Identification of higher brain centres that may encode the cardiorespiratory response to exercise in humans (original) (raw)
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Acta Physiologica, 2012
Aim: The neural structures responsible for the coupling between ventilatory control and pulmonary gas exchange during exercise have not been fully identified. Suprapontine mechanisms have been hypothesized but not formally evidenced. Because the involvement of a premotor circuitry in the compensation of inspiratory mechanical loads has recently been described, we looked for its implication in exercise-induced hyperpnea. Methods: Electroencephalographical recordings were performed to identify inspiratory premotor potentials (iPPM) in eight physically fit normal men during cycling at 40 and 70% of their maximal oxygen consumption ( _ VO 2max ). Relaxed pedalling (0 W) and voluntary sniff manoeuvres were used as negative and positive controls respectively. Results: Voluntary sniffs were consistently associated with iPPMs. This was also the case with voluntarily augmented breathing at rest (in three subjects tested). During the exercise protocol, no respiratory-related activity was observed whilst performing bouts of relaxed pedalling. Exercise-induced hyperpnea was also not associated with iPPMs, except in one subject. Conclusion: We conclude that if there are cortical mechanisms involved in the ventilatory adaptation to exercise in physically fit humans, they are distinct from the premotor mechanisms activated by inspiratory load compensation.
Identifying cardiorespiratory neurocircuitry involved in central command during exercise in humans
The Journal of Physiology, 2006
For almost one hundred years, the exact role of human brain structures controlling the cardiorespiratory response to exercise ('central command') has been sought. Animal experiments and functional imaging studies have provided clues, but the underlying electrophysiological activity of proposed relevant neural sites in humans has never been measured. In this study, local field potentials were directly recorded in a number of 'deep' brain nuclei during an exercise task designed to dissociate the exercise from peripheral feedback mechanisms. Several patient groups had electrodes implanted sterotaxically for the treatment of movement disorder or chronic pain. Fast Fourier transform analysis was applied to the neurograms to identify the power of fundamental spectral frequencies. Anticipation of exercise resulted in increases in heart rate, blood pressure and ventilation. The greatest neural changes were found in the periaqueductal grey area (PAG) where anticipation of exercise was accompanied by an increase of 43% in the power of the 12-25 Hz frequency band (P = 0.007). Exercise increased the activity by 87% compared to rest (P = 0.006). Changes were also seen in the 60-90 Hz band when anticipation or exercise increased power by 32% (P = 0.006) and 109% (P < 0.001), respectively. In the subthalamic nucleus there was a reduction in the power of the beta frequency during both anticipation (7.6 ± 0.68% P = 0.001) and exercise (17.3 ± 0.96% P < 0.001), whereas an increase was seen with exercise only at higher frequencies (93 ± 1.8% P = 0.007). No significant changes were seen in the globus pallidus during anticipation of exercise. We provide direct electrophysiological evidence highlighting the PAG as an important subcortical area in the neural circuitry of the cardiorespiratory response to exercise, since stimulation of this structure is known to alter blood pressure in awake humans.
1989
To investigate the relative contributions of the central and peripheral neural drive to hyperventilation at the onset of muscular exercise, five volunteers were tested during the first ten breaths while performing both voluntary (VM) and passive (PM) ankle rotations with a frequency of 1 Hz and through an angle of 10°. Resulting breathing patterns for the two movements were compared. Hypocapnic hyperventilation, found in both PM and VM, indicated its neural origin. Respiratory changes were higher in VM than in PM. In both experimental conditions, increases in ventilation ( dotVE\dot V_E dotVE ) depended more on respiratory frequency (f) than on tidal volume (V T). Moreover, increases inV T adapted, breath-by-breath, to values lower than the initial ones, while increases inf rose progressively. Expiratory time was reduced more than inspiratory time (T I); increases in inspiratory flow (V T/T I) depended to the same extent on changes in bothT I andV T. Increases in expiratory tidal volume were initially higher than in inspiratory tidal volume, thereby producing a reduction in functional residual capacity. Because PM respiratory changes could be considered to be of nervous reflex origin only, the identical breathing patterns in PM and VM indicated that the hyperventilation found also in VM was mainly of reflex origin. The increase in dotVE\dot V_E dotVE was considered to be dependent on a greater stimulus from muscle proprioreceptors.
Respiratory response to passive limb movement is suppressed by a cognitive task
Journal of Applied Physiology, 2004
Bell, Harold J., and James Duffin. Respiratory response to passive limb movement is suppressed by a cognitive task. Feedback from muscles stimulates ventilation at the onset of passive movement. We hypothesized that central neural activity via a cognitive task source would interact with afferent feedback, and we tested this hypothesis by examining the fast changes in ventilation at the transition from rest to passive leg movement, under two conditions: 1) no task and 2) solving a computer-based puzzle. Resting breathing was greater in condition 2 than in condition 1, evidenced by an increase in mean Ϯ SE breathing frequency (18.2 Ϯ 1.1 vs. 15.0 Ϯ 1.2 breaths/min, P ϭ 0.004) and ventilation (10.93 Ϯ 1.16 vs. 9.11 Ϯ 1.17 l/min, P Ͻ 0.001). In condition 1, the onset of passive movement produced a fast increase in mean Ϯ SE breathing frequency (change of 2.9 Ϯ 0.4 breaths/min, P Ͻ 0.001), tidal volume (change of 233 Ϯ 95 ml, P Ͻ 0.001), and ventilation (change of 6.00 Ϯ 1.76 l/min, P Ͻ 0.001). However, in condition 2, the onset of passive movement only produced a fast increase in mean Ϯ SE breathing frequency (change of 1.3 Ϯ 0.4 breaths/min, P ϭ 0.045), significantly smaller than in condition 1 (P ϭ 0.007). These findings provide evidence for an interaction between central neural cognitive activity and the afferent feedback mechanism, and we conclude that the performance of a cognitive task suppresses the respiratory response to passive movement. exercise hyperpnea; wakefulness drive; afferent feedback Address for reprint requests and other correspondence: J. Duffin,
The Japanese Journal of Physiology, 1987
The possible influence of neurogenic factors on respiratory and circulatory responses to continuous static (CSE), rhythmic static (RSE), and dynamic (DE) exercises was studied in 15 healthy young men. Ventilation (VE), oxygen uptake (Vo 2), cardiac output (Q), and blood pressure (BP) were measured during the steady-state of the exercise. For a given V02, VE, and respiratory frequency (f) enhanced significantly with increasing frequency of RSE, and for the same frequency, the responses of these variables to RSE were significantly higher than those for DE. Although a similar trend was observed in heart rate (HR) and Q responses to exercises, it was not as strong as for ventilatory responses. These results lead to the conclusion that ventilation and circulation during exercise may be influenced by some neurogenic factors mediated either centrally or peripherally.
A review of the control of breathing during exercise
European Journal of Applied Physiology and Occupational Physiology, 1995
During the past 100 years many experimental investigations have been carried out in an attempt to determine the control mechanisms responsible for generating the respiratory responses observed during incremental and constant-load exercise tests. As a result of these investigations a number of different and contradictory control mechanisms have been proposed to be the sole mediators of exercise hyperpnea. However, it is now becoming evident that none of the proposed mechanisms are solely responsible for eliciting the exercise respiratory response. The present-day challenge appears to be one of synthesizing the proposed mechanisms, in order to determine the role that each mechanism has in controlling ventilation during exercise. This review, which has been divided into three primary sections, has been designed to meet this challenge. The aim of the first section is to describe the changes in respiration that occur during constant-load and incremental exercise. The second section briefly introduces the reader to traditional and contemporary control mechanisms that might be responsible for eliciting at least a portion of the exercise ventilatory response during these types of exercise. The third section describes how the traditional and contemporary control mechanisms may interact in a complex fashion to produce the changes in breathing associated with constant-load exercise, and incorporates recent experimental evidence from our laboratory.
The role of central command in ventilatory control during static exercise
European Journal of Applied Physiology and Occupational Physiology, 1994
The role of central command in the respiratory response to 15 min of rhythmic-static (isometric) exercise was studied in humans. Voluntary exercise (VE) was compared with electrically induced exercise (EE) at three different work intensities, i.e. 5%, 15% and 25% of maximal voluntary contraction. A group of 12 volunteers participated in the study and each of them performed six sessions. A session consisted of at least 5 min rest, 15 min rhythmic-static single leg exercise (4 s contraction/12 s relaxation) and at least 5 min recovery..Force, minute ventilation (VE) and oxygen uptake (V02) were measured. In EE, both l~ E and VO2 increased continuously during the entire exercise period after an initial rapid increase at all three work intensities. Correlation between I?E and 1202 was highly significant during EE. During all three work intensities of VE, VE and 1202 achieved a steady-state after the initial increase: During VE, I?E did not correlate as closely with 1202 as during EE. All these findings indicate that central command was not imperative for an adequate ventilatory response to exercise within all three work intensities investigated. Without the influence of central command, correlation between I?E and 1202 was even better than during VE.
Modulation of the ventilatory increase at the onset of exercise in humans
Respiration physiology, 1997
The fast initial increase in ventilation at the start of exercise is generally assumed to be of reflex origin (exercising limbs) and/or caused by a 'feedforward' mechanism increasing breathing via brainstem respiratory centres or cortical areas controlling respiratory muscles. We wanted to test whether this ventilatory increase is in part a learned response which can be modified. Eleven subjects did two 20 min low-intensity arm-cranking exercise bouts on eight different days. Seven subjects were assigned to the experimental group which performed exercise paired with an 1.5 L external dead space. Before and after their eight exercise 'training'-days, these subjects did the same exercise without dead space. At the beginning of the first post-training exercise test (without dead space), the ventilatory increase at the start of exercise (sum of the first four breaths) was significantly increased (31.1 +/- 4.1 L . min-1) compared to the pre-training test session (24.4 +/-...
Advances in experimental medicine and biology, 2010
The present study examined the regional differences of cortical oxygenation in the frontal lobe by near-infrared spectroscopy (NIRS) during incremental exercise tests and the precise location of NIRS was examined by brain magnetic resonance imaging (MRI). Pulmonary gas exchange and NIRS measurement during incremental cycling ergometry tests were investigated in 14 men. In 7 of these subjects, the right middle cerebral artery mean velocity (MCA Vmean) was simultaneously measured by transcranial Doppler (TCD). In the right medial of the frontal lobe cortex, Tissue Oxygenation Index (TOI) increased by 8.8% with its peak value at respiratory compensation threshold (RCT) and Normalized Tissue Hemoglobin Index (nTHI) increased until endpoint by 16.2%. During incremental exercise tests, the changing pattern of TOI was different according to the distribution of the probes. Volitional exhaustion by exercise induced the deteriorated TOI and MCA Vmean, whereas nTHI increased.
1995
Abstract 1. The cardiorespiratory response to imagination of previously performed treadmill exercise was measured in six competitive sportsmen and six non-athletic males. This was compared with the response to a control task (imaging letters) and a task not involving imagination ('treadmill sound only'). 2. In athletes, imagined exercise produced increases in ventilation which varied within and between subjects. The mean maximal increase (11.71 min-1) was approximately 20% of the ventilatory response to actual exercise.