scholarly journals Influence of menstrual phase on ventilatory response to submaximal exercise

2006 ◽  
Vol 18 (2) ◽  
pp. 31 ◽  
Author(s):  
T Oosthuiyse ◽  
AN Bosch

Objectives. To determine whether an increase in respiratory drive, due to elevated progesterone and oestrogen concentration during various menstrual phases, persists throughout prolonged submaximal exercise and potentially contributes to fatigue. Furthermore, to determine whether the difference in the ventilatory response to exercise from one menstrual phase to another is correlated to the ovarian hormone concentrations. Design. We compared the change in ventilatory parameters during 90 min exercise at 60%VO2max between the early follicular (EF) and mid-luteal (ML) phase (N = 9) and between the EF and late follicular (LF) phase (N = 5) in eumenorrhoeic women. Main outcome measures. Menstrual phase comparisons and correlations between the change in ventilatory parameters (minute ventilation (VE), respiratory rate (RR), tidal volume) from the EF to ML or from the EF to LF phase and ovarian hormone concentration. Results. The difference in RR between EF and ML phases correlated to progesterone concentration in the ML phase (r = 0.7, p = 0.04). In addition, RR was higher during exercise in the ML compared with EF phase for the full duration of exercise by on average 2.3 ± 2.1 breaths/min (p < 0.05). However, no difference in submaximal VO2 between menstrual phases was evident. No significant difference in exercising-VE was observed between menstrual phases, but the change in VE from EF to ML correlated to oestrogen (r = 0.8, p = 0.02) and progesterone (r = 0.7, p = 0.04) concentration in the ML phase. South African Journal of Sports Medicine Vol. 18 (2) 2006: pp. 31-37

2009 ◽  
Vol 18 (2) ◽  
pp. 31 ◽  
Author(s):  
T Oosthuiyse ◽  
AN Bosch

Objectives. To determine whether an increase in respiratory drive, due to elevated progesterone and oestrogen concentration during various menstrual phases, persists throughout prolonged submaximal exercise and potentially contributes to fatigue. Furthermore, to determine whether the difference in the ventilatory response to exercise from one menstrual phase to another is correlated to the ovarian hormone concentrations. Design. We compared the change in ventilatory parameters during 90 min exercise at 60%VO2max between the early follicular (EF) and mid-luteal (ML) phase (N = 9) and between the EF and late follicular (LF) phase (N = 5) in eumenorrhoeic women. Main outcome measures. Menstrual phase comparisons and correlations between the change in ventilatory parameters (minute ventilation (VE), respiratory rate (RR), tidal volume) from the EF to ML or from the EF to LF phase and ovarian hormone concentration. Results. The difference in RR between EF and ML phases correlated to progesterone concentration in the ML phase (r = 0.7, p = 0.04). In addition, RR was higher during exercise in the ML compared with EF phase for the full duration of exercise by on average 2.3 ± 2.1 breaths/min (p < 0.05). However, no difference in submaximal VO2 between menstrual phases was evident. No significant difference in exercising-VE was observed between menstrual phases, but the change in VE from EF to ML correlated to oestrogen (r = 0.8, p = 0.02) and progesterone (r = 0.7, p = 0.04) concentration in the ML phase. South African Journal of Sports Medicine Vol. 18 (2) 2006: pp. 31-37


1983 ◽  
Vol 54 (4) ◽  
pp. 874-879 ◽  
Author(s):  
D. P. White ◽  
N. J. Douglas ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
C. W. Zwillich

Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.


Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 144
Author(s):  
Hun-Young Park ◽  
Jeong-Weon Kim ◽  
Sang-Seok Nam

We compared the effects of metabolic, cardiac, and hemorheological responses to submaximal exercise under light hypoxia (LH) and moderate hypoxia (MH) versus normoxia (N). Ten healthy men (aged 21.3 ± 1.0 years) completed 30 min submaximal exercise corresponding to 60% maximal oxygen uptake at normoxia on a cycle ergometer under normoxia (760 mmHg), light hypoxia (596 mmHg, simulated 2000 m altitude), and moderate hypoxia (526 mmHg, simulated 3000 m altitude) after a 30 min exposure in the respective environments on different days, in a random order. Metabolic parameters (oxygen saturation (SPO2), minute ventilation, oxygen uptake, carbon dioxide excretion, respiratory exchange ratio, and blood lactate), cardiac function (heart rate (HR), stroke volume, cardiac output, and ejection fraction), and hemorheological properties (erythrocyte deformability and aggregation) were measured at rest and 5, 10, 15, and 30 min after exercise. SPO2 significantly reduced as hypoxia became more severe (MH > LH > N), and blood lactate was significantly higher in the MH than in the LH and N groups. HR significantly increased in the MH and LH groups compared to the N group. There was no significant difference in hemorheological properties, including erythrocyte deformability and aggregation. Thus, submaximal exercise under light/moderate hypoxia induced greater metabolic and cardiac responses but did not affect hemorheological properties.


1995 ◽  
Vol 79 (2) ◽  
pp. 575-580 ◽  
Author(s):  
C. A. Harms ◽  
J. M. Stager

Is inadequate hyperventilation a cause of the exercise-induced hypoxemia observed in some athletes during intense exercise? If so, is this related to low chemoresponsiveness? To test the hypothesis that exercise-induced hypoxemia, inadequate hyperventilation, and chemoresponsiveness are related, 36 nonsmoking healthy men were divided into hypoxemic (Hyp; n = 13) or normoxemic (Nor; n = 15) groups based on arterial oxygen saturation (SaO2; Hyp < or = 90%, Nor > 92%) observed during maximum O2 uptake (VO2max). Men with intermediate SaO2 values (n = 8) were only included in correlation analysis. Ventilatory parameters were collected at rest, during a treadmill maximal oxygen consumption (VO2max) test, and during a 5-min run at 90% VO2max. Chemoresponsiveness at rest was assessed via hypoxic ventilatory response (HVR) and hypercapnic ventilatory response (HCVR). VO2max was not significantly different between Nor and Hyp. SaO2 was 93.8 +/- 0.9% (Nor) and 87.7 +/- 2.0% (Hyp) at VO2max. End-tidal PO2 and the ratio of minute ventilation to oxygen consumption (VE/VO2) were lower while PETCO2 was higher for Hyp (P < or = 0.01). End-tidal PO2, end-tidal PCO2, and VE/VO2 correlated (P < or = 0.05) to SaO2 (r = 0.84, r = -0.70, r = 0.72, respectively), suggesting that differences in oxygenation were due to differences in ventilation. HVR and HCVR were significantly lower for Hyp. HVR was related to VE/VO2 (r = 0.43), and HCVR was related to the ratio of VE to CO2 production at VO2max (r = 0.61)


1983 ◽  
Vol 55 (3) ◽  
pp. 1008-1014 ◽  
Author(s):  
W. A. LaFramboise ◽  
R. D. Guthrie ◽  
T. A. Standaert ◽  
D. E. Woodrum

Dynamic lung compliance (CL), inspiratory pulmonary resistance (RL), and functional residual capacity (FRC) were measured in 10 unanesthetized 48 h-old newborn monkeys and seven 21-day-old infant monkeys during acute exposures to an equivalent level of hypoxemia. End-expiratory airway occlusions were performed and the pressure developed by 200 ms (P0.2) was utilized as an index of central respiratory drive. P0.2 demonstrated a sustained increase throughout the period of hypoxemia on day 2 despite the fact that minute ventilation (VI) initially increased but then fell back to base-line levels. Dynamic lung compliance fell and FRC increased by 5 min of hypoxemia in the newborns. The 21-day-old monkeys exhibited a sustained increase in both VI and P0.2 throughout the hypoxic period with no change in CL and FRC. RL did not change at either postnatal age during hypoxemia. These data indicate that the neonatal monkey is subject to changes in pulmonary mechanics (decreased CL and increased FRC) during hypoxemia and that these changes are eliminated with maturation.


1989 ◽  
Vol 77 (4) ◽  
pp. 431-437 ◽  
Author(s):  
M. A. A. Airlie ◽  
D. C. Flenley ◽  
P. M. Warren

1. In a double-blind placebo-controlled study, we have investigated the effect of the peripheral chemoreceptor stimulant drug almitrine bismesylate on hypoxic ventilatory drive (expressed as the slope of the minute ventilation/arterial oxygen saturation relationship in litres min−1 %−1) as measured by both progressive isocapnic hypoxia at rest and transient hypoxia (three breaths of 100% N2) during moderate exercise, in seven normal men, to determine if the ventilatory response to the transient hypoxic stimulus is a more specific measure of peripheral chemoreceptor sensitivity to hypoxia. 2. Hypoxic ventilatory drive measured using progressive isocapnic hypoxia ranged from −0.13 to −2.65 litres min−1 % −1 after placebo and from − 0.20 to − 6.48 litres min−1 %−1 after almitrine. The response was greater after almitrine in six of the seven subjects, and the difference was significant for the whole group (P < 0.05). 3. Hypoxic ventilatory drive measured using transient hypoxia ranged from −0.19 to −1.59 litres min−1 %−1 after placebo and from −0.09 to −1.62 litres min−1 %−1 after almitrine. The response was not consistently greater after almitrine, and the difference was not significant for the group. 4. Difficulties in accurately quantifying a brief rise in minute ventilation after transient hypoxia, particularly in subjects with a low hypoxic ventilatory drive, may have masked small changes in the slope of the minute ventilation/arterial oxygen saturation relationship with this method. However, the significant increase in the response to progressive isocapnic hypoxia after almitrine suggests that the failure to demonstrate an effect using transient hypoxic stimuli was not solely due to between-day variation in hypoxic ventilatory drive or the small numbers of subjects studied. 5. We conclude that, although transient hypoxia avoids any central depression of ventilation that might result from the prolonged hypoxia used in the conventional steady state or progressive isocapnic methods (thereby leading to underestimation of the hypoxic ventilatory drive), the ventilatory response to such transient stimuli is also affected by factors other than peripheral chemoreceptor activity.


2014 ◽  
Vol 9 ◽  
Author(s):  
Adriano Di Paco ◽  
Giosuè A. Catapano ◽  
Guido Vagheggini ◽  
Stefano Mazzoleni ◽  
Matteo Levi Micheli ◽  
...  

Background: The purpose of this study was to evaluate the role of ventilatory parameters in maximal exercise performance in elite soccer players. Methods: From September 2009 to December 2012, 90 elite soccer players underwent evaluation of lung function test and ergospirometry by means of an incremental symptom-limited treadmill test. Results were analyzed according to i) maximal exercise velocity performed (Hi-M: high-performers, >18.65 km/h; Lo-M: low-performers, <18.65 km/h) and ii) usual role in the team. Results: Hi-M showed higher peak minute ventilation (V_ Epeak: 158.3 ± 19.5 vs 148.0 ± 18.54 L/min, p = 0.0203), and forced expiratory volume at first second (5.28 ± 0.50 vs 4.89 ± 0.52 liters, p < 0.001) than Lo-M, independently of playing role. Moreover, a significant correlation between peak oxygen uptake and V_ E (r = 0.57, p < 0.001) was found. Conclusions: Ventilatory response plays a role in the assessment of exercise capacity in elite soccer players.


1993 ◽  
Vol 74 (4) ◽  
pp. 1916-1920 ◽  
Author(s):  
K. Y. Cao ◽  
M. Berthon-Jones ◽  
C. E. Sullivan ◽  
C. W. Zwillich

In humans the ventilatory [minute ventilation (VI)] response to sustained hypoxia is biphasic: an initial brisk increase followed by a decline is usually seen. However, in adult dogs, the ventilatory response to a similar stimulus shows no decline. To evaluate if central ventilatory drive is altered by sustained hypoxia, we measured the lowest ventilation (nadir) as the lowest moving average of seven sequential breaths within 200 s after transition to hyperoxia (100% O2) after 3 different exposures: room air, 4-min (brief) eucapnic hypoxia (arterial O2 saturation = approximately 80%), and 12-min (prolonged) eucapnic hypoxia. The nadir hyperoxic VI after brief hypoxia (2.7 +/- 0.2 l/min) was similar to that after room air (2.6 +/- 0.2 l/min; P > 0.05), with both less than prior room air mean VI (P < 0.05). The nadir after prolonged hypoxia (3.5 +/- 0.3 l/min) was significantly greater than that after brief hypoxia (P < 0.05). This suggests that central ventilatory drive increases in conscious dogs after sustained eucapnic hypoxia. The reason for the difference in central ventilatory response to hypoxia between conscious dogs and adult humans is unexplained.


Author(s):  
Joel L. Prowting ◽  
Scott Maresh ◽  
Sarah Vaughan ◽  
Elizabeth Kruppe ◽  
Bander Alsabri ◽  
...  

Studies in those with spinal cord injury (SCI) have demonstrated that medications targeting serotonin receptors may decrease the susceptibility to central sleep-disordered breathing (SDB). We hypothesized that mirtazapine would decrease the propensity to develop hypocapnic central sleep apnea (CSA) during sleep. We performed a single-blind pilot study on a total of 10 men with SDB (seven with chronic SCI and three non-injured) aged 52.0±11.2 years. Participants were randomly assigned to either mirtazapine (15mg) or a placebo for at least one week followed by a seven-day washout period before crossing over to the other intervention. Study nights included polysomnography and induction of hypocapnic CSA using a non-invasive ventilation (NIV) protocol. The primary outcome was CO2 reserve, defined as the difference between eupneic and end of NIV PETCO2 preceding induced hypocapneic CSA. Secondary outcomes included controller gain (CG), other ventilatory parameters, and SDB severity. CG was defined as the ratio of change in minute ventilation (V̇e) between control and hypopnea to the change in CO2 during sleep. CO2 reserve was significantly widened on mirtazapine compared to placebo (-3.8±1.2 vs. -2.0±1.5mmHg; p=0.015). CG was significantly decreased on mirtazapine compared to placebo (2.2±0.7 vs. 3.5±1.9L/(mmHg*min); p=0.023). There were no significant differences for other ventilatory parameters assessed or SDB severity between mirtazapine and placebo trials. These findings suggest that the administration of mirtazapine can decrease the susceptibility to central apnea by reducing chemosensitivity and increasing CO2 reserve, however considering the lack of changes in AHI, further research is required to understand this finding's significance.


1981 ◽  
Vol 51 (5) ◽  
pp. 1169-1174 ◽  
Author(s):  
W. A. LaFramboise ◽  
T. A. Standaert ◽  
D. E. Woodrum ◽  
R. D. Guthrie

End-expiratory airway occlusions were performed in eight unanesthetized premature newborn monkeys during acute hypoxemia to investigate mechanisms involved in the newborn's biphasic ventilatory response to hypoxia. Two-day-old monkeys demonstrated an immediate increase in minute ventilation (VI) and a decrease in PaCO2 followed within 5 min by a return of VI and PaCO2 to base-line levels. The decline in VI was associated with a decrease in tidal volume (VT) and inspiratory flow (VT/TI) and an increase in respiratory frequency. Occlusion pressures (PO.2) remained elevated throughout the hypoxic stimulus, and end-expiratory lung volume increased during the late response. “Effective” impedance (P0.1/V0.1, P0.2/V0.2, etc.) and “effective” elastance (Pmax/VT) were also elevated. At 21 days of age, the monkeys demonstrated a sustained ventilatory response as VI, VT, VT/TI, and P0.2 remained elevated throughout the period of hypoxemia. End-expiratory lung volume increases as on day 2, but effective impedance and effective elastance did not change. These data suggest that the biphasic response to hypoxia in the newborn may result from a change in respiratory timing and an alteration in respiratory mechanics and is not due to a decrease in central respiratory drive.


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