Centenarians, who have escaped or survived lethal diseases earlier in life, may be considered a spontaneous model of healthy ageing. The gut microbial composition of centenarians has consistently been reported to differ in phylogenetic composition from that of younger people. Interestingly, within centenarian populations, species have been reported to display regional characteristics, further supporting that environmental and/or lifestyle factors including the diet, shape microbial composition.

For example, in an Italian cohort, the centenarian microbiome was found to be dominated by the same two microbial families as in the other age groups (<75 years old) of the population, namely Veillonellaceae and Ruminococcaceae (Firmicutes phylum), but was specifically enriched in the genera Akkermansia, Bifidobacterium, and Christensenella. In contrast, the Chinese Hainan Centenarian Cohort was dominated by Bacteroides (Bacteroidetes phylum) and Escherichia (Proteobacteria phylum). Long-term elderly care residents in the Irish ELDERMET Cohort also had a gut microbiome dominated by Bacteroidetes. Importantly, although the aggregate faecal microbiome in ELDERMET was dominated by Bacteroidetes, the residents showed extraordinary inter-individual variation with 3-92% Bacteroidetes and 7-94% Firmicutes, hinting at a long-term effect of their dietary habits.

The results of the Italian study are also in contrast to those of another Chinese Centenarian Cohort from the Guangxi region, who harboured significantly higher abundance of the genera Escherichia and Roseburia, and reduced abundance of Akkermansia, Lactobacillus, Faecalibacterium, Parabacteroides, Butyricimonas, Coprococcus, Megamonas, Mitsuokella, and Sutterella. A Korean centenarian study found trends similar to both Italian and Guangxi Chinese centenarians, with higher abundance of Akkermansia and Christensenella, and Escherichia, respectively. They also displayed increased abundance of Clostridium and Collinsella, and reduced abundance of Faecalibacterium and Prevotella compared to the general population.

At present, we do not have a good understanding to explain these geographical variations in the centenarian gut microbial composition or to unequivocally answer if there are certain microbial species globally associated with longevity. In the reviewed studies, some microbial genera associated with healthy elderly populations include Roseburia, Escherichia, Akkermansia, Christensenella, Bifidobacterium, and Clostridium, but they are all highly variable across populations. Based on these cross-sectional observations, it seems unlikely that a universal pro-longevity gut microbiome exists. Rather, the optimal microbiome for healthspan appears to be conditional on the microbial functionality acting on regional- and ethnicity-specific trends driven by cultural food context.

Today FDA approved Aduhelm (aducanumab) to treat patients with Alzheimer's disease using the Accelerated Approval pathway, under which the FDA approves a drug for a serious or life-threatening illness that may provide meaningful therapeutic benefit over existing treatments when the drug is shown to have an effect on a surrogate endpoint that is reasonably likely to predict a clinical benefit to patients and there remains some uncertainty about the drug's clinical benefit.

We are well-aware of the attention surrounding this approval. We understand that Aduhelm has garnered the attention of the press, the Alzheimer's patient community, our elected officials, and other interested stakeholders. The late-stage development program for Aduhelm consisted of two phase 3 clinical trials. One study met the primary endpoint, showing reduction in clinical decline. The second trial did not meet the primary endpoint. In all studies in which it was evaluated, however, Aduhelm consistently and very convincingly reduced the level of amyloid plaques in the brain in a dose- and time-dependent fashion. It is expected that the reduction in amyloid plaque will result in a reduction in clinical decline.

We know that the Peripheral and Central Nervous System Drugs Advisory Committee, which convened in November 2020 to review the clinical trial data and discuss the evidence supporting the Aduhelm application, did not agree that it was reasonable to consider the clinical benefit of the one successful trial as the primary evidence supporting approval. As mentioned above, treatment with Aduhelm was clearly shown in all trials to substantially reduce amyloid beta plaques. This reduction in plaques is reasonably likely to result in clinical benefit. After the Advisory Committee provided its feedback, our review and deliberations continued, and we decided that the evidence presented in the Aduhelm application met the standard for Accelerated Approval.

The need for treatments is urgent: right now, more than 6 million Americans are living with Alzheimer's disease and this number is expected to grow as the population ages. Alzheimer's is the sixth leading cause of death in the United States. Although the Aduhelm data are complicated with respect to its clinical benefits, FDA has determined that there is substantial evidence that Aduhelm reduces amyloid beta plaques in the brain and that the reduction in these plaques is reasonably likely to predict important benefits to patients.

Older people with COVID-19 infection often suffer a severe form of interstitial pneumonia accompanied to an excessive human immune response with a hyper-inflammatory condition characterized by the increase of many plasma cytokines, including IL-6, interleukin 8 (IL-8), interferon (IFN), and tumor necrosis factor levels increase, particularly of IL-6 (the so-called "cytokine storm"). What drives such intense hyper-inflammation in COVID-19 is not yet known; however, the upregulation of IL-6 seems the pivotal pro-inflammatory function is contributing to COVID-19 severity.

Herein, we suggest that the preexisting upregulation of cytokine expression of inflammaging may trigger, and also support, the excessive hyper-inflammatory state in older people. Indeed, the superimposed SARS-CoV-2 infection in older adults may acutely exaggerate the already present pro-inflammatory background of inflammaging, predisposing older people to greater COVID-19 disease severity and mortality. The co-occurrence of the COVID-19 infection, constituting a second-hit to the preexisting pro-inflammatory condition of inflammaging, leading to a dysregulation of inflammation, which becomes harmful, reaching a severe pathological threshold.

We must also consider the impact of a pro-inflammatory state on coagulation because of the crosstalk between inflammation and coagulation. It is well established that the systemic inflammatory state of elderly people and coagulation disorder are closely linked, a phenomenon which here we refer to as "coagul-aging". Physiological aging is associated with increased plasma levels of many proteins of blood coagulation together with fibrinolysis impairment; this may be of great concern in view of the known association between vascular and thromboembolic diseases and aging, a condition which, here we suggest, may also contribute to the co-occurrence of the high incidence of coagulopathy in older COVID-19 patients.

In the future, we hope to carry out more studies on inflammaging and coagul-aging, which will enable us to understand the mechanism in-depth and find measures to intervene in the corresponding processes. More studies will not only help elderly patients with severe infections like COVID-19, but can also have the potential to intervene in the aging-associated pro-inflammatory state and the senescence process itself.

Populations are ageing worldwide. Globally, the proportion of those aged 65 and over has increased by 9% in the last two decades, and is expected to grow by a further 16% by 2050. This demographic shift will require societies to adapt. If longer lives are spent in poor health, governments face the challenge of providing accessible, high quality and sustainable long-term care. The growth in life expectancy is a positive, but with this comes a responsibility to ensure people have the support they need as they age, and to facilitate ageing in place.

In 2019, the World Health Organisation (WHO) renewed its commitment to support countries to achieve longer and healthier lives with the Decade of Healthy Ageing 2020-2030 strategy. A critical part of achieving longevity is understanding whether longer lives are typified by more years spent in good health (compression of disability) or poor health (expansion of disability). This has important implications for the provision of health and care services to respond to the needs of people as they age. It is, therefore, crucial to keep abreast of trends, specifically how the growth in life expectancy is matched by a growth in years spent in good health.

Metrics to assess this most commonly include healthy life expectancy and disability-free life expectancy. Both provide an estimate of life expectancy spent in good health, but differ slightly with respect to their measurement. Healthy life expectancy tends to rely on single item questions of self-reported health, and is thus subject to fluctuations as expectations of health change over time. Disability-free life expectancy is often calculated from multiple items about activity limitations and/or dependencies, and therefore does not bear the same limitations as that of healthy life expectancy.

Previous reviews have summarised trends in total, healthy, and disability-free life expectancy, the most recently in 2016. Typically, such evidence shows that while people are living longer, gains in life expectancy are not consistently matched by a growth in the number of years lived in good health and free of disability. Nevertheless, this is an evolving evidence base requiring ongoing scrutiny.

This systematic review was undertaken to update our current understanding of trends in health expectancies in OECD high-income countries. The principal finding is that changes in health expectancies have not kept pace with the growth in life expectancy in a number of high-income countries. One clear exception was Sweden, where gains in women's disability-free life expectancy were greater than gains in life expectancy over a period of almost 20 years. In conclusion, a number of high-income countries, changes in health expectancies over time have not kept pace with the growth in life expectancy. That is, people are living longer but disability and poor health are occupying an increasing proportion of later life. Our findings suggest that countries still need to make significant progress to achieve the WHO's Decade of Healthy Ageing goal of healthier, longer lives for all.

Growth hormone (GH) and its receptor (GHR) are not only important for regulating growth, they have many other important biological functions that include response to nutrients, regulation of metabolism, and controlling physiological processes related to the hepatobiliary, cardiovascular, renal, gastrointestinal, and reproductive systems. Growth hormone signaling is an important regulator of aging. GH deficiency leads to slower growth, delayed maturation, reduced body size, and can result in attenuation of the rate of aging, increased health-span, and increased longevity. Key to this are evolutionarily conserved pathways of insulin/insulin-like growth factors and mechanistic target of rapamycin, where there are trade-offs between anabolic processes/growth and lifespan.

We have reported a significant negative association between height and longevity in our large cohort of American men of Japanese ancestry. More recently, in a case-control study of 13 single nucleotide polymorphisms (SNPs) of GHR in this cohort, SNP rs4130113 was associated with greater lifespan of nonagenarian men aged ≥ 95 years. In the present longitudinal study, we tested the hypothesis that genetic variation in GHR affects lifespan at least in part by protection against the detrimental effects of one or more aging-related diseases, namely diabetes, hypertension, coronary heart disease, and/or cancer.

The present study has found that the longevity-associated AA genotype (frequency 35.3%), but also the GG genotype (frequency 17.1%), of GHR SNP rs4130113 is associated with protection against risk of mortality in hypertensive elderly American men of Japanese ancestry. As a result, those individuals lived longer, whereas individuals with the AG genotype (frequency 47.6%) died sooner. Moreover, the survival curve for hypertensive AA/GG subjects did not differ significantly from the survival curve for normotensive subjects with the AA/GG genotype. This indicated that possession of the GHR longevity-associated genotype can mitigate the adverse effects on lifespan of having hypertension.

Accumulating evidence suggests that the sympathetic nervous system (SNS) overactivity plays a crucial role in age-related increase in the risk for cardiovascular diseases such as hypertension, myocardial infarction, stroke, and heart diseases. Previous studies indicate that neuroinflammation in key brainstem regions that regulate sympathetic outflow plays a pathogenic role in aging-mediated sympathoexcitation. However, the molecular mechanisms underlying this phenomenon are not clear. While senescent cells and their secretory phenotype (SASP) have been implicated in the pathogenesis of several age-related diseases, their role in age-related neuroinflammation in the brainstem and SNS overactivity has not been investigated.

To test this, we isolated brainstems from young (2-4 months) and aged (24 months) male C57BL/6J mice and assessed senescence using a combination of RNA-in situ hybridization, PCR analysis, multiplex assay, and SA-β gal staining. Our results show significant increases in p16Ink4a expression, increased activity of SA-β gal and increases in SASP levels in the aged brainstem, suggesting age-induced senescence in the brainstem. Further, analysis of senescence markers in glial cells enriched fraction from fresh brainstem samples demonstrated that glial cells are more susceptible to senesce with age in the brainstem. In conclusion, our study suggests that aging induces glial senescence in the brainstem which likely causes inflammation and SNS overactivity.

Researchers have studied brain activity and blood flow in the hippocampus of mice. The team used simulations to predict that the amount of oxygen supplied to hippocampal neurons furthest from blood vessels is only just enough for the cells to keep working normally. "These findings are an important step in the search for preventative measures and treatments for Alzheimer's, because they suggest that increasing blood flow in the hippocampus might be really effective at preventing damage from happening. If it's right that increasing blood flow in the hippocampus is important in protecting the brain from diseases like Alzheimer's, then it will throw further weight behind the importance of regular exercise and a low-cholesterol diet to long-term brain health."

"We think that the hippocampus exists at a watershed. It's just about OK normally, but when anything else happens to decrease brain blood flow, oxygen levels in the hippocampus reduce to levels that stop neurons working. We think that's probably why Alzheimer's disease first causes memory problems - because the early decrease in blood flow stops the hippocampus from working properly. The same factors that put you at risk of having a heart attack make you more likely to develop dementia. That's because our brains need enough blood flow to provide energy - in the form of oxygen and glucose - so brain cells can work properly, and because blood flow can clear away waste products such as the beta amyloid proteins that build up in Alzheimer's disease. Now we want to discover whether the lower blood flow and oxygen levels in the hippocampus are what causes beta amyloid to start to build up in Alzheimer's disease. Understanding what causes early damage will be really important to help us learn how to treat or prevent disease."

Researchers are preparing to launch clinical trials of a lozenge that contains an engineered peptide, or chain of amino acids, along with phosphorus and calcium ions, which are building blocks of tooth enamel. The peptide is derived from amelogenin, the key protein in the formation of tooth enamel, the tooth's crown. It is also key to the formation of cementum, which makes up the surface of the tooth root.

Each lozenge deposits several micrometers of new enamel on the teeth via the peptide, which is engineered to bind to the damaged enamel to repair it while not affecting the mouth's soft tissue. The new layer also integrates with dentin, the living tissue underneath the tooth's surface. Two lozenges a day can rebuild enamel, while one a day can maintain a healthy layer.

The lozenge produces new enamel that is whiter than what tooth-whitening strips or gels produce. It has another distinct advantage: Conventional whitening treatments rely on hydrogen peroxide, a bleaching agent that can weaken tooth enamel after prolonged use. Since tooth enamel can't regrow spontaneously, the underlying dentin can be exposed, with results ranging from hypersensitivity to cavities or even gum disease. The lozenge, on the other hand, strengthens, rebuilds, and protects teeth.

In addition, the researchers are investigating a gel or solution with the engineered peptide to treat hypersensitive teeth. This problem results from weakness in the enamel that makes the underlying dentin and nerves more vulnerable to heat or cold. Most common products currently on the market can put a layer of organic material on the tooth and numb nerve endings with potassium nitrate, but the relief is only temporary. The peptide, however, addresses the problem permanently at its source by strengthening the enamel.

Researchers have discovered a new mechanism of Alzheimer's disease that disorganises the blood vessels around amyloid plaques, one of the characteristic features of the disease. The mechanism put forward in this study is mediated by the dysfunction of a physiological process, angiogenesis. This mechanism is important during development to form the vessels of the brain and in adulthood to revert possible damage to pre-existing vessels. The study shows that Alzheimer's disease induces angiogenesis dysfunction that causes the loss of vessels instead of the formation of new ones, undoubtedly aggravating the pathology. By identifying the molecular pathways involved, new therapeutic strategies to alleviate the effects of this disease can be rationally designed.

A characteristic feature of Alzheimer's patients is the accumulation of highly toxic substances in their brains, known as senile plaques. The brain has the capacity to clean these toxic substances via transport through the blood. Thus the fact that the plaques cause the loss of the vessels constitutes a vicious circle: having fewer vessels reduces the ability to clean the brain thus allowing more toxic substances to accumulate, which in turn continue to destroy the vessels and worsen the situation. The brain consumes much of the body's oxygen and nutrients. Thus a local reduction in the supply of these substances through the blood represents an additional strain above and beyond the existing strain from the accumulation of toxic substances.

Cellular senescence is a cell fate response characterized by a permanent cell cycle arrest driven primarily the by cell cycle inhibitor and tumor suppressor proteins p16Ink4a and p21Cip1/Waf1. In mice, the p21Cip1/Waf1 encoding locus, Cdkn1a, is known to generate two transcripts that produce identical proteins, but one of these transcript variants is poorly characterized. We show that the Cdkn1a transcript variant 2, but not the better-studied variant 1, is selectively elevated during natural aging across multiple mouse tissues.

Importantly, mouse cells induced to senescence in culture by genotoxic stress (ionizing radiation or doxorubicin) upregulated both transcripts, but with different temporal dynamics: variant 1 responded nearly immediately to genotoxic stress, whereas variant 2 increased much more slowly as cells acquired senescent characteristics. Upon treating mice systemically with doxorubicin, which induces widespread cellular senescence in vivo, variant 2 increased to a larger extent than variant 1. Variant 2 levels were also more sensitive to the senolytic drug ABT-263 in naturally aged mice. Thus, variant 2 is a novel and more sensitive marker than variant 1 or total p21Cip1/Waf1 protein for assessing the senescent cell burden and clearance in mice.

The axolotl, a Mexican salamander that is now all but extinct in the wild, is a favorite model in regenerative medicine research because of its one-of-a-kind status as nature's champion of regeneration. While most salamanders have some regenerative capacity, the axolotl can regenerate almost any body part. Since mammalian embryos and juveniles have the ability to regenerate - for instance, human infants can regenerate heart tissue and children can regenerate fingertips - it's likely that adult mammals retain the genetic code for regeneration, raising the prospect that pharmaceutical therapies could be developed to encourage humans to regenerate tissues and organs lost to disease or injury instead of forming a scar.

Researchers compared immune cells called macrophages in the axolotl to those in the mouse with the goal of identifying the quality in axolotl macrophages that promotes regeneration. The research builds on earlier studies in which it was found that macrophages are critical to regeneration: when they are depleted, the axolotl forms a scar instead of regenerating, just like mammals. The recent research found that although macrophage signaling in the axolotl and in the mouse were similar when the organisms were exposed to pathogens, when it came to exposure to injury it was a different story: the macrophage signaling in the axolotl promoted the growth of new tissue while that in the mouse promoted scarring.

Specifically, the signaling response of a class of proteins called toll-like receptors (TLRs), which allow macrophages to recognize a threat such an infection or a tissue injury and induce a pro-inflammatory response, were unexpectedly divergent in response to injury in the axolotl and the mouse. The finding offers an intriguing window into the mechanisms governing regeneration in the axolotl. The discovery of an alternative signaling pathway that is compatible with regeneration could ultimately lead to regenerative medicine therapies for humans.

While the definition of sarcopenia is an evolving concept that started with a classification based on muscle mass alone, this has progressively moved to a more operational definition that includes the loss not only of muscle mass but also of muscle strength, with a risk of adverse outcomes such as physical disability, poor quality of life, and even death. However, as recognized by recent definitions of sarcopenia, low muscle mass or quality is a determinant factor for confirming sarcopenia in the presence of low muscle strength, otherwise known as dynapenia. Hence, the measurement of muscle mass remains a key requirement for the clinical diagnosis of sarcopenia. Typically, this has been achieved using dual X-ray absorptiometry (DXA), MRI, or bioelectrical impedance. The use of these methods has been widespread and has been instrumental for the diagnosis of sarcopenia in clinical settings.

In 2003, we reported for the first time that the loss of muscle mass associated with sarcopenia not only entails a decrease in muscle cross-sectional area and volume but also alterations in the spatial arrangement of muscle fibres within the muscle. Knowledge of the spatial arrangement of muscle fibres within a muscle is particularly important because muscle architecture is one of the most important determinants of muscle force and velocity. Using ultrasonography, we were able to show, for several locomotor muscles, that the key parameters of muscle architecture are significantly altered in sarcopenic muscle.

If changes in muscle architecture were to scale harmonically with the decrease in muscle volume due to sarcopenia, one would expect the ratio of fascicle length (Lf) to muscle thickness (Tm) to remain constant. However, muscle length (and thus fascicle length) is constrained by its connections into the proximal and distal tendons that insert into bony structures. Although fascicle length has been found to decrease with ageing, this effect should be limited by the proximal and distal tendon insertions into bone, unless tendons were to elongate, which is most unlikely. Hence, the reduction in muscle mass with ageing should be due more to a decrease in muscle thickness than in fascicle length, that is, it should involve a greater loss of sarcomeres in parallel than in series. Recent observations made in our laboratory in different populations of older individuals (active, sedentary, and mobility impaired) seem to confirm this assumption: with increasing degree of sarcopenia, the decrease in muscle thickness (Tm) exceeds that of fascicle length (Lf).

These findings prompted us to formulate the hypothesis that the Lf/Tm ratio, which we shall refer to as 'ultrasound sarcopenia index' (USI), may be used as a marker of the loss of muscle mass associated with sarcopenia. An important advantage of using a marker based on an anatomical ratio rather than on absolute values is its independence from gender and body dimensions. Further, there are several important advantages to be considered regarding the use of ultrasound for assessing muscle architecture, both for clinical and practical purposes. Ultrasound can be delivered at a fraction of the cost of MRI, and has a very good reliability and reproducibility when performed by properly trained personnel.

Chronic sub-clinical inflammation of aging, resulting from lifetime exposures to pathogens in concert with impaired immune responses, poses an obstinate challenge to the health span of the growing elderly population. Several factors contribute to the increased morbidity/mortality of older adults, including loss of naïve lymphocytes, exhaustion of adaptive immunity, and a skew toward proinflammatory responses. Additionally, loss of intestinal homeostasis and perturbations in epithelial barrier protective immune functions have recently emerged as key factors underlying chronic inflammation and age-related comorbidities.

Defense of epithelial barriers against invading pathogens and maintenance of mucosal homeostasis mainly relies on the Th17-type immunity, also known as type-17 and Th3 immunity, which is characterized by IL-17/IL-22 cytokine production. IL-17 predominantly triggers the influx of neutrophils and tissue repair, while IL-22 stimulates proliferation of epithelial cells, and regulates epithelial permeability, production of mucus, antimicrobial proteins, and complement to help maintain barrier integrity.

Our laboratory has shown that systemic inflammation in older macaques was associated with reduced Th17-type cytokine functions of CD161+ immune cells. This correlated with circulating biomarkers of leaky gut and microbial translocation, suggesting a link between intestinal barrier dysfunction and inflammaging. There is significant evidence showing that Th17-type immunity and epithelial barrier functions have an important role in the immune response and inflammation of aging; however, the precise cellular and molecular mechanisms underlying altered Th17-type responses in aging humans remain to be elucidated.

The health and diversity of our microbiome and how it influences Th17-type responses should also be of value for mucosal immunity in the context of aging. A clear understanding of epithelial barrier protective Th17-type responses will aid the development of targeted therapies, specifically tailored for the elderly.

People are living longer, staying healthier longer and accomplishing things late in life that once seemed possible only at younger ages. And it's not just superstars. The fraction of over-85s in the U.S. classified as disabled dropped by a third between 1982 and 2005, while the share who were institutionalized fell nearly in half. As a whole, Americans seem to be aging more slowly than before. Researchers compared how men 60 to 79 years old aged in 1988 to 1994 and in 2007 to 2010. They found that in those later years, the men they studied had a biological age four years less than the men in the earlier years, in part because of improvements in lifestyle and medications. This suggests that not only are people living longer, they're also staying healthier longer.

On one level, greater health and longevity is an old story. In 1900, life expectancy in the U.S. was about 47 years and now it's about 78. But we may also be on the cusp of something new. Over the course of the 20th century, we primarily aided longevity by tackling disease. In the first half of the century vaccines and other innovations prevented people from dying young of communicable diseases. In the second half, improvements in lifestyle and other medical breakthroughs prevented many people from dying in middle age of things like heart attacks and cancer.

But while these improvements have made it more likely that people will live to be 65, after that, aging itself takes an inexorable toll. Even if you beat lung cancer or survive a heart attack, your body's deterioration will finish you off before too long. The average 80-year-old suffers from around five diseases. That's why even if we could totally cure cancer, it would add less than three years to average life expectancy. A total cure for heart disease would give us at best two extra years. To keep the longevity train rolling it may not be enough to cure diseases. We may also need to address the underlying condition of aging itself, which is, after all, the primary risk factor for late-life decline.

S. Jay Olshansky has said "While there are no documented interventions that have been proven safe and effective in slowing aging in humans today, we are on the verge of a breakthrough." For example, as we age, we build up more and more "senescent" cells, which secrete inflammatory molecules that can effectively accelerate aging. In 2011, researchers removed these cells from mice and extended their life spans. Clinical trials on people began in 2018. It's likely that all Americans could be living longer, healthier lives. I imagine an 80-year-old bounding from bed, biking in the morning and playing softball in the afternoon. We're all on borrowed time. More time is more life, and more of it will be sweet.

Cross-sectional and interventional studies suggest that high-intensity strength and impact-type training provide a powerful osteogenic stimulus even in old age. However, longitudinal evidence on the ability of high-intensity training to attenuate age-related bone deterioration is currently lacking. This follow-up study assessed the role of continued strength and sprint training on bone aging in 40- to 85-year-old male sprinters (n = 69) with a long-term training background.

Peripheral quantitative computed tomography (pQCT)-derived bone structural, strength, and densitometric parameters of the distal tibia and tibia midshaft were assessed at baseline and 10 years later. The groups of well-trained (actively competing, sprint training including strength training ≥2 times/week; n = 36) and less-trained (less than 2 times/week, no strength training, switched to endurance training; n = 33) athletes were formed according to self-reports at follow-up. Longitudinal changes in bone traits in the two groups were examined.

Over the 10-year period, group-by-time interactions were found for distal tibia total bone mineral content (BMC), trabecular volumetric bone mineral density (vBMD), and compressive strength index, and for mid-tibia cortical cross-sectional area, medullary area, total BMC, and BMC at the anterior and posterior sites. These interactions reflected maintained (distal tibia) or improved (mid-tibia) bone properties in the well-trained and decreased bone properties in the less-trained athletes over the 10-year period. Depending on the bone variable, the difference in change in favor of the well-trained group ranged from 2% to 5%.

In conclusion, our longitudinal findings indicate that continued strength and sprint training is associated with maintained or even improved tibial properties in middle-aged and older male sprint athletes, suggesting that regular, intensive exercise counteracts bone aging.