scholarly journals Sex differences in diaphragmatic fatigue: the cardiovascular response to inspiratory resistance

2018 ◽  
Vol 596 (17) ◽  
pp. 4017-4032 ◽  
Author(s):  
Joseph F. Welch ◽  
Bruno Archiza ◽  
Jordan A. Guenette ◽  
Christopher R. West ◽  
A. William Sheel
2007 ◽  
Vol 103 (4) ◽  
pp. 1402-1411 ◽  
Author(s):  
Savio W. Wong ◽  
Derek S. Kimmerly ◽  
Nicholas Massé ◽  
Ravi S. Menon ◽  
David F. Cechetto ◽  
...  

In general, cardiac regulation is dominated by the sympathetic and parasympathetic nervous systems in men and women, respectively. Our recent study had revealed sex differences in the forebrain network associated with sympathoexcitatory response to baroreceptor unloading. The present study further examined the sex differences in forebrain modulation of cardiovagal response at the onset of isometric exercise. Forebrain activity in healthy men ( n = 8) and women ( n = 9) was measured using functional magnetic resonance imaging during 5 and 35% maximal voluntary contraction handgrip exercise. Heart rate (HR), mean arterial pressure (MAP), and muscle sympathetic nerve activity (MSNA) were collected in a separate recording session. During the exercise, HR and MAP increased progressively, while MSNA was suppressed ( P < 0.05). Relative to men, women demonstrated smaller HR (8 ± 2 vs. 18 ± 3 beats/min) and MAP (3 ± 2 vs. 11 ± 2 mmHg) responses to the 35% maximal voluntary contraction trials ( P < 0.05). Although a similar forebrain network was activated in both groups, the smaller cardiovascular response in women was reflected in a weaker insular cortex activation. Nevertheless, men did not show a stronger deactivation at the ventral medial prefrontal cortex, which has been associated with modulating cardiovagal activity. In contrast, the smaller cardiovascular response in women related to their stronger suppression of the dorsal anterior cingulate cortex activity, which has been associated with sympathetic control of the heart. Our findings revealed sex differences in both the physiological and forebrain responses to isometric exercise.


1997 ◽  
Vol 73 (2) ◽  
pp. 405-417 ◽  
Author(s):  
Rex A. Wright ◽  
Janie B. Murray ◽  
Parker L. Storey ◽  
Barry J. Williams

2013 ◽  
Vol 305 (7) ◽  
pp. H1098-H1103 ◽  
Author(s):  
Kiril A. Ahtarovski ◽  
Kasper K. Iversen ◽  
Jacob T. Lønborg ◽  
Per L. Madsen ◽  
Thomas Engstrøm ◽  
...  

Men and women are known to react differently to stress. Thus, stress cardiomyopathy almost solely strikes women. Stress cardiomyopathy is suggested to relate to sex differences in catecholamine reaction. Left heart function during dobutamine stress is well described, but sex-specific inotropic and lusitropic response to abrupt termination of dobutamine stress is not. We aimed to investigate sex differences in left ventricular (LV) and atrial (LA) function during and after dobutamine stress. We enrolled 20 healthy elderly subjects (60–70 yr, 10 females) and measured their LV and LA volumes throughout the cardiac cycle by cardiac magnetic resonance imaging at rest, during dobutamine stress (15 μg·kg−1·min−1), 15 min after termination (T15), and 30 min after termination (T30) of dobutamine stress. We calculated LV ejection fractions, LV stroke volumes, LV peak filling rates, and LA passive, active, and conduit volumes. Sex differences were not observed at rest or during dobutamine stress. Compared with prestress values, at T15 a rebound decrease in LV peak filling rate was observed in women (−22 ± 3%, P < 0.001) but not in men. This was reflected in reduced LA passive emptying volume (−40 ± 3%, P < 0.001) and a corresponding increase in LA active emptying volume (36 ± 2%, P < 0.001). At T30 there were no differences between the sexes. We conclude that dobutamine causes greater stress to the female heart. This is revealed after termination of dobutamine stress where the left heart recovers in men, whereas women experience rebound LV stiffening with reduced diastolic relaxation. This is the first report of a sex-specific transient rebound phenomenon in cardiovascular response to catecholamines.


2018 ◽  
Vol 315 (1) ◽  
pp. R68-R75 ◽  
Author(s):  
Eliza Prodel ◽  
Thales C. Barbosa ◽  
Antonio C. Nóbrega ◽  
Lauro C. Vianna

We sought to investigate the possibility that there are sex differences in the cardiovascular responses to trigeminal nerve stimulation (TGS) with cold exposure to the face at rest and during dynamic exercise. In 9 healthy men (age: 28 ± 3 yr; height: 178 ± 1 cm; weight: 77 ± 8 kg) and 13 women (age 26 ± 5 yr; height 164 ± 3 cm; weight 63 ± 7 kg) beat-to-beat heart rate (HR) and blood pressure were recorded. Mean arterial pressure (MAP), stroke volume (SV), cardiac index (CI), and total vascular resistance index (TVRI) were calculated. TGS was applied for 3 min at rest and in-between 10-min steady-state cycling exercise at a HR of 110 beats/min, the measurements were obtained during the last minute of each period. At rest, TGS increased MAP (men: Δ18 ± 8 mmHg; women: Δ23 ± 8 mmHg; means ± SD), TVRI (men: Δ1.1 ± 0.6 mmHg·l−1·min·m−2; women: Δ1.2 ± 1.2 mmHg·l−1·min·m−2) and SV (men: Δ19 ± 15 ml; women: Δ16 ± 11 ml) in both groups. CI increased with TGS in women but not in men. However, men presented a bradycardic response to TGS (Δ−11 ± 8 beats/min) that was not significant in women compared with baseline. Cycling exercise increased HR, MAP, SV, and CI and decreased TVRI in men and women. TGS during exercise further increased MAP in men and women and did not change CI in either group. SV and TVRI increased with TGS during exercise only in women. TGS during exercise evoked bradycardia in men (Δ−7 ± 9 beats/min), whereas HR was unchanged in women. Our findings indicate sex differences in TGS-related cardiovascular responses at rest and during exercise.


2019 ◽  
Vol 17 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Zewen Chen ◽  
Lei Wang ◽  
Jun Ke ◽  
Daliao Xiao

Background: Epidemiological studies and experimental studies have demonstrated that intrauterine adverse environment increases the risk of Cardiovascular Disease (CVD) in adulthood. However, whether an individual develops a cardiovascular dysfunctional phenotype may depend on genetic background, age, and sex. </P><P> Methods: In this review, we summarize some of the recent experimental animal studies in the developmental programming of adult CVD with an emphasis on sex differences and the potential role of estrogen in mediating sexual dimorphism. </P><P> Results: Few epidemiological studies report the effect of sex on the developmental programming of CVD. However, numerous experimental animal studies have shown a sex difference in fetal programming of adult cardiovascular dysfunction. Most of the animal studies indicate that male offspring develop cardiovascular dysfunction and CVD in adulthood, whereas adult females appear to be protected. Estrogen is one of the key factors that contributes to the sex difference of adult CVD. Estrogen/its Receptor (ER) may interact with the RAS system by changes of DNA methylation patterns at the target gene promoter, serve as an antioxidant to counteract the prenatal insults-induced heightened ROS, and function as an eNOS activator to increase vasodilation, resulting in the protection of female offspring from the development of hypertension and other CVDs. </P><P> Conclusion: These studies suggest that estrogen/ER may contribute to sex differences in cardiovascular response to an adverse intrauterine environment and play a significant role in modulating the cardiovascular response in adulthood.


Author(s):  
Jordan A. Guenette ◽  
Lee M. Romer ◽  
Jordan S. Querido ◽  
Romeo Chua ◽  
Neil D. Eves ◽  
...  

2018 ◽  
Vol 596 (19) ◽  
pp. 4579-4580
Author(s):  
Christina D. Bruce ◽  
Alexandra F. Yacyshyn ◽  
Luca Ruggiero

2016 ◽  
Vol 16 (C) ◽  
pp. 89
Author(s):  
Wesley K. Lefferts ◽  
Jacqueline A. Augustine ◽  
Kayla M. Nunemacher ◽  
Kevin S. Heffernan

1979 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
D. Gross ◽  
A. Grassino ◽  
W. R. Ross ◽  
P. T. Macklem

We studied the effect of breathing at various levels of transdiaphragmatic pressure (Pdi) on the EMG power spectrum of the diaphragm. The diaphragmatic EMG was measured simultaneously with a bipolar esophageal electrode (EE) and surface electrode (SE) placed on the ventral portion of the sixth and seventh intercostal spaces in five normal subjects breathing at functional residual capacity (FRC) against an inspiratory resistance. During each fatigue run the subjects generated a Pdi, with each inspiration, that was 25, 50, or 75% of maximum Pdi (Pdimax) for a period up to 15 min. During runs at 50 and 75% of the Pdimax, which are known to produce fatigue, we found for both EE and SE a progressive increase in the amplitude of the low-frequency (L = 20-46.7 Hz) and a decrease in the high-frequency (H = 150-350 Hz) component of the EMG. These changes were not seen at 25% of Pdimax. The diaphragmatic H/L ratio was independent of Pdi when the diaphragm was not fatigued. H/L fell while the diaphragm performed fatiguing work and this was more rapid at higher Pdi's. It was thus concluded that frequency spectrum analysis of the EMG can detect diaphragmatic fatigue reliably, prior to the time when the diaphragm fails as a pressure generator.


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