Long-term intermittent hypoxia increases sympathetic activity and chemosensitivity during acute hypoxia in humans

被引:83
作者
Lusina, Sarah-Jane C.
Kennedy, Paul M.
Inglis, J. Timothy
McKenzie, Donald C.
Ayas, Najib T.
Sheel, A. William
机构
[1] Univ British Columbia, Sch Human Kinet, Vancouver, BC V5Z 1M9, Canada
[2] Univ British Columbia, Fac Med, Vancouver, BC V5Z 1M9, Canada
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2006年 / 575卷 / 03期
关键词
D O I
10.1113/jphysiol.2006.114660
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We determined the effects of 10 daily exposures of intermittent hypoxia (IH; 1 h day(-1); oxyhaemoglobin saturation = 80%) on muscle sympathetic nerve activity ( MSNA, peroneal nerve) and the hypoxic ventilatory response (HVR) before, during and after an acute 20 min isocapnic hypoxic exposure. We also assessed the potential parallel-modulation of the ventilatory and sympathetic systems following IH. Healthy young men (n = 11; 25 +/- 1 years) served as subjects and pre- and post-IH measures of MSNA were obtained on six subjects. The IH intervention caused HVR to significantly increase (pre-IH = 0.30 +/- 0.03; post-IH= 0.61 +/- 0.12 l min(-1) % S-aO2(-1)). During the 20 min hypoxic exposure sympathetic activity was significantly greater than baseline and remained above baseline after withdrawal of the hypoxic stimulus, even though oxyhaemoglobin saturation had normalized and ventilation and blood pressure had returned to baseline levels. When compared to the pre- IH trial, burst frequency increased (P < 0.01), total MSNA trended towards higher values ( P = 0.06), and there was no effect on burst amplitude ( P = 0.82) during the post-IH trial. Following IH the rise in MSNA burst frequency was strongly related to the change in HVR (r = 0.79, P < 0.05) suggesting that these sympathetic and ventilatory responses may have common central control.
引用
收藏
页码:961 / 970
页数:10
相关论文
共 43 条
[1]  
Asano K, 1997, AVIAT SPACE ENVIR MD, V68, P104
[2]  
BHATTACH.J, 1973, J PHYSIOL-LONDON, V234, pP112
[3]   Interaction of chemoreceptor and baroreceptor reflexes by hypoxia and hypercapnia - a mechanism for promoting hypertension in obstructive sleep apnoea [J].
Cooper, VL ;
Pearson, SB ;
Bowker, CM ;
Elliott, MW ;
Hainsworth, R .
JOURNAL OF PHYSIOLOGY-LONDON, 2005, 568 (02) :677-687
[4]   Hypoxia-mediated prolonged elevation of sympathetic nerve activity after periods of intermittent hypoxic apnea [J].
Cutler, MJ ;
Swift, NM ;
Keller, DM ;
Wasmund, WL ;
Smith, ML .
JOURNAL OF APPLIED PHYSIOLOGY, 2004, 96 (02) :754-761
[5]  
Dwinell MR, 2000, ADV EXP MED BIOL, V475, P477
[6]   REPETITIVE, EPISODIC HYPOXIA CAUSES DIURNAL ELEVATION OF BLOOD-PRESSURE IN RATS [J].
FLETCHER, EC ;
LESSKE, J ;
WEI, Q ;
MILLER, CC ;
UNGER, T .
HYPERTENSION, 1992, 19 (06) :555-561
[7]   CAROTID CHEMORECEPTORS, SYSTEMIC BLOOD-PRESSURE, AND CHRONIC EPISODIC HYPOXIA MIMICKING SLEEP-APNEA [J].
FLETCHER, EC ;
LESSKE, J ;
BEHM, R ;
MILLER, CC ;
STAUSS, H ;
UNGER, T .
JOURNAL OF APPLIED PHYSIOLOGY, 1992, 72 (05) :1978-1984
[8]   Effects of enhanced human chemosensitivity on ventilatory responses to exercise [J].
Foster, GE ;
McKenzie, DC ;
Sheel, AW .
EXPERIMENTAL PHYSIOLOGY, 2006, 91 (01) :221-228
[9]   Effects of two protocols of intermittent hypoxia on human ventilatory, cardiovascular and cerebral responses to hypoxia [J].
Foster, GE ;
McKenzie, DC ;
Milsom, WK ;
Sheel, AW .
JOURNAL OF PHYSIOLOGY-LONDON, 2005, 567 (02) :689-699
[10]   Effects of intermittent hypoxia on the isocapnic hypoxic ventilatory response and erythropoiesis in humans [J].
Garcia, N ;
Hopkins, SR ;
Powell, FL .
RESPIRATION PHYSIOLOGY, 2000, 123 (1-2) :39-49