Training and Oxygen Conductance in the Elderly I. The Respiratory System

Niinimaa, V.; Shephard, Roy J.

doi:10.1093/geronj/33.3.354

Cited by 37 publications

(17 citation statements)

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“…These findings are in line with animal studies showing that chronic exercise training does not affect pulmonary diffusion capacity (58,59,456) or the morphological dimensions of the pulmonary diffusion surface (456). Static lung volumes of endurance trained subjects are also not different compared to those of sedentary individuals (67,330,342), and physical training does not cause significant changes in these parameters (391,442,485).…”

Section: Lungs and Airwayssupporting

confidence: 88%

Ventilation and Respiratory Mechanics

Sheel

Romer

2012

Comprehensive Physiology

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During dynamic exercise, the healthy pulmonary system faces several major challenges, including decreases in mixed venous oxygen content and increases in mixed venous carbon dioxide. As such, the ventilatory demand is increased, while the rising cardiac output means that blood will have considerably less time in the pulmonary capillaries to accomplish gas exchange. Blood gas homeostasis must be accomplished by precise regulation of alveolar ventilation via medullary neural networks and sensory reflex mechanisms. It is equally important that cardiovascular and pulmonary system responses to exercise be precisely matched to the increase in metabolic requirements, and that the substantial gas transport needs of both respiratory and locomotor muscles be considered. Our article addresses each of these topics with emphasis on the healthy, young adult exercising in normoxia. We review recent evidence concerning how exercise hyperpnea influences sympathetic vasoconstrictor outflow and the effect this might have on the ability to perform muscular work. We also review sex-based differences in lung mechanics.

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Section: Lungs and Airwayssupporting

confidence: 88%

Ventilation and Respiratory Mechanics

Sheel

Romer

2012

Comprehensive Physiology

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“…Other investigators have reported that the decline in fat free mass accounts for ∼35% of the decline in VO 2 max [9]. It is clear that the maximal cardiac output declines with aging but whether muscle oxidative capacity (which is a major determinant of A-VO 2 difference) declines with aging is a question that is presently under scientific debate.The results of early studies of aerobic exercise training in the elderly suggested that there was little adaptation in aerobic capacity [10][11][12][13]. These early studies have been criticized as a result of the exercise intensity being inadequate to stimulate adaptation.…”

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confidence: 99%

Adaptations to Aerobic and Resistance Exercise in the Elderly

Lambert

Evans

2005

Rev Endocr Metab Disord

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Maximal aerobic exercise capacity (VO 2 max) is the product of maximal cardiac output (Q) and the maximal arteriovenous oxygen difference (A-VO 2 diff) (VO 2 = Q X A-VO 2 ). Generally speaking, cardiac output represents oxygen delivery to the working muscle and A-VO 2 difference is oxygen extraction at the muscle tissue level. Maximal Q is product of stroke volume (SV), the amount of blood pumped per heart beat, and heart rate (HR) or the number of times the heart beats/min (Q = SV X HR).VO 2 max declines ∼1%/year after the age of 25 in non-training individuals [1][2][3]. Thus, the VO 2 max of an untrained elderly individual is significantly lower than that of an untrained young individual. However, this decline in maximal oxygen consumption is ∼0.5%/year in master athletes who participate in aerobic activities [4]. Further, Pollock et al. [5] reported that there was a non-significant 1.7% decline in VO 2 max over 10.1 years in master athletes who remained competitive and maintained their training intensity while in other master athletes who continued to train but reduced their training intensity there was a significant 12.6% decline in VO 2 max over the 10.1 year period. The reason for the decline in maximal aerobic capacity in sedentary individuals is likely due to 3 major factors. A decline in maximal cardiac output [6], a decline in muscle oxidative capacity due to aging and/or inactivity [7], and a decline in metabolically active muscle mass with a concomitant increase in metabolically inactive fat mass [8]. To examine the effect of the reduction in muscle mass/and increase in fat mass in the elderly on VO 2 max, Proctor et al.[8] expressed VO 2 max relative to appendicular muscle mass. These investigators reported that ∼50% of the decline in VO 2 max with aging was accounted for by the decline in muscle mass and increase in fat mass. Thus, the other ∼50% was related to a decline in oxygen delivery and/or oxygen extraction. Other investigators have reported that the decline in fat free mass accounts for ∼35% of the decline in VO 2 max [9]. It is clear that the maximal cardiac output declines with aging but whether muscle oxidative capacity (which is a major determinant of A-VO 2 difference) declines with aging is a question that is presently under scientific debate.The results of early studies of aerobic exercise training in the elderly suggested that there was little adaptation in aerobic capacity [10][11][12][13]. These early studies have been criticized as a result of the exercise intensity being inadequate to stimulate adaptation. Subsequent studies with relatively high exercise intensities suggested that the magnitude of the adaptation in fitness level of elderly individuals is similar to that of younger individuals [14][15][16][17][18]. In a seminal study, Kohrt et al. [17] had elderly individuals (age 60-71) exercise 4 days/wk, 45 min/day for 9-12 months with exercise intensity gradually increasing from 76% of heart rate maximum to ∼83% of heart rate maximum over the training period. These investigat...

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“…The values obtained both in absolute terms and expressed in terms of body weight fit well into the ex pected range for elderly men [Benestad, 1965;Niinimaa and Shephard, 1978], Since we do not know with certainty whether the asymp totic relationship of fH to VO2 applies to elderly subjects [cf. Benestad, 1965] it is pos sible that we have overestimated VO2 max and underestimated the relative work-load.…”

Section: Discussionmentioning

confidence: 54%

Effects of Dynamic Exercise on Muscle Function in Elderly Men, Aged 70 Years

Davies¹,

White²

1983

Gerontology

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The maximal electrically evoked and voluntary contractions of the triceps surae were measured, before and after 30 min of continuous uphill walking, in 8 elderly men aged 67–71 years. The exercise was performed on a motor-driven treadmill and corresponded to 66–74% of their predicted maximal aerobic power output. During the control period, before exercise, twitch tension (P_t), time-to-peak tension (TPT) and half relaxation time (½RT) of the maximal twitch response were 102 ± 29 N, 156 ± 15 ms and 98 ± 11 ms; the tetanic responses at frequencies of 10 Hz (Po₁₀) and 20 Hz (Po₂₀) and the maximal voluntary contraction (MVC) averaged 600 ± 103, 766 ± 106 and 1,225 ± 185 N, respectively. The fatigue index in response to a 2-min test involving repeated tetanisation of the triceps surae was 0.40 ± 0.14. None of these variables (except TPT which was decreased to 145 ± 11 ms, p < 0.001) was significantly changed following exercise. It was concluded that exercise of relatively high intensity and duration in healthy elderly men does not impair the force-generating capacity of the lower leg muscles nor increase their fatigability.

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Training and Oxygen Conductance in the Elderly I. The Respiratory System

Cited by 37 publications

References 0 publications

Ventilation and Respiratory Mechanics

Ventilation and Respiratory Mechanics

Adaptations to Aerobic and Resistance Exercise in the Elderly

Effects of Dynamic Exercise on Muscle Function in Elderly Men, Aged 70 Years

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