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Physical and cognitive performances change across lifespan. Studying cohorts of individuals in specific age ranges and athletic abilities remains essential in assessing the underlying physiological mechanisms that result in such a drop in performance. This decline is now viewed as a unique phenotypic biomarker and a hallmark of the aging process. The rates of decline are well documented for sets of traits such as running or swimming but only a limited number of studies have examined the developmental and senescent phases together. Moreover, the few attempts to do so are merely descriptive and do not include any meaningful biological features. Here we propose an averaged and deterministic model, based on cell population dynamics, replicative senescence and functionality loss. It describes the age-related change of performance in 17 time-series phenotypic traits, including human physical and cognitive skills, mouse lemur strength, greyhound and thoroughbred speed, and mouse activity. We demonstrate that the estimated age of peak performance occurs in the early part of life (20.5% ± 6.6% of the estimated lifespan) thus emphasizing the asymmetrical nature of the relationship. This model is an initial attempt to relate performance dynamics to cellular dynamics and will lead to more sophisticated models in the future.

Background Aging is associated with a progressive decline in skeletal muscle mass and strength as well as an increase in adiposity. These changes may have devastating impact on the quality of life of older adults. Mitochondrial dysfunctions have been implicated in aging‐related and obesity‐related deterioration of muscle function. Impairments in mitochondrial quality control processes (biogenesis, fusion, fission, and mitophagy) may underlie this accumulation of mitochondrial dysfunction. High‐intensity interval training (HIIT) was shown to improve muscle and mitochondrial function in healthy young and old adults and to improve body composition in obese older adults. Recent studies also positioned citrulline (CIT) supplementation as a promising intervention to counter obesity‐related and aging‐related muscle dysfunction. In the present study, our objectives were to assess whether HIIT, alone or with CIT, improves muscle function, functional capacities, adipose tissue gene expression, and mitochondrial quality control processes in obese older adults. Methods Eighty‐one‐old and obese participants underwent a 12 week HIIT with or without CIT on an elliptical trainer [HIIT‐CIT: 20 men/25 women, 67.2 ± 5.0 years; HIIT‐placebo (PLA): 18 men/18 women, 68.1 ± 4.1 years]. Handgrip and quadriceps strength, lower limb muscle power, body composition, waist circumference, and functional capacities were assessed pre and post intervention. Vastus lateralis muscle biopsies were performed in a subset of participants to quantify markers of mitochondrial content (TOM20 and OXPHOS subunits), biogenesis (TFAM), fusion (MFN1&2, OPA1), fission (DRP1), and mitophagy (Parkin). Subcutaneous abdominal adipose tissue biopsies were also performed to assess the expression of genes involved in lipid metabolism. Results HIIT‐PLA and HIIT‐CIT displayed improvements in functional capacities (P < 0.05), total (mean ± SD: HIIT‐PLA: +1.27 ± 3.19%, HIIT‐CIT: +1.05 ± 2.91%, P < 0.05) and leg lean mass (HIIT‐PLA: +1.62 ± 3.85%, HIIT‐CIT: +1.28 ± 4.82%, P < 0.05), waist circumference (HIIT‐PLA: −2.2 ± 2.9 cm, HIIT‐CIT: −2.6 ± 2.5 cm, P < 0.05), and muscle power (HIIT‐PLA: +15.81 ± 18.02%, HIIT‐CIT: +14.62 ± 20.02%, P < 0.05). Only HIIT‐CIT decreased fat mass (−1.04 ± 2.42%, P < 0.05) and increased handgrip and quadriceps strength (+4.28 ± 9.36% and +10.32 ± 14.38%, respectively, P < 0.05). Both groups increased markers of muscle mitochondrial content, mitochondrial fusion, and mitophagy (P < 0.05). Only HIIT‐CIT decreased the expression of the lipid droplet‐associated protein CIDEA (P < 0.001). Conclusions High‐intensity interval training is effective in improving functional capacities, lean mass, muscle power, and waist circumference in obese older adults. HIIT also increases markers of mitochondrial biogenesis, mitochondrial fusion, and mitophagy. Importantly, adding CIT to HIIT results in a greater increase in muscle strength and a significant decrease in fat mass. The present study therefore positions HIIT combined with CIT as an effective intervention to improve the health status of obese older adults.

The purpose of this study was to quantify training loads (TL) of high intensity sessions through original methods (TRIMP; session-RPE; Work-Endurance-Recovery) and their updated alternatives (TRIMP.sub.cumulative ; RPE.sub.alone ; New-WER). Ten endurance athletes were requested to perform five sessions until exhaustion. Session 1 composed by a 800m maximal performance and four intermittent sessions performed at the 800m velocity, three sessions with 400m of interval length and work:recovery ratios of 2:1, 1:1 and 1:2 and one with 200m intervals and 1:1. Total TL were quantified from the sessions' beginning to the cool-down period and an intermediate TL (TL.sub.800) was calculated when 800m running was accumulated within the sessions. At the end of the sessions high and similar RPE were reported (effect size, [eta].sup.2 = 0.12), while, at the intermediate 800m distance, the higher interval distances and work:recovery ratios the higher the RPE ([eta].sup.2 = 0.88). Our results show marked differences in sessions' total TL between original (e.g., lowest TL for the 800m and highest for the 200m-1:1 sessions) and alternative methods (RPE.sub.alone and New-WER; similar TL for each session). Differences appear in TL.sub.800 notably between TRIMP and other methods which are negatively correlated. All TL report light to moderate correlations between original methods and their alternatives, original methods are strongly correlated together, as observed for alternative methods. Differences in TL quantification between original and alternative methods underline that they are not interchangeable. Because of high exercise volume influence, original methods markedly enhance TL of sessions with higher exercise volumes although these presented the easiest interval distances and work-recovery ratios. Alternative methods based on exhaustion level (New-WER) and exertion (RPE.sub.alone) provided a new and promising point of view of TL quantification where exhaustion determines the highest TL whatever the exercise. This remains to be tested with more extended populations submitted to wider ranges of exercises.

The emergence and circulation of a novel coronavirus (2019-nCoV)—Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)—set off a global health crisis. SARS-CoV-2 spreads faster than its two ancestors, SARS-CoV and MERS-CoV. Several modes of transmission have been identified: via respiratory droplets, contact with infected people or contaminated surfaces, and potentially, bioaerosols. Various countries have taken preventive measures that may include partial or total lockdowns lasting weeks. The physical inactivity associated with lockdowns may promote cardiometabolic or other diseases, while physical activity may play a critical role in preventing them. Here we develop the hypothesis of the involvement of aerosols in the contamination process, the role of angiotensin converting enzyme 2 (ACE2), the potential benefits and harm of physical activity during lockdowns, and we suggest directions for future research. Highlights • Physical inactivity during COVID-19 lockdowns may damage health. • Risk of contamination by aerosols is higher during high-intensity urban outdoor exercise. • Angiotensin converting enzyme 2 (ACE2) could play key role in SARS-CoV-2 transmission during exercise. • How ACE2 serum concentration changes as function of exercise intensity and duration must be studied to elucidate role of this enzyme.

The age-performance relationship describes changes in the organism’s structural and functional capabilities over the course of the lifespan. The typical, empirical pattern is an asymmetrical inverted-U shape association with peak capacity occurring early in life. This process is well described in the literature, with an increasing interest in features that characterize this pattern, such as the rate of growth, age of peak performance, and rate of decline with aging. This is usually examined in cohorts of individuals followed over time with repeat assessments of physical or cognitive abilities. This framework ought to be integrated into public health programs, embedding the beneficial (such as physical or cognitive training) or adverse effects (such as chronic diseases or injuries) that respectively sustain or limit capabilities. The maintenance of physical or cognitive performances at older ages would result in both optimal health and promote resistance to disabling conditions and chronic diseases, such as obesity and type 2 diabetes. The causes of accelerated degeneration of health optima are mainly: sedentary and unhealthy lifestyles -including poor nutrition-, exposure to environmental pollutants, and heterogeneity in aging. Better knowledge of optima, compatible with or required for good health, should also allow for establishing ideal conditions for longevity.

Low levels of the neurotransmitter serotonin have been associated with the onset of depression. While traditional treatments include antidepressants, physical exercise has emerged as an alternative for patients with depressive disorders. Yet there remains the fundamental question of how exercise is sensed by the brain. The existence of a muscle–brain endocrine loop has been proposed: according to this scenario, exercise modulates metabolization of tryptophan into kynurenine within skeletal muscle, which in turn affects the brain, enhancing resistance to depression. But the breakdown of tryptophan into kynurenine during exercise may also alter serotonin synthesis and help limit depression. In this study, we investigated whether peripheral serotonin might play a role in muscle–brain communication permitting adaptation for endurance training. We first quantified tryptophan metabolites in the blood of 4 trained athletes before and after a long-distance trail race and correlated changes in tryptophan metabolism with physical performance. In parallel, to assess exercise capacity and endurance in trained control and peripheral serotonin–deficient mice, we used a treadmill incremental test. Peripheral serotonin–deficient mice exhibited a significant drop in physical performance despite endurance training. Brain levels of tryptophan metabolites were similar in wild-type and peripheral serotonin–deficient animals, and no products of muscle-induced tryptophan metabolism were found in the plasma or brains of peripheral serotonin–deficient mice. But mass spectrometric analyses revealed a significant decrease in levels of 5-hydroxyindoleacetic acid (5-HIAA), the main serotonin metabolite, in both the soleus and plantaris muscles, demonstrating that metabolization of tryptophan into serotonin in muscles is essential for adaptation to endurance training. In light of these findings, the breakdown of tryptophan into peripheral but not brain serotonin appears to be the rate-limiting step for muscle adaptation to endurance training. The data suggest that there is a peripheral mechanism responsible for the positive effects of exercise, and that muscles are secretory organs with autocrine-paracrine roles in which serotonin has a local effect.

Background: Iron excess has been proposed as an essential factor in skeletal muscle wasting. Studies have reported correlations between muscle iron accumulation and atrophy, either through ageing or by using experimental models of secondary iron overload. However, iron treatments performed in most of these studies induced an extra-pathophysiological iron overload, more representative of intoxication or poisoning. The main objective of this study was to determine the impact of iron excess closer to pathophysiological conditions on structural and metabolic adaptations (i) in differentiated myotubes and (ii) in skeletal muscle exhibiting oxidative (i.e. the soleus) or glycolytic (i.e. the gastrocnemius) metabolic phenotypes.Methods: The impact of iron excess was assessed in both in vitro and in vivo models. Murine differentiated myotubes were exposed to ferric ammonium citrate (FAC) (i.e. 10 and 50 μM) for the in vitro component. The in vivo model was achieved by a single iron dextran subcutaneous injection (1 g/kg) in mice. Four months after the injection, soleus and gastrocnemius muscles were harvested for analysis.Results: In vitro, iron exposure caused dose-dependent increases of iron storage protein ferritin (P < 0.01) and dose-dependent decreases of mRNA TfR1 levels (P < 0.001), which support cellular adaptations to iron excess. Extra-physiological iron treatment (50 μM FAC) promoted myotube atrophy (P = 0.018), whereas myotube size remained unchanged under pathophysiological treatment (10 μM FAC). FAC treatments, whatever the doses tested, did not affect the expression of proteolytic markers (i.e. NF-κB, MurF1, and ubiquitinated proteins). In vivo, basal iron content and mRNA TfR1 levels were significantly higher in the soleus compared with the gastrocnemius (+130% and +127%; P < 0.001, respectively), supporting higher iron needs in oxidative skeletal muscle. Iron supplementation induced muscle iron accumulation in the soleus and gastrocnemius muscles (+79%, P < 0.001 and +34%, P = 0.002, respectively), but ferritin protein expression only increased in the gastrocnemius (+36%, P = 0.06). Despite iron accumulation, muscle weight, fibre diameter, and myosin heavy chain distribution remained unchanged in either skeletal muscle.Conclusions: Together, these data support that under pathophysiological conditions, skeletal muscle can protect itself from the related deleterious effects of excess iron.

Acute kidneys injuries (AKIs) have been described in marathon and trail running. The currently available data allows assessment of before/after comparisons but does not allow an analysis of what happens during the race. A multidisciplinary assessment protocol was performed during the first trail of Clécy (Normandy France) in November 2021. This allowed an initial assay to be carried out, then at the end of each of the 6 loops of 26 km, and finally after 24 h of recovery. The race extends over 156 km in hilly terrain and 6000 m of elevation gain (D+). The level of impairment according to the RIFLE classification was defined for each runner at each assay. Fifty‐five runners were at the start, and the per protocol analysis involved 36 runners (27 men and 9 women, 26 finishers). Fifteen (41.7%) of the riders presented at least one result corresponding to a “RIFLE risk” level. After 24 h of rest, only one runner still had a “RIFLE Risk”. The distance around the marathon seems to be the moment of greatest risk. For the first time, we find an association between this renal risk and the probability of abandonment. Many runners are vulnerable to kidney damage during long‐duration exercise, which is why it's important to limit risk situations, such as the use of potentially toxic drugs or hydration disorders. The consumption of NSAIDs (nonsteroidal anti‐inflammatory drugs) before or during an ultra‐distance race should therefore be prohibited. Attention should be paid to hydration disorders.

Physical activity can be effective in preventing some of the adverse effects of aging on health. High-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) are beneficial interventions for the quality of life of obese older individuals. The understanding of all possible metabolic mechanisms underlying these beneficial changes has not yet been established. The aim of this study was to analyze changes in the serum metabolome after 12 weeks of HIIT and MICT in obese older adults. Thirty-eight participants performed either HIIT (n = 26) or MICT (n = 12) three times per week for 12 weeks. Serum metabolites as well as clinical and biological parameters were assessed before and after the 12-week intervention. Among the 364 metabolites and ratio of metabolites identified, 51 metabolites changed significantly following the 12-week intervention. Out of them, 21 significantly changed following HIIT intervention and 18 significantly changed following MICT. Associations with clinical and biological adaptations revealed that changes in acyl-alkyl-phosphatidylcholine (PCae) (22:1) correlated positively with changes in handgrip strength in the HIIT group (r = 0.52, p < 0.01). A negative correlation was also observed between 2-oxoglutaric acid and HOMA-IR (r = −0.44, p < 0.01) when considering both groups together (HIIT and MICT). This metabolite also correlated positively with quantitative insulin-sensitivity check index (QUICKI) in both groups together (r = 0.46, p < 0.01) and the HIIT group (r = 0.51, p < 0.01). Additionally, in the MICT group, fumaric acid was positively correlated with triglyceride levels (r = 0.73, p < 0.01) and acetylcarnitine correlated positively with low-density lipoprotein (LDL) cholesterol (r = 0.81, p < 0.01). These four metabolites might represent potential metabolites of interest concerning muscle strength, glycemic parameters, as well as lipid profile parameters, and hence, for a potential healthy aging. Future studies are needed to confirm the association between these metabolites and a healthy aging.

The growing interest of the scientific community in trail running has highlighted the acute effects of practice at the time of these races on isolated aspects of physiological and structural systems; biological, physiological, cognitive, and muscular functions; and the psychological state of athletes. However, no integrative study has been conducted under these conditions with so many participants and monitoring of pre-, per-, and postrace variables for up to 10 days over a distance close to 100 miles. The aim of this study was to evaluate the kinetics of the performance parameters during a 156 km trail run and 6000 m of elevation gain in pre-, per-, and postrace conditions. The general hypothesis is based on significant alterations in the psychological, physiological, mechanical, biological, and cognitive parameters. The Trail Scientifique de Clécy took place on November 11, 2021. This prospective experimental study provides a comprehensive exploration of the constraints and adaptations of psychophysiological and sociological variables assessed in real race conditions during a trail running of 156 km on hilly ground and 6000 m of elevation gain (D+). The study protocol allowed for repeatability of study measurements under the same experimental conditions during the race, with the race being divided into 6 identical loops of 26 km and 1000 m D+. Measurements were conducted the day before and the morning of the race, at the end of each lap, after a pit stop, and up to 10 days after the race. A total of 55 participants were included, 43 (78%) men and 12 (22%) women, who were experienced in ultra-trail-running events and with no contraindications to the practice of this sport. The launch of the study was authorized on October 26, 2021, under the trial number 21-0166 after a favorable opinion from the Comité de Protection des Personnes Ouest III (21.09.61/SIRIPH 2G 21.01586.000009). Of the 55 runners enrolled, 41 (75%) completed the race and 14 (25%) dropped out for various reasons, including gastric problems, hypothermia, fatigue, and musculoskeletal injuries. All the measurements for each team were completed in full. The race times (ie, excluding the measurements) ranged from 17.8206 hours for the first runner to 35.9225 hours for the last runner. The average time to complete all measurements for each lap was 64 (SD 3) minutes. The Trail Scientifique de Clécy, by its protocol, allowed for a multidisciplinary approach to the discipline. This approach will allow for the explanation of the studied parameters in relation to each other and observation of the systems of dependence and independence. The initial results are expected in June 2022. RR1-10.2196/38027.