Recovery from cycling exercise: effects of carbohydrate and protein beverages.

The effects of different carbohydrate-protein (CHO + Pro) beverages were compared during recovery from cycling exercise. Twelve male cyclists (VO(2peak): 65 ± 7 mL/kg/min) completed ~1 h of high-intensity intervals (EX1). Immediately and 120 min following EX1, subjects consumed one of three calorically-similar beverages (285-300 kcal) in a cross-over design: carbohydrate-only (CHO; 75 g per beverage), high-carbohydrate/low-protein (HCLP; 45 g CHO, 25 g Pro, 0.5 g fat), or low-carbohydrate/high-protein (LCHP; 8 g CHO, 55 g Pro, 4 g fat). After 4 h of recovery, subjects performed subsequent exercise (EX2; 20 min at 70% VO(2peak) + 20 km time-trial). Beverages were also consumed following EX2. Blood glucose levels (30 min after beverage ingestion) differed across all treatments (CHO > HCLP > LCHP; p < 0.05), and serum insulin was higher following CHO and HCLP ingestion versus LCHP. Peak quadriceps force, serum creatine kinase, muscle soreness, and fatigue/energy ratings measured pre- and post-exercise were not different between treatments. EX2 performance was not significantly different between CHO (48.5 ± 1.5 min), HCLP (48.8 ± 2.1 min) and LCHP (50.3 ± 2.7 min). Beverages containing similar caloric content but different proportions of carbohydrate/protein provided similar effects on muscle recovery and subsequent exercise performance in well-trained cyclists.

Selective impairment in dendritic cell function and altered antigen-specific CD8+ T-cell responses in diet-induced obese mice infected with influenza virus.

There is a clear link between obesity and metabolic disorders; however, little is known about the effect of obesity on immune function, particularly during an infection. We have previously reported that diet-induced obese mice are more susceptible to morbidity and mortality during influenza infection than lean mice. Obese mice displayed aberrant innate immune responses characterized by minimal induction of interferon (IFN)-alpha/beta, delayed expression of pro-inflammatory cytokines and chemokines, and impaired natural killer cell cytotoxicity. To further examine the abnormal immune response of diet-induced obese mice, we analysed the cellularity of their lungs during influenza virus infection. We found delayed mononuclear cell entry with a marked decrease in dendritic cells (DCs) throughout the infection. Given the critical role of the DC in activating the cell-mediated immune response, we also analysed the functional capacity of DCs from obese mice. We found that, while obesity did not interfere with antigen uptake and migration, it did impair DC antigen presentation. This was probably attributable to an altered cytokine milieu, as interleukin (IL)-2, IL-12, and IL-6 were differentially regulated in the obese mice. Overall, this did not impact the total number of virus-specific CD8(+) T cells that were elicited, but did affect the number and frequency of CD3(+) and CD8(+) T cells in the lung. Thus, obesity interferes with cellular responses during influenza infection, leading to alterations in the T-cell population that ultimately may be detrimental to the host.

Diet-induced obese mice have increased mortality and altered immune responses when infected with influenza virus.

Obesity is associated with an impaired immune response, an increased susceptibility to bacterial infection, and a chronic increase in proinflammatory cytokines such as IL-6 and TNFalpha. However, few studies have examined the effect of obesity on the immune response to viral infections. Because infection with influenza is a leading cause of morbidity and mortality worldwide, we investigated the effect of obesity on early immune responses to influenza virus exposure. Diet-induced obese and lean control C57BL/6 mice were infected with influenza A/PR8/34, and lung pathology and immune responses were examined at d 0 (uninfected), 3, and 6, postinfection. Following infection, diet-induced obese mice had a significantly higher mortality rate than the lean controls and elevated lung pathology. Antiviral and proinflammatory cytokine mRNA production in the lungs of the infected mice was markedly different between obese and lean mice. IFNalpha and beta were only minimally expressed in the infected lungs of obese mice and there was a notable delay in expression of the proinflammatory cytokines IL-6 and TNFalpha. Additionally, obese mice had a substantial reduction in NK cell cytotoxicity. These data indicate that obesity inhibits the ability of the immune system to appropriately respond to influenza infection and suggests that obesity may lead to increased morbidity and mortality from viral infections.