The improvement in VO2max following endurance training is a linear function of Qmax, but not Ca-vO2max, through healthy ageing.

Neutrophil pathogen-killing mechanism termed neutrophil extracellular traps (NETs) has been recently identified. NETs consist of chromatin and histones along with serine proteases and myeloperoxidase and are induced by a great variety of infectious and non-infectious stimuli. NETosis is a kind of programmed neutrophil death characterized by chromatin decondensation and release of nuclear granular contents, mainly driven by peptidylarginine deiminase 4 citrullination of histones. Although classically related to the protection against infectious pathogens, nowadays NETs have been described as a player of several pathophysiological processes. Neutrophil dysregulation has been demonstrated in the pathogenesis of most representative vascular diseases, such as acute coronary syndrome, stroke and venous thrombosis. Indeed, NETs have been identified within atherosclerotic lesions and arterial thrombi in both human beings and animal models. Moreover, an imbalance in this mechanism has been proposed as a critical source of modified and/or externalized autoantigens in autoimmune and inflammatory diseases. Finally, an update on the role of NETs in the pathogenesis of cancer has been included. In the present review, based on papers released on PubMed and MEDLINE up to July 2017, we point to update the knowledge on NETs, from their structure to their roles in infectious diseases as well as in cardiovascular diseases, autoimmunity, metabolic disorders and cancer, with a look to future perspectives and therapeutic opportunities.

Based on a relatively small number of studies, improvement in V˙O2max following 5-13 wk of ET is associated with increase in Qmax, but not in a-V˙O2diff, in previously untrained to moderately trained healthy young individuals.

Aims Intrinsic sex differences in fundamental blood attributes have long been hypothesized to contribute to the gap in cardiorespiratory fitness between men and women. This study experimentally assessed the role of blood volume and oxygen (O2) carrying capacity on sex differences in cardiac function and aerobic power. Methods and results Healthy women and men (n = 60) throughout the mature adult lifespan (42-88 yr) were matched by age and physical activity levels. Transthoracic echocardiography, central blood pressure and O2 uptake were assessed throughout incremental exercise (cycle ergometry). Main outcomes such as left ventricular end-diastolic volume (LVEDV), stroke volume (SV), cardiac output (Q), and peak O2 uptake (VO2peak), as well as blood volume (BV) were determined with established methods. Measurements were repeated in men following blood withdrawal and O2 carrying capacity reduction matching women’s levels. Prior to blood normalization, BV and O2 carrying capacity were markedly reduced in women compared with men (P < 0.001). Blood normalization resulted in a precise match of BV (82.36 ± 9.83 vs. 82.34 ± 7.70 ml·kg−1, P = 0.993) and O2 carrying capacity (12.0 ± 0.6 vs. 12.0 ± 0.7 g·dl−1, P = 0.562) between women and men. Body size-adjusted cardiac filling and output (LVEDV, SV, Q) during exercise as well as VO2peak (30.8 ± 7.5 vs. 35.6 ± 8.7 ml·min−1·kg−1, P < 0.001) were lower in women compared with men prior to blood normalization. VO2peak did not differ between women and men after blood normalization (30.8 ± 7.5 vs. 29.7 ± 7.4 ml·min−1·kg−1, P = 0.551). Conclusions Sex differences in cardiorespiratory fitness are abolished when blood attributes determining O2 delivery are experimentally matched between adult women and men. Translational Perspective Low cardiorespiratory fitness is strongly associated with all-cause and cardiovascular mortality in asymptomatic adults independently of traditional risk factors, relationships seemingly enhanced in middle-aged and older women. Yet, whether the primary hematological determinants of cardiorespiratory fitness that were established in studies comprising men explain the difference between sexes remains uncertain. Importantly, blood attributes are amenable to modification and thus potentially translated into effective targets to improve or preserve cardiovascular health in the general population. The present experimental study demonstrates that blood normalization between men and women eliminate sex differences in cardiorespiratory fitness.