Ingestion of a moderate dose of alcohol enhances physical exercise-induced changes in blood lactate concentration

The consumption of alcoholic beverages influences carbohydrate and lipid metabolism, although it is not yet clear whether metabolism during physical exercise at different intensities is also affected. This was the objective of the present study. Eight young and healthy volunteers performed a treadmill test to identify the running speed corresponding to a lactate concentration of 4 mM (S4mM). At least 48 h later, they were subjected to two experimental trials (non-alcohol or alcohol) in which they performed two 1-km running sessions at the following intensities: 1) S4mM; 2) 15% above S4mM. In both trials, blood lactate, triglycerides, and glucose concentrations were measured before and after exercise. The acute alcohol intake increased triglycerides, but not lactate concentration under resting conditions. Interestingly, alcohol intake enhanced the exercise-induced increase in lactate concentration at the two intensities: S4mM (non-alcohol: 4.2±0.3 mM vs alcohol: 4.8±0.9 mM; P=0.003) and 15% above S4mM trial (P=0.004). When volunteers ingested alcohol, triglycerides concentration remained increased after treadmill running (e.g., at S4mM - at rest; non-alcohol: 0.2±0.5 mM vs alcohol: 1.3±1.3 mM; P=0.048). In contrast, glucose concentration was not modified by either alcohol intake, exercise, or their combination. We concluded that an acute alcohol intake changed lactate and lipid metabolism without affecting blood glucose concentration. In addition, the increase in lactate concentration caused by alcohol was specifically observed when individuals exercised, whereas augmented triglycerides concentration was already observed before exercise and was sustained thereafter.

Identificação do limiar anaeróbio em indivíduos com diabetes tipo-2 sedentários e fisicamente ativos / Identification of the anaerobic threshold in sedentary and physically active individuals with type 2 diabetes

OBJETIVO: Comparar intensidades de limiar anaeróbio (LA) obtidas a partir do lactato, ventilação e glicemia em diabéticos tipo-2 ativos (DA) e sedentários (DS) e não-diabéticos ativos (NDA), e correlacionar variáveis metabólicas, hemodinâmicas e de composição corporal com o LA. METODOLOGIA: Grupos de DS (n= 09, 56,7 ± 11,9 anos), DA (n= 09, 50,6 ± 12,7 anos) e NDA (n= 10, 48,1 ± 10,8 anos) foram submetidos a um teste em cicloergômetro com incrementos de 15W até a exaustão. Freqüência cardíaca, pressão arterial (PA), percepção de esforço, lactato, glicemia e variáveis ventilatórias foram mensuradas nos 20seg finais de cada estágio de 3min para determinação dos limiares de lactato, ventilatório e glicêmico. RESULTADOS: As intensidades associadas ao LA identificado pelos diferentes métodos não diferiram entre si (p> 0,05). As intensidades absolutas foram menores para o grupo DS em relação aos grupos ativos (p< 0,05), não sendo observadas diferenças entre os grupos para as intensidades relativas ao consumo máximo de oxigênio ( por centoVO2 pico) e potência máxima ( por centoPpico) de ocorrência do LA. Observou-se correlação significativa entre LA e o percentual de gordura (r= -0,52), com tendência à correlação entre o LA e a glicemia ambulatorial (r= -0,33). Variáveis hemodinâmicas e LA não demonstraram correlações. CONCLUSÃO: O LA foi identificado a partir das técnicas estudadas em diabéticos tipo-2 e não-diabéticos. Apesar das diferenças entre grupos para as intensidades absolutas (Watts), a patologia pareceu não influenciar as intensidades relativas em que o LA foi observado. O LA apresentou correlação com a composição corporal e tendência a se correlacionar com a glicemia ambulatorial, sugerindo-se, com isso, o LA como um parâmetro importante na avaliação clínica destes pacientes.

OBJECTIVE: To compare anaerobic threshold (AT) intensities determined from blood lactate, blood glucose and ventilatory responses among sedentary (SD) and physically active (AD) type-2 diabetics and active non-diabetics (AND), and to correlate metabolic, hemodynamic and body composition variables with the AT. METHOD: The SD (n= 9, 56.7 ± 11.9 years), AD (n= 9, 50.6 ± 12.7 years) and AND (n= 10, 48.1 ± 10.8 years) groups performed a cycle ergometer test with increases of 15 watts every three minutes until exhaustion. Heart rate, arterial pressure, perceived exertion, blood lactate, blood glucose and ventilatory variables were measured during the last 20 seconds of each incremental stage, to determine the lactate, ventilatory and glucose thresholds. RESULTS: The AT intensities identified by the different methods did not differ from each other (p> 0.05). However, the absolute intensities were lower for SD than for the active groups (p< 0.05). No differences in intensity were found between the groups in relation to maximum oxygen consumption ( percentVO2 peak) and maximum power ( percentPpeak) at which the AT was observed. There was a significant correlation between AT and percentage fat (r= -0.52), and there was a trend towards correlation between AT and ambulatory blood glucose (r= -0.33). The hemodynamic variables did not show any correlations with AT. CONCLUSION: The AT was identified by means of the techniques studied, among type 2 diabetics and non-diabetics. Despite the differences between the groups with regard to absolute intensities (watts), diabetes did not appear to influence the relative intensities at which the AT was observed. The AT presented a correlation with body composition and a trend towards correlation with ambulatory blood glucose, thus suggesting that the AT is an important parameter in clinical assessments for such patients.

Impact of initial exposure to calcineurin inhibitors on kidney graft function of patients at high risk to develop delayed graft function

We conducted a retrospective analysis of the influence of full doses of calcineurin inhibitors [8-10 mg kg-1 day-1 cyclosporine (N = 80), or 0.2-0.3 mg kg-1 day-1 tacrolimus (N = 68)] administered from day 1 after transplantation on the transplant outcomes of a high-risk population. Induction therapy was used in 13 percent of the patients. Patients also received azathioprine (2 mg kg-1 day-1, N = 58) or mycophenolate mofetil (2 g/day, N = 90), and prednisone (0.5 mg kg-1 day-1, N = 148). Mean time on dialysis was 79 ± 41 months, 12 percent of the cases were re-transplants, and 21 percent had panel reactive antibodies >10 percent. In 43 percent of donors the cause of death was cerebrovascular disease and 27 percent showed creatinine above 1.5 mg/dL. The incidence of slow graft function (SGF) and delayed graft function (DGF) was 15 and 60 percent, respectively. Mean time to last dialysis and to nadir creatinine were 18 ± 15 and 34 ± 20 days, respectively. Mean creatinine at 1 year after transplantation was 1.48 ± 0.50 mg/dL (DGF 1.68 ± 0.65 vs SGF 1.67 ± 0.66 vs immediate graft function (IGF) 1.41 ± 0.40 mg/dL, P = 0.089). The incidence of biopsy-confirmed acute rejection was 22 percent (DGF 31 percent, SGF 10 percent, IGF 8 percent). One-year patient and graft survival was 92.6 and 78.4 percent, respectively. The incidence of cytomegalovirus disease, post-transplant diabetes mellitus and malignancies was 28, 8.1, and 0 percent, respectively. Compared to previous studies, the use of initial full doses of calcineurin inhibitors without antibody induction in patients with SGF or DGF had no negative impact on patient and graft survival.

Relationship of cyclosporin and sirolimus blood concentrations regarding the incidence and severity of hyperlipidemia after kidney transplantation

The influence of drug concentrations on the development of persistent posttransplant hyperlipidemia was investigated in 82 patients who received cyclosporin A (CsA) and prednisone plus sirolimus (SRL) (52) or azathioprine (AZA) (30) during the first year after transplantation. Blood levels of CsA and SRL, daily doses of AZA and prednisone, and cholesterol, triglyceride, and glucose concentrations were determined during each visit (pretransplant and 30, 60, 90, 120, 180, and 360 days posttransplant). Persistent hyperlipidemia was defined as one-year average steady-state cholesterol (CavCHOL) or triglyceride (CavTG) concentrations above 240 and 200 mg/dL, respectively. Mean cholesterol and triglyceride concentrations increased after transplantation (P < 0.01) and were higher in patients receiving SRL compared to AZA (P < 0.001). Patients receiving SRL showed a significantly higher number of cholesterol (>229 or >274 mg/dL) and triglyceride (>198 or >282 mg/dL) determinations in the upper interquartile ranges. CsA and SRL interquartile ranges correlated with cholesterol concentrations (P = 0.001) whereas only SRL interquartile ranges correlated with triglyceride concentrations (P < 0.0001). Only pretransplant cholesterol concentration >205 mg/dL was independently associated with development of persistent hypercholesterolemia (CavCHOL >240 mg/dL, relative risk (RR) = 20, CI 3.8-104.6, P = 0.0004) whereas pretransplant triglyceride concentration >150 mg/dL (RR = 7.2, CI 1.6-32.4, P = 0.01) or >211 mg/dL (RR = 19.8, CI 3.6-107.9, P = 0.0006) and use of SRL (RR = 3, CI 1.0-8.8, P = 0.0049) were independently associated with development of persistent hypertriglyceridemia (CavTG >200 mg/dL). Persistent hypercholesterolemia was more frequent among patients with higher pretransplant cholesterol concentrations and was dependent on both CsA and SRL concentrations. Persistent hypertriglyceridemia was more frequent among patients with higher pretransplant triglyceride concentrations and was dependent on SRL concentrations.