Altered ventilatory responses to exercise testing in young adult men with obstructive sleep apnea

Laboratory for Health and Exercise Science, Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
Respiratory medicine (Impact Factor: 2.92). 02/2009; 103(7):1063-9. DOI: 10.1016/j.rmed.2009.01.010
Source: PubMed

ABSTRACT Obstructive sleep apnea (OSA) is a disorder characterized by repetitive obstructions of the upper airway. Individuals with OSA experience intermittent hypoxia, hypercapnia, and arousals during sleep, resulting in increased sympathetic activation. Chemoreflex activation, arising from the resultant oscillatory disturbances in blood gases from OSA, exerts control over ventilation, and may induce increases in sympathetic vasoconstriction, contributing to increased long-term risks for hypertension (HTN) and cardiovascular disease (CVD).
To evaluate whether OSA elicits exaggerated ventilatory responses to exercise in young men, 14 overweight men with OSA and 16 overweight men without OSA performed maximal ramping cycle ergometer exercise tests. Oxygen consumption (VO(2)), ventilation, (V(E)), ventilatory equivalents for oxygen (V(E)/VO(2)) and carbon dioxide (V(E)/VCO(2)), and V(E)/VCO(2) slope were measured.
The VO(2) response to exercise did not differ between groups. The V(E), V(E)/VCO(2), V(E)/VO(2) were higher (p< 0.05, 0.002, and p<0.02, respectively) in the OSA group across all workloads. The V(E)/VCO(2) slope was greater in the OSA group (p<0.05). The V(E)/VCO(2) slope and AHI were significantly correlated (r=0.56, p<0.03). Thus, young, overweight men with OSA exhibit increased ventilatory responses to exercise when compared to overweight controls. This may reflect alterations in chemoreflex sensitivity, and contribute to increased sympathetic drive and HTN risk.


Available from: William G Herbert, Jan 14, 2014
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obese subjects commonly suffer from exertional dyspnea and exercise intolerance. Preliminary evidence suggests that treatment with nocturnal continuous positive airway pressure (nCPAP) may improve dyspnea in obese patients with obstructive sleep apnea (OSA), but the effect on exercise tolerance is unknown. This study sought to investigate whether nCPAP improves exercise tolerance and exertional dyspnea in obese patients with OSA. Obese patients prescribed nCPAP for moderate/severe OSA and without cardiopulmonary disease were recruited. Patients completed a constant-load exercise test and Baseline and Transitional Dyspnea Index questionnaires (BDI/TDI) at baseline and after one and three months of nCPAP. Primary outcome was change in constant-load exercise time from baseline to one and three months. Secondary outcomes included changes in isotime dyspnea, isotime leg fatigue and BDI/TDI score at one and three months. Fifteen subjects (body mass index = 43 kg m(-2), apnea-hypopnea index = 49(.)hr(-1)) were studied. Constant-load exercise time increased by 2.0 min (40%, p = 0.02) at one month and 1.8 min (36%, p = 0.04) at three months. At one and three months, isotime dyspnea decreased by 1.4 (p = 0.17) and 2 units (p = 0.04), and leg fatigue decreased by 1.2 (p = 0.18) and 2 units (p = 0.02), respectively. BDI/TDI scores were 2.7 (p = 0.001) and 4.5 points (p < 0.001) at one and three months. Peak oxygen consumption and static pulmonary function were unchanged. Nocturnal CPAP improves exercise tolerance and dyspnea in obese patients with OSA. Effects on exercise time and chronic dyspnea were seen after one and three months of nCPAP, while exertional dyspnea was only improved at three months.
    Respiratory medicine 10/2011; 105(10):1565-71. DOI:10.1016/j.rmed.2011.06.007
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is a national health issue in the US. Among the many physiological changes induced by obesity, it also presents a unique challenge to ventilatory control during exercise due to increased metabolic demand of moving larger limbs, increased work of breathing due to extra weight on the chest wall, and changes in breathing mechanics. These challenges to ventilatory control in obesity can be inconspicuous or overt among obese adults but for the most part adaptation of ventilatory control during exercise in obesity appears remarkably unnoticed in the majority of obese people. In this brief review, the changes to ventilatory control required for maintaining normal ventilation during exercise will be examined, especially the interaction between respiratory neural drive and ventilation. Also, gaps in our current knowledge will be discussed.
    Respiratory Physiology & Neurobiology 05/2013; 189(2). DOI:10.1016/j.resp.2013.05.019
  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: Obstructive sleep apnea (OSA) predisposes individuals to cardiovascular morbidity, and cardiopulmonary exercise test (CPET) markers prognostic for cardiovascular disease have been found to be abnormal in adults with OSA. Due to the persistence of OSA and its cardiovascular consequences, whether the cardiovascular adaptations normally conferred by exercise are blunted in adults not utilizing established OSA treatment is unknown. The aims of this study were to document whether OSA participants have abnormal CPET responses and determine whether exercise modifies these CPET markers in individuals with OSA. METHODS: The CPET responses of 43 sedentary, overweight adults (body mass index [BMI]>25) with untreated OSA (apnea-hypopnea index [AHI]≥15) were compared against matched non-OSA controls (n=9). OSA participants were then randomized to a 12-week exercise training (n=27) or stretching control treatment (n=16), followed by a post-intervention CPET. Measures of resting, exercise, and post-exercise recovery heart rate (HRR), blood pressure, and ventilation, as well as peak oxygen consumption (VO(2peak)), were obtained. RESULTS: OSA participants had blunted HRR compared to non-OSA controls at 1 (P=.03), 3 (P=.02), and 5-min post-exercise (P=.03). For OSA participants, exercise training improved VO(2peak) (P=.04) and HRR at 1 (P=.03), 3 (P<.01), and 5-min post-exercise (P<.001) compared to control. AHI change was associated with change in HRR at 5-min post-exercise (r=-.30, P<.05), but no other CPET markers. CONCLUSIONS: These results suggest that individuals with OSA have autonomic dysfunction, and that exercise training, by increasing HRR and VO(2peak), may attenuate autonomic imbalance and improve functional capacity independent of OSA severity reduction.
    International journal of cardiology 05/2012; 167(4). DOI:10.1016/j.ijcard.2012.04.108