Central command generated prior to arbitrary motor execution induces muscle vasodilatation at the beginning of dynamic exercise.

The purpose of this study was to examine the role of central command, generated prior to arbitrary motor execution, in cardiovascular and muscle blood flow regulation during exercise. Thirty two subjects performed 30 s of two-legged cycling or 1 min of one-legged cycling (66 ± 4% and 35% of the maximal exercise intensity, respectively), which was started arbitrarily or abruptly by a verbal cue (arbitrary vs. cued start). We measured the cardiovascular variables during both exercises and the relative changes in oxygenated-hemoglobin concentration (Oxy-Hb) of noncontracting vastus lateralis muscles as index of tissue blood flow and femoral blood flow to nonexercising leg during one-legged cycling. Two-legged cycling with arbitrary start caused a decrease in total peripheral resistance (TPR), which was smaller during the exercise with cued start. The greater reduction of TPR with arbitrary start was also recognized at the beginning of one-legged cycling. Oxy-Hb of noncontracting muscle increased by 3.6 ± 1% (P < 0.05) during one-legged cycling with arbitrary start, whereas such increase in Oxy-Hb was absent with cued start. The increases in femoral blood flow and vascular conductance of nonexercising leg were evident (P < 0.05) at 10 s from the onset of one-legged cycling with arbitrary start, whereas those were smaller or absent with cued start. It is likely that when voluntary exercise is started arbitrarily, central command is generated prior to motor execution and then contributes to muscle vasodilatation at the beginning of exercise. Such centrally induced muscle vasodilatation may be weakened and/or masked in the case of exercise with cued start.

Increased oxygenation of the cerebral prefrontal cortex prior to the onset of voluntary exercise in humans.

To determine whether output from the forebrain (termed central command) may descend early enough to increase cardiac and renal sympathetic outflows at the onset of voluntary exercise, we examined the changes in regional tissue blood flows of bilateral prefrontal cortices with near-infrared spectroscopy, precisely identifying the onset of voluntary ergometer 30-s exercise at 41 ± 2% of the maximal exercise intensity in humans. Prefrontal oxygenated-hemoglobin (Oxy-Hb) concentration was measured as index of regional blood flow unless deoxygenated-hemoglobin concentration remained unchanged. Prefrontal Oxy-Hb concentration increased significantly (P < 0.05) 5 s prior to the onset of exercise with arbitrary start, whereas such increase in prefrontal Oxy-Hb was absent before exercise abruptly started by a verbal cue. Furthermore, the increase in prefrontal Oxy-Hb observed at the initial 15-s period of exercise was greater with arbitrary start than cued start. The prefrontal Oxy-Hb, thereafter, decreased during the later period of exercise, irrespective of either arbitrary or cued start. The reduction in prefrontal Oxy-Hb had the same time course and response magnitude as that during motor-driven passive exercise. Cardiac output increased at the initial period of exercise, whereas arterial blood pressure and total peripheral resistance decreased. The depressor response was more pronounced (P < 0.05) with arbitrary start than cued start. Taken together, it is suggested that the increase in prefrontal Oxy-Hb observed prior to the onset of voluntary exercise may be in association with central command, while the later decrease in the Oxy-Hb during exercise may be in association with feedback stimulated by mechanical limb motion.

Coactivation of renal sympathetic neurons and somatic motor neurons by chemical stimulation of the midbrain ventral tegmental area.

We examined whether neurons in the midbrain ventral tegmental area (VTA) play a role in generating central command responsible for autonomic control of the cardiovascular system in anesthetized rats and unanesthetized, decerebrated rats with muscle paralysis. Small volumes (60 nl) of an N-methyl-D-aspartate receptor agonist (L-homocysteic acid) and a GABAergic receptor antagonist (bicuculline) were injected into the VTA and substantia nigra (SN). In anesthetized rats, L-homocysteic acid into the VTA induced short-lasting increases in renal sympathetic nerve activity (RSNA; 66 ± 21%), mean arterial pressure (MAP; 5 ± 2 mmHg), and heart rate (HR; 7 ± 2 beats/min), whereas bicuculline into the VTA produced long-lasting increases in RSNA (130 ± 45%), MAP (26 ± 2 mmHg), and HR (66 ± 6 beats/min). Bicuculline into the VTA increased blood flow and vascular conductance of the hindlimb triceps surae muscle, suggesting skeletal muscle vasodilatation. However, neither drug injected into the SN affected all variables. Renal sympathetic nerve and cardiovascular responses to chemical stimulation of the VTA were not essentially affected by decerebration at the premammillary-precollicular level, indicating that the ascending projection to the forebrain from the VTA was not responsible for evoking the sympathetic and cardiovascular responses. Furthermore, bicuculline into the VTA in decerebrate rats produced long-lasting rhythmic bursts of RSNA and tibial motor nerve discharge, which occurred in good synchrony. It is likely that the activation of neurons in the VTA is capable of eliciting synchronized stimulation of the renal sympathetic and tibial motor nerves without any muscular feedback signal.

Central command does not decrease cardiac parasympathetic efferent nerve activity during spontaneous fictive motor activity in decerebrate cats.

To examine whether withdrawal of cardiac vagal efferent nerve activity (CVNA) predominantly controls the tachycardia at the start of exercise, the responses of CVNA and cardiac sympathetic efferent nerve activity (CSNA) were directly assessed during fictive motor activity that occurred spontaneously in unanesthetized, decerebrate cats. CSNA abruptly increased by 71 ± 12% at the onset of the motor activity, preceding the tachycardia response. The increase in CSNA lasted for 4-5 s and returned to the baseline, even though the motor activity was not ended. The increase of 6 ± 1 beats/min in heart rate appeared with the same time course of the increase in CSNA. In contrast, CVNA never decreased but increased throughout the motor activity, in parallel with a rise in mean arterial blood pressure (MAP). The peak increase in CVNA was 37 ± 9% at 5 s after the motor onset. The rise in MAP gradually developed to 21 ± 2 mmHg and was sustained throughout the spontaneous motor activity. Partial sinoaortic denervation (SAD) blunted the baroreflex sensitivity of the MAP-CSNA and MAP-CVNA relationship to 22-33% of the control. Although partial SAD blunted the initial increase in CSNA to 53% of the control, the increase in CSNA was sustained throughout the motor activity. In contrast, partial SAD almost abolished the increase in CVNA during the motor activity, despite the augmented elevation of 31 ± 1 mmHg in MAP. Because afferent inputs from both muscle receptors and arterial baroreceptors were absent or greatly attenuated in the partial SAD condition, only central command was operating during spontaneous fictive motor activity in decerebrate cats. Therefore, it is likely that central command causes activation of cardiac sympathetic outflow but does not produce withdrawal of cardiac parasympathetic outflow during spontaneous motor activity.

The effects of adrenalectomy and autonomic blockades on the exercise tachycardia in conscious rats.

Heart rate (HR) during exercise is controlled by cardiac sympathetic (CSNA) and vagal (CVNA) efferent nerve activity and plasma catecholamines. To determine their relative contribution to the exercise tachycardia, we examined the effects of adrenalectomy (ADX) and autonomic blockades on the HR response during treadmill exercise for 32min in 13 conscious rats. The baseline HR was not influenced by ADX, suggesting no significant role of adrenal catecholamines on the baseline HR. Since the baseline HR was increased 61beats/min by atropine methyl nitrate (1.5mg/kg) and decreased 26beats/min by atenolol (3mg/kg), CVNA determined the baseline HR more than CSNA. ADX did not affect the immediate increase in HR at 0-12s from the exercise onset but reduced the subsequent increase in HR at 13-30s. These increases in HR at the early period of exercise were more blunted by atenolol than atropine. On the other hand, the peak tachycardia response of 99+/-8beats/min at the end of exercise, which was the same between the intact and ADX conditions, was blunted to 73% by atenolol, to 77% by atropine, and to 35% by combined atenolol and atropine, respectively. In conclusion, it is likely that the tachycardia at the beginning of dynamic exercise is predominantly determined by the cardiac autonomic nerve activity, especially by a prompt increase in CSNA, and that the hormonal mechanism due to adrenal epinephrine contributes to a further increase in HR approximately in 13s from the onset of exercise.