Recovery Kinetics of Oxygen Uptake Is Abnormally Prolonged in Patients with Mustard/Senning Repair for Transposition of the Great Arteries (original) (raw)
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Jendzjowsky NG, Tomczak CR, Lawrance R, Taylor DA, Tymchak WJ, Riess KJ, Warburton DE, Haykowsky MJ. Impaired pulmonary oxygen uptake kinetics and reduced peak aerobic power during small muscle mass exercise in heart transplant recipients. We examined peak and reserve cardiovascular function and skeletal muscle oxygenation during unilateral knee extension (ULKE) exercise in five heart transplant recipients (HTR, mean Ϯ SE; age: 53 Ϯ 3 years; years posttransplant: 6 Ϯ 4) and five age-and body mass-matched healthy controls (CON). Pulmonary oxygen uptake (V O2p), heart rate (HR), stroke volume (SV), cardiac output (Q ), and skeletal muscle deoxygenation (HHb) kinetics were assessed during moderate-intensity ULKE exercise. Peak exercise and reserve V O2p, Q , and systemic arterial-venous oxygen difference (a-vO 2diff) were 23-52% lower (P Ͻ 0.05) in HTR. The reduced Q and a-vO 2diff reserves were associated with lower HR and HHb reserves, respectively. The phase II V O2p time delay was greater (HTR: 38 Ϯ 2 vs. CON: 25 Ϯ 1 s, P Ͻ 0.05), while time constants for phase II V O2p (HTR: 54 Ϯ 8 vs. CON: 31 Ϯ 3 s), Q (HTR: 66 Ϯ 8 vs. CON: 28 Ϯ 4 s), and HHb (HTR: 27 Ϯ 5 vs. CON: 13 Ϯ 3 s) were significantly slower in HTR. The HR half-time was slower in HTR (113 Ϯ 21 s) vs. CON (21 Ϯ 2 s, P Ͻ 0.05); however, no significant difference was found between groups for SV kinetics (HTR: 39 Ϯ 8 s vs. CON 31 Ϯ 6 s). The lower peak V O2p and prolonged V O2p kinetics in HTR were secondary to impairments in both cardiovascular and skeletal muscle function that result in reduced oxygen delivery and utilization by the active muscles.
Chest, 2001
Background: The time required for oxygen uptake (V O 2) to return to baseline level (recovery kinetics) is prolonged in patients with reduced ventricular function, and the degree to which it is prolonged is related to the severity of heart failure, markers of abnormal ventilation, and prognosis. In the present study, we sought to determine the effect of exercise training on V O 2 recovery kinetics in patients with reduced ventricular function. Methods: Twenty-four male patients with reduced ventricular function after a myocardial infarction were randomized to either a 2-month high-intensity residential exercise training program or to a control group. V O 2 kinetics in recovery from maximal exercise were calculated before and after the study period and expressed as the slope of a single exponential relation between V O 2 and time during the first 3 min of recovery. Results: Peak V O 2 increased significantly in the exercise group (19.4 ؎ 3.0 mL/kg/min vs 25.1 ؎ 4.7 mL/kg/min, p < 0.05), whereas no change was observed in control subjects. The V O 2 half-time in recovery was reduced slightly after the study period in both groups (108.7 ؎ 33.1 to 102.1 ؎ 50.5 s in the exercise group and 122.3 ؎ 68.7 to 107.5 ؎ 36.0 s in the control group); neither the change within or between groups was significant. The degree to which V O 2 was prolonged in recovery was inversely related to measures of exercise capacity (peak V O 2 , watts achieved, and exercise time; r ؍ ؊ 0.48 to ؊ 0.57; p < 0.01) and directly related to the peak ventilatory equivalents for oxygen (r ؍ 0.59, p < 0.01) and carbon dioxide (r ؍ 0.57, p < 0.01). Conclusion: Two months of high-intensity training did not result in a faster recovery of V O 2 in patients with reduced ventricular function. This suggests that adaptations to exercise training manifest themselves only during, but not in, recovery from exercise.
Electronic Journal of General Medicine, 2011
Aim: One major cause of postoperative respiratory complications is pulmonary atelectasis. Atelectasis and the associated loss of functional alveolar units has been recognized as a major pathophysiological mechanism responsible for postoperative hypoxemia after coronary artery bypass graft (CABG). The aim of this study was to determine which therapeutic breathing method from incentive spirometry (IS), non-invasive intermittent positive pressure breathing (IPPB) and continuous positive airway pressure breathing (CPAP) in addition to postoperative pulmonary physiotherapy obtain the best improvement in blood gases in phase I of cardiac rehabilitation program after CABG. Method: Thirty six patients of both sexes who underwent CABG divided into three groups. Group (A) received breathing training with IS (5 minutes 5 times per day) in addition the chest physiotherapy program for patients after CABG and Group (B) received breathing training with CPAP (10 cmH2O for 15 minutes once daily) in addition to the chest physiotherapy program for patients after CABG., where Group(C) received breathing training with IPPB (maximum 15 cmH2O for 15 minutes once daily) in addition to the chest physiotherapy program for patients after CABG. Measurements of blood gases were done before the study in the first post operative day and repeated at the end of the study in the tenth postoperative day. Result: Blood gases were improved in all groups in addition to a significant difference between IS & CPAP and IS & IPPB groups. Where there was no significant difference between CPAP & IPPB groups. Conclusion: Incentive spirometry in addition to the usual respiratory physical therapy is recommended for patients in phase I of cardiac rehabilitation program after CABG.
Türk fizyoterapi ve rehabilitasyon dergisi, 2022
Purpose: Exercise capacity is associated with diastolic function. The aim of our study is to investigate the shortterm effects of cardiopulmonary rehabilitation and NMES on functional capacity and myocardial tissue doppler (MTD) after coronary artery surgery. Methods: Forty patients with coronary artery bypass graft were randomly divided into two groups: CPR+NMES and CPR. Functional capacity were analyzed through 2 minutes walk test (2MWT) and sit to stand test (SST), left ventricular (LV) diastolic functions were analyzed with MTD and thoracic expansion was analyzed with chest wall measurement on the 2nd and 7th postoperative days. Results: Statistically significant difference was identified between the groups in 2MWT distance (CPR+NMES, Zt*p=0.000*), SST (CPR, Zt*p=0.000*), E' (CPR+NMES, Zt*p=0.002*), E (CPR+NMES, Zt*p=0.025*), E/E' (CPR+NMES, Zt*p=0.007*), A (CPR, Zt*p=0.006*) (p<0.05). Statistically significant difference has been observed in group comparisons in E' (CPR+NMES, G*p=0.000*) ve E/E'(CPR+NMES, G*p=0.007* postoperative 2nd day; G*p=0.019* postoperative 7th day) (p<0.05). The temporal changes of 2MWT distance, heart rate, blood pressures, respiratory frequency, saturation and Borg dyspnea-fatigue measurements did not show a statistically significant difference between groups (p>0.05), except for E'(Zg*p=0.000*), E/E' (Zg*p=0.003*) parameters (p<0.05). Conclusion: It was seen that NMES, which we applied in addition to early cardiopulmonary rehabilitation, made a positive contribution to LV filling pressure and LV filling rate in the CPR+NMES group. Additionally, in the intergroup comparisons of the CPR+NMES group, it was observed that there was a statistically significant increase in the 2 MWT distance on the postoperative 7th day compared to the postoperative 2nd day.
Circulation, 1999
Background-Dyspnea and fatigue are the main causes of exercise limitation in chronic heart failure (CHF) patients, whose peak inspiratory (Pi max ) and expiratory pressures (Pe max ) are often reduced. The aim of this study was to examine the relationship between respiratory muscle performance and oxygen kinetics. Methods and Results-A total of 55 patients (NYHA class I to III) and 11 healthy subjects underwent cardiopulmonary exercise tests (CPET) on a treadmill. In 45 of the 55 patients (group I) and in healthy subjects (group II), pulmonary function tests, Pi max , and Pe max were measured before and 10 minutes after exercise, and oxygen kinetics were monitored throughout and during early recovery from CPET. The first degree slope of oxygen consumption (V O 2 ) decline during early recovery (V O 2 /t-slope) and V O 2 half-time (T 1/2 ) were calculated. In 10 of the 55 CHF patients (group III), the measurements of Pi max were repeated 2, 5, and 10 minutes after CPET. A Ͼ10% reduction in Pi max after CPET (subgroup IA) was measured in 11 of 45 patients. In contrast, 34 of 45 CHF patients (subgroup IB) and all control subjects (group II) had Pi max Ͼ90% of baseline value after CPET. Subgroup IA patients had significantly lower peak V O 2 (13.5Ϯ2.1 versus 17.8Ϯ5.6 mL ⅐ kg Ϫ1 ⅐ min Ϫ1 ; PϽ0.001), lower anaerobic thresholds (10.1Ϯ2.4 versus 13.6Ϯ4.6 mL ⅐ kg Ϫ1 ⅐ min Ϫ1 ; Pϭ0.003) and lower V O 2 /t-slopes (0.365Ϯ0.126 versus 0.519Ϯ0.227 L ⅐ min Ϫ1 ⅐ min Ϫ1 ; Pϭ0.008) than subgroup IB patients. Conclusions-The reduction of Pi max after exercise is associated with prolonged early recovery of oxygen kinetics, which may explain, in part, the role played by respiratory muscles in exercise intolerance in CHF patients. (Circulation. 1999;100:503-508.)
Heart Rate Recovery and Oxygen Kinetics After Exercise in Obstructive Sleep Apnea Syndrome
Clinical Cardiology, 2010
BackgroundPatients who suffer from obstructive sleep apnea (OSA) have a decreased exercise capacity and abnormal autonomic nervous function. However, the kinetics of early oxygen (O2) and heart rate recovery (HRR) have not been described.Patients who suffer from obstructive sleep apnea (OSA) have a decreased exercise capacity and abnormal autonomic nervous function. However, the kinetics of early oxygen (O2) and heart rate recovery (HRR) have not been described.Materials and MethodsWe evaluated 21 men with moderate to severe OSA (mean age: 48 ± 11 yrs, mean apnea-hypopnea index [AHI]: 55 ± 13) and without known heart disease and 10 healthy men matched for age and body mass index (BMI; controls). Men with OSA underwent overnight polysomnography, and both groups underwent symptom-limited incremental cardiopulmonary exercise testing (CPET). We recorded the CPET parameters including peak O2 uptake (VO2p), kinetics of early O2 recovery by the first degree slope of VO2 during the first minute (VO2/t slope), the time required for a 50% decline of VO2p during recovery (T1/2), and early heart rate recovery (HRR = HR at maximal exercise − HR at 1 min of recovery), as well as the chronotropic reserve to exercise ([CR] = [peak HR − resting HR/220 − age − resting HR] × 100). Patients with OSA had a lower VO2p (28.7 ± 4.0 vs 34.7 ± 6.2 mL/kg/min), VO2/t slope (1.04 ± 0.3 vs 1.4 ± 0.17 mL/kg/min2), and T1/2 (74 ± 10 vs 56 ± 6 sec) compared to controls (all P < 0.001). In addition, both HRR and CR were lower in the OSA group (22.0 ± 7.0 vs 31.0 ± 6.0 bpm, P:0.003, and 79.0% ± 15% vs 99.0% ± 13.0%, P:0.01, respectively).We evaluated 21 men with moderate to severe OSA (mean age: 48 ± 11 yrs, mean apnea-hypopnea index [AHI]: 55 ± 13) and without known heart disease and 10 healthy men matched for age and body mass index (BMI; controls). Men with OSA underwent overnight polysomnography, and both groups underwent symptom-limited incremental cardiopulmonary exercise testing (CPET). We recorded the CPET parameters including peak O2 uptake (VO2p), kinetics of early O2 recovery by the first degree slope of VO2 during the first minute (VO2/t slope), the time required for a 50% decline of VO2p during recovery (T1/2), and early heart rate recovery (HRR = HR at maximal exercise − HR at 1 min of recovery), as well as the chronotropic reserve to exercise ([CR] = [peak HR − resting HR/220 − age − resting HR] × 100). Patients with OSA had a lower VO2p (28.7 ± 4.0 vs 34.7 ± 6.2 mL/kg/min), VO2/t slope (1.04 ± 0.3 vs 1.4 ± 0.17 mL/kg/min2), and T1/2 (74 ± 10 vs 56 ± 6 sec) compared to controls (all P < 0.001). In addition, both HRR and CR were lower in the OSA group (22.0 ± 7.0 vs 31.0 ± 6.0 bpm, P:0.003, and 79.0% ± 15% vs 99.0% ± 13.0%, P:0.01, respectively).ConclusionsPatients with OSA demonstrate reduced exercise capacity, delayed oxygen kinetics, and reduced HRR. These data point to abnormal oxygen delivery and/or oxidative function of the peripheral muscles and impaired autonomic nervous activity in OSA patients. Copyright © 2010 Wiley Periodicals, Inc.Patients with OSA demonstrate reduced exercise capacity, delayed oxygen kinetics, and reduced HRR. These data point to abnormal oxygen delivery and/or oxidative function of the peripheral muscles and impaired autonomic nervous activity in OSA patients. Copyright © 2010 Wiley Periodicals, Inc.