Decline In Maximal Aerobic Capacity Research Articles

Influence of high affinity haemoglobin on the response to normoxic and hypoxic exercise.

Theoretical models suggest there is no benefit of high affinity haemoglobin to preserve maximal oxygen uptake in acute hypoxia but the comparative biology literature has many examples of species that are evolutionarily adapted to hypoxia and have high affinity haemoglobin. We studied humans with high affinity haemoglobin and compensatory polycythaemia. These subjects performed maximal exercise tests in normoxia and hypoxia to determine how their altered haemoglobin affinity impacts hypoxic exercise tolerance. The high affinity haemoglobin participants demonstrated an attenuated decline in maximal aerobic capacity in acute hypoxia. Those with high affinity haemoglobin had no worsening of pulmonary gas exchange during hypoxic exercise but had greater lactate and lower pH than controls for all exercise bouts. High affinity haemoglobin and compensatory polycythaemia mitigated the decline in exercise performance in acute hypoxia through a higher arterial oxygen content and an unchanged pulmonary gas exchange. The longstanding dogma is that humans exhibit an acute reduction in haemoglobin (Hb) binding affinity for oxygen that facilitates adaptation to moderate hypoxia. However, many animals have adapted to high altitude through enhanced Hb binding affinity for oxygen. The objective of the study was to determine whether high affinity haemoglobin (HAH) affects maximal and submaximal exercise capacity. To accomplish this, we recruited individuals (n=11, n=8 females) with HAH (P50 =16±1mmHg), had them perform normoxic and acute hypoxic (15% inspired oxygen) maximal exercise tests, and then compared their results to matched controls (P50 =26±1, n=14, n=8 females). Cardiorespiratory and arterial blood gases were collected throughout both exercise tests. Despite no difference in end-exercise arterial oxygen tension in hypoxia (59±6 vs. 59±9mmHg for controls and HAH, respectively), the HAH subjects' oxyhaemoglobin saturation ( ) was ∼7% higher. Those with HAH had an attenuated decline in maximal oxygen uptake ( ) (4±5% vs. 12±%, p<0.001) in hypoxia and the change in between trials was related to the change in (r=-0.75, p<0.0001). Compared to normoxia, the controls' alveolar-to-arterial oxygen gradient significantly increased during hypoxic exercise, whereas pulmonary gas exchange in HAH subjects was unchanged between the two exercise trials. However, arterial lactate was significantly higher and arterial pH significantly lower in the HAH subjects for both exercise trials. We conclude that HAH attenuates the decline in maximal aerobic capacity and preserves pulmonary gas exchange during acute hypoxic exercise. Our data support the comparative biology literature indicating that HAH is a positive adaptation to acute hypoxia.

Aging, Fitness, and Marathon Times in a 91 Year-old Man Who Competed in 627 Marathons.

Aging is associated with a decline in maximal aerobic capacity (VO2max) that may be attenuated by chronic endurance exercise. This case study chronicles the changes in marathon times in a 91 year old man who completed 627 marathons and 117 ultramarathons over 42 years. He began running marathons at age 48. His yearly best times remained fairly constant at ~240 minutes from age 50 – 64 years and then gradually rose to about 260 minutes in his early seventies followed by a curvilinear deterioration as he approached his ninth decade. His times plateaued at ~ 600 minutes in his late eighties. Between ages 68 and 89 his VO2max declined from 43 to 20 ml/kg/min. His marathon times were highly correlated with his VO2max (r2=0.87). The decline in marathons times and VO2max may reflect the contributions of biological aging, changes in exercise training volume and intensity, injuries, and comorbid disease.

Resveratrol and Exercise May Improve Kidney Disease Co-morbidities in a Model of Uremia

PURPOSE: Excessive inflammation and oxidative stress in chronic kidney disease (CKD) promote muscle wasting, and vascular disease. Two therapies that have shown promise in treating these conditionings are resveratrol, which is enriched in polyphenolic compounds with anti-oxidant and anti-inflammatory properties, and exercise, which has been shown to have anti-inflammatory and anti-atherogenic effects. The purpose of this study was to test the efficacy of exercise (EXE) and resveratrol (RSV) on CKD co-morbidities in uremic mice. METHODS: Female ApoE-/- mice (n=24) with surgically-induced uremia were randomly assigned to the following dietary groups for 16 weeks: control diet/sedentary (CON), control diet supplemented with resveratrol at 0.04%/sedentary (RSV), control diet/exercise (EXE). The exercise protocol consisted of treadmill running 45min/day, 5 days/week at 15 m/min. One week before sacrifice, maximal aerobic capacity (VO2max) was assessed by treadmill test to measure physical function. At sacrifice, atherosclerosis (Oil Red O staining) and calcification (Arizarin Red staining) in the proximal aorta were quantified using image analysis software at 3 sites, the coronary cusps, the orifices of the coronary arteries, and the ascending aorta. All statisrical tests used a two-tailed significance alpha =0.05, and independent sample t-tests were used to assess group differences in atherosclerotic lesion size. RESULTS: Aortic atherosclerotic lesion area did not differ between groups at any site, but aortic calcification was significantly reduced in RSV compared to CON in the section of the proximal aorta corresponding to the orifices of the coronary arteries. In addition, VO2max was reduced by 16% in CON (p<0.05) and 29.5% in EXE groups (p<0.05), but did not change in RSV group, suggesting that RSV attenuates uremia-associated decline in maximal aerobic capacity. CONCLUSIONS: These data suggest that RSV and, in part EXE, may be beneficial in the treatment of a cardiovascular disease and physical functions associated with CKD.

Potential Application of Essential Amino Acid Supplementation to Treat Sarcopenia in Elderly People

Aging is universally associated with a progressive decline in both physical and metabolic function across a diverse rangeofspeciesfromnematodestohumans.Moreover,progressive reductions in skeletal muscle mass, strength, and quality (referred to as sarcopenia) are often observed with aging. An associated problem is decline in maximal aerobic capacity, and all of these factors together contribute to the physical frailty of older people. In light of the rapidly expanding aging population, sarcopenia and related disorders are emerging as a major public health problem of the 21st century. This is particularly pertinent considering the loss of independence that is associated with frailty and falls that increase the risk of fractures. Another consequence of the sarcopenia of aging is a deleterious change in body composition resulting in many metabolic alterations leading on to metabolic syndrome and increased cardiovascular disease risk. Indeed, sarcopenia has received considerable attention by both researchers and clinicians over the last two decades. Muscle changes with age include reduction in fiber numbers, motor units, and a relative loss of type II fibers with a preservation of type I fibers (1) that may result from reductions in transcript levels of myosin heavy chain isoforms IIa and IIx without any decline of isoform I as reported in older people (2). Thus, a relative increase of type I fibers occurs with age, but these fibers are lower in abundance of mitochondria (3) than those in longdistance runners who also have a relatively high proportion of type I fibers but with high abundance of mitochondria. Reductionsinskeletalmuscleproteinabundances(thebalancebetween protein synthesis and degradation) are a key contributing factor to the development of sarcopenia. Mechanistically, it has been extensively reported that skeletal muscle protein synthesis is reduced in aging adults (2, 4, 5). The reduction in skeletal muscle mitochondrial protein synthesis (6) occurs in conjunction with reducedmitochondrialcapacityforATPproduction(3).Thank

Adaptations to Aerobic and Resistance Exercise in the Elderly

Maximal aerobic exercise capacity (VO2 max) is the product of maximal cardiac output (Q) and the maximal arteriovenous oxygen difference (A-VO2diff) (VO2 = Q X AVO2). Generally speaking, cardiac output represents oxygen delivery to the working muscle and A-VO2 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). VO2 max declines ∼1%/year after the age of 25 in non-training individuals [1–3]. Thus, the VO2 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 VO2 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 VO2 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 VO2 max, Proctor et al. [8] expressed VO2 max relative to appendicular muscle mass. These investigators reported that ∼50% of the decline in VO2 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 VO2 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-VO2 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 [10–13]. 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 [14–18]. 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 investigators reported a significant improvement of VO2 max of 24%. When subjects were grouped by age (60–62, 63–66, and 67–71 years) there were no differences between groups in the improvement of VO2 max. Similar increases in VO2 max have been observed by other investigators utilizing strenuous aerobic exercise training [14–16]. Elderly women appear to adapt to exercise training with similar increases in VO2 max as elderly men. Interestingly, however, the mechanism by which elderly men and women increase their VO2 max appears to be different. Using a similar exercise training paradigm as Kohrt et al. [17], Spina et al. [19] reported that ∼66% of the improvement in VO2 max in elderly men was due to an increase in cardiac output and more specifically stroke volume. However, in elderly women these investigators reported that the improvement in VO2 max was due to an enhanced A-VO2 difference with no change in cardiac output. Spina et al. [20,21] using echocardiography, the drug atropine (which releases vagal tone) and the β-adrenergic agonist isoproterenol reported that the endurance exercise training in women had no effect on left ventricular function or left

Aging and marathon times in an 81-Year-Old man who competed in 591 marathons

Aging and marathon times in an 81-Year-Old man who competed in 591 marathons

Greater rate of decline in maximal aerobic capacity with age in endurance-trained than in sedentary men.

To determine the relation between habitual endurance exercise status and the age-associated decline in maximal aerobic capacity [i.e., maximal O(2) consumption (Vo(2 max))] in men, we performed a well-controlled cross-sectional laboratory study on 153 healthy men aged 20-75 yr: 64 sedentary and 89 endurance trained. Vo(2 max) (ml. kg(-1). min(-1)), measured by maximal treadmill exercise, was inversely related to age in the endurance-trained (r = -0.80) and sedentary (r = -0.74) men but was higher in the endurance-trained men at any age. The rate of decline in Vo(2 max) with age (ml. kg(-1). min(-1)) was greater (P < 0.001) in the endurance-trained than in the sedentary men. Whereas the relative rate of decline in Vo(2 max) (percent decrease per decade from baseline levels in young adulthood) was similar in the two groups, the absolute rate of decline in Vo(2 max) was -5.4 and -3.9 ml. kg(-1). min(-). decade(-1) in the endurance-trained and sedentary men, respectively. Vo(2 max) declined linearly across the age range in the sedentary men but was maintained in the endurance-trained men until approximately 50 yr of age. The accelerated decline in Vo(2 max) after 50 yr of age in the endurance-trained men was related to a decline in training volume (r = 0.46, P < 0.0001) and was associated with an increase in 10-km running time (r = -0.84, P < 0.0001). We conclude that the rate of decline in maximal aerobic capacity during middle and older age is greater in endurance-trained men than in their sedentary peers and is associated with a marked decline in O(2) pulse.

Meta-analysis of the age-associated decline in maximal aerobic capacity in men: relation to training status.

Based on cross-sectional data, we recently reported that, in contrast to the prevailing view, the rate of decline in maximal oxygen consumption (VO(2 max)) with age is greater in physically active compared with sedentary healthy women. We tested this hypothesis in men using a meta-analytic study of VO(2 max) values in the published literature. A total of 242 studies (538 subject groups and 13,828 subjects) met the inclusion criteria and were arbitrarily separated into sedentary (214 groups, 6,231 subjects), active (159 groups, 5,621 subjects), and endurance-trained (165 groups, 1,976 subjects) populations. Body fat percent increased with age in sedentary and active men (P < 0.001), whereas no change was observed in endurance-trained men. VO(2 max) was inversely and strongly related to age within each population (r = -0.80 to -0.88, all P < 0. 001) and was highest in endurance-trained and lowest in sedentary populations at any age. Absolute rates of decline in VO(2 max) with age were not different (P > 0.05) in sedentary (-4.0 ml. kg(-1). min(-1). decade(-1)), active (-4.0), and endurance-trained (-4.6) populations. Similarly, there were no group differences (P > 0.05) in the relative (%) rates of decline in VO(2 max) with advancing age (-8.7, -7.3, and -6.8%/decade, respectively). Maximal heart rate was inversely related to age within each population (r = -0.88 to -0.93, all P < 0.001), but the rate of age-related reduction was not different among the populations. There was a significant decline in running mileage and speed with advancing age in the endurance-trained men. The present cross-sectional meta-analytic findings do not support the hypothesis that the rate of decline in VO(2 max) with age is related to habitual aerobic exercise status in men.

SIMILAR AGE-RELATED DECLINES IN MAXIMAL AEROBIC CAPACITY IN SEDENTARY HISPANIC AND CAUCASIAN WOMEN

1427 Hispanic women may demonstrate greater age-related declines in physical functional capacity and functional disability compared with non-Hispanic, Caucasian women. The responsible physiological mechanism(s) are unknown, but a greater rate of decline in maximal aerobic capacity with age could contribute. We tested this hypothesis in 120 healthy sedentary Hispanic (H) and Caucasian (C) adult females aged 20-75 years (n=42 H and n=77 C). The groups were matched across the age range for body mass, fat-free mass, BMI, estimated physical activity-related energy expenditure, and education-based socio-economic status (SES). Maximal respiratory exchange ratio, rating of perceived exertion, and heart rate (% predicted maximal heart rate) were similar across age and ethnicity, suggesting equivalent maximum voluntary efforts in all subjects. Maximal oxygen consumption (V̇O2max) expressed in l·min−1, as well as when normalized for body mass (ml·kg−1·min−1) and fat-free mass (ml·kg FFM−1·min−1), was inversely related to age in both H (r=−0.60, p<0.01; r=−0.69, p<0.01; and r=−0.63, p<0.01) and C (r=−0.64, p<0.01; r=−0.66, p<0.01; and r=−0.79, p<0.01). The absolute unit/decade and %/decade (∼8%) rates of decline in VO2max were similar in H and C (p>0.05). Maximal heart rate was inversely related to age in both H (r=−0.79, p<0.01) and C (r=−0.66, p<0.01); the rates of decline with age (∼6 beats·min−1·decade−1) were similar in the two groups (p>0.05). The present cross-sectional findings suggest that the rate of decline in maximal aerobic capacity with age is not different in H and C healthy sedentary women matched for SES. Support: NIH AG06537, HL03840, AG13038 and NIA Minority Supplement

Role of central circulatory factors in the fat-free mass-maximal aerobic capacity relation across age.

Fat-free mass (FFM) (primarily skeletal muscle mass) is related to maximal aerobic capacity among healthy humans across the adult age range. The basis for this physiological association is assumed to be a direct relation between skeletal muscle mass and its capacity to consume oxygen. We tested the alternative hypothesis that FFM exerts its influence on maximal aerobic capacity in part via an association with central circulatory function. To do so, we analyzed data from 103 healthy sedentary adults aged 18-75 yr. FFM was strongly and positively related to maximal oxygen consumption (r = 0.80, P < 0. 001). FFM was also strongly and positively related to supine resting levels of blood volume (r = 0.79, P < 0.001) and stroke volume (r = 0.75, P < 0.001). Statistically controlling for the collective influences of blood volume and stroke volume abolished the tight relation between FFM and maximal oxygen consumption (r = 0.12, not significant). These results indicate that 1) FFM may be an important physiological determinant of blood volume and stroke volume among healthy sedentary adult humans of varying age; and 2) this relation between FFM and central circulatory function appears to represent the primary physiological basis for the strong association between FFM and maximal aerobic capacity in this population. Our findings suggest that sarcopenia (loss of skeletal muscle mass with aging) may contribute to the age-related decline in maximal aerobic capacity primarily via reductions in blood volume and stroke volume rather than a direct effect on the oxygen-consuming potential of muscle per se.

Age-related declines in maximal aerobic capacity in regularly exercising vs. sedentary women: a meta-analysis.

Our purpose was to determine the relationship between habitual aerobic exercise status and the rate of decline in maximal aerobic capacity across the adult age range in women. A meta-analytic approach was used in which mean maximal oxygen consumption (VO2 max) values from female subject groups (ages 18-89 yr) were obtained from the published literature. A total of 239 subject groups from 109 studies involving 4,884 subjects met the inclusion criteria and were arbitrarily separated into sedentary (groups = 107; subjects = 2,256), active (groups = 69; subjects = 1, 717), and endurance-trained (groups = 63; subjects = 911) populations. VO2 max averaged 29.7 +/- 7.8, 38.7 +/- 9.2, and 52.0 +/- 10.5 ml . kg-1 . min-1, respectively, and was inversely related to age within each population (r = -0.82 to -0.87, all P < 0.0001). The rate of decline in VO2 max with increasing subject group age was lowest in sedentary women (-3.5 ml . kg-1 . min-1 . decade-1), greater in active women (-4.4 ml . kg-1 . min-1 . decade-1), and greatest in endurance-trained women (-6.2 ml . kg-1 . min-1 . decade-1) (all P < 0.001 vs. each other). When expressed as percent decrease from mean levels at age approximately 25 yr, the rates of decline in VO2 max were similar in the three populations (-10.0 to -10.9%/decade). There was no obvious relationship between aerobic exercise status and the rate of decline in maximal heart rate with age. The results of this cross-sectional study support the hypothesis that, in contrast to the prevailing view, the rate of decline in maximal aerobic capacity with age is greater, not smaller, in endurance-trained vs. sedentary women. The greater rate of decline in VO2 max in endurance-trained populations may be related to their higher values as young adults (baseline effect) and/or to greater age-related reductions in exercise volume; however, it does not appear to be related to a greater rate of decline in maximal heart rate with age.

Longitudinal variations in maximal oxygen intake with age and activity.

Longitudinal variations in maximal oxygen intake with age and activity.