Abstract

In goats, repeated exposure to moderate steady-state exercise with an added deadspace has been shown to alter the ventilatory response to subsequent exercise tests [1], a phenomenon termed long-term modulation (LTM). There are few relevant studies in humans, but it has been proposed that LTM can be achieved by a form of associative conditioning involving exercise and hypercapnia [2]. However, such data as there is would appear to be conflicting [3,4]. We have further investigated this phenomenon in humans in an attempt to resolve the disparity. After providing informed consent as approved by the Local Ethics Committee, and familiarisation, 16 subjects (9 female, age 22.4 ± 2.7 years) were randomly divided into two groups; a control group (8 subjects, 5 female) and an intervention group (8 subjects, 4 female). The Intervention protocol consisted an initial (pre) steady-state exercise bout (100 W, 5 min) on a cycle ergometer, followed by a 'conditioning session' of 10 repeated bouts of steady-state exercise (100 W) while breathing through an additional deadspace (+VD = 1.35 l). Two post-conditioning steady-state exercise tests (100 W, 5 min) were performed, one 7 min after (post1) and one 1 h after (post2) the end of the last conditioning bout. Each bout was interposed by a 7-min period of unencumbered rest. The control group protocol was identical to the Intervention protocol, except that at no time was exercise associated with an added deadspace. Breath-by-breath recordings for ventilatory parameters and respired gases (including PetCO2) were measured during exercise (Morgan Benchmark, Kent). The results are given in Table ​Table11. Table 1 Changes in exercise response following conditioning. Post-conditioning ventilation was not augmented in either group. Respiratory frequency was increased significantly in both groups post-conditioning, whilst both tidal volume and PetCO2 were reduced in both groups. The magnitude of the changes in the pattern of breathing and the PetCO2 were similar between groups at both post-conditioning assessments. The mechanisms underlying these changes are not immediately obvious, but the results do not support the concept of a LTM of exercise ventilation dependant on associative conditioning.

Highlights

  • To be effective, inspiratory muscles on the left and right sides must contract together

  • We have found that a prominent gap in the column of ventral respiratory group (VRG) The nucleus tractus solitarii (NTS) relays information from primary related parvalbumin cells [2] likely corresponds to the pBc since visceral receptors to the central nervous system and is critically parvalbumin cells are rare in this zone and never co-localize with involved in the reflex control of autonomic functions

  • The specific protein(s) necessary for longterm facilitation (LTF) is unknown, we recently found that episodic hypoxia and LTF are associated with elevations in ventral spinal concentrations of brain derived neurotrophic factor (BDNF)

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Summary

Introduction

Inspiratory muscles on the left and right sides must contract together. The left and right halves of the diaphragm are synchronised because a bilateral population of medullary premotor neurones [1] simultaneously excites left and right phrenic motoneurones. Transection studies demonstrate that each side of the brainstem is capable of generating respiratory rhythm independently [2], so that left and right medullary inspiratory neurones must themselves be synchronised. The interconnections and common excitation that accomplish such synchronisation are unknown in rats. The respiratory rhythm of hypoglossal (XII) nerve discharge in transverse medullary slice preparations from neonatal rats is thought to originate in the region of the ventral respiratory group (VRG); generated there by a combination of “pacemaker” neurones [1] and their interactions with other respiratory neurones. Our goal was to discover interconnections between left and right VRG neurones as well as their connections to XII motoneurones

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