Physical Detraining Research Articles

Chronic effects of training and subsequent physical detraining on histology and morphometry of adipose tissue in adult Wistar rats

Chronic effects of training and subsequent physical detraining on histology and morphometry of adipose tissue in adult Wistar rats

Importance of physical detraining in functional capacity of individuals with chronic peripheral arterial occlusive disease: a cross-sectional pilot study.

BackgroundPhysical training is a well-established strategy for rehabilitation of the functional capacity of individuals with chronic peripheral arterial occlusive disease (PAOD). However, some individuals quit training after participating in a physical training program, undergoing detraining. There is scant literature on the effects of physical detraining in individuals with PAOD and it is therefore important to investigate the effects of this phenomenon.ObjectivesThe objective of this article was to evaluate the effects of physical detraining on functional capacity in individuals with PAOD.MethodsCross-sectional study with 22 individuals. Participants were divided into two groups: a detraining group (DG) and a control group (CG). The distance covered in the 6-minute walk test (6MWTD) and the pain-free walking distance (PFWD) were evaluated. The PFWD is the distance covered until claudication begins, i.e., the distance covered without pain.ResultsMean age was 66 ± 8 in the DG and 67 ± 7 in the CG. There were no differences between the groups in either the 6MWTD or the PFWD (p = 0.428; p = 0.537, respectively).ConclusionsThe present pilot study allows us to conclude that the functional capacity of individuals with PAOD who participated in a physical training program and subsequently underwent detraining was not superior in relation to individuals who did not participate in a physical training program. The results of the present study serve to encourage maintenance of physical exercise, since physical training is no longer effective if detraining occurs.

The mechanisms involved in the increased adiposity induced by interruption of regular physical exercise practice

AimsWe investigated the effects of physical detraining on lipogenesis/lipolysis and cellularity (apoptosis/adipogenesis) in rat subcutaneous (inguinal; SC) and visceral (retroperitoneal; RP) white adipose depots. Main methodsThree groups of male Wistar rats (6-wk old) were studied: (1) (T) trained for 12 weeks; (2) (D) trained for 8 weeks and detrained for 4 weeks; and (3) (S) age-matched sedentary. Training consisted of treadmill running sessions (1 h/day, 5 days/week, 50–60% maximal race capacity). Key findingsPhysical detraining increased glucose oxidation, lipogenesis, and adipocyte size in the SC and RP depots. The number of apoptotic SC adipocytes was reduced by 53% in the T (p < 0.0001) and by 43% in the D (p < 0.001) as compared with S. RP adipocyte apoptosis in the T and D was 9.48% and 10.9% greater compared to the S, respectively (p < 0.05). In the SC stromal vascular fraction (SVF) of D rats, adiponectin, sterol regulatory element binding protein (SREBP)-1c, Peroxisome proliferator-activated receptor gamma (PPARγ), and Perilipin A mRNA expressions were more pronounced than S group, suggesting a more intense adipogenesis. This putative adipogenic effect was not observed in the RP depot. The physical detraining promoted rapid increase in the SC and RP depots however not through the same mechanisms. SignificancePhysical detraining induced fat cell hypertrophy (increase of lipogenesis) in both SC and RP whereas hyperplasia (increase of adipogenesis and reduction of apoptosis) was found in SC only. These results indicate the mechanism associated with obesogenic effects of detraining varies with the fat depot.

Aerobic capacity of wistar rats: the effects of training and physical detraining at middle-aged

It has been shown that engaging in regular physical exercise yields short- and long-term health benefits, primarily by mitigating the risk for cardiovascular disease, but little information is known about physical deconditioning at aging process. The aim of the present study was to analyze the aerobic capacity, through maximal lactate steady state (MLSS), in Wistar rats of different ages (2,4, 6 e 12 months ) and physical conditioning deconditioning responses in middle-aged rats. The results were significant for weight gain in the sedentary (588 ± 71 g) and detraining animals (576 ± 62 g) at 12 months, whereas the conditioned group maintained their original body weights – BW (515 ± 72 g), similar at four (455 ±17 g) and six months of age (471 ± 37 g). MLSS decreased with age (2 months sedentary (8.4 ± 1% Body Weight, 4 months sedentary (6.4 ± 0.6% BW), 6 months sedentary (5.8 ± 1% BW), 12 months sedentary (5.1 ± 0.7% BW), but physical exercise was effective in attenuating the age-related loss of aerobic capacity after 12 months (5.8 ± 1.3% BW). The physical detraining was (5.3 ± 0.4% BW) was similar at 12 months trained. The physical training in long term protected against the increased of the body weight and fat depots caused by aging, but, this effect was found by deconditioning physical. Additionally, the physical training attenuated the aerobic capacity loss due to aging process and this effect was maintained after detraining physical.

Muscular glucose metabolism in middle-age trained rats

Aging decreases the normal organism physiological functions. On the other hand, physical exercise shows health benefits, but little information is known about physical deconditioning at aging. The aim of the present study was to analyze the glucose muscle metabolism in middle-age Wistar rats in response to conditioning and physical deconditioning. The study included three groups: Control (C)—not performed physical training; Trained (T)—performed physical training from 4 to 12 months—swimming exercise for 1 h per day, 5 days per week at 80% of maximal lactate stead state—MLSS; Detrained (D)—performed to physical training from 4 to 8 months and assessed at 12 months (D). Physical training at submaximal intensities induced decreases in body weight (C 588 ± 71, T 515 ± 72, D 576 ± 62 g), and the weight of mesenteric adipose tissue (C 4399 ± 643, T 3007 ± 811, D 4085 ± 540 mg/g), and increases in exercise workload in MLSS intensity (C 4.6 ± 0.4, T 5.8 ± 1.3, D 5.3 ± 0.4% body weight), glucose tolerance (C 12314 ± 1122, T 8428 ± 853, D 9433 ± 1200 mg/dL 120 min), glycogen deposits (C 0.48 ± 0.07, T 0.66 ± 0.18, D 0.46 ± 0.10 mg/100 mg) and glucose uptake by skeletal muscle (C 1.96 ± 0.54, T 3.28 ± 0.53, D 2.55 ± 0.35 μmol/g/h) in trained animals. Additionally, the improvement in exercise load in MLSS, glucose tolerance and glucose uptake was maintained after physical detraining. In summary, the physical training promotes alterations in body weight, fat tissue, aerobic capacity and muscular glucose metabolism in middle-age rats. However, only the aerobic capacity and muscular glucose metabolism were maintained after detraining.

Fat gain with physical detraining is correlated with increased glucose transport and oxidation in periepididymal white adipose tissue in rats

As it is a common observation that obesity tends to occur after discontinuation of exercise, we investigated how white adipocytes isolated from the periepididymal fat of animals with interrupted physical training transport and oxidize glucose, and whether these adaptations support the weight regain seen after 4 weeks of physical detraining. Male Wistar rats (45 days old, weighing 200 g) were divided into two groups (n=10): group D (detrained), trained for 8 weeks and detrained for 4 weeks; and group S (sedentary). The physical exercise was carried out on a treadmill for 60 min/day, 5 days/week for 8 weeks, at 50-60% of the maximum running capacity. After the training protocol, adipocytes isolated from the periepididymal adipose tissue were submitted to glucose uptake and oxidation tests. Adipocytes from detrained animals increased their glucose uptake capacity by 18.5% compared with those from sedentary animals (P<0.05). The same cells also showed a greater glucose oxidation capacity in response to insulin stimulation (34.55%) compared with those from the S group (P<0.05). We hypothesize that, owing to the more intense glucose entrance into adipose cells from detrained rats, more substrate became available for triacylglycerol synthesis. Furthermore, this increased glucose oxidation rate allowed an increase in energy supply for triacylglycerol synthesis. Thus, physical detraining might play a role as a possible obesogenic factor for increasing glucose uptake and oxidation by adipocytes.

D-17 Thematic Poster - Sex Hormones and Musculoskeletal Effects

Physical detraining (PD) is associated with increased fat mass, body weight gain and changes in protein metabolism. One of the nutritional strategies used to minimize the increase in adipose mass is caloric restriction (CR). This strategy may potentiate the loss of muscle mass, as observed in PD. The supplementation with essential amino acids, particularly leucine, can be used to mitigate these changes. PURPOSE:Evaluate the effect of leucine supplementation on the expression of myofibrillar proteins, particularly slow myosin heavy chain (MyHC-7), in detrained rats undergoing CR. METHODS:40 adult male Sprague-Dawley rats were assigned to 2 groups: Sedentary (SED, n = 8) and Trained (TRAIN, n = 32); the animals of the latter group underwent training on a treadmill for 8 weeks. TRAIN animals were then re-distributed into four groups: Trained (TRAIN, n = 8): animals who continued following the physical training protocol; Detrained (DT, n = 8): animals who stopped training and had free access to food; Detrained + CR (CR + DT): animals who stopped training and consumed 70% of DT caloric intake; Detrained + Leucine + CR (CR + DT + LEU): animals who stopped training and consumed 70% of DT caloric intake, and received 5% leucine supplementation. Body weight and food consumption were measured weekly. After 14 weeks the animals were euthanized, body composition was assessed using carcass chemical analysis, and the soleum tissue was used to assess the expression of MyHC-7 through imunoblotting. ANOVA was used for group comparison, along with Tukey test, considering a 5% significance level. RESULTS:Statistically significant difference was observed in body fat in CR+DT (16.08±6.98g) and CR+DT+LEU (15.98±7.74g) groups compared to DT (56.16±18.01g). No statistical difference was observed in fat-free mass (%) and relative protein (%) in the leucine-supplemented group. Additionally, a statistically significant difference was seen in the expression of MyHC-7 between TRAIN and SED groups (TRAIN 1.29±0.39, SED .44±0.12; p < 0.05), there was no difference when comparing groups DT, CR + DT and CR + DT + LEU. CONCLUSION:Leucine supplementation was not effective to minimize the loss of lean body mass and specifically to mitigate the decreased expression of MyHC-7 in detrained animals under CR. Acknowledgements to FAPESP

Cessation of physical exercise changes metabolism and modifies the adipocyte cellularity of the periepididymal white adipose tissue in rats

All of the adaptations acquired through physical training are reversible with inactivity. Although significant reductions in maximal oxygen uptake (Vo2max) can be observed within 2 to 4 wk of detraining, the consequences of detraining on the physiology of adipose tissue are poorly known. Our aim was therefore to investigate the effects of discontinuing training (physical detraining) on the metabolism and adipocyte cellularity of rat periepididymal (PE) adipose tissue. Male Wistar rats, aged 6 wk, were divided into three groups and studied for 12 wk under the following conditions: 1) trained (T) throughout the period; 2) detrained (D), trained during the first 8 wk and detrained during the remaining 4 wk; and 3) age-matched sedentary (S). Training consisted of treadmill running sessions (1 h/day, 5 days/wk, 50-60% Vo2max). The PE adipocyte size analysis revealed significant differences between the groups. The adipocyte cross-sectional area (in μm(2)) was significantly larger in D than in the T and S groups (3,474 ± 68.8; 1,945.7 ± 45.6; 2,492.4 ± 49.08, respectively, P < 0.05). Compared with T, the isolated adipose cells (of the D rats) showed a 48% increase in the ability to perform lipogenesis (both basal and maximally insulin-stimulated) and isoproterenol-stimulated lipolysis. No changes were observed with respect to unstimulated lipolysis. A 15% reduction in the proportion of apoptotic adipocytes was observed in groups T and D compared with group S. The gene expression levels of adiponectin and PPAR-gamma were upregulated by factors of 3 and 2 in D vs. S, respectively. PREF-1 gene expression was 3-fold higher in T vs. S. From these results, we hypothesize that adipogenesis was stimulated in group D and accompanied by significant adipocyte hypertrophy and an increase in the lipogenic capacity of the adipocytes. The occurrence of apoptotic nuclei in PE fat cells was reduced in the D and T rats; these results raise the possibility that the adipose tissue changes after detraining are obesogenic.

Detraining Differentially Preserved Beneficial Effects of Exercise on Hypertension: Effects on Blood Pressure, Cardiac Function, Brain Inflammatory Cytokines and Oxidative Stress

AimsThis study sought to investigate the effects of physical detraining on blood pressure (BP) and cardiac morphology and function in hypertension, and on pro- and anti-inflammatory cytokines (PICs and AIC) and oxidative stress within the brain of hypertensive rats.Methods and ResultsHypertension was induced in male Sprague-Dawley rats by delivering AngiotensinII for 42 days using implanted osmotic minipumps. Rats were randomized into sedentary, trained, and detrained groups. Trained rats underwent moderate-intensity exercise (ExT) for 42 days, whereas, detrained groups underwent 28 days of exercise followed by 14 days of detraining. BP and cardiac function were evaluated by radio-telemetry and echocardiography, respectively. At the end, the paraventricular nucleus (PVN) was analyzed by Real-time RT-PCR and Western blot. ExT in AngII-infused rats caused delayed progression of hypertension, reduced cardiac hypertrophy, and improved diastolic function. These results were associated with significantly reduced PICs, increased AIC (interleukin (IL)-10), and attenuated oxidative stress in the PVN. Detraining did not abolish the exercise-induced attenuation in MAP in hypertensive rats; however, detraining failed to completely preserve exercise-mediated improvement in cardiac hypertrophy and function. Additionally, detraining did not reverse exercise-induced improvement in PICs in the PVN of hypertensive rats; however, the improvements in IL-10 were abolished.ConclusionThese results indicate that although 2 weeks of detraining is not long enough to completely abolish the beneficial effects of regular exercise, continuing cessation of exercise may lead to detrimental effects.

Deconditioning and Fibromyalgia: A Pilot Study

This pilot, multiple case study primarily examined deconditioning effects on four physical fitness components in eight participants with fibromyalgia syndrome (FMS). Fitness results after training were contrasted with fitness results immediately following two periods of inactivity. These preliminary data suggest that aspects of physical deconditioning among people with FMS may be highly individualized; therefore, making any generalizations about physical detraining in this population requires more study. Also, results regarding FMS symptoms and psychosocial factors following training versus no training on these eight participants suggest that deconditioning on these factors is very individualized. Knowledge of data-based, deconditioning information relative to FMS is important for professionals who work with older adult patients, especially activity directors who coordinate/direct recreational exercise programs or physical rehabilitation programs that involve exercise in nursing homes. Deconditioning effects from program closings, activity staff absences, or missing sessions for any reason may potentially affect fitness, FMS symptoms, psychosocial function, and possibly activities of daily living (ADL). This potential negative effect on ADL can increase workload and place much more stress on the nursing staff. All of this requires more research for a more thorough understanding.

The beneficial effects of exercise in rodents are preserved after detraining: a phenomenon unrelated to GLUT4 expression

BackgroundAlthough exercise training has well-known cardiorespiratory and metabolic benefits, low compliance with exercise training programs is a fact, and the harmful effects of physical detraining regarding these adaptations usually go unnoticed. We investigated the effects of exercise detraining on blood pressure, insulin sensitivity, and GLUT4 expression in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY).MethodsStudied animals were randomized into sedentary, trained (treadmill running/5 days a week, 60 min/day for 10 weeks), 1 week of detraining, and 2 weeks of detraining. Blood pressure (tail-cuff system), insulin sensitivity (kITT), and GLUT4 (Western blot) in heart, gastrocnemius and white fat tissue were measured.ResultsExercise training reduced blood pressure (19%), improved insulin sensitivity (24%), and increased GLUT4 in the heart (+34%); gastrocnemius (+36%) and fat (+22%) in SHR. In WKY no change in either blood pressure or insulin sensitivity were observed, but there was an increase in GLUT4 in the heart (+25%), gastrocnemius (+45%) and fat (+36%) induced by training. Both periods of detraining did not induce any change in neither blood pressure nor insulin sensitivity in SHR and WKY. One-week detraining reduced GLUT4 in SHR (heart: -28%; fat: -23%) and WKY (heart: -19%; fat: -22%); GLUT4 in the gastrocnemius was reduced after a 2-week detraining (SHR: -35%; WKY: -25%). There was a positive correlation between GLUT4 (gastrocnemius) and the maximal velocity in the exercise test (r = 0.60, p = 0.004).ConclusionsThe study findings show that in detraining, despite reversion of the enhanced GLUT4 expression, cardiorespiratory and metabolic beneficial effects of exercise are preserved.

Evaluación de la tolerancia al ejercicio en pacientes con schistosomiasis crónica sin evidencias clínicas de compromiso cardiopulmonar tratados con praziquantel

The purpose of this study was to evaluate whether a progressive cycle ergometer test (PCET) can detect minimal functional abnormalities that might indicate compromise of the pulmonary vascular bed in patients treated with praziquantel for chronic schistosomiasis who have no clinical signs of cardiopulmonary impairment. We studied 9 patients (whose mean (SD) age was 38 (18) years and 10 control subjects aged 32 (14) years. Both groups were evaluated by spirometry and a PCET to determine maximum oxygen consumption, heart rate, minute ventilation and gas exchange. Echocardiograms were used to rule out the presence of associated heart disease. Lung function was similar among patients and controls. Slight decreases in maximum oxygen consumption and heart rate reserve were observed with effort during the PCET, with normal respiratory response. No echocardiographic abnormalities that might indicate the presence of pulmonary vascular occlusive disease were observed. The results showed that the resting lung function is normal in these patients. However, there was a slight decrease in exercise tolerance, probably related to physical detraining. The data obtained during exercise indicated that pulmonary vascular occlusive disease is unlikely in these patients. Abnormalities may appear in later stages of the disease or in patients who do not receive early medical treatment.

Effects of physical detraining on athlete performance: a review about skeletal muscle and cardiovascular changes

As adaptações cardiovasculares e metabólicas adquiridas com o treinamento físico de “endurance” podem ser revertidas quando o atleta é submetido a um período de inatividade física, devido ao reajuste dos sistemas corporais às alterações dos estímulos fisiológicos induzidos pelo treinamento físico. Reduções significantes do consumo máximo de oxigênio (V02max) parecem ocorrer dentro de duas a quatro semanas de destreinamento físico, provocando um grande declínio da “performance” do atleta em esportes de “endurance”! A queda inicial do V02max está associada à redução do débito cardíaco conseqüente da redução do volume sistólico, haja visto que a freqüência cardíaca permanece praticamente inalterada. O destreinamento físico também provoca alterações das adaptações do músculo esquelético que resultam em uma redução significante da diferença artério-venosa máxima de oxigênio contribuindo também para a redução do V02max Se a condição física elevada de um atleta pode ser obtida após alguns anos seguidos de treinamento físico efetivo, preparadores físicos e técnicos devem estar atentos para que possíveis eventualidades que impeçam a continuidade da preparação física do atleta não resultem em prejuízos na sua “performance” Sendo assim, esta revisão tem como objetivo descrever o curso temporal e a magnitude de perda das adaptações fisiológicas adquiridas com o treinamento físico, bem como os mecanismos envolvidos nas mesmas

31P-nuclear magnetic resonance evidence of abnormal skeletal muscle metabolism in patients with chronic lung disease and congestive heart failure

The development of 31P-nuclear magnetic resonance (NMR) has enabled direct and non-invasive measurements of muscle metabolism. Serial measurements of the phosphocreatine/inorganic phosphate (PCr/Pi) ratio, which is closely related to the adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio and pH during and after forearm exercise were performed in 11 patients with chronic lung disease (CLD), nine patients with chronic heart failure (CHF) and eight control subjects. As compared with control subjects, the PCr/Pi ratio in the patients with CLD or CHF was lower during the recovery period and significantly lower at three and 4 min exercise. The pH values after exercise were lower in patients with CLD or CHF compared to control subjects. The PCr/Pi ratio at 4 min after exercise in the patients with CLD or CHF did not correlate with parameters of cardiac function or arterial and mixed venous oxygen tension. The arterial oxygen content and output in patients with CLD and CHF were significantly lower than that of control subjects. Nutritional parameters were not statistically different among the three groups. These observations suggest that metabolic abnormalities may be present in the skeletal muscles of patients with CLD and CHF that are not due to under-nutrition. These may result from reduced arterial oxygen output and, partially, from physical detraining.