Exercise training improves sleep pattern and metabolic profile in elderly people in a time-dependent manner.

Aging and physical inactivity are two factors that favors the development of cardiovascular disease, metabolic syndrome, obesity, diabetes, and sleep dysfunction. In contrast, the adoption a habitual of moderate exercise may present a non-pharmacological treatment alternative for sleep and metabolic disorders. We aimed to assess the effects of moderate exercise training on sleep quality and on the metabolic profile of elderly people with a sedentary lifestyle. Fourteen male sedentary, healthy, elderly volunteers performed moderate training for 60 minutes/day, 3 days/week for 24 wk at a work rate equivalent to the ventilatory aerobic threshold. The environment was kept at a temperature of 23 ± 2 °C, with an air humidity 60 ± 5%. Blood and polysomnographs analysis were collected 3 times: at baseline (1 week before training began), 3 and 6 months (after 3 and 6 months of training). Training promoted increasing aerobic capacity (relative VO2, time and velocity to VO2max; p < 0.05), and reduced serum NEFA, and insulin concentrations as well as improved HOMA index (p < 0.05), and increased adiponectin levels (p < 0.05), after 3 months of training when compared with baseline data. The sleep parameters, awake time and REM sleep latency were decreased after 6 months exercise training (p < 0.05) in relation baseline values. Our results demonstrate that the moderate exercise training protocol improves the sleep profile in older people, but the metabolism adaptation does not persist. Suggesting that this population requires training strategy modifications as to ensure consistent alterations regarding metabolism.

Physiological and lipid profile response to acute exercise at different intensities in individuals with spinal cord injury.

STUDY DESIGN: Experimental and cross-sectional study. OBJECTIVE: To assess the immediate effect of exercise on heart rate (HR), oxygen uptake (VO2), pulmonary ventilation (PV), oxygen pulse (OP), glucose and lipids of wheelchair basketball players with spinal cord injury (SCI). SETTING: Center of Studies in Psychobiology and Exercise-São Paulo, Brazil. METHODS: In all, nine wheelchair basketball players with SCI and nine able-bodied controls (C) performed three exercise sessions at different intensities: ventilatory threshold 1 (VT1), 15% below VT1 and 15% above VT1 with a duration of ~24-34 min. HR, VO2, PV, OP, glucose and lipids were analyzed. RESULTS: VO2, PV and OP were significantly lower in the players with SCI compared to C during the same intensity exercise sessions. However, the individuals with SCIs demonstrated increases in HR, PV and OP at similar rates to C. Triglycerides of the SCI group were elevated 30 min after the exercise session at VT1 compared to values before the exercise session (P=0.017); this elevation was not observed in group C. For the exercise sessions 15% above VT1, only glucose (P=0.040) and low-density lipoprotein (P=0.012) 30 min after the exercise were elevated in the SCI group compared to group C. CONCLUSION: We conclude that the SCI group demonstrated increases in HR, PV and OP but not VO2 with increased intensity of exercise at similar rates as in group C.

Exercise intensity modulation of hepatic lipid metabolism.

Lipid metabolism in the liver is complex and involves the synthesis and secretion of very low density lipoproteins (VLDL), ketone bodies, and high rates of fatty acid oxidation, synthesis, and esterification. Exercise training induces several changes in lipid metabolism in the liver and affects VLDL secretion and fatty acid oxidation. These alterations are even more conspicuous in disease, as in obesity, and cancer cachexia. Our understanding of the mechanisms leading to metabolic adaptations in the liver as induced by exercise training has advanced considerably in the recent years, but much remains to be addressed. More recently, the adoption of high intensity exercise training has been put forward as a means of modulating hepatic metabolism. The purpose of the present paper is to summarise and discuss the merit of such new knowledge.

Hypothalamic inflammation is reversed by endurance training in anorectic-cachectic rats.

AIM: We tested the effects of a cancer cachexia-anorexia sydrome upon the balance of anti and pro-inflammatory cytokines in the hypothalamus of sedentary or trained tumour-bearing (Walker-256 carcinosarcoma) rats. METHODS: Animals were randomly assigned to a sedentary control (SC), sedentary tumour-bearing (ST), and sedentary pair-fed (SPF) groups or, exercised control (EC), exercised tumour-bearing (ET) and exercised pair-fed (EPF) groups. Trained rats ran on a treadmill (60%VO2max) for 60 min/d, 5 days/wk, for 8 wks. We evaluated food intake, leptin and cytokine (TNF-α, IL1ß) levels in the hypothalamus. RESULTS: The cumulative food intake and serum leptin concentration were reduced in ST compared to SC. Leptin gene expression in the retroperitoneal adipose tissue (RPAT) was increased in SPF in comparison with SC and ST, and in the mesenteric adipose tissue (MEAT) the same parameter was decreased in ST in relation to SC. Leptin levels in RPAT and MEAT were decreased in ST, when compared with SC. Exercise training was also able to reduce tumour weight when compared to ST group. In the hypothalamus, IL-1ß and IL-10 gene expression was higher in ST than in SC and SPF. Cytokine concentration in hypothalamus was higher in ST (TNF-α and IL-1ß, p < 0.05), compared with SC and SPF. These pro-inflammatory cytokines concentrations were restored to control values (p < 0.05), when the animals were submitted to endurance training. CONCLUSION: Cancer-induced anorexia leads towards a pro-inflammatory state in the hypothalamus, which is prevented by endurance training which induces an anti-inflammatory state, with concomitant decrease of tumour weight.

ß-Hydroxy-ß-methylbutyrate (HMß) supplementation stimulates skeletal muscle hypertrophy in rats via the mTOR pathway.

ß-Hydroxy-ß-methylbutyrate (HMß) supplementation is used to treat cancer, sepsis and exercise-induced muscle damage. However, its effects on animal and human health and the consequences of this treatment in other tissues (e.g., fat and liver) have not been examined. The purpose of this study was to evaluate the effects of HMß supplementation on skeletal muscle hypertrophy and the expression of proteins involved in insulin signalling. Rats were treated with HMß (320 mg/kg body weight) or saline for one month. The skeletal muscle hypertrophy and insulin signalling were evaluated by western blotting, and hormonal concentrations were evaluated using ELISAs. HMß supplementation induced muscle hypertrophy in the extensor digitorum longus (EDL) and soleus muscles and increased serum insulin levels, the expression of the mammalian target of rapamycin (mTOR) and phosphorylation of p70S6K in the EDL muscle. Expression of the insulin receptor was increased only in liver. Thus, our results suggest that HMß supplementation can be used to increase muscle mass without adverse health effects.