Cardiovascular System

Lakatta, Edward G.

doi:10.1002/cphy.cp110117

Cited by 16 publications

(26 citation statements)

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“…It is well documented that maximal oxygen uptake (VO 2max ) decreases with age in humans and horses (Pollock et al 1987;Stamford 1988;Holloszy and Kohrt 1995;Lakatta 1995;Dempsey and Seals 1995;McKeever and Malinowski 1997). Studies of man, horses and other species have demonstrated that the decline in aerobic capacity is the result of ageing-induced decreases in both peripheral and central mechanisms affecting the ability to transport and utilise oxygen (McKeever and Malinowski 1997;Holloszy and Kohrt 1995;Lakatta 1995;Kenney 1995;Dempsey and Seals 1995;Stamford 1988;Pollock et al 1987). Human studies have suggested that, centrally, this age-related decrease in VO 2max is due to a decline in maximal cardiac output (Raven and Mitchell 1980;Seals et al 1984;Lakatta 1995).…”

Section: Introductionmentioning

confidence: 99%

“…Studies of man, horses and other species have demonstrated that the decline in aerobic capacity is the result of ageing-induced decreases in both peripheral and central mechanisms affecting the ability to transport and utilise oxygen (McKeever and Malinowski 1997;Holloszy and Kohrt 1995;Lakatta 1995;Kenney 1995;Dempsey and Seals 1995;Stamford 1988;Pollock et al 1987). Human studies have suggested that, centrally, this age-related decrease in VO 2max is due to a decline in maximal cardiac output (Raven and Mitchell 1980;Seals et al 1984;Lakatta 1995). In man, this decline in maximal cardiac output appears to be the result of both a decline in factors affecting stroke volume and a decrease in maximal heart rate (Cooper et al 1977;Sheffield et al 1978;Londeree and Moeschberger 1984;Lakatta 1995).…”

Section: Introductionmentioning

confidence: 99%

“…Human studies have suggested that, centrally, this age-related decrease in VO 2max is due to a decline in maximal cardiac output (Raven and Mitchell 1980;Seals et al 1984;Lakatta 1995). In man, this decline in maximal cardiac output appears to be the result of both a decline in factors affecting stroke volume and a decrease in maximal heart rate (Cooper et al 1977;Sheffield et al 1978;Londeree and Moeschberger 1984;Lakatta 1995). Studies of other species, especially man, have demonstrated that, in middle-aged individuals, factors affecting stroke volume remain adaptable to exercise training, allowing for a slowing of the decline in VO 2max seen in old individuals (Seals et al 1984;Haskell and Phillips 1995;Lakatta 1995;Kenney 1995).…”

Section: Introductionmentioning

confidence: 99%

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Effects of ageing and training on maximal heart rate and V̇O_2max

Betros

McKeever

Kearns

et al. 2002

Equine Veterinary Journal

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The purpose of this study was to test the hypotheses that ageing would result in a decline in maximal heart rate (HRmax) and maximal aerobic capacity (VO2max) and, secondarily, that those effects would be reversible with training. Eighteen, healthy, unfit Standardbred mares representing 3 age groups: young (Y = mean +/- s.e. 6.8 +/- 0.4 years, n = 6); middle-aged (MA = 15.2 +/- 0.4 years, n = 6); and old (O = 27.0 +/- 0.2 years, n = 6) were used. HRmax, VO2max and oxygen pulse at VO2max (OPmax) and the velocities producing HRmax (VHRmax) and VO2max (VVO2max) were measured during pretraining and post-training incremental exercise tests (GXT). During training, mares exercised 3 days/week (Weeks 1-8) and 4 days/week (Weeks 9-12) at a submaximal intensity (approximately 60% HRmax) for approximately 30 min/day. There were no differences (P>0.05) between Y and MA, before (218 +/- 2 vs. 213 +/- 3 beats/min; 116 +/- 3 vs. 109 +/- 3 ml/kg bwt/min; 0.55 +/- 0.01 vs. 0.52 +/- 0.02 ml/kg/beat; 9.0 +/- 0.3 vs. 9.3 +/- 0.2 ms; 8.8 +/- 0.2 vs. 8.8 +/- 0.2 m/s) or after training (224 +/- 2 vs. 218 +/- 2 beats/min; 131 +/- 3 vs. 120 +/- 2 ml/kg bwt/min; 0.58 +/- 0.01 vs. 0.55 +/- 0.01 ml/kg/beat; 10.5 +/- 0.2 vs. 9.5 +/- 0.1 ms; 10.6 +/- 0.2 vs. 9.5 +/- 0.1 m/s) for HRmax, VO2max, OPmax, VHRmax or VVO2max, respectively. Old horses had lower HRmax, VO2max and OPmax and reached them at lower velocities compared to Y and MA (P<0.05), both before (193 +/- 3 beats/min; 83.2 +/- 2.0 ml/kg bwt/min; 0.43 +/- 0.01 ml/kg/beat; 7.8 +/- 0.1 m/s; 7.2 +/- 0.1 m/s) and after training (198 +/- 2 beats/min; 95 +/- 2 ml/kg bwt/min; 0.48 +/- 0.01 ml/kg/beat; 8.2 +/- 0.2 m/s; 8.0 +/-0.2 m/s). Training did not alter HRmax in any age group (P>0.05) but did cause increases in VO2max, OPmax and VVO2max for all groups (P<0.05). Interestingly, training increased VHRmax only in Y (P<0.05). These data demonstrate that there is a reduction in HRmax, VO2max, OPmax, VHRmax and VVO2max in old horses, and that training can partially reverse some effects of ageing.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of ageing and training on maximal heart rate and V̇O_2max

Betros

McKeever

Kearns

et al. 2002

Equine Veterinary Journal

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“…There is considerable heterogeneity in the cardiovascular changes secondary to aging [8,13–15]. Cardiovascular function is effected by atherosclerotic cardiovascular disease and it is difficult to separate its effect from the effects of aging.…”

Section: Pathophysiologic Considerations In the Elderly With Criticalmentioning

confidence: 99%

Critical Illness in the Elderly: Review of Pathophysiology of Aging and Outcome of Intensive Care

Chelluri¹

2001

J Intensive Care Med

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The goal of this article is to review the literature on age and its influence on the pathophysiology of critical illness, outcome after critical illness, and end of life decision making in critically ill elderly patients. Sources for this review included the MEDLINE database and bibliographies of original articles, reviews, and book chapters. The population is aging and the need for medical care and its costs increase with increasing age. A majority of the elderly lead independent lives, although some need help with various functional activities related to daily living. It is difficult to separate the effects of aging from the effects of the comorbidities that develop with increasing age. The physiologic reserve decreases in the elderly and they may not be able to tolerate a critical injury or illness as well as a younger individual. As the elderly are usually on multiple medications, they are prone to have more drug interactions and side effects, and need close monitoring of the drugs and adjustment of the dosage. Mortality after a critical illness in the elderly is higher compared to younger patients, and it is more related to the acuity of physiologic disturbance than age alone. The effect of age alone on long‐term outcome is not well studied, but individuals with poor functional status and/or increased comorbidities have a poor short‐term outcome. Functional status usually deteriorates after critical illness, but the long‐term survivors usually recover functional abilities, and they are satisfied with their quality of life. Decision making at the end of life is difficult because of the paucity of data on long‐term mortality and quality of life, lack of information about patient wishes, and the uncertainty of the prognosis. Because many elderly patients survive critical illness and may return to their previous lifestyle, age alone should not weigh heavily in end of life decisions. As with other age groups, end of life decisions in the elderly should be made after considering long‐term outcomes, patient goals, and the benefits and burdens of life‐sustaining technology.

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“…; Fitzgerald et al . ) and although this decline is, in part, attributable to a diminution of maximal cardiac output (Lakatta, ), age‐induced reductions in muscle blood flow during exercise (Proctor et al . ; Lawrenson et al .…”

Section: Introductionmentioning

confidence: 99%

Heterogeneous ageing of skeletal muscle microvascular function

Muller‐Delp

2015

The Journal of Physiology

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The distribution of blood flow to skeletal muscle during exercise is altered with advancing age. Changes in arteriolar function that are muscle specific underlie age-induced changes in blood flow distribution. With advancing age, functional adaptations that occur in resistance arterioles from oxidative muscles differ from those that occur in glycolytic muscles. Age-related adaptations of morphology, as well as changes in both endothelial and vascular smooth muscle signalling, differ in muscle of diverse fibre type. Age-induced endothelial dysfunction has been reported in most skeletal muscle arterioles; however, unique alterations in signalling contribute to the dysfunction in arterioles from oxidative muscles as compared with those from glycolytic muscles. In resistance arterioles from oxidative muscle, loss of nitric oxide signalling contributes significantly to endothelial dysfunction, whereas in resistance arterioles from glycolytic muscle, alterations in both nitric oxide and prostanoid signalling underlie endothelial dysfunction. Similarly, adaptations of the vascular smooth muscle that occur with advancing age are heterogeneous between arterioles from oxidative and glycolytic muscles. In both oxidative and glycolytic muscle, late-life exercise training reverses age-related microvascular Judy Muller-Delp received her PhD in Physiology from the University of Missouri in 1992, where her work focused on coronary microvascular adaptations to exercise training. She trained as a postdoctoral research associate at Texas A&M University and at the University of Missouri. She is currently a Professor of Biomedical Sciences at Florida State University. Research in her laboratory focuses on understanding microvascular adaptations to ageing and interventional exercise training in cardiac and skeletal muscle, with a major emphasis on assessing the cellular mechanisms that underlie age-induced dysfunction of the endothelium and vascular smooth muscle in resistance arteries.This review was presented at the symposium "Limitations of skeletal muscle oxygen supply in ageing", which took place at Ageing and Degeneration: A Physiological Perspective in Edinburgh, UK, 10-11 April 2015. Abstract figure legend In the skeletal muscle resistance vasculature, muscle-specific signals from nerves, muscle metabolites, intraluminal flow and transmural pressure change with age and declining activity. Resulting vascular adaptations in the endothelium include changes in signalling through nitric oxide, prostanoids and reactive oxygen species. In the vascular smooth muscle, age induces hyperplasia, reduced expression of contractile proteins and alterations in receptor expression. These changes in both the endothelium and the vascular smooth muscle are muscle and fibre type specific.

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Cardiovascular System

Abstract: The sections in this article are: Cardiovascular Structure in Younger and Older Humans Arterial Structure and Mechanical Properties Cardiac Structure Ventricular–Vascular Coupling Myocardial and Cardiac Pump Function at Rest Integrated Regulation of Cardiac Function Card… Show more

Cited by 16 publications

References 461 publications

Effects of ageing and training on maximal heart rate and V̇O_2max

Effects of ageing and training on maximal heart rate and V̇O_2max

Critical Illness in the Elderly: Review of Pathophysiology of Aging and Outcome of Intensive Care

Heterogeneous ageing of skeletal muscle microvascular function

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Cardiovascular System

Abstract: The sections in this article are: Cardiovascular Structure in Younger and Older Humans Arterial Structure and Mechanical Properties Cardiac Structure Ventricular–Vascular Coupling Myocardial and Cardiac Pump Function at Rest Integrated Regulation of Cardiac Function Card… Show more

Cited by 16 publications

References 461 publications

Effects of ageing and training on maximal heart rate and V̇O2max

Effects of ageing and training on maximal heart rate and V̇O2max

Critical Illness in the Elderly: Review of Pathophysiology of Aging and Outcome of Intensive Care

Heterogeneous ageing of skeletal muscle microvascular function

Contact Info

Product

Resources

About

Effects of ageing and training on maximal heart rate and V̇O_2max

Effects of ageing and training on maximal heart rate and V̇O_2max