Speeding of VO2 kinetics in response to endurance-training in older and young women

Murias, Juan M.; Kowalchuk, John M.; Paterson, Donald H.

doi:10.1007/s00421-010-1649-6

Cited by 62 publications

(66 citation statements)

References 37 publications

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“…For instance, a slower rate of adjustment of the oxidative phosphorylation has been shown to be partly determined by impairments in blood flow distribution (24,25) and has been proposed to disturb cellular homeostasis and reduce exercise tolerance due to an increase in metabolic by-products associated with nonoxidative metabolism (4). This rapid improvement in vascular responses might improve O 2 provision to the active tissues and thus reduce exercise-related fatigue.…”

Section: Discussionmentioning

confidence: 99%

Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific

Murias¹,

Grisé²,

Jiang³

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Murias JM, Grise KN, Jiang M, Kowalchuk H, Melling CWJ, Noble EG. Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific. Am J Physiol Regul Integr Comp Physiol 304: R574 -R580, 2013. First published December 12, 2012 doi:10.1152/ajpregu.00508.2012.-The dynamic adjustment and amplitude of the endothelium-dependent vasorelaxation of the carotid, aorta, iliac, and femoral vessels were measured in response to acute low-(LI) or high-intensity (HI) endurance exercise. Vasorelaxation to 10 Ϫ4 M ACh was evaluated in 10 control, 10 LI, and 10 HI rats. Two-millimeter sections of carotid, aorta, iliac, and femoral arteries were mounted onto a myography system. Vasorelaxation responses were modeled as a monoexponential function. The overall (control, 10.5 Ϯ 6.0 s; LI, 10.4 Ϯ 5.7 s; HI, 11.0 Ϯ 6.9 s) and time-to-steady-state (control, 47.6 Ϯ 24.0 s; LI, 46.2 Ϯ 22.8 s; HI, 49.1 Ϯ 28.3 s) was similar in LI, HI, and control (P Ͼ 0.05). The overall (average of four vessel-type) % vasorelaxation was larger in LI (73 Ϯ 16%) and HI (73 Ϯ 16%) than in control (66 Ϯ 19%) (P Ͻ 0.05). The overall rate of vasorelaxation was greater in LI (1.9 Ϯ 0.9%·s Ϫ1) and HI (1.9 Ϯ 1.1%·s Ϫ1) compared with control (1.6 Ϯ 0.7%·s Ϫ1 ) (P Ͻ 0.05). The vessel-specific responses (average response for the three conditions) showed that carotid displayed a slower adjustment (, 18.9 Ϯ 4.4 s; time-to-steady-state, 80.4 Ϯ 18.4 s) compared with the aorta (, 10.3 Ϯ 3.8 s; time-to-steady-state, 46.3 Ϯ 15.2 s), the iliac (, 6.3 Ϯ 2.1 s; time-to-steady-state, 30.3 Ϯ 9.0 s), and the femoral (, 6.0 Ϯ 1.9 s; time-to-steady-state, 29.3 Ϯ 8.4 s). The % vasorelaxation was larger in the carotid (82 Ϯ 14%) than in the aorta (67 Ϯ 16%), iliac (61 Ϯ 13%), and femoral (71 Ϯ 19%) (P Ͼ 0.05). The rate of vasorelaxation was carotid (1.1 Ϯ 0.2%·s, and femoral (2.6 Ϯ 1.0%·s Ϫ1 ). In conclusion, an acute bout of endurance exercise increased vascular responsiveness. The dynamic and percent adjustments were vessel-specific with vessel function likely determining the response. endothelium-dependent vasorelaxation; vessel myography; vascular responsiveness; vascular kinetics THE MATCHING OF BLOOD FLOW to the metabolic demands for oxygen and other nutrients throughout different organs is of critical importance to maintain cellular energetics and homeostasis (2). In this regard, relaxation of the vascular smooth muscle through diffusion of nitric oxide (NO) produced in the endothelial cells through the activation of endothelial NO synthase (e-NOS) has been shown to be fundamental (6,9,29). Although the positive effects of endurance exercise training on vascular responsiveness (and more specifically endothelium-dependent vasodilation) have been demonstrated (12,13,15,28), the effects of an acute bout of exercise on vascular responsiveness are poorly understood. For instance, an early study by Delp and Laughlin (5) showed no changes in the vasorelaxation response to a given dose of ACh in the aorta arteries of rats 24 h after a single, 1-h bout of...

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Section: Discussionmentioning

confidence: 99%

Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific

Murias¹,

Grisé²,

Jiang³

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

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“…Although technical limitations make the measurement of rapid changes in blood flow within the muscle challenging in humans, recent studies have shown that an estimation of changes in muscle O 2 delivery can be obtained using near-infrared spectroscopy (NIRS) derived deoxyhaemoglobin concentration (DHHb) data in combination with measures of VO 2 (DiMenna et al 2010;Harper et al 2008;Murias et al 2010a;Murias et al 2010b). Using this methodology, temporal adjustments in muscle O 2 delivery during periods of work and recovery can be derived and insights can be gained into the mechanisms controlling the adjustments in muscle O 2 utilization during intermittent exercise.…”

Section: Introductionmentioning

confidence: 99%

The effects of short recovery duration on VO2 and muscle deoxygenation during intermittent exercise

et al. 2011

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This study compared the oxygen uptake (VO(2)) and muscle deoxygenation (∆HHb) of two intermittent protocols to responses during continuous constant load cycle exercise in males (24 year ± 2, n = 7). Subjects performed three protocols: (1) 10 s work/5 s active recovery (R), R at 20 W (INT1): (2) 10 s work/5 s R, R at moderate intensity (INT2); and (3) continuous exercise (CONT), all for 10 min, on separate days. The work rate of CONT and the 10 s work of INT1 and INT2 were set within the heavy intensity domain. VO(2) and ∆HHb data were filtered and averaged to 5 s bins. Average VO(2) (80-420 s) was highest during CONT (3.77 L/min), lower in INT2 (3.04 L/min), and lowest during INT1 (2.81 L/min), all (p < 0.05). Average ∆HHb (80-420 s) was higher during CONT (p < 0.05) than both INT exercise protocols (CONT; 25.7 ± 0.9 a.u. INT1; 16.4 ± 0.8 a.u., and INT2; 15.8 ± 0.8 a.u.). The repeated changes in metabolic rate elicited oscillations in ΔHHb in both intermittent protocols, whereas oscillations in VO(2) were only observed during INT1. The greater ΔHHb during CONT suggests a reduction in oxygen delivery compared to oxygen consumption relative to INT. The higher VO(2) for INT 2 versus INT 1 and similar ΔHHb during INT suggests an increase in oxygen delivery during INT 2. Thus the different demands of INT1, INT2, and CONT protocols elicited differing physiological responses to a similar heavy intensity power output. These intermittent exercise models seem to elicit an elevated O(2) delivery condition compared to CONT.

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“…In healthy skeletal muscle, faster V O 2 kinetics after endurance exercise training results primarily from improved oxidative capacity and/or allosteric regulation of mitochondrial respiration (i.e., 1"parallel activation"; Refs. 18,35,36,86,133,207,221,222,242,338,339) (see also Figs. 6 and 7).…”

Section: Muscle V O 2 (V Mo 2 )mentioning

confidence: 99%

Exercise training in chronic heart failure: improving skeletal muscle O₂transport and utilization

Hirai

Musch

Poole

2015

American Journal of Physiology-Heart and Circulatory Physiology

142

156

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Hirai DM, Musch TI, Poole DC. Exercise training in chronic heart failure: improving skeletal muscle O 2 transport and utilization. Am J Physiol Heart Circ Physiol 309: H1419 -H1439, 2015. First published August 28, 2015; doi:10.1152/ajpheart.00469.2015.-Chronic heart failure (CHF) impairs critical structural and functional components of the O 2 transport pathway resulting in exercise intolerance and, consequently, reduced quality of life. In contrast, exercise training is capable of combating many of the CHF-induced impairments and enhancing the matching between skeletal muscle O 2 delivery and utilization (Q mO 2 and V mO 2 , respectively). The Q mO 2 /V mO 2 ratio determines the microvascular O2 partial pressure (PmvO 2 ), which represents the ultimate force driving blood-myocyte O 2 flux (see Fig. 1). Improvements in perfusive and diffusive O2 conductances are essential to support faster rates of oxidative phosphorylation (reflected as faster V mO 2 kinetics during transitions in metabolic demand) and reduce the reliance on anaerobic glycolysis and utilization of finite energy sources (thus lowering the magnitude of the O 2 deficit) in trained CHF muscle. These adaptations contribute to attenuated muscle metabolic perturbations (e.g., changes in [PCr], [Cr], [ADP], and pH) and improved physical capacity (i.e., elevated critical power and maximal V mO 2 ). Preservation of such plasticity in response to exercise training is crucial considering the dominant role of skeletal muscle dysfunction in the pathophysiology and increased morbidity/mortality of the CHF patient. This brief review focuses on the mechanistic bases for improved Q mO 2 /V mO 2 matching (and enhanced PmvO 2 ) with exercise training in CHF with both preserved and reduced ejection fraction (HFpEF and HFrEF, respectively). Specifically, O 2 convection within the skeletal muscle microcirculation, O 2 diffusion from the red blood cell to the mitochondria, and muscle metabolic control are particularly susceptive to exercise training adaptations in CHF. Alternatives to traditional whole body endurance exercise training programs such as small muscle mass and inspiratory muscle training, pharmacological treatment (e.g., sildenafil and pentoxifylline), and dietary nitrate supplementation are also presented in light of their therapeutic potential. Adaptations within the skeletal muscle O 2 transport and utilization system underlie improvements in physical capacity and quality of life in CHF and thus take center stage in the therapeutic management of these patients.

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Speeding of VO2 kinetics in response to endurance-training in older and young women

Cited by 62 publications

References 37 publications

Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific

Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific

The effects of short recovery duration on VO2 and muscle deoxygenation during intermittent exercise

Exercise training in chronic heart failure: improving skeletal muscle O₂transport and utilization

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Speeding of VO2 kinetics in response to endurance-training in older and young women

Cited by 62 publications

References 37 publications

Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific

Acute endurance exercise induces changes in vasorelaxation responses that are vessel-specific

The effects of short recovery duration on VO2 and muscle deoxygenation during intermittent exercise

Exercise training in chronic heart failure: improving skeletal muscle O2transport and utilization

Contact Info

Product

Resources

About

Exercise training in chronic heart failure: improving skeletal muscle O₂transport and utilization