Adaptation of the respiratory controller contributes to the attenuation of exercise hyperpnea in endurance-trained athletes |
| |
Authors: | Email author" target="_blank">Tadayoshi?MiyamotoEmail author Masashi?Inagaki Hiroshi?Takaki Toru?Kawada Toshiaki?Shishido Atsunori?Kamiya Masaru?Sugimachi |
| |
Institution: | (1) Faculty of Health Sciences, Morinomiya University of Medical Sciences, 1-26-16 Nanko-Kita, Suminoe-Ku, Osaka City Osaka, 559-0034, Japan;(2) Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center Research Institute, Suita City Osaka, 565-8565, Japan |
| |
Abstract: | We have reported that minute ventilation
(V)\dot]\textE \dot{V}_{\text{E}} ] and end-tidal CO2 tension
P\textETCO 2 P_{{{\text{ETCO}}_{ 2} }} ] are determined by the interaction between central controller and peripheral plant properties. During exercise, the controller
curve shifts upward with unchanged central chemoreflex threshold to compensate for the plant curve shift accompanying increased
metabolism. This effectively stabilizes
P\textETCO 2 P_{{{\text{ETCO}}_{ 2} }} within the normal range at the expense of exercise hyperpnea. In the present study, we investigated how endurance-trained
athletes reduce this exercise hyperpnea. Nine exercise-trained and seven untrained healthy males were studied. To characterize
the controller, we induced hypercapnia by changing the inspiratory CO2 fraction with a background of hyperoxia and measured the linear
P\textETCO 2 - (V)\dot]\textE P_{{{\text{ETCO}}_{ 2} }} - \dot{V}_{\text{E}} relation
(V)\dot]\textE = S (P\textETCO2 - B) \dot{V}_{\text{E}} = S\, (P_{{{\text{ETCO}}_{2} }} - {\rm B}) ]. To characterize the plant, we instructed the subjects to alter
(V)\dot]\textE \dot{V}_{\text{E}} voluntarily and measured the hyperbolic
(V)\dot]\textE - P\textETCO 2 \dot{V}_{\text{E}} - P_{{{\text{ETCO}}_{ 2} }} relation (
P\textETCO 2 = A/(V)\dot]\textE + C P_{{{\text{ETCO}}_{ 2} }} = A/\dot{V}_{\text{E}} + C ). We characterized these relations both at rest and during light exercise. Regular exercise training did not affect the characteristics
of either controller or plant at rest. Exercise stimulus increased the controller gain (S) both in untrained and trained subjects.
On the other hand, the
P\textETCO 2 P_{{{\text{ETCO}}_{ 2} }} -intercept (B) during exercise was greater in trained than in untrained subjects, indicating that exercise-induced upward shift of the
controller property was less in trained than in untrained subjects. The results suggest that the additive exercise drive to
breathe was less in trained subjects, without necessarily a change in central chemoreflex threshold. The hyperbolic plant
property shifted rightward and upward during exercise as predicted by increased metabolism, with little difference between
two groups. The
(V)\dot]\textE \dot{V}_{\text{E}} during exercise in trained subjects was 21% lower than that in untrained subjects (P < 0.01). These results indicate that an adaptation of the controller, but not that of plant, contributes to the attenuation
of exercise hyperpnea at an iso-metabolic rate in trained subjects. However, whether training induces changes in neural drive
originating from the central nervous system, afferents from the working limbs, or afferents from the heart, which is additive
to the chemoreflex drive to breathe, cannot be determined from these results. |
| |
Keywords: | |
本文献已被 PubMed SpringerLink 等数据库收录! |
|