Are oxygen uptake kinetics in chronic heart failure limited by oxygen delivery or oxygen utilization?

Kemps, Hareld; Schep, Goof; Zonderland, M. L.; Thijssen, Eric J. M.; Vries, W. R. de; Wessels, Bart; Doevendans, Pieter A.; Wijn, Pff Pieter

doi:10.1016/j.ijcard.2008.12.088

Cited by 43 publications

(49 citation statements)

References 31 publications

(42 reference statements)

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“…24,25 Additionally, the degree of tissue oxygenation and/or capacity for O 2 utilization may be responsible for different O 2 uptake kinetics in hypertensive and non-hypertensive subjects. 26 Hypertension and protection against oxidation Hypertension is a condition with a permanent shift in redox balance and diminished capacity of the antioxidant defense system. 14,15 Findings from our study indicate that patients with long-term hypertension have an attenuated SOD level before and after exercise, which is inadequate compared with subjects without hypertension.…”

Section: Mechanisms Underlying Reduced Exercise Tolerance In Hypertenmentioning

confidence: 99%

“…Attenuated antioxidant defense in hypertensive patients with mild LVDD may be related to changed energetic reserves, oxygen kinetics and uptake. 26 Insufficient antioxidant response could be particularly important for understanding the complex and interactive mechanisms underlying the progression from asymptomatic to symptomatic LVDD. 3,4 Study limitations Although we did not perform exercise echocardiography for evaluating actual diastolic dynamics during exercise, we used CPET, which allowed us to assess the contribution of ventilation to functional capacity.…”

Section: Mechanisms Underlying Reduced Exercise Tolerance In Hypertenmentioning

confidence: 99%

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Cardiopulmonary exercise testing and its relation to oxidative stress in patients with hypertension

et al. 2012

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An increase in reactive oxygen species has been implicated in the pathologies of hypertension. This study was designed to evaluate antioxidant activity in hypertensive patients and to assess the relationship between oxidative stress and exercise tolerance in hypertensive patients with mild left ventricular diastolic dysfunction (LVDD). A total of 42 patients, aged 51 ± 9 years, with a long history of hypertension and mild LVDD (mitral flow velocities-E/A o1, deceleration time of E 4220 ms, and preserved ejection fraction-EF 450%), and 30 controls without cardiovascular disease, aged 50 ± 7 years, underwent cardiopulmonary exercise testing (CPET). Peak oxygen uptake (peak VO 2 ), oxygen pulse (VO 2 /heart rate (HR)) and ventilatory anaerobic threshold (VAT) were obtained during CPET. Antioxidant activity of superoxide dismutase (SOD) and glutathione peroxidase in the blood was measured before and after exercise. Reduced peak VO 2 (1715 ± 426 vs. 2083±465 ml min À1 , Po0.001), VO 2 /HR (12.0±2.8 vs. 14.6±3.3 ml per beat, Po0.001) and percentage of peak VO 2 at VAT (55.5 ± 15.8% vs. 64.5 ± 14.7%, P ¼ 0.007) were observed in hypertensive patients, compared with controls. Antioxidant protection was significantly attenuated in hypertensive patients, compared with controls, before (945 vs. 1006, P ¼ 0.012) and after exercise (954 vs. 1051, Po0.001). The level of SOD before and after exercise was significantly associated with LVDD in hypertensive patients (P ¼ 0.012 and 0.02, respectively). In addition, the degree of LVDD before exercise (E/A) influenced the degree of exercise capability (peak VO 2 ) (P ¼ 0.016). Asymptomatic hypertensive patients with mild LVDD had reduced cardiopulmonary capacity, accurately identified by CPET. The redox state in hypertensive patients was significantly related to LVDD and exercise tolerance. Attenuated antioxidant protection was associated with long-term hypertension.

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Section: Mechanisms Underlying Reduced Exercise Tolerance In Hypertenmentioning

confidence: 99%

Section: Mechanisms Underlying Reduced Exercise Tolerance In Hypertenmentioning

confidence: 99%

Cardiopulmonary exercise testing and its relation to oxidative stress in patients with hypertension

et al. 2012

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“…To investigate oxygen kinetics, the data were visually inspected for the rise time from baseline to the plateau in oxygen uptake during the reading task. This variable may provide insight into the phenomenon of fatigue, specifically, neuromuscular inefficiency (Kemps et al, 2010).…”

Section: Descriptive Exploration Of Raw Data (Supplement To Sa 1)mentioning

confidence: 99%

“…First is the question of oxygen uptake kinetics. Slower oxygen uptake kinetics at the onset of exercise and the delay to reach steady state to supply the demands of the task via aerobic means may be attributable to poor oxygen utilization of the working muscles, thus relating to neuromuscular inefficiency (Kemps et al, 2010). Poor oxygen utilization can be explained by the following mechanisms: (a) possible co-contraction of agonist and antagonist muscle groups, (b) increased neuromotor recruitment of more muscles at the same time or differing times for a given task (hyperadduction), (c) decreased blood flow through the capillaries due to increased constriction of working muscles, or (d) muscle membrane repair or damage.…”

Section: Potential Physiological Mechanismsmentioning

confidence: 99%

Metabolic Mechanisms of Vocal Fatigue

2017

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Vocal fatigue is among the most debilitating conditions affecting individuals with voice disorders. Impressions about mechanisms potentially underlying vocal fatigue have varied depending on how fatigue is defined, participants studied, and measures made, thereby impacting the selection of treatment strategies that may alleviate the condition. However, little is currently known about actual metabolic mechanisms of vocal fatigue. The current study aimed to address this issue by investigating the hypothesis that neuromuscular inefficiency, cardiovascular recovery deficits, or both, may play a role in fatigue. The approach replicated well-vetted approaches in exercise physiology.Metabolic profiles of subjects with vocal fatigue were assessed using gas exchange measures in comparison to two non-fatigue groups: vocally healthy and cardiovascular trained individuals, recruited based on results from a newly vetted questionnaire, the Vocal Fatigue Index (VFI) and laryngeal examination. Participants read out loud at two different loudness levels for a duration of 5 minutes for each task with periods of rest between tasks. Metabolic cost for and recovery time from reading were same across all groups. Oxygen uptake and recovery kinetics (EPOC), ratings of perceived exertion revealed interesting patterns in individuals with vocal fatigue compared to cardiovascular trained individuals in particular.Specifically, slow oxygen uptake kinetics in the vocal fatigue compared to the cardiovascular iv trained group pointed to utilization of anaerobic energy source to meet the demands of the reading task in the vocal fatigue group, suggesting neuromuscular inefficiency. In contrast, rapid oxygen uptake kinetics in the cardiovascular trained group pointed to utilization of aerobic energy sources and greater neuromuscular efficiency. Similarly, a greater number of individuals in vocal fatigue and vocally healthy groups showed an increase in oxygen consumption post reading (EPOC) compared to the cardiovascular trained group, indicating possible cardiovascular recovery deficits in the former groups.In addition to uncovering potential mechanisms underlying vocal fatigue, including neuromuscular inefficiency and cardiovascular recovery deficits, results from the present study highlight the potential importance of aerobic training to generate aerobic energy required for vocal task demands for both ease of task performance and recovery from it. In sharp contrast to the situation for voice, fatigue as a common physical phenomenon more generally has received extensive attention in the physical therapy, sports medicine, and exercise physiology literature. Three broad schools of thought identify mechanisms pertaining to the origins of physical fatigue: (1) peripheral mechanisms (Allen, Lamb, & Westerblad, 2008;Asmussen, 1979;Edwards, 1981;Fitts, 1994;Westerblad, Allen, & Lannergren, 2002;Westerblad, Lee, Lannergren, & Allen, 1991), (2) The next pages and chapters provide pertinent background information on vocal fatigue, fatigue as understood ...

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“…Hence, in healthy subjects, oxygen utilisation mechanisms are likely the limiting factor in onset and recovery of exercise. In a recently published paper by Kemps and colleagues, 20 data are presented that suggest that in almost uniquely NYHA-II CHF patients cardiac output and oxygen uptake kinetics are slower than in healthy subjects, but also, that there was no longer a clear difference between the time constants describing oxygen uptake and cardiac output kinetics. This would imply that, in these patients, not only the oxygen delivery and consumption had deteriorated, but also that it seems that oxygen delivery is the limiting factor for oxygen uptake kinetics.…”

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confidence: 99%