Lifelong Endurance Exercise Research Articles

Fast and slow myofiber nuclei, satellite cells, and size distribution with lifelong endurance exercise in men and women.

We previously observed lifelong endurance exercise (LLE) influenced quadriceps whole-muscle and myofiber size in a fiber-type and sex-specific manner. The current follow-up exploratory investigation examined myofiber size regulators and myofiber size distribution in vastus lateralis biopsies from these same LLE men (n = 21, 74 ± 1 years) and women (n = 7, 72 ± 2 years) as well as old, healthy nonexercisers (OH; men: n = 10, 75 ± 1 years; women: n = 10, 75 ± 1 years) and young exercisers (YE; men: n = 10, 25 ± 1 years; women: n = 10, 25 ± 1 years). LLE exercised ~5 days/week, ~7 h/week for the previous 52 ± 1 years. Slow (myosin heavy chain (MHC) I) and fast (MHC IIa) myofiber nuclei/fiber, myonuclear domain, satellite cells/fiber, and satellite cell density were not influenced (p > 0.05) by LLE in men and women. The aging groups had ~50%-60% higher proportion of large (>7000 μm2) and small (<3000 μm2) myofibers (OH; men: 44%, women: 48%, LLE; men: 42%, women: 42%, YE; men: 27%, women: 29%). LLE men had triple the proportion of large slow fibers (LLE: 21%, YE: 7%, OH: 7%), while LLE women had more small slow fibers (LLE: 15%, YE: 8%, OH: 9%). LLE reduced by ~50% the proportion of small fast (MHC II containing) fibers in the aging men (OH: 14%, LLE: 7%) and women (OH: 35%, LLE: 18%). These data, coupled with previous findings, suggest that myonuclei and satellite cell content are uninfluenced by lifelong endurance exercise in men ~60-90 years, and this now also extends to septuagenarian lifelong endurance exercise women. Additionally, lifelong endurance exercise appears to influence the relative abundance of small and large myofibers (fast and slow) differently between men and women.

Effects of Lifelong Exercise on Body Composition and Bone Density

Objective: The purpose of this study was to compare body composition and bone density among young exercisers (YE), lifelong exercisers (LLE), and old healthy non-exercisers (OH), as well as between men (M) and women (W). Hypothesis: A hierarchal pattern will emerge (YE &gt; LLE &gt; OH) for healthy body composition and bone density. Both body composition and bone density will differ between M and W. Methods: Healthy adults were separated into three groups: YE (n=20, 10M, 25±1yr, 67±10kg), LLE (n=28, 21M, 74±2yr, 75±12kg), and OH (n=20, 10M, 74±2yr, 77±14kg). Daily physical activity was indirectly assessed using a pedometer (YE: ~10,000steps/day; LLE: ~9,000steps/day; OH: ~6,000steps/day). LLE individuals completed aerobic exercise regularly ~5 days/week (~7 hrs/week) for 52±1yr. Further analysis was done between men and women to investigate potential sex differences (M: n=41, 62±25yr, 80±10kg; W: n=27, 58±28yr, 62±7kg). Dual X-ray absorptiometry (DXA) was used to assess body composition (fat and lean mass) and bone mineral density. Results: There was a hierarchal pattern of beneficial body composition related to total body fat (YE: 21±6% &lt; LLE: 25±6% &lt; OH: 37±7%; p&lt;0.05) and lean mass (YE: 79±6% &gt; LLE: 74±6% &gt; OH: 62±7%; p&lt;0.05). In addition, there were sex differences for both total body fat (M: 24±7%; W: 32±9%; p&lt;0.05) and lean mass (M: 75±7%; W: 67±10%; p&lt;0.05). Bone mineral density was not different among the three groups (YE: 1.26±0.10g/cm2; LLE: 1.27±0.18g/cm2; OH: 1.22±0.14g/cm2; P&gt;0.05) but was different between men and women (M: 1.33±0.12g/cm2; W: 1.14±0.11g/cm2; p&lt;0.05). Conclusion: These data suggest lifelong endurance exercise was beneficial for body fat and lean mass in both men and women. Bone mineral density, generally thought to decrease with age, was not impacted by aging or exercise status in this cohort. Women had lower bone mineral density compared to men, regardless of age, which may be related to distinct hormonal regulation between the sexes. Funding Sources: This research was supported by the National Institutes of Health Grant R01-AG038576 and the Ball State University Human Bioenergetics Program. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Fast and slow muscle fiber transcriptome dynamics with lifelong endurance exercise.

We investigated fast and slow muscle fiber transcriptome exercise dynamics among three groups of men: lifelong exercisers (LLE, n = 8, 74 ± 1 yr), old healthy nonexercisers (OH, n = 9, 75 ± 1 yr), and young exercisers (YE, n = 8, 25 ± 1 yr). On average, LLE had exercised ∼4 day·wk-1 for ∼8 h·wk-1 over 53 ± 2 years. Muscle biopsies were obtained pre- and 4 h postresistance exercise (3 × 10 knee extensions at 70% 1-RM). Fast and slow fiber size and function were assessed preexercise with fast and slow RNA-seq profiles examined pre- and postexercise. LLE fast fiber size was similar to OH, which was ∼30% smaller than YE (P < 0.05) with contractile function variables among groups, resulting in lower power in LLE (P < 0.05). LLE slow fibers were ∼30% larger and more powerful compared with YE and OH (P < 0.05). At the transcriptome level, fast fibers were more responsive to resistance exercise compared with slow fibers among all three cohorts (P < 0.05). Exercise induced a comprehensive biological response in fast fibers (P < 0.05) including transcription, signaling, skeletal muscle cell differentiation, and metabolism with vast differences among the groups. Fast fibers from YE exhibited a growth and metabolic signature, with LLE being primarily metabolic, and OH showing a strong stress-related response. In slow fibers, only LLE exhibited a biological response to exercise (P < 0.05), which was related to ketone and lipid metabolism. The divergent exercise transcriptome signatures provide novel insight into the molecular regulation in fast and slow fibers with age and exercise and suggest that the ∼5% weekly exercise time commitment of the lifelong exercisers provided a powerful investment for fast and slow muscle fiber metabolic health at the molecular level.NEW & NOTEWORTHY This study provides the first insights into fast and slow muscle fiber transcriptome dynamics with lifelong endurance exercise. The fast fibers were more responsive to exercise with divergent transcriptome signatures among young exercisers (growth and metabolic), lifelong exercisers (metabolic), and old healthy nonexercisers (stress). Only lifelong exercisers had a biological response in slow fibers (metabolic). These data provide novel insights into fast and slow muscle fiber health at the molecular level with age and exercise.

Can lifelong endurance exercise improve ageing through beneficial effects on circadian timing function, muscular performance and health status in men? Protocol for a comparative cross-sectional study.

A well-synchronized circadian system is a manifestation of an individual's health. A gradual weakening of the circadian timing function characterizes aging. Regular exercise has been suggested as a modality to improve many detrimental changes associated with aging. Therefore, we aim to examine the benefits and risks of lifelong endurance exercise on age-dependent changes in the circadian time-keeping function, the performance of the muscular system and health status. The study protocol has a comparative cross-sectional design, including groups of senior (65 to 75 years old, n=16) and young (20-30 years old, n=16) endurance runners and triathletes. Age-matched groups of young and elderly sedentary men are included as controls. The circadian function is evaluated mainly by measurement of urinary 6-sulphatoxymelatonin, a metabolite of the hormone melatonin shown to participate in the modulation of sleep cycles. The 6-sulphatoxymelatonin will be assessed in urine samples collected upon awakening in the morning and in the late evening, as a marker of melatonin production. In addition, sleep/activity rhythms and sleep quality will be measured by wrist actigraphy. Performance of the muscular system will be assessed by examination of muscular strength and quantifying of gene expression in the skeletal muscle tissue samples. Health status and age-induced reduction in immune function are to be analysed via the balance of pro- and anti-inflammatory immune markers in the plasma and skeletal muscle, body composition, bone density and physical fitness.

Impact of Aging and Lifelong Exercise Training on Mitochondrial Function and Network Connectivity in Human Skeletal Muscle.

Aging is associated with metabolic decline in skeletal muscle, which can be delayed by physical activity. Moreover, both lifelong and short-term exercise training have been shown to prevent age-associated fragmentation of the mitochondrial network in mouse skeletal muscle. However, whether lifelong endurance exercise training exerts the same effects in human skeletal muscle is still not clear. Therefore, the aim of the present study was to examine the effect of volume-dependent lifelong endurance exercise training on mitochondrial function and network connectivity in older human skeletal muscle. Skeletal muscle complex I+II-linked mitochondrial respiration per tissue mass was higher, but intrinsic complex I+II-linked mitochondrial respiration was lower in highly trained older subjects than in young untrained, older untrained, and older moderately trained subjects. Mitochondrial volume and connectivity were higher in highly trained older subjects than in untrained and moderately trained older subjects. Furthermore, the protein content of the ADP/ATP exchangers ANT1 + 2 and VDAC was higher and of the mitophagic marker parkin lower in skeletal muscle from the highly trained older subjects than from untrained and moderately trained older subjects. In contrast, H2O2 emission in skeletal muscle was not affected by either age or exercise training, but SOD2 protein content was higher in highly trained older subjects than in untrained and moderately trained older subjects. This suggests that healthy aging does not induce oxidative stress or mitochondrial network fragmentation in human skeletal muscle, but high-volume exercise training increases mitochondrial volume and network connectivity, thereby increasing oxidative capacity in older human skeletal muscle.

What's all the hype with fibre type? Selective single fibre adaptations with lifelong endurance exercise.

What's all the hype with fibre type? Selective single fibre adaptations with lifelong endurance exercise.

Single muscle fibre contractile characteristics with lifelong endurance exercise.

A hallmark trait of ageing skeletal muscle health is a reduction in size and function, which is most pronounced in the fast muscle fibres. We studied older men (74±4years) with a history of lifelong (>50years) endurance exercise to examine potential benefits for slow and fast muscle fibre size and contractile function. Lifelong endurance exercisers had slow muscle fibres that were larger, stronger, faster and more powerful than young exercisers (25±1years) and age-matched non-exercisers (75±2years). Limited benefits with lifelong endurance exercise were noted in the fast muscle fibres. These findings suggest that additional exercise modalities (e.g. resistance exercise) or other therapeutic interventions are needed to target fast muscle fibres with age. We investigated single muscle fibre size and contractile function among three groups of men: lifelong exercisers (LLE) (n=21, 74±4years), old healthy non-exercisers (OH) (n=10, 75±2years) and young exercisers (YE) (n=10, 25±1years). On average, LLE had exercised ∼5 daysweek-1 for ∼7 hweek-1 over the past 53±6years. LLE were subdivided based on lifelong exercise intensity into performance (LLE-P) (n=14) and fitness (LLE-F) (n=7). Muscle biopsies (vastus lateralis) were examined for myosin heavy chain (MHC) slow (MHC I) and fast (MHC IIa) fibre size and function (strength, speed, power). LLE MHC I size (7624±2765μm2 ) was 25-40% larger (P<0.001) than YE (6106±1710μm2 ) and OH (5476±2467μm2 ). LLE MHC I fibres were ∼20% stronger, ∼10% faster and ∼30% more powerful than YE and OH (P<0.05). By contrast, LLE MHC IIa size (6466±2659μm2 ) was similar to OH (6237±2525μm2 ; P=0.854), with both groups ∼20% smaller (P<0.001) than YE (7860±1930μm2 ). MHC IIa contractile function was variable across groups, with a hierarchical pattern (OH > LLE > YE; P<0.05) in normalized power among OH (16.7±6.4WL-1 ), LLE (13.9±4.5WL-1 ) and YE (12.4±3.5WL-1 ). The LLE-P and LLE-F had similar single fibre profiles with MHC I power driven by speed (LLE-P) or force (LLE-F), suggesting exercise intensity impacted slow muscle fibre mechanics. These data suggest that lifelong endurance exercise benefited slow muscle fibre size and function. Comparable fast fibre characteristics between LLE and OH, regardless of training intensity, suggest other exercise modes (e.g. resistance training) or myotherapeutics may be necessary to preserve fast muscle fibre size and performance with age.

Young at heart: lifelong endurance exercise confers cardiovascular benefits for older women.

Young at heart: lifelong endurance exercise confers cardiovascular benefits for older women.

The effect of lifelong endurance exercise on cardiovascular structure and exercise function in women.

The beneficial effects of sustained or lifelong (>25years) endurance exercise on cardiovascular structure and exercise function have been largely established in men. The current findings indicate that committed (≥4weekly exercise sessions) lifelong exercise results in substantial benefits in exercise capacity ( ), cardiovascular function at submaximal and maximal exercise, left ventricular mass and compliance, and blood volume compared to similarly aged or even younger (middle-age) untrained women. Endurance exercise training should be considered a key strategy to prevent cardiovascular disease with ageing in women as well as men. This study was a retrospective, cross-sectional analysis of exercise performance and left ventricular (LV) morphology in 70 women to examine whether women who have performed regular, lifelong endurance exercise acquire the same beneficial adaptations in cardiovascular structure and function and exercise performance that have been reported previously in men. Three groups of women were examined: (1) 35 older (>60years) untrained women (older untrained, OU), (2) 13 older women who had consistently performed four or more endurance exercise sessions weekly for at least 25years (older trained, OT), and (3) 22middle-aged (range 35-59years) untrained women (middle-aged untrained, MU) as a reference control for the appropriate age-related changes. Oxygen uptake ( ) and cardiovascular function (cardiac output ( ); stroke volume (SV) acetylene rebreathing) were examined at rest, steady-state submaximal exercise and maximal exercise (maximal oxygen uptake, ). Blood volume (CO rebreathing) and LV mass (cardiac magnetic resonance imaging), plus invasive measures of static and dynamic chamber compliance were also examined. (p<0.001) and maximal exercise and SV were larger in older trained women compared to the two untrained groups (∼17% and ∼27% for and SV, respectively, versus MU; ∼40% and ∼38% versus OU, all p<0.001). Blood volume (mLkg-1 ) and LV mass index (gm-2 ) were larger in OT versus OU (∼11% and ∼16%, respectively, both P≤0.015) Static LV chamber compliance was greater in OT compared to both untrained groups (median (25-75%): MU: 0.065 (0.049-0.080); OU: 0.085 (0.061-0.138); OT: 0.047 (0.031-0.054), P≤0.053). Collectively, these findings indicate that lifetime endurance exercise appears to be extremely effective at preserving or even enhancing cardiovascular structure and function with advanced age in women.

Lifelong Endurance Exercise as a Countermeasure Against Age-Related [Formula: see text] Decline: Physiological Overview andInsights from Masters Athletes.

Maximum oxygen consumption ([Formula: see text]) is not only an indicator of endurance performance, but also a strong predictor of cardiovascular disease and mortality. This physiological parameter is known to decrease with aging. In turn, physical exercise might attenuate the rate of aging-related decline in [Formula: see text], which in light of the global population aging is of major clinical relevance, especially at advanced ages. In this narrative review, we summarize the evidence available from masters athletes about the role of lifelong endurance exercise on aging-related [Formula: see text] decline, with examples of the highest [Formula: see text] values reported in the scientific literature for athletes across different ages (e.g., 35ml·kg-1·min-1 in a centenarian cyclist). These data suggest that a linear decrease in [Formula: see text] might be possible if physical exercise loads are kept consistently high through the entire life span, with [Formula: see text] values remaining higher than those of the general population across all ages. We also summarize the main physiological changes that occur with inactive aging at different system levels-pulmonary and cardiovascular function, blood O2 carrying capacity, skeletal muscle capillary density and oxidative capacity-and negatively influence [Formula: see text], and review how lifelong exercise can attenuate or even prevent most-but apparently not all (e.g., maximum heart rate decline)-of them. In summary, although aging seems to be invariably associated with a progressive decline in [Formula: see text], maintaining high levels of physical exercise along the life span slows the multi-systemic deterioration that is commonly observed in inactive individuals, thereby attenuating age-related [Formula: see text] decline.

Impact of Lifelong Exercise Training Dose on Ventricular-Arterial Coupling.

The dynamic Starling mechanism, as assessed by beat-by-beat changes in stroke volume and left ventricular end-diastolic pressure, reflects ventricular-arterial coupling. It deteriorates with age, and is preserved in highly trained masters athletes. Currently, it remains unclear how much exercise over a lifetime is necessary to preserve efficient ventricular-arterial coupling. The purpose of this study was to assess the dose-dependent relationship between lifelong exercise training and the dynamic Starling mechanism in healthy seniors. One hundred two seniors were recruited and stratified into 4 groups based on 25 years of exercise training history: sedentary subjects (n=27, <2 sessions/week), casual exercisers (n=25, 2-3 sessions/week), committed exercisers (n=25, 4-5 sessions/week), and competitive Masters Athletes (n=25, 6-7 sessions/week). The dynamic Starling mechanism was estimated by transfer function gain between beat-by-beat changes in diastolic pulmonary artery pressure, a surrogate for left ventricular end-diastolic pressure, and stroke volume index. The transfer function gain of pulmonary artery pressure-stroke volume index was markedly enhanced in committed and competitive exercisers compared with more sedentary seniors and correlated with higher peak oxygen uptake (Vo2) and lower left ventricular stiffness. The power spectral density of pulmonary artery pressure was greater in sedentary adults than in committed and competitive exercisers, whereas the power spectral density of stroke volume index was greater in competitive exercisers than in the other groups. There is a graded, dose-dependent improvement in ventricular-arterial coupling with increasing amounts of lifelong regular exercise in healthy older individuals. Our data suggest that the optimal dose of lifelong endurance exercise to preserve ventricular-arterial coupling with age appears to be at least 4 to 5 sessions per week.

Expression Of Markers Of Browning In White Adipose Tissue In Life-long Endurance Trained Athletes

Physical exercise and training results in adaptations in adipose tissue. Such adaptations may in part be mediated through “cross-talk” with skeletal muscle. One of these adaptations potentially relevant to energy metabolism in endurance athletes is the beiging of white adipose tissue (WAT). Beiging is the process by which WAT shows characteristics of brown adipose tissue (BAT), possibly increasing basal metabolic rate. While the process of beiging in rodents and the existence of BAT in humans has been shown previously, it is unknown if and how life-long endurance exercise influences beiging of WAT depots. PURPOSE: To study the influence of life-long training on adipose tissue markers of beiging and metabolic performance, the uncoupling protein 1 (UCP-1), CIDEA and PPAR-γ in white adipose tissue (WAT) in sub-elite athletes. METHODS: Periumbilical subcutaneous adipose tissue biopsies were collected from 14 life-long trained sub-elite endurance athletes (8 male, 6 female; VO max performance over 90th percentile for their age group) and 13 age-matched controls (6 male 7 female). Gene expression was analyzed on extracted RNA. Fold induction was statistically analyzed by Student’s-test. RESULTS: UCP-1 gene expression was significantly higher in trained women compared with the control group (p=0.046). No significant difference was found in men when comparing UCP-1 expression (p=0.257). Expression of CIDEA was, again, significantly higher compared with controls (p=0.049), but also in men (p=0.024). Finally, expression of PPAR-γ was significantly higher in trained women (p=0.005). Again no differences were found in men (p=0.924). CONCLUSION: Life-long endurance training results in a higher expression of brown adipose tissue markers in periumbilical WAT in women, in men only in expression of CIDEA, a factory closely associated with metabolic health. Previous results in rodents show a higher susceptibility of females to upregulate BAT markers following β-adrenergic signaling. A similar mechanism might be possible in humans. This effect might also be caused by differences in body fat distribution and functionality, with women having a higher prevalence for BAT.

Endurance exercise prevents high-fat-diet induced heart and mobility premature aging and dsir2 expression decline in aging Drosophila.

High-Fat-Diet (HFD)-induced obesity is a major contributor to heart and mobility premature aging and mortality in both Drosophila and humans. The dSir2 genes are closely related to aging, but there are few directed reports showing that whether HFD could inhibit the expression dSir2 genes. Endurance exercise can prevent fat accumulation and reverse HFD-induced cardiac dysfunction. Endurance also delays age-relate functional decline. It is unclear whether lifetime endurance exercise can combat lifetime HFD-induced heart and mobility premature aging, and relieve the harmful HFD-induced influence on the dSir2 gene and lifespan yet. In this study, flies are fed a HFD and trained from when they are 1 week old until they are 5 weeks old. Then, triacylglycerol levels, climbing index, cardiac function, lifespan, and dSir2 mRNA expressions are measured. We show that endurance exercise improves climbing capacity, cardiac contraction, and dSir2 expression, and it reduces body and heart triacylglycerol levels, heart fibrillation, and mortality in both HFD and aging flies. So, lifelong endurance exercise delays HFD-induced accelerated age-related locomotor impairment, cardiac dysfunction, death, and dSir2 expression decline, and prevents HFD-induced premature aging in Drosophila.

Are There Deleterious Cardiac Effects of Acute and Chronic Endurance Exercise?

Multiple epidemiological studies document that habitual physical activity reduces the risk of atherosclerotic cardiovascular disease (ASCVD), and most demonstrate progressively lower rates of ASCVD with progressively more physical activity. Few studies have included individuals performing high-intensity, lifelong endurance exercise, however, and recent reports suggest that prodigious amounts of exercise may increase markers for, and even the incidence of, cardiovascular disease. This review examines the evidence that extremes of endurance exercise may increase cardiovascular disease risk by reviewing the causes and incidence of exercise-related cardiac events, and the acute effects of exercise on cardiovascular function, the effect of exercise on cardiac biomarkers, including "myocardial" creatine kinase, cardiac troponins, and cardiac natriuretic peptides. This review also examines the effect of exercise on coronary atherosclerosis and calcification, the frequency of atrial fibrillation in aging athletes, and the possibility that exercise may be deleterious in individuals genetically predisposed to such cardiac abnormalities as long QT syndrome, right ventricular cardiomyopathy, and hypertrophic cardiomyopathy. This review is to our knowledge unique because it addresses all known potentially adverse cardiovascular effects of endurance exercise. The best evidence remains that physical activity and exercise training benefit the population, but it is possible that prolonged exercise and exercise training can adversely affect cardiac function in some individuals. This hypothesis warrants further examination.

Left ventricular atrioventricular plane displacement is preserved with lifelong endurance training and is the main determinant of maximal cardiac output.

Age-related decline in cardiac function can be prevented or postponed by lifelong endurance training. However, effects of normal ageing as well as of lifelong endurance exercise on longitudinal and radial contribution to stroke volume are unknown. The aim of this study was to determine resting longitudinal and radial pumping in elderly athletes, sedentary elderly and young sedentary subjects. Furthermore, we aimed to investigate determinants of maximal cardiac output in elderly. Eight elderly athletes (63 ± 4 years), seven elderly sedentary (66 ± 4 years) and ten young sedentary subjects (29 ± 4 years) underwent cardiac magnetic resonance imaging. All subjects underwent maximal exercise testing and for elderly subjects maximal cardiac output during cycling was determined using a dye dilution technique. Longitudinal and radial contribution to stroke volume did not differ between groups (longitudinal left ventricle (LV) 52-65%, P = 0.12, right ventricle (RV) 77-87%, P = 0.16, radial 7.9-8.6%, P = 1.0). Left ventricular atrioventricular plane displacement (LVAVPD) was higher in elderly athletes and young sedentary compared with elderly sedentary subjects (14 ± 3, 15 ± 2 and 11 ± 1 mm, respectively, P < 0.05). There was no difference between groups for RVAVPD (P = 0.2). LVAVPD was an independent predictor of maximal cardiac output (R(2) = 0.61, P < 0.01, β = 0.78). Longitudinal and radial contributions to stroke volume did not differ between groups. However, how longitudinal pumping was achieved differed; elderly athletes and young sedentary subjects showed similar AVPD whereas this was significantly lower in elderly sedentary subjects. Elderly sedentary subjects achieved longitudinal pumping through increased short-axis area of the ventricle. Large AVPD was a determinant of maximal cardiac output and exercise capacity.

Life-long endurance exercise in humans: Circulating levels of inflammatory markers and leg muscle size

Human aging is associated with a loss of skeletal muscle and an increase in circulating inflammatory markers. It is unknown whether endurance training (Tr) can prevent these changes. Therefore we studied 15 old trained (O-Tr) healthy males and, for comparison, 12 old untrained (O-Un), 10 Young-Tr (Y-Tr) and 12 Young-Un (Y-Un). Quadriceps size, VO2 peak, CRP, IL-6, TNF-α and its receptors, suPAR, lipid profile, leucocytes and glucose homeostasis were measured. Tr was associated with an improved insulin profile (p<0.05), and lower leucocyte (p<0.05) and triglyceride levels (p<0.05), independent of age. Aging was associated with poorer glucose control (p<0.05), independent of training. The age-related changes in waist circumference, VO2 peak, cholesterol, LDL, leg muscle size, CRP and IL-6 were counteracted by physical activity (p<0.05). A significant increase in suPAR with age was observed (p<0.05). Most importantly, life-long endurance exercise was associated with a lower level of the inflammatory markers CRP and IL-6 (p<0.05), and with a greater thigh muscle area (p<0.05), compared to age-matched untrained counterparts. These findings in a limited group of individuals suggest that regular physical endurance activity may play a role in reducing some markers of systemic inflammation, even within the normal range, and in maintaining muscle mass with aging.

Effects of Lifelong Endurance Exercise on Cardiovascular Response to Orthostatic Stress in The Elderly Athletes

BackgroundYoung endurance athletes have a greater decrease in stroke volume (SV) during orthostatic stress than age‐matched controls, due to a more compliant left ventricle (LV). Elderly athletes with lifelong training (EA) also have more compliant LV compared to elderly controls (C). However, it is unclear if the decrease in SV during orthostatic stress is greater in EA relative to C.MethodsFifty five subjects (EA 27, C 28) underwent right heart catheterization to measure pulmonary capillary wedge (PCWP) and right atrial (RAP) pressures, and SV at baseline and −15 and −30 mmHg lower body negative pressures (LBNP). To minimize the effect of external constraint on the LV, transmural pressure (TMP), which is the true preload for the LV, was calculated as PCWP‐RAP.ResultsAt baseline, SV index was larger in EA than C. PCWP appeared to be lower in EA, while TMP was similar between EA and C (3.4±1.4 vs. 3.5±1.4 mmHg, p=0.87). LBNP similarly lowered PCWP and TMP in EA and C (interaction p ≥ 0.56), while a greater decrease in SV index from baseline was observed in EA than C at −30 mmHg LBNP (17 vs. 12 ml/m2, p &lt;0.01).ConclusionTMP was similarly regulated in EA and C at all loading conditions. EA had greater decrease in SV during orthostatic stress, probably due to a more compliant LV. Thus, similar to young athletes, EA may be more susceptible to orthostatic intolerance.

Mitochondrial biogenesis and angiogenesis in skeletal muscle of the elderly

The aim of this study was to test the hypotheses that 1) skeletal muscles of elderly subjects can adapt to a single endurance exercise bout and 2) endurance trained elderly subjects have higher expression/activity of oxidative and angiogenic proteins in skeletal muscle than untrained elderly people. To investigate this, lifelong endurance trained elderly (ET; n = 8) aged 71.3 ± 3.4 years and untrained elderly subjects (UT; n = 7) aged 71.3 ± 4 years, performed a cycling exercise bout at 75% VO 2max with vastus lateralis muscle biopsies obtained before (Pre), immediately after exercise (0h) and at 2 h of recovery. Capillarization was detected histochemically and oxidative enzyme activities were determined on isolated mitochondria. GLUT4, HKII, Cyt c and VEGF protein expression was measured on muscle lysates from Pre-biopsies, phosphorylation of AMPK and P38 on lysates from Pre and 0h biopsies, while PGC-1α, VEGF, HKII and TFAM mRNA content was determined at all time points. ET had ~ 40% higher PDH, CS, SDH, α-KG-DH and ATP synthase activities and 27% higher capillarization than UT, reflecting increased skeletal muscle oxidative capacity with lifelong endurance exercise training. In addition, acute exercise increased in UT PGC-1α mRNA 11-fold and VEGF mRNA 4-fold at 2 h of recovery, and AMPK phosphorylation ~ 5-fold immediately after exercise, relative to Pre, indicating an ability to adapt metabolically and angiogenically to endurance exercise. However, in ET PGC-1α mRNA only increased 5 fold and AMPK phosphorylation ~ 2-fold, while VEGF mRNA remained unchanged after the acute exercise bout. P38 increased similarly in ET and UT after exercise. In conclusion, the present findings suggest that lifelong endurance exercise training ensures an improved oxidative capacity of skeletal muscle, and that skeletal muscle of elderly subjects maintains the ability to respond to acute endurance exercise.

Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes

This study examined the cardiac structure and function of a unique cohort of documented lifelong, competitive endurance veteran athletes (>50 yr). Twelve lifelong veteran male endurance athletes [mean ± SD (range) age: 56 ± 6 yr (50-67)], 20 age-matched veteran controls [60 ± 5 yr; (52-69)], and 17 younger male endurance athletes [31 ± 5 yr (26-40)] without significant comorbidities underwent cardiac magnetic resonance (CMR) imaging to assess cardiac morphology and function, as well as CMR imaging with late gadolinium enhancement (LGE) to assess myocardial fibrosis. Lifelong veteran athletes had smaller left (LV) and right ventricular (RV) end-diastolic and end-systolic volumes (P < 0.05), but maintained LV and RV systolic function compared with young athletes. However, veteran athletes had a significantly larger absolute and indexed LV and RV end-diastolic and systolic volumes, intraventricular septum thickness during diastole, posterior wall thickness during diastole, and LV and RV stroke volumes (P < 0.05), together with significantly reduced LV and RV ejection fractions (P < 0.05), compared with veteran controls. In six (50%) of the veteran athletes, LGE of CMR indicated the presence of myocardial fibrosis (4 veteran athletes with LGE of nonspecific cause, 1 probable previous myocarditis, and 1 probable previous silent myocardial infarction). There was no LGE in the age-matched veteran controls or young athletes. The prevalence of LGE in veteran athletes was not associated with age, height, weight, or body surface area (P > 0.05), but was significantly associated with the number of years spent training (P < 0.001), number of competitive marathons (P < 0.001), and ultraendurance (>50 miles) marathons (P < 0.007) completed. An unexpectedly high prevalence of myocardial fibrosis (50%) was observed in healthy, asymptomatic, lifelong veteran male athletes, compared with zero cases in age-matched veteran controls and young athletes. These data suggest a link between lifelong endurance exercise and myocardial fibrosis that requires further investigation.

Cardiovascular function and the veteran athlete

The cardiovascular benefits of exercise are well known. In contrast, the impact of lifelong endurance exercise is less well understood. Long-term high-intensity endurance exercise is associated with changes in cardiac morphology together with electrocardiographic alterations that are believed to be physiologic in nature. Recent data however has suggested a number of deleterious adaptive changes in cardiac structure, function and electrical activity, together with peripheral and cerebral vascular structure and function. This review serves to detail knowledge in relation to; (1) Cardiac structure and function in veteran endurance athletes focusing on the differentiation of physiological and pathological changes in cardiac remodelling; (2) Cardiac electrical activity and the veteran endurance athlete with attention to arrhythmias, the substrate for arrhythmia generation and the clinical significance of such arrhythmias; (3) Peripheral and cerebral vascular structure and function in ageing and endurance-trained individuals; and (4) directions for future research.