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LETTER TO THE EDITOR
Ventilation and locomotion coupling (entrainment) has been observed and described in rowers during incremental exercise protocols but not during simulated race conditions. The purpose of this descriptive study was to examine ventilation and locomotion entrainment on a breath-by-breath and stroke-by-stroke basis in varsity male rowers during a maximal 2,000-m ergometer test. Eight of eleven rowers entrained ventilation at integral multiples of stroke rate (1:1, 2:1, or 3:1) for at least 120 consecutive seconds, with a 2:1 entrainment pattern being most common. In all 2:1-entrained subjects, inspiration occurred at catch and finish and expiration occurred during the latter portions of drive and recovery. In entrained and unentrained breaths from all rowers, peak flow rates and tidal volumes varied depending on when the breath was initiated during the stroke cycle. Entrained rowers made use of these differences and breathed in a pattern by which they avoided initiating breaths that resulted in reduced tidal volumes. The present data indicated that ventilation was impaired at stroke finish and not at catch, as hypothesized by some previous researchers. Ventilation also appeared to be subordinate to consistent locomotive patterns under race conditions.
To the Editor: Entrainment between cyclic movement and respiration has been observed in a wide variety of locomotor activities, including walking and running, manual wheelchair propulsion, and rowing. To date, however, few generic mechanisms for the occurrence of locomotion-respiration coupling (LRC) have been identified. In search of such causal principles, we reanalyzed recently published data showing LRC in rowing (4). In addition to the frequency doubling in respiration reported by Siegmund et al. (4), detailed time-resolved (cross-)spectral analyses revealed decreases in the stability of entrainment in the vicinity of bifurcations (abrupt changes in frequency relations) as well as switches in the relative phase between the rowing strokes and respiration.
What is causing these patterns of synchronization, the loss of their stability, and subsequent switches to other entrainment forms? We submit that a single physiological although mechanically constrained quantity may be sufficient to explain preferences of frequency and phase locking between locomotion and respiration: energy or, more specifically, the effective value of oxygen concentration in the lungs. Oscillations in abdominal pressure (3) modulate the self-sustaining rhythmic respiration (2), superimposing on the total lung pressure, and cause (local) maxima at integer frequency ratios between movement (rowing strokes) and respiration. Hence, optimization of the effective oxygen concentration can be seen as a driving mechanism that forces respiration to synchronize with rhythmic movement. Because the rowing movements are constrained in a cadence, the optimization is realized by varying the respiration frequency and/or phase. One can model this adaptation dynamically as a stable limit cycle oscillator ("free" respiration) coupled to a periodic force (movement). The explicit coupling is given via the maximization of the effective oxygen level in the lungs. Indeed, such a model can exhibit the empirically observed synchronization patterns. In addition, it provides hints at certain distinct mechanisms that may induce switches between different modes of entrainment (1). In particular, amplitude and phase relations between respiration and movement affect the stability of specific frequency locking ratios and may therefore be seen as the corresponding bifurcation parameters. When searching for a maximal energy transfer, these parameters have to be adjusted properly. If the adjustment is limited and, consequently, the proper frequency relation can no longer be maintained, then the intrinsic structure of lung pressure modulation readily implies a spontaneous switch to another (sub)optimal rational frequency locking state because integer ratios always reflect (local) maxima of effective oxygen concentration.
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The model proposed by Huys et al. fails to consider many alternate possibilities, and the notion that optimization of the oxygen concentration in the lung drives LRC appears overly simplistic given the complexity of the relationship between exercise and ventilation. The mechanisms that mediate the ventilatory responses to exercise have been studied for more than a century and remain controversial. Forster (3) suggested this was because investigators have not yet devised an ideal preparation for its study. Most investigators have agreed on a three-component model to explain the regulation of exercise ventilation: a central medullary rhythm generator/integrator, neural inputs into this integrator from higher locomotor areas of the central nervous system and from the periphery, and the regulation of the distribution of efferent motor output to the muscles of respiration.
Although LRC has been documented in humans engaged in a variety of exercise modalities and in many exercising mammals, little is known about the neural or biomechanical basis for it (1). Evidence for a locomotor-linked neural stimuli to hyperpnea has emerged from animal models with simulated locomotion (2, 5). A feed-forward mechanism ("central command") originates in locomotor areas of the higher central nervous system; this is capable of producing parallel activation of medullary respiratory neurons and motor pathways to limb locomotor muscles and requires no feedback from the periphery. However, direct evidence for central command activation of ventilation during dynamic exercise in humans is lacking, although the rapid increase in ventilation at the onset of exercise supports the concept. Another locomotor-linked ventilatory stimulus is related to the chemical and mechanical conditions of the working muscle. Stimulation of thinly myelinated (group III) or unmyelinated (group IV) muscle afferents provokes powerful ventilatory and circulatory effects. These slowly conducting afferents respond to mechanical, chemical, and thermal stimuli (4).
Clearly, the causal mechanism for LRC in humans is complex and not well understood. Although Huys et al. have proposed one possible mechanism, it is not clear how this fits into the general model of control of exercise hyperpnea.
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