Blood pressure remained elevated during PEMI after all exercise conditions (P < 0.05 vs. rest), whereas cardiac output and ACA V(mean) were not different from rest (P > 0.05). Pet(CO2) was unchanged from rest throughout. These data suggest that selective activation of skeletal muscle afferents (i.e., stretch, PEMI, or stimulated exercise) does not increase ACA V(mean) and that increases in ACA V(mean) during volitional contractions of an exercising calf muscle are dependent on the presence of central command.
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Vianna et al. (2009) studied this question.
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