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Introduction: Quadriceps weakness and decreased muscle mass in chronic obstructive pulmonary disease(COPD)patients is related with mortality.We planned a pilot study to investigate the relationship between increase in rectus femoris cross-sectional area and walking distance and quality of life. Methods: COPD patients who received pulmonary rehabilitation (PR)were assessed for exercise capacity with incrimental shuttle walking test, quality of life questionnaire before and after the PR program.Rectus femoris sectional area(RFCSAmm2 )were measured by ultrasonography before and after the PR program.Patients received upper and lower extremity strengthening exercises, cycling, treadmill accompanied by a physical therapist.Patients were taken a total of 2 days per week for 8 week program. Results: Mean age of patients is 66.3±5 years(1male,2 females)and mean duration of COPD is 8.6±5.5 years.Patients data before and after PR are shown in and Conclusion: The rectus femoris cross-sectional area measurements with ultrasound may be a candidate for non-invasive method of measuring muscle mass change in PR patients.We wish to present the early results of 3 cases in this pilot study.

The aim of the study was to assess the effect of a polyunsaturated omega-3 fatty acids (PUFA) supplementation on the parameters of body composition, muscle strength and physical performance in elderly people with decreased muscle mass (DMM). Fifty three elderly people with an ALM index (the ratio of appendicular lean mass to squared height) either below (−2SD: low muscle mass-LMM) or between (−1SD and −2SD: the risk of LMM-rLMM) the ALM index for the young Polish reference population were randomly assigned to PUFA-treated groups (LMM-PUFA, rLMM-PUFA) or control groups (LMM-control, rLMM-control). PUFA-treated groups received capsules containing 1.3 g of PUFA and 10 mg of vitamin E, while the control groups received 11 mg of vitamin E daily for 12 weeks. Body composition (BIA analysis), muscle strength (hand grip measured with dynamometer) and physical performance (Timed Up and Go test-TUG) were assessed before and after supplementation. No statistically significant differences were observed either in muscle mass or in the hand grip and TUG in any group. The post-pre difference (mean ± SD) in ALM index was as follows (kg/m2): LMM-PUFA: 0.00 ± 0.30, rLMM-PUFA: 0.00 ± 0.22, LMM-control: 0.03 ± 0.36, rLMM-control: –0.03 ± 0.20. In our study, a 12 week supplementation of PUFA did not affect the evaluated parameters in elderly individuals with DMM.

Loss of muscle mass and function is a common occurrence in both patients with decompensated cirrhosis and those undergoing liver transplantation. Sarcopenia is associated with morbidity and mortality before and after liver transplantation. The ability of skeletal muscle mass to recover after transplant is questionable, and long term adverse events associated with persistent sarcopenia have not been well studied. Limited data is available examining mechanisms by which decreased muscle mass might develop. It is not clear which interventions might reduce the prevalence of sarcopenia and associated health burdens. However, measures to either decrease portal hypertension or improve nutrition appear to have benefit. Research on sarcopenia in the liver transplant setting is hampered by differing methodology to quantify muscle mass and varied thresholds determining the presence of sarcopenia. One area highlighted in this review is the heterogeneity used when defining sarcopenia. The health consequences, clinical course and potential pathophysiologic mechanisms of sarcopenia in the setting of cirrhosis and liver transplantation are further discussed.

The frailty syndrome refers to the concurrence of a number of specific clinical manifestations that include unintentional weight loss, decreased muscle mass (sarcopenia), exhaustion, reduced physical strength and activity, and slow ambulation. It involves multiple systems, is an increasing problem in elderly populations, and is strongly associated with increases in both morbidity and mortality. Despite its recognition clinically, the frailty syndrome is not often identified in forensic situations and is only infrequently mentioned in the associated literature. As there is a direct relationship between the frailty syndrome and significant adverse health outcomes the syndrome has clear medicolegal significance.

Random urine Ca/creatinine (UCa/Cr) is used to estimate 24-hour Ca excretion. However, due to decreased urine creatinine excretion in children with decreased muscle mass (DMM), UCa/Cr overestimates their Ca excretion.To evaluate whether in children with DMM random urine Ca/osmolality (UCa/Osm) can accurately predict hypercalciuria (24-hour urine Ca4.0 mg/kg) and at which "cutoff" value.19 children with DMM and 29 with normal muscle mass (NMM), ages 6 - 17 years, were studied. DMM was diagnosed based on clinical findings and decreased serum creatinine, and confirmed by low urine creatinine excretion. Over 24 hours, subjects collected each void separately. After each sample was analyzed, samples of each participant were combined to form a 24-hour specimen from which an aliquot (AL) was obtained; 24-hour urine Ca was first correlated with the corresponding AL Ca/Cr and Ca/Osm. As an internal control, a similar assessment ofproteinuria was conducted. In the next step, AL data were compared with individual urine samples to identify the time of day when a random sample best correlates with AL.The correlation coefficient between 24-hour Ca and AL Ca/Cr in all children was 0.61, in NMM 0.96, and in DMM 0.69 (in all p0.001). The correlation coefficient between 24-hour urine Ca and AL Ca/Osm in all children was 0.90, in NMM 0.90, and in DMM 0.91 (in all p0.001). In children with DMM, the correlation coefficient of 24-hour protein with AL protein/Cr was 0.75, and with protein/Osm 0.98 (both p0.001). Receiver operating characteristic curves showed UCa/Cr as a better predictor of 24-hour Ca4.0 mg/kg in NMM, whereas UCa/Osm was a better predictor of hypercalciuria in DMM patients. In NMM, UCa/Cr ratio0.20 had sensitivity of 88% and specificity of 96% in detecting 24-hour Ca4.0 mg/kg, whereas in those with DMM UCa/Osm (x 10) ratio of0.25 had sensitivity of 100% and specificity of 93% in detecting hypercalciuria. It was further found that random urine specimens collected between 9:00 a.m. and 2:00 p.m. best represented 24-hour urine data.In children with DMM, UCa/Osm can successfully replace UCa/Cr as a screening tool for hypercalciuria.

Chronic kidney disease is commonly accompanied by disturbances in the hypothalamic-pituitary-gonadal axis. Such disturbances in men give rise to hypogonadism and low circulating testosterone levels. The deficiency in testosterone can contribute to clinical outcomes such as sexual dysfunction, decreased bone mineralization, malnutrition and decreased muscle mass, and anemia. The administration of androgens to nonuremic hypogonadal men is usually effective in treating such outcomes. By contrast, the response to therapy in uremic men tends to be much less predictable. This variability in response is not surprising, because these same clinical outcomes can be the result of other aspects of the uremic state or the comorbid conditions that are frequently present in men with chronic kidney disease. Although further studies are needed, testosterone therapy may prove most useful as an adjunct to other more general therapies designed to address the uremic state.

Men generally have an inherent performance advantage over women due to their average greater height and muscle mass and power, as the result of correspondingly different exposures to androgens. Therefore, it is considered fair that in sports men and women compete in separate categories. The question now emerging is whether reassigned transsexuals can compete in fairness with others of their new sex. The pertinent question is how far the previous effects of testosterone in male-to-female transsexuals (M-F) are reversible upon androgen deprivation so that M-F have no advantage over women, and, vice versa, what the effects are of androgen exposure in female-to-male transsexuals (F-M) on variables relevant to competition in sports. Before puberty, boys and girls do not differ in height, muscle and bone mass. Recent information shows convincingly that actual levels of circulating testosterone determine largely muscle mass and strength, though with considerable interindividual diversity. This study analyzed the effects of androgen deprivation in 19 M-F and of androgen administration to 17 F-M on muscle mass, hemoglobin (Hb) and insulin-like growth factor-1 (IGF-1). Before cross-sex hormone administration, there was a considerable overlap in muscle mass between M-F and F-M. In both M-F and F-M, height was a strong predictor of muscle mass. Androgen deprivation of M-F decreased muscle mass, increasing the overlap with untreated F-M, but mean muscle mass remained significantly higher in M-F than in F-M. Androgen administration to F-M increased muscle mass without inducing an advantage over nontreated M-F. The conclusion is that androgen deprivation in M-F increases the overlap in muscle mass with women but does not reverse it, statistically. The question of whether reassigned M-F can fairly compete with women depends on what degree of arbitrariness one wishes to accept, keeping in mind, for instance, that similar blood testosterone levels in men have profoundly different biologic effects on muscle properties, rendering competition in sports intrinsically a matter of how nature endows individuals for this competition.

Aging is associated with progressive loss of neuromuscular function that often leads to progressive disability and loss of independence. The term sarcopenia is now commonly used to describe the loss of skeletal muscle mass and strength that occurs in concert with biological aging. By the seventh and eighth decade of life, maximal voluntary contractile strength is decreased, on average, by 20-40% for both men and women in proximal and distal muscles. Although age-associated decreases in strength per unit muscle mass, or muscle quality, may play a role, the majority of strength loss can be accounted for by decreased muscle mass. Multiple factors lead to the development of sarcopenia and the associated impact on function. Loss of skeletal muscle fibers secondary to decreased numbers of motoneurons appears to be a major contributing influence, but other factors, including decreased physical activity, altered hormonal status, decreased total caloric and protein intake, inflammatory mediators, and factors leading to altered protein synthesis, must also be considered. The prevalence of sarcopenia, which may be as high as 30% for those ≥60 yr, will increase as the percentage of the very old continues to grow in our populations. The link between sarcopenia and disability among elderly men and women highlights the need for continued research into the development of the most effective interventions to prevent or at least partially reverse sarcopenia, including the role of resistance exercise and other novel pharmacological and nutritional interventions.

The influence of decreased muscle mass and reduced food intake on diaphragm structure and contractility in male Wistar rats was determined after triamcinolone acetate treatment (TR: 0.5mg per kg per day for 4 weeks) and two degrees of undernutrition (PW: pair-weight, which resulted in a similar (41%) reduction of body weight as TR; PF: pair-fed, which resulted in a moderate (13%) reduction of body weight) and a free-fed control group (FF, with an increase (9%) in body weight). Energy intake of TR decreased, but based on daily measurements of food intake and body weight, energy expenditure of the TR rats was increased compared with the other groups. Body (BW) and muscle weights were reduced in proportion to the extent of undernutrition in the nutritionally deprived rats (i.e. BW and diaphragm weight of PF animals were reduced 21% and 16% respectively compared with FF, v. a 48% and 41% reduction in the PW group). Triamcinolone-induced atrophy was limited to type II fibres (30% of type IIa and 45% of type IIx/b, p

Growth abnormalities are uniquely associated with autism spectrum disorders (ASD); however, the extent to which growth abnormalities are present has hardly been investigated. The current study aims to compare the differences in anthropometric parameters in a group of autistic Egyptian children and the healthy normal population. We recruited 100 children with ASD from the Outpatient Clinic for “Autistic Children” at the Medical Research Hospital of Excellence, National Research Centre in Cairo, Egypt. They were diagnosed by DSM-IV criteria of the American Psychiatric Association, Autism Diagnostic Interview-Revised, and Childhood Autism Rating Scale. Of these children at age of 3–10 years, 71 were males and 29 females. Eight anthropometric parameters were assessed in view of data of the healthy Egyptians of pertinent sex and age. Weight and body mass index increased because of a significant increase in subcutaneous fat thickness. This tendency with a probable decrease in muscle mass was more evident in male or in older children, likely resulting from sedentary life style and food selectivity. The Z head circumference score and its variance significantly increased especially in males or older children, suggesting the relative overgrowth of the brain in a substantial percentage of Egyptian children with autism. We concluded that increased fat composition in Egyptian autistic children with decreased muscle mass necessitates tailoring a specially designed food supplementation program to ameliorate the severity of autism symptoms.

In addition to the primary symptoms arising from inflammatory processes in the joints, muscle weakness and impaired work capacity are commonly reported by patients with rheumatoid arthritis (RA). Reduced muscle strength has always been more or less synonymous with decreased muscle mass. However, our data show that muscle weakness associated with RA is not only a result of atrophic muscles. Instead, intracellular (intrinsic) muscle dysfunction appears as important factors behind arthritis-induced muscle weakness. Our data suggests that the impaired capacity to produce force is the result of free radical (reactive oxygen/nitrogen species (ROS/RNS)) signaling altering the intracellular Ca2+ release and contractile proteins (myosin and actin) inside the skeletal muscle fibers. Here our latest data on the mechanisms behind arthritis-induced skeletal muscle weakness from animal studies and patients with RA will be presented. Altered contractile function induced by the RNS peroxynitrite (ONOO-) and the prospective of using antioxidant treatment to counteract muscle weakness in inflammatory conditions will be discussed. Disclosure of Interest None declared

Testosterone is the major circulating androgen in men with a physiological age-related decline in the aging male. Late-onset hypogonadism or Androgen Deficiency Syndrome (ADS) is a “syndromic” diagnosis including both, persistent low testosterone concentrations together with clinical symptoms including erectile dysfunction, low libido, decreased muscle mass and strength, increased body fat, decreased vitality, and depressed mood. But due to its unspecific symptoms, treatment goals, and monitoring parameters, there are many uncertainties concerning the diagnosis, therapy, and monitoring of ADS to date. The present work intends to introduce the application of metabolomics as a novel and promising tool for the improved diagnosis, therapy, and monitoring of ADS. We will outline the current uncertainties and limitations in the diagnosis and therapy of ADS to subsequently explore the scientific opportunities of metabolomics to account for the specific metabolic requirements and characteristics of the individual patient, better understand the metabolic deviations in testosterone deficiency, and monitor the biochemical changes induced by testosterone replacement therapy. We also discuss the potential of metabolomics to optimize the effectiveness and safety of individualized testosterone replacement therapy, and to thereby significantly reduce the side effects and associated health care costs of ADS treatment.

Publisher Summary This chapter discusses the various aspects of growth hormone (GH). GH, which primarily exerts its somatotropic and metabolic effects by stimulating production of insulin-like growth factor-1 (IGF-I), initiates a wide range of cellular effects. The production of GH and IGF-I and the important interplay of these two proteins are quite complex and are altered in individuals with renal insufficiency. The alterations in the GH/IGF-I axis seen in renal failure can lead to profound effects. In children with renal disease, GH and IGF-I abnormalities may result in impaired linear growth, decreased muscle mass, decreased bone mass, impaired neurocognitive development, and disordered plasma lipids. In adults with renal insufficiency, GH and IGF-I abnormalities have also been identified and may lead to decreased muscle mass, decreased bone mass, altered plasma lipids, and altered metabolism. Exogenous recombinant human GH (rGH) therapy is safe and effective in the treatment of children with chronic kidney disease (CKD) who have growth failure. The benefit of rGH therapy for the other GH/IFGF-I-mediated clinical problems seen in CKD is not proven, but some of these may become important indicators in the future.

Denervation or inactivity is known to decrease the mass and alter the phenotype of muscle. The mechanical response of tendon to inactivity that has been determined experimentally differs from what is reported by patients. We investigated the hypothesis that this difference was the result of artifacts of the testing process and did not represent what occurred in vivo. To test this hypothesis, a novel approach was used to determine the mechanical properties of the tibialis anterior (TA) tendon by optically measuring the end-to-end mechanical strains as well as the local strains at specific regions of excised TA tendon units. When the end-to-end strain of normal TA tendon is determined, stress-strain response curves show considerably more extensibility than when strain is measured across only the midsection of the tendon (mid-tendon). The strain experienced by the region close to the muscle (muscle tendon) is five times greater than the strain in either the mid-tendon or near the bone (bone-tendon). Five weeks of denervation decreased muscle mass by 67%; increased tendon mass by 10%; and changed the entire shape of the nonlinear response curve, including a loss in regional variation in strain, a 3.9-fold increase in end-to-end tangent modulus, and a 70% reduction in the toe region, as a result of a drastic reduction of the extensibility in the muscle-tendon region. The stress-strain response in the mid-tendon region of a normal TA tendon is therefore not indicative of its overall ability to deform in vivo as it transmits forces from muscle to bone.

Hypercalciuria in children with decreased muscle mass—urine calcium : osmolality versus urine calcium : creatinine

Obesity is growing in prevalence among older Americans and is accompanied by an unfortunate burden of chronic disease, functional decline, and poor quality of life. Elevated past or current body mass index (BMI) is strongly associated with increased self-reported functional limitations. Supportive findings have also related decreased physical performance test scores with elevated BMI. Body composition analyses have explored which body compartment is most strongly associated with obesity-related functional impairments. Studies have suggested possible contributions of decreased muscle mass and increased fat mass. Weight reduction intervention studies that have examined functional outcomes among older persons are limited.

The osteogenic response to mechanical stress is blunted with aging. It has been postulated that this decline in responsiveness is related to (a) a limited ability to engender the strain necessary to reach the bone modeling threshold, due to decreased muscle mass and strength, and/or (b) a decline in certain hormones or growth factors that may interact with mechanical signals to change the sensitivity of bone cells to strain. There is reason to believe that both of these factors contribute to the reduced ability to increase bone mass through exercise with advancing age. Weight-bearing endurance exercise and resistance exercise have both been found to increase bone mass in older women and men. However, exercise training studies involving older individuals have generally resulted in increased bone mineral density only when the exercise is quite vigorous. There is also evidence that the osteogenic response to mechanical loading is enhanced by estrogens. Whether age-related changes in other factors (e.g., other hormones, growth factors, cytokines) also contribute to the reduced responsiveness of the aged skeleton to mechanical loading remains to be investigated.

We studied 174 patients with SIRS criteria, 45 with sepsis, eight with severe sepsis and 13 with septic shock. Serum TNF-alpha, IL-6, IL-8 and IL-10 levels were raised in SIRS patients, even in those cases in which an infection could not be documented, and more intensely in severe sepsis and in patients who died (11%). The slope of the regression line between IL-10 and TNF-alpha was sharper in patients with severe sepsis and in those who died; an imbalance between pro- and anti-inflammatory cytokines may be related to poor prognosis. Increased IL-6 and IL-10, decreased muscle mass, raised BUN and low body temperature were all independently related to prognosis.

Objectives: Age related decline in sex hormone levels has been associated with decreased muscle mass, bone density, and changes in metabolism in both males and females[1-3]. Although the effect of estrogen levels on tendon size and architecture has been studied in females [4,5], the influence of testosterone levels on tendons in males is unknown. The purpose of the present study was to retrospectively compare free testosterone (FT) and total testosterone (TT) level in males diagnosed with Achilles tendon rupture and healthy normal historical data as a means of evaluating if decreased sex hormone level is a risk factor for tendon injury. We hypothesized males diagnosed with Achilles tendon ruptures will have lower FTand TT levels than age-matched normal levels in the literature. Methods: 22 males diagnosed with Achilles injury that had their FT (nmol/L) and TT (nmol/L) levels measured as part of their initial clinical evaluation were retrospectively identified. The FT and TT levels of these injured men were directly compared to age matched historical data [5-7]. The mean FT and TT levels, and 95% confidence intervals were then compared. The difference of means was reported as statistically significant if the confidence interval for the difference in means test did not include zero. Results: Six males age 24-33, ten age 34-43, four age 44-53 and two males age 54-63 had FT and TT levels recorded as part of their care. For each age group, the mean FT and TT levels of males with Achilles tendon rupture were lower than the respective age-matched normal controls reported in the literature. Males in their 30s, 40s and 50s had statistically significant lower FT and TT levels compared to normal controls in the literature (Figure 1a, b, * indicates difference of means test statistically significant, PConclusion: Our study showed the average FT and TT levels of males with Achilles tendon rupture were lower than corresponding age-matched historical data for each age group. Males in their 30s, 40s and 50s had statistically significant lower FT and TT levels compared to normal controls in the literature. Past studies have shown there is an increased incidence of Achilles tendon rupture for males during this same decade of life [8]. Overall, we believe our findings suggest low hormone levels maybe associated with the risk of Achilles tendon rupture. The main limitation of this retrospective study design is fact that the FT and TT levels were not redrawn to account for the impact of injury on these hormone levels. Future studies will be repeated with larger sample size, and include albumin and sex-binding globulin levels to help adjust for other biological factors that may influence these measures. Cited1.Tenover. Testosterone and the aging male. Journal of andrology, 1997. 2. Clarke. Archives of biochemistry and biophysics, 2010. 3.Figueroa. The journals of gerontology. Series A, Biological sciences and medical sciences, 2003 4.Cook.Scandinavian journal of medicine & science in sports, 2007. 5.Finni. Journal of applied physiology, 2009 6.Mohr.Clinical endocrinology, 2005. 7.Vermeulen.The Journal of clinical endocrinology and metabolism, 1996. 8. Halmenschlager. International urology and nephrology, 2012.

Source Citation Wannamethee SG, Shaper AG, Lennon L, Whincup PH. Decreased muscle mass and increased central adiposity are independently related to mortality in older men. Am J Clin Nutr. 2007;86:1...

Objectives: To document the time course of recovery of the targeted muscle after botulinum toxin type A (BTX) injection. Design: Basic science study using a rat model. Setting: University medical center research laboratory. Animals: Twenty-four 1-month old Sprague-Dawley rats. Intervention: BTX-A was injected into the left gastrocnemius muscle of 24 rats (6U/kg of body weight). Equal volume of saline was injected into the right gastrocnemius muscle (control). Main Outcome Measures: Muscle mass, motor evoked action potentials (latency, amplitude), and muscle force generation (single twitch, tetanus) were evaluated at different follow-up intervals. Results: In the BTX group, muscle mass was reduced by 31.5% of the control side within 2 weeks of injection and recovered to 92% at 6 months. Latency was prolonged to 144.9% at 3 days and recovered to 101% at 6 months. Amplitude, single twitch, and tetanus were significantly reduced at 1 week, but recovered to >94% at 6 months. Conclusions: BTX injection at 6U/kg of body weight effectively decreased muscle mass and muscle electrophysiologic parameters with peak onset 1 to 2 weeks after injection and with >90% functional recovery at 6 months.

Muscle and plasma concentrations of free and acylated carnitine (short-chain acylcarnitine and long-chain acylcarnitine) were determined by employing an optimized radiochemical-enzymatic assay in 14 healthy volunteers and in 10 patients with oesophageal carcinoma prior to elective operation. No significant correlations between total carnitine and its subfractions in muscle and plasma were observed and no sex differences were apparent. The estimated total carnitine pool in the patients (75.0 +/- 27 mmol) was significantly reduced compared to controls (130 +/- 24.3 mmol). The reduction was still present when expressed per kg muscle tissue (3.5 +/- 1.0 mmol versus 4.5 +/- 0.7 mmol) in order to consider age related decreased muscle mass in the patients. The muscular ratio of acylcarnitines to free carnitine was higher in the patients (0.23 +/- 0.10) than in healthy subjects (0.15 +/- 0.07), whereas the corresponding plasma quotient in the patients (0.22 +/- 0.09) was lowered compared to controls (0.30 +/- 0.10), indicating that instead of glucose, oxidation of fatty acids can be maintained, resulting in a preservation of the glycogen stores and thus an energy-conserving metabolic adaptation as a response to prolonged energy deficit.

Available data have established that the female athlete is particularly vulnerable to various stress syndromes and noncontact ligament sprains of the knee. Although anatomic differences such as decreased muscle mass and increased joint laxity exist, the primary reason for this disparity appears to be an inadequate level of basic motor skills. The average female athlete has less training and conditioning than the male and has paid less attention to preparticipation fitness. Normal motor function has been defined in terms of required flexibility and coordination so that simple clinical testing can be performed. Normal flexibility may be defined as the unimpeded range of motion at each joint required for running. Coordination is normal when posture and movement are efficient and self-protective. This results from the action of primary neuromuscular mechanisms, which are anthropologic developments to support the unique posture of humans. Poor motor training or reflex inhibition causes secondary, less efficient mechanisms to be substituted for the primary ones, resulting in faulty coordination. These changes can be detected on clinical examination. Assessment of flexibility and coordination are the most important parts of the evaluation of the female athlete, since they relate directly to her most common injury patterns. The underlying neuromuscular physiology governing postural control and movement needs to be considered in planning therapeutic measures.

No abnormality of exocrine function of the pancreas was found in 10 patients with amyotrophic lateral sclerosis. Eight patients showed abnormal glucose metabolism, attributed to the effects of age, malnutrition, diminished physical activity, and decreased muscle mass.

A male infant born at term to a mother with myotonic dystrophy had sufficient evidence of the disease to enable the diagnosis to be made on the first day of postnatal life. Clinical manifestations included profound hypotonia, feeble respiratory efforts, elevation of the right hemidiaphragm, decreased muscle mass in the lower extremities, hirsutism of the lower legs, thin and hypomineralized ribs and long bones, cryptorchidism, and talipes equinovarus. Death occurred at 90 hours of age from respiratory insufficiency. This case further demonstrates that features of myotonic dystrophy can be prenatal in onset.

The Fontan operation is the anticipated palliative strategy for children born with single-ventricle type of congenital heart disease. As a result of important circulatory limitations, a series of end-organ complications are now increasingly recognized. Elevated central venous pressure and impaired cardiac output are the hallmarks of cavo-pulmonary flow, which result in a cascade of pathophysiological consequences. The Fontan circulation likely impacts all organ systems in an indolent and relentless manner, with progressive decline in functionality likely to occur in many. Liver fibrosis, altered bone density, decreased muscle mass, renal dysfunction, lymphatic insufficiency, and a host of other conditions are present. Standardized screening and evaluation of survivors as they grow through childhood and beyond is indicated and can be facilitated through dedicated multidisciplinary clinical programs. Invasive assessment at specific milestones can provide important actionable information to optimize individual status. More detailed characterization and understanding of these end-organ complications is necessary to contribute to the goal of achieving a normal duration and quality of life for these unique individuals.

With increasing age, it appears that masters athletes competing in anaerobic events (10–100 s) decline linearly in performance until 70 years of age, after which the rate of decline appears to accelerate. This decline in performance appears strongly related to a decreased anaerobic work capacity, which has been observed in both sedentary and well-trained older individuals. Previously, a number of factors have been suggested to influence anaerobic work capacity including gender, muscle mass, muscle fiber type, muscle fiber size, muscle architecture and strength, substrate availability, efficiency of metabolic pathways, accumulation of reaction products, aerobic energy contribution, heredity, and physical training. The effects of sedentary aging on these factors have been widely discussed within literature. Less data are available on the changes in these factors in masters athletes who have continued to train at high intensities with the aim of participating in competition. The available research has reported that these masters athletes still demonstrate age-related changes in these factors. Specifically, it appears that morphological (decreased muscle mass, type II muscle fiber atrophy), muscle contractile property (decreased rate of force development), and biochemical changes (changes in enzyme activity, decreased lactate production) may explain the decreased anaerobic performance in masters athletes. However, the reduction in anaerobic work capacity and subsequent performance may largely be the result of physiological changes that are an inevitable result of the aging process, although their effects may be minimized by continuing specific high-intensity resistance or sprint training.

In kwashiorkor the heart is clinically and radiologically small. This study utilises echocardiography, a tool not previously used in this disease, to show that this is due to decreased muscle mass.

At postmortem examination decreased muscle mass and body fat and an empty gastrointestinal tract are evident.