Determinants of VO2 max decline with aging: an integrated perspective

2008 ◽  
Vol 33 (1) ◽  
pp. 130-140 ◽  
Author(s):  
Andrew C. Betik ◽  
Russell T. Hepple
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Output ◽  
Oxygen Delivery ◽  
Dominant Role ◽  
Oxidative Capacity ◽  
Oxygen Utilization ◽  
Critical Perspective ◽  
Progressive Decline ◽  
Muscle Oxygen ◽  
Capillary Bed

Aging is associated with a progressive decline in the capacity for physical activity. Central to this decline is a reduction in the maximal rate of oxygen utilization, or VO2 max. This critical perspective examines the roles played by the factors that determine the rate of muscle oxygen delivery versus those that determine the utilization of oxygen by muscle as a means of probing the reasons for VO2 max decline with aging. Reductions in muscle oxygen delivery, principally due to reduced cardiac output and perhaps also a maldistribution of cardiac output, appear to play the dominant role up until late middle age. On the other hand, there is a decline in skeletal muscle oxidative capacity with aging, due in part to mitochondrial dysfunction, which appears to play a particularly important role in extreme old age (senescence) where skeletal muscle VO2 max is observed to decline by approximately 50% even under conditions of similar oxygen delivery as young adult muscle. It is noteworthy that at least the structural aspects of the capillary bed do not appear to be reduced in a manner that would compromise the capacity for muscle oxygen diffusion even in senescence.

Soothing the sleeping giant: improving skeletal muscle oxygen kinetics and exercise intolerance in HFpEF

2015 ◽  
Vol 119 (6) ◽  
pp. 734-738 ◽  
Author(s):  
Satyam Sarma ◽  
Benjamin D. Levine
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Functional Capacity ◽  
Oxidative Capacity ◽  
Exercise Intolerance ◽  
Aerobic Performance ◽  
Muscle Oxygen ◽  
Oxygen Kinetics ◽  
Patients With Heart Failure

Patients with heart failure with preserved ejection fraction (HFpEF) have similar degrees of exercise intolerance and dyspnea as patients with heart failure with reduced EF (HFrEF). The underlying pathophysiology leading to impaired exertional ability in the HFpEF syndrome is not completely understood, and a growing body of evidence suggests “peripheral,” i.e., noncardiac, factors may play an important role. Changes in skeletal muscle function (decreased muscle mass, capillary density, mitochondrial volume, and phosphorylative capacity) are common findings in HFrEF. While cardiac failure and decreased cardiac reserve account for a large proportion of the decline in oxygen consumption in HFrEF, impaired oxygen diffusion and decreased skeletal muscle oxidative capacity can also hinder aerobic performance, functional capacity and oxygen consumption (V̇o2) kinetics. The impact of skeletal muscle dysfunction and abnormal oxidative capacity may be even more pronounced in HFpEF, a disease predominantly affecting the elderly and women, two demographic groups with a high prevalence of sarcopenia. In this review, we 1) describe the basic concepts of skeletal muscle oxygen kinetics and 2) evaluate evidence suggesting limitations in aerobic performance and functional capacity in HFpEF subjects may, in part, be due to alterations in skeletal muscle oxygen delivery and utilization. Improving oxygen kinetics with specific training regimens may improve exercise efficiency and reduce the tremendous burden imposed by skeletal muscle upon the cardiovascular system.

scholarly journals Distinguishing the effects of convective and diffusive O2 delivery on V̇o2 on-kinetics in skeletal muscle contracting at moderate intensity

2013 ◽  
Vol 305 (5) ◽  
pp. R512-R521 ◽  
Author(s):  
Jessica Spires ◽  
L. Bruce Gladden ◽  
Bruno Grassi ◽  
Matthew L. Goodwin ◽  
Gerald M. Saidel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Demand ◽  
Experimental Studies ◽  
Moderate Intensity ◽  
Oxygen Utilization ◽  
Muscle Oxygen ◽  
Mean Response Time ◽  
Convective Oxygen Delivery ◽  
Dynamics Simulations ◽  
O2 Delivery

With current techniques, experimental measurements alone cannot characterize the effects of oxygen blood-tissue diffusion on muscle oxygen uptake (V̇o2) kinetics in contracting skeletal muscle. To complement experimental studies, a computational model is used to quantitatively distinguish the contributions of convective oxygen delivery, diffusion into cells, and oxygen utilization to V̇o2 kinetics. The model is validated using previously published experimental V̇o2 kinetics in response to slowed blood flow (Q) on-kinetics in canine muscle (τQ = 20 s, 46 s, and 64 s) [Goodwin ML, Hernández A, Lai N, Cabrera ME, Gladden LB. J Appl Physiol. 112:9–19, 2012]. Distinctive effects of permeability-surface area or diffusive conductance ( PS) and Q on V̇o2 kinetics are investigated. Model simulations quantify the relationship between PS and Q, as well as the effects of diffusion associated with PS and Q dynamics on the mean response time of V̇o2. The model indicates that PS and Q are linearly related and that PS increases more with Q when convective delivery is limited by slower Q dynamics. Simulations predict that neither oxygen convective nor diffusive delivery are limiting V̇o2 kinetics in the isolated canine gastrocnemius preparation under normal spontaneous conditions during transitions from rest to moderate (submaximal) energy demand, although both operate close to the tipping point.

scholarly journals Understanding near infrared spectroscopy and its application to skeletal muscle research

2019 ◽  
Vol 126 (5) ◽  
pp. 1360-1376 ◽  
Author(s):  
Thomas J. Barstow
Keyword(s):  
Skeletal Muscle ◽  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Oxygen Delivery ◽  
Near Infrared ◽  
Control Mechanisms ◽  
Oxygen Utilization ◽  
Muscle Research ◽  
Athletic Field ◽  
Nirs Data

Near infrared spectroscopy (NIRS) is a powerful noninvasive tool with which to study the matching of oxygen delivery to oxygen utilization and the number of new publications utilizing this technique has increased exponentially in the last 20 yr. By measuring the state of oxygenation of the primary heme compounds in skeletal muscle (hemoglobin and myoglobin), greater understanding of the underlying control mechanisms that couple perfusive and diffusive oxygen delivery to oxidative metabolism can be gained from the laboratory to the athletic field to the intensive care unit or emergency room. However, the field of NIRS has been complicated by the diversity of instrumentation, the inherent limitations of some of these technologies, the associated diversity of terminology, and a general lack of standardization of protocols. This Cores of Reproducibility in Physiology (CORP) will describe in basic but important detail the most common methodologies of NIRS, their strengths and limitations, and discuss some of the potential confounding factors that can affect the quality and reproducibility of NIRS data. Recommendations are provided to reduce the variability and errors in data collection, analysis, and interpretation. The goal of this CORP is to provide readers with a greater understanding of the methodology, limitations, and best practices so as to improve the reproducibility of NIRS research in skeletal muscle.

Body mass-normalized moderate dose of dietary nitrate intake improves endothelial function and walking capacity in patients with peripheral artery disease

2021 ◽  
Author(s):  
Elizabeth J. Pekas ◽  
TeSean K. Wooden ◽  
Saantosh Yadav ◽  
Song-Young Park
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Function ◽  
Body Mass ◽  
Walking Distance ◽  
Moderate Dose ◽  
Peripheral Artery ◽  
Oxygen Utilization ◽  
Muscle Oxygen ◽  
Walking Capacity ◽  
Artery Disease

Peripheral artery disease (PAD) is characterized by the accumulation of atherosclerotic plaques in the lower extremity conduit arteries, which impairs blood flow and walking capacity. Dietary nitrate has been used to reduce blood pressure (BP) and improve walking capacity in PAD. However, a standardized dose for PAD has not been determined. Therefore, we sought to determine the effects of a body mass-normalized moderate dose of nitrate (0.11 mmol nitrate/kg) as beetroot juice on serum nitrate/nitrite, vascular function, walking capacity, and tissue oxygen utilization capacity in patients with PAD. 11 patients with PAD received either nitrate supplement or placebo in a randomized crossover design. Total serum nitrate/nitrite, resting BP, brachial and popliteal artery endothelial function (flow-mediated dilation, FMD), arterial stiffness (pulse-wave velocity, PWV), augmentation index (AIx), maximal walking distance and time, claudication onset time, and skeletal muscle oxygen utilization were measured pre-and-post-nitrate and placebo intake. There were significant group x time interactions (p<0.05) for serum nitrate/nitrite, FMD, BP, walking distance and time, and skeletal muscle oxygen utilization. The nitrate group showed significantly increased serum nitrate/nitrite (Δ1.32μM), increased brachial and popliteal FMD (Δ1.3% and Δ1.7%, respectively), reduced peripheral and central systolic BP (Δ-4.7mmHg and Δ-8.2mmHg, respectively), increased maximal walking distance (Δ92.7m) and time (Δ56.3s), and reduced deoxygenated hemoglobin during walking. There were no changes in PWV, AIx, or claudication (p>0.05). These results indicate that a body-mass normalized moderate dose of nitrate may be effective and safe for reducing BP, improving endothelial function, and improving walking capacity in patients with PAD.

Limits for oxygen and substrate transport in mammals.

1998 ◽  
Vol 201 (8) ◽  
pp. 1051-1064 ◽  
Author(s):  
H Hoppeler ◽  
E R Weibel
Keyword(s):  
Skeletal Muscle ◽  
Muscle Tissue ◽  
Oxygen Demand ◽  
Muscle Cells ◽  
Oxidative Capacity ◽  
Important Variable ◽  
Lipid Transfer ◽  
Work Intensity ◽  
Muscle Mitochondria ◽  
Muscle Oxygen

Environmental oxygen is transported by the respiratory cascade to the site of oxidation in active tissues. Under conditions of heavy exercise, it is ultimately the working skeletal muscle cells that set the aerobic demand because over 90 % of energy is spent in muscle cells. The pathways for oxygen and substrates converge in muscle mitochondria. In mammals, a structural limitation of carbohydrate and lipid transfer from the microvascular system to the muscle cells is reached at a moderate work intensity (i.e. at 40-50 % of VO2max). At higher work rates, intracellular substrate stores must be used for oxidation. Because of the importance of these intracellular stores for aerobic work, we find larger intramyocellular substrate stores in 'athletic' species as well as in endurance-trained human athletes. The transfer limitations for carbohydrates and lipids at the level of the sarcolemma imply that the design of the respiratory cascade from lungs to muscle mitochondria reflects primarily oxygen demand. Comparative studies indicate that the oxidative capacity of skeletal muscle tissue, and hence maximal oxygen demand, is adjusted by varying mitochondrial content. At the level of microcirculatory oxygen supply, it is found that muscle tissue capillarity is adjusted to muscle oxygen demand but that the capillary erythrocyte volume also plays a role. Oxygen delivery by the heart has long been recognized to be a key link in the oxygen transport chain. In allometric variation it is heart rate and in adaptive variation it is essentially stroke volume, and hence heart size, that determines maximal cardiac output. Again, haematocrit is an important variable that allows the heart of athletic species to generate higher flux rates for oxygen. The pulmonary gas exchanger offers only a negligible resistance to oxygen flux to the periphery. However, in contrast to all other steps in the respiratory cascade, the lungs have only a minimal phenotypical plasticity and appear, therefore, to be built with considerable structural redundancy in all but the most athletic species. Because of the lack of malleability, the lungs may ultimately become limiting for VO2max when adaptive processes have maximized O2 flux through the malleable downstream elements of the respiratory system: the heart, microcirculation and muscle mitochondria.

In vivo effects on human skeletal muscle oxygen delivery and metabolism of cardiopulmonary bypass and perioperative hemodilution

2011 ◽  
Vol 38 (3) ◽  
pp. 413-421 ◽  
Author(s):  
R. A. De Blasi ◽  
E. Tonelli ◽  
R. Arcioni ◽  
M. Mercieri ◽  
L. Cigognetti ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiopulmonary Bypass ◽  
Oxygen Delivery ◽  
Human Skeletal Muscle ◽  
Muscle Oxygen ◽  
In Vivo Effects

scholarly journals Muscle oxygen transport and utilization in heart failure: implications for exercise (in)tolerance

2012 ◽  
Vol 302 (5) ◽  
pp. H1050-H1063 ◽  
Author(s):  
David C. Poole ◽  
Daniel M. Hirai ◽  
Steven W. Copp ◽  
Timothy I. Musch
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Cardiac Output ◽  
Uptake Kinetics ◽  
Exercise Intolerance ◽  
Transport Pathway ◽  
Muscle Oxygen ◽  
Patient Morbidity ◽  
Oxidative Function ◽  
Factor Α

The defining characteristic of chronic heart failure (CHF) is an exercise intolerance that is inextricably linked to structural and functional aberrations in the O2 transport pathway. CHF reduces muscle O2 supply while simultaneously increasing O2 demands. CHF severity varies from moderate to severe and is assessed commonly in terms of the maximum O2 uptake, which relates closely to patient morbidity and mortality in CHF and forms the basis for Weber and colleagues' ( 167 ) classifications of heart failure, speed of the O2 uptake kinetics following exercise onset and during recovery, and the capacity to perform submaximal exercise. As the heart fails, cardiovascular regulation shifts from controlling cardiac output as a means for supplying the oxidative energetic needs of exercising skeletal muscle and other organs to preventing catastrophic swings in blood pressure. This shift is mediated by a complex array of events that include altered reflex and humoral control of the circulation, required to prevent the skeletal muscle “sleeping giant” from outstripping the pathologically limited cardiac output and secondarily impacts lung (and respiratory muscle), vascular, and locomotory muscle function. Recently, interest has also focused on the dysregulation of inflammatory mediators including tumor necrosis factor-α and interleukin-1β as well as reactive oxygen species as mediators of systemic and muscle dysfunction. This brief review focuses on skeletal muscle to address the mechanistic bases for the reduced maximum O2 uptake, slowed O2 uptake kinetics, and exercise intolerance in CHF. Experimental evidence in humans and animal models of CHF unveils the microvascular cause(s) and consequences of the O2 supply (decreased)/O2 demand (increased) imbalance emblematic of CHF. Therapeutic strategies to improve muscle microvascular and oxidative function (e.g., exercise training and anti-inflammatory, antioxidant strategies, in particular) and hence patient exercise tolerance and quality of life are presented within their appropriate context of the O2 transport pathway.

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