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Postprandial hyperglycemia is assumed to have a negative impact on flow-mediated dilation (FMD), an index of endothelial function, and blood flow of the peripheral conduit arteries. This study aimed to determine whether the enhancement of postprandial hyperglycemia by skipping breakfast accelerates endothelial dysfunction and reduces the blood flow in the brachial artery in young men. Using a randomized cross-over design, ten healthy men completed two trials: with and without breakfast (Eating and Fasting trials, respectively). Venous blood sampling and brachial FMD tests were conducted before, 30, 60, 90, and 120 min after a 75-g oral glucose tolerance test (OGTT). Skipping breakfast boosted post-OGTT glucose levels than having breakfast (P = 0.01). The magnitude of the decrease in FMD via OGTT did not vary between trials (main effect of trial P = 0.55). Although brachial blood flow tended to decrease after OGTT in both trials (interaction and main effect of time P = 0.61 and P = 0.054, respectively), the decrease in blood flow following OGTT was greater in the Fasting trial than in the Eating trial (main effect of trial, mean difference =  − 15.8 mL/min [95%CI =  − 25.6 to − 6.0 mL/min], P < 0.01). Skipping breakfast did not enhance the magnitude of the decrease in FMD following glucose loading, but did accelerate hyperglycemia-induced reduction in brachial blood flow. Current findings suggest that even missing one breakfast has negative impacts on the blood flow regulation of the peripheral conduit arteries in young men who habitually eat breakfast.

We evaluated effects of age and rowing on concentrations of lipids and lipoprotein cholesterols in the blood. Maximal oxygen uptake (VO2max), and concentrations of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured in 17 oarsmen [mean (SD)] [age 64 (4) years, body mass 69 (6) kg] and in sedentary men [age 65 (3) years, body mass 70 (7) kg] who were matched on the basis of body size. Also the variables were obtained from young oarsmen [age 22 (2) years, body mass 70 (4) kg] and young sedentary men [age 22 (3) years, body mass 69 (7) kg]. The percentage body fat of the older oarsmen was lower than that of the older sedentary men [18 (4)% compared to 23 (4)%, P<0.05], but it was similar to that of the young sedentary men [17 (4)%]. Although older oarsmen possessed a lower VO2max than the young oarsmen [3.0 (0.4) l·min–1 compared to 4.1 (0.3) l·min–1, P<0.01], they showed a VO2max similar to that of the young sedentary men [3.1 (0.5) l·min–1] but a higher value than obtained from the older sedentary men [2.2 (0.3) l·min–1, P<0.05]. Although the indices of risk factors for coronary artery disease in the older oarsmen were higher than those in the young oarsmen [LDL-C/HDL-C 1.7 (0.2) compared to 1.3 (0.4), TC/HDL-C 3.1 (0.2) compared to 2.6(0.4), P<0.05], they were lower than those in both the older [2.1 (0.3), 3.6 (0.3), P<0.05] and the young sedentary men [2.1 (0.4), 3.5 (0.4), P<0.05]. The results suggest that rowing is an appropriate type of exercise for the promotion of health.

The purpose of the present work was to study whether long-term alcohol consumption in man affects the develeopment of brown adipose tissue. The adipose tissue around the thoracic aorta and common carotid arteries was collected at medicolegal autopsies on adults with a positive record of heavy alcohol consumption. Adults without any evident history of alcohol consumption served as controls. Histochemical reactions of the oxidative mitochondrial enzymes, cytochrome oxidase and succinate dehydrogenase were studied in samples of this adipose tissue and the activities of the enzymes were measured biochemically. There was histological evidence of some multilocular adipose tissue around the thoracic aorta and common carotid arteries of the alcohol consumers, whereas the adipose tissue from the non-drinkers was mostly unilocular resembling white adipose tissue. Histochemical evidence of brown adipose tissue was found in all alcohol consumers, but also in some of the controls. Biochemical cytochrome oxidase (CYO) and succinate dehydrogenase measurements in isolated mitochondria showed activity in 70% of the cases of drinkers and in one of the eight controls. Activity of CYO was measurable in the mitochondria from two other controls. The protein content of the samples from the alcoholics was twice that of the controls. The results suggest that chronic alcohol intake may induce a change in the white adipose tissue around the thoracic aorta and common carotid arteries of human adults into brown fat.

This study characterized the profile of near-infrared spectroscopy (NIRS)-derived muscle deoxygenation (Δ[HHb]) and the tissue oxygenation index (TOI) as a function of absolute (POABS) and normalized power output (%PO) or oxygen consumption (%VO2) during incremental cycling exercise. Eight men (24 ± 5 year) each performed two fatigue-limited ramp incremental cycling tests (20 W min−1), during which pulmonary VO2, Δ[HHb] and TOI were measured continuously. Responses from the two tests were averaged and the TOI (%) and normalized Δ[HHb] (%Δ[HHb]) were plotted against %VO2, %PO and POABS. The overall responses were modelled using a sigmoid regression (y = f 0  + A/(1 + e−(−c+dx))) and piecewise ‘double-linear’ function of the predominant adjustment of %Δ[HHb] or TOI observed throughout the middle portion of exercise and the ‘plateau’ that followed. In ~85% of cases, the corrected Akaike Information Criterion (AICC) was smaller (suggesting one model favoured) for the ‘double-linear’ compared with the sigmoid regression for both %Δ[HHb] and TOI. Furthermore, the f 0 and A estimates from the sigmoid regressions of %Δ[HHb] yielded unrealistically large projected peak (f 0  + A) values (%VO2p 114.3 ± 17.5; %PO 113.3 ± 9.5; POABS 113.5 ± 9.8), suggesting that the sigmoid model does not accurately describe the underlying physiological responses in all subjects and thus may not be appropriate for comparative purposes. Alternatively, the present study proposes that the profile of %Δ[HHb] and TOI during ramp incremental exercise may be more accurately described as consisting of three distinct phases in which there is little adjustment early in the ramp, the predominant increase in %Δ[HHb] (decrease in TOI) is approximately linear and an approximately linear ‘plateau’ follows.

Previous evidence from surface electromyograms (EMGs) suggests that exercise-induced muscle damage (EIMD) may manifest unevenly within the muscle. Here we investigated whether these regional changes were indeed associated with EIMD or if they were attributed to spurious factors often affecting EMGs. Ten healthy male subjects performed 3 × 10 eccentric elbow flexions. Maximal voluntary contraction (MVC), muscle soreness and ultrasound images from biceps brachii distal and proximal regions were measured immediately before (baseline) and during each of the following 4 days after the exercise. Moreover, 64 monopolar surface EMGs were detected while 10 supramaximal pulses were applied to the musculocutaneous nerve. The innervation zone (IZ), the number of electrodes detecting largest M-waves and their centroid longitudinal coordinates were assessed to characterize the spatial distribution of the M-waves amplitude. The MVC torque decreased (~ 25%; P < 0.001) while the perceived muscle soreness scale increased (~ 4 cm; 0 cm for no soreness and 10 cm for highest imaginable soreness; P < 0.005) across days. The echo intensity of the ultrasound images increased at 48 h (71%), 72 h (95%) and 96 h (112%) for both muscle regions (P < 0.005), while no differences between regions were observed (P = 0.136). The IZ location did not change (P = 0.283). The number of channels detecting the greatest M-waves significantly decreased (up to 10.7%; P < 0.027) and the centroid longitudinal coordinate shifted distally at 24, 48 and 72 h after EIMD (P < 0.041). EIMD consistently changed supramaximal M-waves that were detected mainly proximally from the biceps brachii, suggesting that EIMD takes place locally within the biceps brachii.