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Effective storage of excess energy in abdominal subcutaneous adipose tissue during periods of overeating may help attenuate weight-gain-related insulin resistance. The objective of this study was to assess changes in the expression of factors regulating abdominal subcutaneous adipose tissue storage capacity in response to a brief exposure to overeating in nonobese adults. Because exercise can alter the expression of genes involved in regulating adipose tissue storage capacity, we compared the responses to overeating in regular exercisers (EX, n  = 11) and nonexercisers (nonEX, n  = 11). Abdominal subcutaneous adipose tissue samples and oral glucose tolerance tests were performed before and after participants ate 30% above their estimated daily energy requirements for 1 week. Both EX and nonEX gained ∼1 kg ( P  < 0.01), and Matsuda insulin sensitivity index was reduced ∼15% ( P  = 0.04) in both groups. Gene expression of factors involved in lipid metabolism ( HSL, ATGL, DGAT , and PPARγ ) and angiogenesis ( HIF1α and KDR ) were increased ( P  < 0.05), with no differences observed between EX and nonEX. In contrast, protein abundance of these factors did not change. The modest overeating stimulus did not increase markers of inflammation in the systemic circulation or adipose tissue. Overall, our findings indicate that a brief and modest overeating stimulus can impair insulin sensitivity and upregulate genes involved in abdominal adipose tissue storage capacity similarly in exercisers and nonexercisers. ClinicalTrials.gov ID#: NCT02701738.

Dehydration is a common event associated with exercise. However, few studies have examined the effects of dehydration on plasma redox status in humans. Eighty-two athletes were recruited and baseline anthropometrics and blood samples were obtained. Athletes then engaged in a dehydration protocol, training until 3% of preweight body mass was lost. Athletes returned to the lab and had postdehydration blood collected. Athletes then consumed an isotonic drink until pre-exercise body weight was reestablished. Blood was then recollected (1 h post full rehydration (PFR)). Samples were centrifuged and the plasma snap frozen in liquid nitrogen and stored at -80 °C. Lipid and protein oxidative stress was determined by measuring F 2 -isoprostanes and protein carbonyls (PC), respectively. Antioxidant capacity was determined by the ferric reducing ability of plasma (FRAP) and trolox equivalent antioxidant capacity (TEAC) assays. Plasma osmolality was determined using an osmometer. Statistical analysis utilized a 1-way ANOVA with posthoc testing. Values are reported as mean ± SD. Plasma osmolality was significantly elevated immediately postdehydration (p ≤ 0.001) but decreased to baseline at PFR. Plasma TEAC increased immediately postdehydration and at PFR (p ≤ 0.001). FRAP increased immediately postdehydration (p ≤ 0.001) and decreased to below baseline at PFR (p ≤ 0.05). Conversely, F 2 -isoprostanes declined significantly from baseline to immediately postdehydration and then significantly rose at PFR (p ≤ 0.001), whereas PC declined at PFR (p ≤ 0.01). This study indicates that dehydration and exercise cause a significant increase in plasma osmolality and antioxidant potential immediately postexercise. We propose dehydration significantly elevates antioxidant concentration which suppresses F 2 -isoprostanes and PC.

Beer is promoted by popular media as a good choice for rehydration, but there is limited support for the claim. To assess the effect of beer alcohol on rehydration and motor control, 11 young (24.4 ± 3.7 years old) males of legal drinking age were dehydrated to 2.12% ± 0.20% body mass (mean ± SD) by exercising in a climatic chamber (31.7 ± 1.6 °C, 55.0% ± 8.3% relative humidity) on 3 different days, 1 week apart, and rehydrated with 100% of their sweat loss using water (WATER), 4.6% alcohol beer (BEER), or low-alcohol beer (LAB), in random order. Urine output, blood alcohol content (BAC), reaction time (RT), and balance (as measured by center of pressure velocity (VCoP)) were measured every 30 min over 3 h and compared via 2-way, repeated-measures analyses of variance (ANOVAs). After consuming ≈1.6 L in 1 h, urine output was greater for BEER (1218 ± 279 mL) than for LAB (745 ± 313 mL, p = 0.007) and WATER (774 ± 304 mL, p = 0.043). BAC remained at 0 with WATER and LAB; with BEER, BAC reached 0.857 g/L (95% confidence intervals [0.752, 0.963]) immediately postrehydration. RT was longer for BEER (0.314 ± 0.039 s) than for LAB (0.294 ± 0.034 s, p = 0.009), but was no different from WATER (0.293 ± 0.049 s, p = 0.077). VCoPx was significantly higher for BEER (0.0284 ± 0.0020 m/s) compared with LAB (0.0233 ± 0.0010 m/s) or WATER (0.0238 ± 0.0010 m/s) (p = 0.022), but VCoPy was not different among beverages. In conclusion, rehydration with BEER resulted in higher diuresis, slower RT, and impaired VCoP than rehydration with LAB or WATER.