Compliance of a cobalt chromium coronary stent alloy – the COVIS trial

Aim

Female cardiac transplant recipients' aerobic capacity is 60% lower than sex and age-predicted values. The effect of exercise training on restoring the impaired aerobic endurance and muscle strength in female cardiac transplant recipients is not known. This study examined the effect that aerobic and strength training have on improving aerobic endurance and muscle strength in female cardiac transplant recipients.

Methods

20 female cardiac transplant recipients (51 ± 11 years) participated in this investigation. The subjects performed a baseline six-minute walk test and a leg-press strength test when they were discharged following cardiac transplantation. The subjects then participated in a 12-week exercise program consisting of aerobic and lower extremity strength training. Baseline assessments were repeated following completion of the exercise intervention.

Results

At baseline, the cardiac transplant recipients' aerobic endurance was 50% lower than age-matched predicted values. The training program resulted in a significant increase in aerobic endurance (pre-training: 322 ± 104 m vs. post-training: 501 ± 99 m, p < 0.05) and leg-press strength (pre-training: 48 ± 16 kg. vs. post-training: 78 ± 27 kg, p < 0.05).

Conclusion

Aerobic and strength training are effective interventions that can partially restore the impaired aerobic endurance and strength found in female cardiac transplant recipients.     

Heart Rate Dynamics after Combined Strength and Endurance Training in Middle-Aged Women: Heterogeneity of Responses

The loss of complexity in physiological systems may be a dynamical biomarker of aging and disease. In this study the effects of combined strength and endurance training compared with those of endurance training or strength training alone on heart rate (HR) complexity and traditional HR variability indices were examined in middle-aged women. 90 previously untrained female volunteers between the age of 40 and 65 years completed a 21 week progressive training period of either strength training, endurance training or their combination, or served as controls. Continuous HR time series were obtained during supine rest and submaximal steady state exercise. The complexity of HR dynamics was assessed using multiscale entropy analysis. In addition, standard time and frequency domain measures were also computed. Endurance training led to increases in HR complexity and selected time and frequency domain measures of HR variability (P<0.01) when measured during exercise. Combined strength and endurance training or strength training alone did not produce significant changes in HR dynamics. Inter-subject heterogeneity of responses was particularly noticeable in the combined training group. At supine rest, no training-induced changes in HR parameters were observed in any of the groups. The present findings emphasize the potential utility of endurance training in increasing the complex variability of HR in middle-aged women. Further studies are needed to explore the combined endurance and strength training adaptations and possible gender and age related factors, as well as other mechanisms, that may mediate the effects of different training regimens on HR dynamics.     

Skeletal muscle fiber area alterations in two opposing modes of resistance-exercise training in the same individual

The purpose of this study was to observe fiber area changes that might occur in the same subject from two opposing resistance-exercise training regimes isolating the quadriceps muscle group. Twelve college-age men divided into two groups participated in each of two 7.5-week regimens; one performed a muscular strength program (high-resistance, low-repetition) 4 days a week on a resistance-exercise apparatus, while the other performed a muscular endurance (low-resistance, high-repetition) program. After a 5.5-week hiatus, the groups changed regimens for the second 7.5 weeks. Closed-needle biopsies of the dominant vastus lateralis and isokinetic dynamometer evaluations were made before and at the end of each training period. The muscle samples were analyzed for area changes. In both groups the initial exercise stimulus, whether for strength or endurance, increased the area of fibers of all three major types (I, IIA, and IIB). Subjects doing strength exercises as their second treatment showed a further increase in the area of type I and IIB fibers, whereas those doing endurance exercises showed a decrease in all fiber types. From the first to the last biopsy all fiber areas were decreased (P less than 0.05) in the control-strength-endurance group and increased (P less than 0.05) in the control-endurance-strength group. These results suggested that endurance exercise preceding strength exercise in an isolated muscle group maximized fiber area adaptations to exercise stress. Consideration should thus be given in exercise and rehabilitation programs to the muscle cellular adaptations evidenced in different orders of training, particularly if muscular strength is considered important.     

Exercise training improves aerobic endurance and musculoskeletal fitness in female cardiac transplant recipients

Aim

Female cardiac transplant recipients'' aerobic capacity is 60% lower than sex and age-predicted values. The effect of exercise training on restoring the impaired aerobic endurance and muscle strength in female cardiac transplant recipients is not known. This study examined the effect that aerobic and strength training have on improving aerobic endurance and muscle strength in female cardiac transplant recipients.

Methods

20 female cardiac transplant recipients (51 ± 11 years) participated in this investigation. The subjects performed a baseline six-minute walk test and a leg-press strength test when they were discharged following cardiac transplantation. The subjects then participated in a 12-week exercise program consisting of aerobic and lower extremity strength training. Baseline assessments were repeated following completion of the exercise intervention.

Results

At baseline, the cardiac transplant recipients'' aerobic endurance was 50% lower than age-matched predicted values. The training program resulted in a significant increase in aerobic endurance (pre-training: 322 ± 104 m vs. post-training: 501 ± 99 m, p < 0.05) and leg-press strength (pre-training: 48 ± 16 kg. vs. post-training: 78 ± 27 kg, p < 0.05).

Conclusion

Aerobic and strength training are effective interventions that can partially restore the impaired aerobic endurance and strength found in female cardiac transplant recipients.Exercise training is an effective intervention that can partially restore the impaired aerobic capacity and musculoskeletal fitness (i.e. muscle strength) found in cardiac transplant recipients [1,2]. However, previous reports have focused exclusively on the effects of exercise training in men. Therefore, the effect of exercise training on these outcomes in female cardiac transplant recipients is not known [2-7]. Importantly, a majority of female cardiac transplant recipients do not engage in regular physical activity leading to increased levels of fatigue, poor functional status and reduced exercise capacity [8-10]. Based on this rationale, the aim of this study is to examine the effect that exercise training has on improving aerobic endurance (i.e. distance walked in six-minutes) and lower extremity muscle strength in female cardiac transplant recipients. We hypothesized that exercise training would be a feasible and effective intervention to improve aerobic endurance and lower extremity strength in female cardiac transplant recipients.     

Exercise‐stimulated interleukin‐15 is controlled by AMPK and regulates skin metabolism and aging

Aging is commonly associated with a structural deterioration of skin that compromises its barrier function, healing, and susceptibility to disease. Several lines of evidence show that these changes are driven largely by impaired tissue mitochondrial metabolism. While exercise is associated with numerous health benefits, there is no evidence that it affects skin tissue or that endocrine muscle‐to‐skin signaling occurs. We demonstrate that endurance exercise attenuates age‐associated changes to skin in humans and mice and identify exercise‐induced IL‐15 as a novel regulator of mitochondrial function in aging skin. We show that exercise controls IL‐15 expression in part through skeletal muscle AMP‐activated protein kinase (AMPK), a central regulator of metabolism, and that the elimination of muscle AMPK causes a deterioration of skin structure. Finally, we establish that daily IL‐15 therapy mimics some of the anti‐aging effects of exercise on muscle and skin in mice. Thus, we elucidate a mechanism by which exercise confers health benefits to skin and suggest that low‐dose IL‐15 therapy may prove to be a beneficial strategy to attenuate skin aging.     

Effects of endurance exercise-training on single-fiber contractile properties of insulin-treated streptozotocin-induced diabetic rats.

The purpose of this study was to characterize the contractile properties of individual skinned muscle fibers from insulin-treated streptozotocin-induced diabetic rats after an endurance exercise training program. We hypothesized that single-fiber contractile function would decrease in the diabetic sedentary rats and that endurance exercise would preserve the function. In the study, 28 rats were assigned to either a nondiabetic sedentary, a nondiabetic exercise, a diabetic sedentary, or a diabetic exercise group. Rats in the diabetic groups received subcutaneous intermediate-lasting insulin daily. The exercise-trained rats ran on a treadmill at a moderate intensity for 60 min, five times per week. After 12 wk, the extensor digitorum longus and soleus muscles were dissected. Single-fiber diameter, Ca(2+)-activated peak force, specific tension, activation threshold, and pCa(50) as well as the myosin heavy chain isoform expression (MHC) were determined. We found that in MHC type II fibers from extensor digitorum longus muscle, diameters were significantly smaller from diabetic sedentary rats compared with nondiabetic sedentary rats (P < 0.001). Among the nondiabetic rats, fiber diameters were smaller with exercise (P = 0.038). The absolute force-generating capacity of single fibers was lower in muscles from diabetic rats. There was greater specific tension (force normalized to cross-sectional area) by fibers from the rats that followed an endurance exercise program compared with sedentary. From the results, we conclude that alterations in the properties of contractile proteins are not implicated in the decrease in strength associated with diabetes and that endurance-exercise training does not prevent or increase muscle weakness in diabetic rats.     

Regular Multicomponent Exercise Increases Physical Fitness and Muscle Protein Anabolism in Frail,Obese, Older Adults

Aging is associated with a decline in strength, endurance, balance, and mobility. Obesity worsens the age‐related impairment in physical function and often leads to frailty. The American College of Sports Medicine recommends a multicomponent (strength, endurance, flexibility, and balance) exercise program to maintain physical fitness. However, the effect of such an exercise program on physical fitness in frail, obese older adults is not known. We therefore determined the effect of a 3‐month long multicomponent exercise training program, on endurance (peak aerobic capacity (VO₂ peak)), muscle strength, muscle mass, and the rate of muscle protein synthesis (basal rate and anabolic response to feeding) in nine 65‐ to 80‐year‐old, moderately frail, obese older adults. After 3 months of training, fat mass decreased (P < 0.05) whereas fat‐free mass (FFM), appendicular lean body mass, strength, and VO₂ peak increased (all P < 0.05). Regular strength and endurance exercise increased the mixed muscle protein fractional synthesis rate (FSR) but had no effect on the feeding‐induced increase in muscle protein FSR (～0.02%/h increase from basal values both before and after exercise training; effect of feeding: P = 0.02; effect of training: P = 0.047; no interaction: P = 0.84). We conclude that: (i) a multicomponent exercise training program has beneficial effects on muscle mass and physical function and should therefore be recommended to frail, obese older adults, and (ii) regular multicomponent exercise increases the basal rate of muscle protein synthesis without affecting the magnitude of the muscle protein anabolic response to feeding.     

The benefits of regular kinesiotherapy once a week for postmenopausal women: an aged-matched study

Regular exercise training improves overall physical fitness and quality of life in postmenopausal women. The exigent training frequency depends on a user-specified training aim. The aim of this study was to confirm the benefits of regular once a week exercise training for the maintenance of fitness in postmenopausal women. The test group included 20 postmenopausal women (65 +/- 3.1 years) who have been attending the exercise training program conducted by the physiotherapist once a week for three years. The age-matched control group included 20 healthy women (65.5 +/- 2.4 years) who did not regularly attend the training program. The outcomes were: right and left lateral trunk flexion, right and left shoulder flexion, right and left grip strength, endurance capacity of the trunk extensors, lower limb muscle strength (1' chair stand test), and balance (one-leg standing duration time with eyes open and closed). Women from the test group achieved statistically significant better results in the following outcomes: right lateral trunk flexion (15.4 cm: 12.6 cm, p < 0.001), left lateral trunk flexion (15.4 cm: 12.6 cm, p = 0.001), trunk extension muscle endurance (53.4 s: 40.5 s, p < 0.001), lower limb muscle strength (28.4 x: 25 x, p < 0.001), and one-leg standing duration time with open eyes (33.5 s: 19.7 s, p < 0.001). The results suggest that a regular once a week exercise training program designed and conducted by the physiotherapist, may be helpful in the improvement or maintenance of flexibility, muscle strength and capacity, and balance in postmenopausal women. The better fitness proved by our study could be a result of other causes and not solely that of the designed training program.     

Deletion of ghrelin prevents aging‐associated obesity and muscle dysfunction without affecting longevity

During aging, decreases in energy expenditure and locomotor activity lead to body weight and fat gain. Aging is also associated with decreases in muscle strength and endurance leading to functional decline. Here, we show that lifelong deletion of ghrelin prevents development of obesity associated with aging by modulating food intake and energy expenditure. Ghrelin deletion also attenuated the decrease in phosphorylated adenosine monophosphate‐activated protein kinase (pAMPK) and downstream mediators in muscle, and increased the number of type IIa (fatigue resistant, oxidative) muscle fibers, preventing the decline in muscle strength and endurance seen with aging. Longevity was not affected by ghrelin deletion. Treatment of old mice with pharmacologic doses of ghrelin increased food intake, body weight, and muscle strength in both ghrelin wild‐type and knockout mice. These findings highlight the relevance of ghrelin during aging and identify a novel AMPK‐dependent mechanism for ghrelin action in muscle.     

Lipid peroxidation and scavenger enzymes during exercise: adaptive response to training

This study was designed to determine whether endurance training would influence the production of lipid peroxidation (LI-POX) by-products as indicated by malondialdehyde (MDA) at rest and after an acute exercise run. Additionally, the scavenger enzymes catalase (CAT) and superoxide dismutase (SOD) were examined to determine whether changes in LIPOX are associated with alterations in enzyme activity both at rest and after exercise. Male Sprague-Dawley rats (n = 32) were randomly assigned to either trained or sedentary groups and were killed either at rest or after 20 min of treadmill running. The training program increased oxidative capacity 64% in leg muscle. After exercise, the sedentary group demonstrated increased LIPOX levels in liver and white skeletal muscle, whereas the endurance-trained group did not show increases in LIPOX after exercise. CAT activity was higher in both red and white muscle after exercise in the trained animals. Total SOD activity was unaffected by either acute or chronic exercise. These data suggest that endurance training can result in a reduction in LIPOX levels as indicated by MDA during moderate-intensity exercise. It is possible that activation of the enzyme catalase and the increase in respiratory capacity were contributory factors responsible for regulating LIPOX after training during exercise.     

Body composition as affected by physical activity and nutrition

Although exercise and/or training can augment maximum oxygen consumption, muscle strength, and endurance, it has not been shown to markedly increase lean body mass (LBM) or to markedly decrease body fat in humans unless androgens are given. Bed rest likewise leads to very modest changes in body composition. Over-nutrition, on the other hand, produces a significant increase in body LBM and fat, and undernutrition a fall in both; hence the evaluation of exercise programs should include assessment of energy intake.     

Effects of exercise on the biomechanical,biochemical and structural properties of tendons

Tendon has been shown to undergo remodeling in response to strength or endurance training, however, compared to muscle, studies of the effects of exercise on tendon are limited and the information is inconsistent. Exercise may influence the structure, chemical composition and/or mechanical properties of tendon. Studies that have examined mechanical changes of tendon in response to endurance training suggest that ultimate failure strength and stiffness increase with training. Available reports indicate that increases in tensile strength and stiffness are probably not associated with increases in collagen concentration or with tendon hypertrophy. The paucity of data renders it impossible to evaluate the response of other structural, chemical and mechanical parameters to training. Furthermore, few investigators have included discrete measures of structural, biomechanical and biochemical variables within a single study. The lack of integrative studies makes it difficult to definitively associate changes in the mechanical properties of tendon with chemical composition and structure.     

Enzyme activities and reduced insulin need with training in streptozotocin-induced diabetic rats

Following a 12-week endurance training program, the SDH activities of gastrocnemius medialis muscle of streptozotocin-induced diabetic animals increased by 50%. On the other hand, a 14% decrease was observed in the same muscle of diabetic animals submitted to power training. No difference between groups, for soleus and gastrocnemius lateralis muscles following the two different training regimens was observed. It can be concluded that streptozotocin-induced diabetic animals controlled by daily insulin demonstrate a normal muscle enzyme adaptation to exercise. These data also demonstrate that regular power and/or endurance exercise can result in reduced exogenous insulin need in streptozotocin-induced diabetic rats (18% and 28% respectively), suggesting a more efficient membrane transport of glucose with induced exercise, and a decreased need for insulin supported transport.     

Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans

Endurance and strength training are established as distinct exercise modalities, increasing either mitochondrial density or myofibrillar units. Recent research, however, suggests that mitochondrial biogenesis is stimulated by both training modalities. To test the training "specificity" hypothesis, mitochondrial respiration was studied in permeabilized muscle fibers from 25 sedentary adults after endurance (ET) or strength training (ST) in normoxia or hypoxia [fraction of inspired oxygen (Fi(O(2))) = 21% or 13.5%]. Biopsies were taken from the musculus vastus lateralis, and cycle-ergometric incremental maximum oxygen uptake (VO(2max)) exercise tests were performed under normoxia, before and after the 10-wk training program. The main finding was a significant increase (P < 0.05) of fatty acid oxidation capacity per muscle mass, after endurance and strength training under normoxia [2.6- and 2.4-fold for endurance training normoxia group (ET(N)) and strength training normoxia group (ST(N)); n = 8 and 3] and hypoxia [2.0-fold for the endurance training hypoxia group (ET(H)) and strength training hypoxia group (ST(H)); n = 7 and 7], and higher coupling control of oxidative phosphorylation. The enhanced lipid oxidative phosphorylation (OXPHOS) capacity was mainly (87%) due to qualitative mitochondrial changes increasing the relative capacity for fatty acid oxidation (P < 0.01). Mitochondrial tissue-density contributed to a smaller extent (13%), reflected by the gain in muscle mass-specific respiratory capacity with a physiological substrate cocktail (glutamate, malate, succinate, and octanoylcarnitine). No significant increase was observed in mitochondrial DNA (mtDNA) content. Physiological OXPHOS capacity increased significantly in ET(N) (P < 0.01), with the same trend in ET(H) and ST(H) (P < 0.1). The limitation of flux by the phosphorylation system was diminished after training. Importantly, key mitochondrial adaptations were similar after endurance and strength training, regardless of normoxic or hypoxic exercise. The transition from a sedentary to an active lifestyle induced muscular changes of mitochondrial quality representative of mitochondrial health.     

Exercise improves impaired ventricular function and alterations of cardiac myofibrillar proteins in diabetic dyslipidemic pigs.

Chronic diabetes is often associated with cardiomyopathy, which may result, in part, from defects in cardiac muscle proteins. We investigated whether a 20-wk porcine model of diabetic dyslipidemia (DD) would impair in vivo myocardial function and yield alterations in cardiac myofibrillar proteins and whether endurance exercise training would improve these changes. Myocardial function was depressed in anesthetized DD pigs (n = 12) compared with sedentary controls (C; n = 13) as evidenced by an approximately 30% decrease in left ventricular fractional shortening and an approximately 35% decrease in +dP/dt measured by noninvasive echocardiography and direct cardiac catheterization, respectively. This depression in myocardial function was improved with chronic exercise as treadmill-trained DD pigs (DDX) (n = 13) had significantly greater fractional shortening and +dP/dt than DD animals. Interestingly, the isoform expression pattern of the myofibrillar regulatory protein, cardiac troponin T (cTnT), was significantly shifted from cTnT1 toward cTnT2 and cTnT3 in DD pigs. Furthermore, this change in cTnT isoform expression pattern was prevented in DDX pigs. Finally, there was a decrease in baseline levels of cAMP-dependent protein kinase-induced phosphorylation of the myofibrillar proteins troponin I and myosin-binding protein-C in DD animals. Overall, these results indicate that 20 wk of DD lead to myocardial dysfunction coincident with significant alterations in myofibrillar proteins, both of which are prevented with endurance exercise training, implying that changes in myofibrillar proteins may contribute, at least in part, to cardiac dysfunction associated with diabetic cardiomyopathy.     

Coenzyme Q₁₀ reverses mitochondrial dysfunction in atorvastatin-treated mice and increases exercise endurance

Statins are cholesterol-lowering drugs widely used in the prevention of cardiovascular diseases; however, they are associated with various types of myopathies. Statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and thus decrease biosynthesis of low-density lipoprotein cholesterol and may also reduce ubiquinones, essential coenzymes of a mitochondrial electron transport chain, which contain isoprenoid residues, synthesized through an HMG-CoA reductase-dependent pathway. Therefore, we hypothesized that statin treatment might influence physical performance through muscular mitochondrial dysfunction due to ubiquinone deficiency. The effect of two statins, atorvastatin and pravastatin, on ubiquinone content, mitochondrial function, and physical performance was examined by using statin-treated mice. Changes in energy metabolism in association with statin treatment were studied by using cultured myocytes. We found that atorvastatin-treated mice developed muscular mitochondrial dysfunction due to ubiquinone deficiency and a decrease in exercise endurance without affecting muscle mass and strength. Meanwhile, pravastatin at ten times higher dose of atorvastatin had no such effects. In cultured myocytes, atorvastatin-related decrease in mitochondrial activity led to a decrease in oxygen utilization and an increase in lactate production. Conversely, coenzyme Q(10) treatment in atorvastatin-treated mice reversed atorvastatin-related mitochondrial dysfunction and a decrease in oxygen utilization, and thus improved exercise endurance. Atorvastatin decreased exercise endurance in mice through mitochondrial dysfunction due to ubiquinone deficiency. Ubiquinone supplementation with coenzyme Q(10) could reverse atorvastatin-related mitochondrial dysfunction and decrease in exercise tolerance.     

Disuse and aging: same problem, different outcomes

Many of the changes that accompany physical inactivity coincide with those that occur during aging. These changes are generally grouped under the term of 'disuse' (or "lack of use" or "inappropriately modulated stimulation"). Studies of long-term space travel have revealed that weightlessness in space also induces changes resembling those of aging and physical inactivity. The relationship between disuse (due to bed rest, insufficient exercise, or lack of gravity) and aging has some definite practical implications. As life expectancy is lenghtened in all populations worldwide, the number of elderly with varying degrees of disability leading to reduced physical activity also increases. Changes induced by bed rest as a consequence of disease may also be superimposed on aging changes and further diminish physiologic reserves and accelerate pathology. Therefore, the study of disuse, irrespective of its etiology, may serve as a model for understanding not only some of the functional changes induced by lack of activity and/or gravity but also some of the disabilities of old age. Indeed, a better understanding of disuse phenomena will make it possible to establish programs of prevention and rehabilitation that will ameliorate both disuse and aging deficits.