English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Ventilation increases rapidly and significantly in proportion to workload or metabolic rate during dynamic exercise. This increase is called “exercise hyperpnea.” During light to moderate step load exercise, ventilation increases from the first breath and reaches a plateau within 20 s (Phase I), during which metabolites do not reach chemoreceptors; thus Phase I is solely caused by neurogenic drives. It is worthwhile to clarify the aspects of Phase I in order to identify the mechanism of neurally mediated exercise hyperpnea. Until 2000, the mechanisms of exercise hyperpnea during light to moderate step load exercise were assumed to have been derived from two conventional neurogenic drives, “central command,” coming from the motor cortex or the hypothalamus, and “peripheral neural reflex,” originating mainly from the mechanoreceptors in muscles through group III afferents. For about a century there have been a large number of experiments trying to illuminate which mechanism is the cause of exercise hyperpnea. Although central command is thought to be the more likely key source, the consensus is that both central and peripheral neurogenic drives operate ventilation redundantly, building a multiple regulation system during exercise. Recent advantages in technology have enabled us to examine exercise hyperpnea in novel ways. Peripheral neurogenic drive through group III and IV afferents again enters into the limelight by using selective blockers for these afferents without augmenting central command. The vascular distension hypothesis has advocated that a rapid increase in peripheral blood flow is sensed as a plethysmometric change by the mechanoreceptors around the venule near the contracting muscles, stimulating the respiratory center through group IV afferents so as to match ventilation with metabolic rate. On the other hand, “learning” is attracting a growing interest from a central neurogenic point of view. Two types of learning have been proposed: “long term modulation (LTM),” serotonin mediated synaptic adaptation to repeated combined exercise and other stimuli such as an increase in dead space, and “volitional control,” a behavioral and learned response with cognitive function by way of the cerebrum and cerebellum. Nevertheless, these two pathways were derived from, not direct, but circumstantial evidence. The question, “What causes ventilation to increase during exercise?” is not likely to be solved in the near future.

Neural regulation of respiration during exercise -Beyond the conventional central command and afferent feedback mechanisms-