Background: Irisin, a recently discovered myokine, has been shown to induce browning of white adipose tissue, enhancing energy expenditure and mediating some of the beneficial effects of exercise. We aimed to estimate the time frame of changes in irisin levels after acute exercise and the effect of different exercise workloads and intensities on circulating irisin levels immediately post-exercise. Methods: In a pilot study, four healthy subjects (22.5G1.7 years) underwent maximal workload exercise (maximal oxygen consumption, VO 2 max ) and blood was drawn at prespecified intervals to define the time frame of pre-and post-exercise irisin changes over a 24-h period. In the main study, 35 healthy, non-smoking (23.0G3.3 years) men and women (nZ20/15) underwent three exercise protocols R48-h apart, in random order: i) maximal workload (VO 2 max ); ii) relative workload (70% of VO 2 max /10 min); and iii) absolute workload (75 W/10 min). Blood was drawn immediately pre-exercise and 3 min post-exercise. Results: In the pilot study, irisin levels increased by 35% 3 min post-exercise, then dropped and remained relatively constant. In the main study, irisin levels post-exercise were significantly higher than those of pre-exercise after all workloads (all, P!0.001). Post-to-pre-exercise differences in irisin levels were significantly different between workloads (PZ0.001), with the greatest increase by 34% following maximal workload (PZ0.004 vs relative and absolute). Conclusions: Circulating irisin levels were acutely elevated in response to exercise, with a greater increase after maximal workload. These findings suggest that irisin release could be a function of muscle energy demand. Future studies need to determine the underlying mechanisms of irisin release and explore irisin's therapeutic potential.

BackgroundStudies showed that long-standing smokers have stiffer arteries at rest. However, the effect of smoking on the ability of the vascular system to respond to increased demands (physical stress) has not been studied. The purpose of this study was to estimate the effect of smoking on arterial stiffness and subendocardial viability ratio, at rest and after acute exercise in young healthy individuals.Methods/ResultsHealthy light smokers (n = 24, pack-years = 2.9) and non-smokers (n = 53) underwent pulse wave analysis and carotid-femoral pulse wave velocity measurements at rest, and 2, 5, 10, and 15 minutes following an exercise test to exhaustion. Smokers were tested, 1) after 12h abstinence from smoking (chronic condition) and 2) immediately after smoking one cigarette (acute condition). At rest, chronic smokers had higher augmentation index and lower aortic pulse pressure than non-smokers, while subendocardial viability ratio was not significantly different. Acute smoking increased resting augmentation index and decreased subendocardial viability ratio compared with non-smokers, and decreased subendocardial viability ratio compared with the chronic condition. After exercise, subendocardial viability ratio was lower, and augmentation index and aortic pulse pressure were higher in non-smokers than smokers in the chronic and acute conditions. cfPWV rate of recovery of was greater in non-smokers than chronic smokers after exercise. Non-smokers were also able to achieve higher workloads than smokers in both conditions.ConclusionChronic and acute smoking appears to diminish the vascular response to physical stress. This can be seen as an impaired ‘vascular reserve’ or a blunted ability of the blood vessels to accommodate the changes required to achieve higher workloads. These changes were noted before changes in arterial stiffness or subendocardial viability ratio occurred at rest. Even light smoking in young healthy individuals appears to have harmful effects on vascular function, affecting the ability of the vascular bed to respond to increased demands.

The objective of this systematic review was to provide insight into the controversy that still abounds as to the impact of acute aerobic exercise on immediate changes in arterial stiffness. Electronic databases were searched to identify articles assessing the effects of acute aerobic exercise on parameters of arterial stiffness. Eligible studies included arterial stiffness measurements before and after acute aerobic exercise in healthy human subjects. Forty-three studies were included. The effect of acute aerobic exercise on arterial stiffness was found to be dependent on the anatomical segment assessed, and on the timing of the measurement post-exercise. Arterial stiffness of the central and upper body peripheral arterial segments was found to be increased relative to resting values immediately post-exercise (0-5 min), whereas, thereafter (>5 min), decreased to a level at or below resting values. In the lower limbs, proximal to the primary working muscles, arterial stiffness decreased immediately post-exercise (0-5 min), which persisted into the recovery period post-exercise (>5 min). This systematic review reveals a differential response to acute exercise in the lower and upper/central arterial segments in healthy adult subjects. We further showed that the effect of acute aerobic exercise on arterial stiffness is dependent on the timing of the measurements post-exercise. Therefore, when assessing the overall impact of exercise on arterial stiffness, it is important to consider the arterial segment being analyzed and measurement time point, as failure to contextualize the measurement can lead to conflicting results and misleading clinical inferences.

There is controversy as to whether there are sex differences in arterial stiffness. Acute physical stress can elicit vascular abnormalities not present at rest. Our objective was to assess sex differences in arterial stiffness at rest and in response to acute physical stress. Healthy young men (n=67) and women (n=55) underwent pulse wave analysis and carotid-femoral pulse wave velocity measurements at rest and 2, 5, 10 and 15 min following an exercise test to exhaustion. At rest, aortic systolic, diastolic, pulse and mean pressures were all significantly higher in men as was aortic pulse pressure at 10 and 15 min post exercise and aortic systolic pressure at 15 min. Carotid-femoral pulse wave velocity was significantly higher in men (6.0±0.7 m s(-1) vs. 5.6±0.6 m s(-1), P=0.03) at rest and at all time points post exercise. Heart rate-adjusted augmentation index was significantly lower (-10.7±10.2% vs. -4.0±10.9, P<0.0001) and subendocardial viability ratio was significantly higher (176.2±43.8% vs. 163.4±40.9, P=0.04) in men at rest. To our knowledge, this is the first study to assess sex differences in the arterial stiffness response to acute physical stress in young men and women. Although we were not able to elicit differences in vascular function after adjustment, which were not present at rest, we found that young men and women exhibit differences in arterial stiffness at rest and after acute physical stress.

In physically fit, surgically naïve students, one bout of aerobic exercise enhanced immediate learning of simple FLS skills but did not have an impact on more complex skills or on retention. The use of exercise in the surgical curriculum, or as a learning tool, warrants further investigation regarding how best to apply it.