Exercise-based cardiac rehabilitation increases daily physical activity of patients following myocardial infarction: subanalysis of two randomised controlled trials.

OBJECTIVE: To assess the effects of an exercise-based cardiac rehabilitation programme on daily physical activity levels of patients following myocardial infarction. DESIGN: Subanalysis of two randomised, prospective controlled trials. SETTING: Outpatient clinic of a secondary hospital. PARTICIPANTS: Fifty consecutive patients randomised to the exercise group {n=25; 23 males; mean age 54 [standard deviation (SD) 9] years} or the control group [n=25; 20 males; mean age 58 (SD 9) years]. INTERVENTIONS: The exercise group participated in an 8-week aerobic exercise programme plus usual medical care and follow-up. The control group received usual medical care and follow-up. MAIN OUTCOME MEASURES: The primary outcome measure was change in time spent undertaking moderate-to-vigorous physical activity per day, assessed by accelerometer over 7 consecutive days. Secondary outcome measures were cardiorespiratory fitness, body mass, and resting blood pressure and heart rate. RESULTS: Moderate-to-vigorous physical activity levels increased significantly in the exercise group [43.2 (SD 36.3) to 53.5 (SD 31.9) minutes/day, P=0.030], and remained unchanged in the control group [40.8 (SD 26.2) to 36.8 (SD 26.5) minutes/day, P=0.241] from baseline to the end of the programme. Cardiorespiratory fitness increased significantly in the exercise group (mean difference 2.8; 95% of the difference 1.3 to 4.4ml/kg/minute, P=0.001) after the 8-week programme. CONCLUSIONS: In patients under optimal medication following myocardial infarction, participation in an 8-week exercise-based cardiac rehabilitation programme was found to improve physical activity levels consistent with health-related benefits. Future studies are needed to determine whether the increase in physical activity is maintained in the long term.

Effect of intestinal colonisation by two Lactobacillus strains on the immune response of gnotobiotic mice.

The effect of intestinal colonisation on the immune system was investigated in germ-free mice monoassociated with Lactobacillus strains isolated from calf faeces. Single doses of Lactobacillus acidophilus L36 or Lactobacillus salivarius L38 were administered to germ-free mice by intragastric gavage. Ten days later, the mice were euthanised. Gene expression levels of interleukin 5 (IL-5), IL-6, IL-10, IL-12b, IL-17a, gamma interferon (IFN-γ), transforming growth factor beta 1 (TGF-ß1), and tumour necrosis factor alpha (TNF-α) were quantified in segments of the small and large intestines by real time quantitative polymerase chain reaction. All the mice were colonised rapidly after Lactobacillus administration with intestinal counts ranging from 6.53 to 8.26 log cfu/g. L. acidophilus L36 administration increased the expression of cytokines involved with the Th2 (IL-5, IL-6 and TGF-ß1) and Th17 (IL-17a, TNF-α and IL-6) inflammatory response, whereas L. salivarius L38 appeared to stimulate a pattern of less diversified cytokines in the intestine. Intragastric gavage of L. acidophilus L36 and L. salivarius L38 induced similar levels of colonisation in the digestive tracts of germ-free mice but stimulated different immune responses in the intestinal mucosa. The different immunomodulation patterns might facilitate the potential use of these lactobacilli as probiotics to treat distinct pathological conditions, for example protection against Citrobacter rodentium infection by stimulating IL-17 production.

VO2 kinetics in 200-m race-pace front crawl swimming.

Studies that aim to characterize oxygen uptake kinetics in efforts above maximal oxygen consumption intensity are scarce. Our aim was to analyze the oxygen kinetics in a maximal 200-m front crawl, all measurements being conducted in swimming pool conditions. 10 high-level male swimmers performed a maximal 200-m bout and oxygen uptake was directly measured through breath-by-breath gas analysis. Mean (±SD) peak oxygen uptake was 68.58 (±5.79) ml.kg(-1).min(-1), evidencing a fast component phase. As expected, peak oxygen uptake presented a direct relationship with mean swimming speed of the first 50-m lap and with the 200-m effort, and was also correlated with the amplitude of the fast component (r=0.75, r=0.72, r=0.73, p<0.05, respectively). The observed mean amplitude value was higher than those observed in the literature for other exercise intensity domains. However, the time for its onset, as well as the duration for attaining the steady state, was shorter, as the peak oxygen uptake was not correlated with these 2 components. Moreover, as previously described for swimming at high intensities, the slow component phenomenon was not observed. Aerobic metabolic pathway accounted for 78.6%, confirming the high aerobic contribution in middle distance swimming events.

Induced differentiation of HL-60 promyelocytic leukemia cells to monocyte/macrophages is inhibited by hydroquinone, a hematotoxic metabolite of benzene.

Chronic exposure of humans to benzene has been shown to have a cytotoxic effect on hematopoietic progenitor cells in intermediate stages of differentiation, which can lead to aplastic anemia and acute myelogenous leukemia. We studied the effect of hydroquinone (HQ), a toxic metabolite of benzene found in the bone marrow, on the human promyelocytic leukemia cell line (HL-60), which can be induced to differentiate to both monocyte and myeloid cells, and thus has been used as a surrogate for a granulocyte/macrophage progenitor cell. Exposure of HL-60 cells to noncytotoxic concentrations of HQ for 3 hours before induction with phorbol myristate acetate (TPA) caused a dose-dependent inhibition of the acquisition of characteristics of monocytic differentiation, such as adherence, nonspecific esterase (NSE) activity, and phagocytosis, but had no effect on cell proliferation. HQ appeared to be affecting maturation beyond the monoblast/promonocyte stages. HQ also prevented differentiation induced by 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]; however, the block occurred after the acquisition of adherence. HQ at concentrations that inhibited monocytic differentiation had no effect on differentiation to granulocytes, suggesting that the block in the differentiation of these bipotential cells is a step unique to the monocytic pathway. HQ was unable to prevent differentiation induced by the macrophage-derived cytokine, interleukin (IL)-1, a differentiation factor for cells of the monocytic lineage.