Department of Kinesiology and Health Sciences, Faculty of Health, University of Waterloo, Waterloo, Ontario, Canada.
Schlegel-UW Research Institute for Aging, Waterloo, Ontario, Canada.
Exp Physiol. 2023 Apr;108(4):636-649. doi: 10.1113/EP090779. Epub 2023 Feb 8.
What is the central question of this study? Is the attenuation of the respiratory muscle metaboreflex preserved after detraining? What is the main finding and its importance? Inspiratory muscle training increased respiratory muscle strength and attenuated the respiratory muscle metaboreflex as evident by lower heart rate and blood pressure. After 5 weeks of no inspiratory muscle training (detraining), respiratory muscle strength was still elevated and the metaboreflex was still attenuated. The benefits of inspiratory muscle training persist after cessation of training, and attenuation of the respiratory metaboreflex follows changes in respiratory muscle strength.
Respiratory muscle training (RMT) improves respiratory muscle (RM) strength and attenuates the RM metaboreflex. However, the time course of muscle function loss after the absence of training or 'detraining' is less known and some evidence suggest the respiratory muscles atrophy faster than other muscles. We sought to determine the RM metaboreflex in response to 5 weeks of RMT and 5 weeks of detraining. An experimental group (2F, 6M; 26 ± 4years) completed 5 weeks of RMT and tibialis anterior (TA) training (each 5 days/week at 50% of maximal inspiratory pressure (MIP) and 50% maximal isometric force, respectively) followed by 5 weeks of no training (detraining) while a control group (1F, 7M; 24 ± 1years) underwent no intervention. Prior to training (PRE), post-training (POST) and post-detraining (DETR), all participants underwent a loaded breathing task (LBT) to failure (60% MIP) while heart rate and mean arterial blood pressure (MAP) were measured. Five weeks of training increased RM (18 ± 9%, P < 0.001) and TA (+34 ± 19%, P < 0.001) strength and both remained elevated after 5 weeks of detraining (MIP-POST vs. MIP-DETR: 154 ± 31 vs. 153 ± 28 cmH2O, respectively, P = 0.853; TA-POST vs. TA-DETR: 86 ± 19 vs. 85 ± 16 N, respectively, P = 0.982). However, the rise in MAP during LBT was attenuated POST (-11 ± 17%, P = 0.003) and DETR (-9 ± 9%, P = 0.007) during the iso-time LBT. The control group had no change in MIP (P = 0.33), TA strength (P = 0.385), or iso-time MAP (P = 0.867) during LBT across all time points. In conclusion, RM and TA have similar temporal strength gains and the attenuation of the respiratory muscle metaboreflex remains after 5 weeks of detraining.
本研究的核心问题是什么？呼吸肌代谢反射的衰减在停训后是否得到保留？主要发现及其重要性是什么？吸气肌训练增加了呼吸肌力量，并降低了心率和血压，从而减弱了呼吸肌代谢反射。经过 5 周的不进行吸气肌训练（停训）后，呼吸肌力量仍然升高，代谢反射仍然减弱。吸气肌训练的益处在停止训练后仍然存在，而呼吸肌力量的变化伴随着代谢反射的减弱。
呼吸肌训练（RMT）可改善呼吸肌（RM）力量并减弱 RM 代谢反射。然而，人们对训练停止后肌肉功能丧失的时间过程知之甚少，并且一些证据表明呼吸肌比其他肌肉更快地萎缩。我们试图确定 5 周 RMT 和 5 周停训后 RM 代谢反射。实验组（2F，6M；26±4 岁）完成了 5 周的 RMT 和胫骨前肌（TA）训练（分别为 50%最大吸气压力（MIP）和 50%最大等长力，每天 5 天/周），随后进行了 5 周的无训练（停训），而对照组（1F，7M；24±1 岁）未进行干预。在训练前（PRE）、训练后（POST）和停训后（DETR），所有参与者在加载呼吸任务（LBT）中达到衰竭（60% MIP），同时测量心率和平均动脉血压（MAP）。5 周的训练增加了 RM（18±9%，P<0.001）和 TA（+34±19%，P<0.001）的力量，并且在 5 周的停训后仍然保持升高（MIP-POST 与 MIP-DETR：154±31 与 153±28 cmH2O，分别，P=0.853；TA-POST 与 TA-DETR：86±19 与 85±16 N，分别，P=0.982）。然而，在等时 LBT 期间，MAP 升高在 POST（-11±17%，P=0.003）和 DETR（-9±9%，P=0.007）期间减弱。对照组在整个时间点的 LBT 期间，MIP（P=0.33）、TA 力量（P=0.385）或等时 MAP（P=0.867）均无变化。总之，RM 和 TA 的力量在时间上具有相似的增长，并且在 5 周的停训后，呼吸肌代谢反射的衰减仍然存在。
