Vascular Ageing and Exercise: Focus on Cellular Reparative Processes

Ageing is associated with an increased risk of developing noncommunicable diseases (NCDs), such as diabetes and cardiovascular disease (CVD). The increased risk can be attributable to increased prolonged exposure to oxidative stress. Often, CVD is preceded by endothelial dysfunction, which carries with it a proatherothrombotic phenotype. Endothelial senescence and reduced production and release of nitric oxide (NO) are associated with “vascular ageing” and are often accompanied by a reduced ability for the body to repair vascular damage, termed “reendothelialization.” Exercise has been repeatedly shown to confer protection against CVD and diabetes risk and incidence. Regular exercise promotes endothelial function and can prevent endothelial senescence, often through a reduction in oxidative stress. Recently, endothelial precursors, endothelial progenitor cells (EPC), have been shown to repair damaged endothelium, and reduced circulating number and/or function of these cells is associated with ageing. Exercise can modulate both number and function of these cells to promote endothelial homeostasis. In this review we look at the effects of advancing age on the endothelium and these endothelial precursors and how exercise appears to offset this “vascular ageing” process

Blood flow restriction exercise attenuates the exercise-induced endothelial progenitor cells in healthy, young men.

Endothelial progenitor cells (EPCs) are a vasculogenic subset of progenitors, which play a key role in maintenance of endothelial integrity. These cells are exercise-responsive, and thus exercise may play a key role in vascular repair and maintenance via mobilization of such cells. Blood flow restriction exercise, due to the augmentation of local tissue hypoxia, may promote exercise-induced EPC mobilization. Nine, healthy, young (18-30yrs) males participated in the study. Participants undertook 2 trials of single leg knee extensor (KE) exercise, at 60% of thigh occlusion pressure (4 sets at 30% maximal torque) (BFR) or non- blood flow restricted (non-BFR), in a fasted state. Blood was taken prior, immediately after, and 30 minutes after exercise. Blood was used for the quantification of haematopoietic progenitor cells (HPCs: CD34+CD45dim), EPCs (CD34+VEGFR2+/CD34+CD45dimVEGFR2+) by flow cytometry. Our results show that unilateral KE exercise did not affect circulating HPC levels (p = 0.856), but did result in increases in both CD34+VEGFR2+ and CD34+CD45dimVEGFR2+ EPCs, but only in the non-BFR trial (CD34+VEGFR2+: 269 ± 42 cells·mL-1 to 573 ± 90 cells·mL-1, pre- to immediately post-exercise, p = 0.008; CD34+CD45dimVEGFR2+: 129 ± 21 cells·mL-1 to 313 ± 103 cells·mL-1, pre- to 30 min post-exercise, p = 0.010). In conclusion, low intensity BFR exercise did not result in significant circulating changes in EPCs in the post-exercise recovery period and may impair exercise-induced EPC mobilization compared to non-BFR exercise

Elite mountain bike enduro competition: a study of rider hand-arm vibration exposure

Limited information is currently available regarding the hand-arm vibration (HAV) exposure 5 for professional off-road cyclists. Previous reports have suggested that commuting and 6 recreational cyclists are at risk of exceeding exposure limit values (ELV) in a single ride. 7 Therefore, further investigation of HAV exposure in competitive mountain biking is 8 warranted. Partial and total eight hour exposure data (Ai(8), A(8), ms⁻²) were computed for a 9 national level mountain bike enduro competitions. Hand-arm vibrations were measured using 10 a tri-axial accelerometer recording at a frequency of 3.2 kHz mounted on the handlebar and 11 accelerations were quantified after frequency weighting filters were applied (Wh). The data 12 presented shows that HAV exposure during one day of competitive enduro mountain bike 13 racing exceeds ELV (mean race exposure = 5.84 ms⁻² , minimum = 5.47ms⁻² , maximum = 14 6.61ms⁻²) and is greater than the HAV exposure observed in recreational cycling. This 15 suggests that further work is required to determine the exposure associated with changes in 16 equipment, technique and international racing events in professional athletes

Lower Resting and Exercise-Induced Circulating Angiogenic Progenitors and Angiogenic T-Cells in Older Men

Ageing is associated with a dysfunctional endothelial phenotype, as well as reduced angiogenic capabilities. Exercise exerts beneficial effects on the cardiovascular system, possibly by increasing/maintaining the number and/or function of circulating angiogenic cells (CACs) that are known to decline with age. However, the relationship between cardiorespiratory fitness (CRF) and age related changes in frequency of CACs, as well as the exercise-induced responsiveness of CACs in older individuals has not yet been determined. One hundred and seven healthy male volunteers, aged 18-75 years, participated in the study 1. CRF was estimated using submaximal cycling ergometer test. Circulating endothelial progenitor cells (EPCs), angiogenic T-cells (TANG) and their CXCR4 cell surface receptor expression were enumerated by flow cytometry using peripheral blood samples obtained under resting conditions prior to the exercise test. Study 2 recruited 17 healthy males (8 young, 18-25yrs; 9 older, 60-75yrs) and these participants undertook a 30-minute cycling exercise bout at 70% V ?O2max, with CACs enumerated pre- and immediately post-exercise. Age was inversely associated with both CD34+ progenitor cells (r2=-0.140, p=0.000) and TANG (r2=-0.176, p=0.000) cells, as well as CXCR4-expressing CACs (CD34+, r2=-0.167, p=0.000; EPCs: r2=-0.098, p=0.001; TANG, r2=-0.053, p=0.015). However, after correcting for age, CRF had no relationship with either CAC subset. In addition, older individuals displayed attenuated exercise-induced increases in CD34+ progenitor cells, TANG, CD4+ TANG, and CD8+CXCR4+ TANG cells. Older men display lower CAC levels, which may contribute to increased CVD risk, and older adults display an impaired exercise-induced responsiveness of these cells

Sleep disruption and its effect on lymphocyte redeployment following an acute bout of exercise

Sleep disruption and deprivation are common in contemporary society and have been linked with poor health, decreased job performance and increased life-stress. The rapid redeployment of lymphocytes between the blood and tissues is an archetypal feature of the acute stress response, but it is not known if short-term perturbations in sleep architecture affect lymphocyte redeployment. We examined the effects of a disrupted night sleep on the exercise-induced redeployment of lymphocytes and their subtypes. 10 healthy male cyclists performed 1 h of cycling at a fixed power output on an indoor cycle ergometer, following a night of undisrupted sleep (US) or a night of disrupted sleep (DS). Blood was collected before, immediately after and 1 h after exercise completion. Lymphocytes and their subtypes were enumerated using direct immunofluorescence assays and 4-colour flow cytometry. DS was associated with elevated concentrations of total lymphocytes and CD3−/CD56+ NK-cells. Although not affecting baseline levels, DS augmented the exercise-induced redeployment of CD8+ T-cells, with the naïve/early differentiated subtypes (KLRG1−/CD45RA+) being affected most. While the mobilisation of cytotoxic lymphocyte subsets (NK cells, CD8+ T-cells γδ T-cells), tended to be larger in response to exercise following DS, their enhanced egress at 1 h post-exercise was more marked. This occurred despite similar serum cortisol and catecholamine levels between the US and DS trials. NK-cells redeployed with exercise after DS retained their expression of perforin and Granzyme-B indicating that DS did not affect NK-cell ‘arming’. Our findings indicate that short-term changes in sleep architecture may ‘prime’ the immune system and cause minor enhancements in lymphocyte trafficking in response to acute dynamic exercise

The impact of acute strenuous exercise on TLR2, TLR4 and HLA.DR expression on human blood monocytes induced by autologous serum

Acute exercise alters the surface expression of toll-like receptors (TLRs) and HLA.DR on blood monocytes, which could transiently compromise immunity. As serum factors might be responsible, we examined the effects of autologous post-exercise serum exposure on TLR2, TLR4 and HLA.DR expression on resting blood monocytes and their subtypes. Eight trained cyclists completed an ergometer 60 km time trial. PBMCs and serum were obtained before, immediately after and 1 h after exercise. TLR2, TLR4 or HLA.DR expression (gMFI) was determined on blood monocyte subtypes expressing combinations of CD14 and CD16 by flow cytometry, and on resting monocytes exposed to 50% autologous serum (pre, immediately after or 1 h after exercise) for 18 h in culture. Immediately after exercise, total monocyte expression of TLR2 and TLR4 increased by 41 and 27%, respectively, while HLA.DR expression was 39% lower than baseline. TLR2 and TLR4 was 53 and 84% greater 1 h after exercise, respectively, while HLA.DR was 48% lower. Changes in TLR2 and TLR4 expression occurred on the CD14++bright/CD16+dim monocyte subtype only, while HLA.DR expression changed on the CD14+dim/CD16++bright subtype. Serum did not affect monocyte TLR2 or TLR4 expression but 1 h post serum increased expression of HLA.DR on total monocytes and the CD14+dim/CD16++bright subtype, which was in contrast to the change observed at this time after exercise. We conclude that a bout of strenuous aerobic exercise alters the surface expression of TLR2, TLR4 and HLA.DR on blood monocytes and some of their subtypes, but these changes appear to be unrelated to blood serum factors

Lymphocyte Apoptosis, Adhesion/activation Molecules And Complement Regulatory Proteins Following Intensive, Moderate And Eccentric Exercise: 1739 11:30 AM - 11:45 AM

No abstract available

Physiological and Anthropometrical Indicators of Backpack Running Performance in ??Elite?? British Soldiers: 1384

PURPOSE: To identify indicators of backpack running performance in “elite” British soldiers using an extensive range of physiological and anthropometrical variables.METHODS: Thirteen male soldiers (mean ± SD: Age: 26 ± 4 yrs; VO2peak: 55.1 ± 5.4) from two “elite” British Army Units completed two backpack running protocols (backpack weight: 20kg) on separate occasions; (1) an incremental treadmill running test to volitional exhaustion and (2) an 8-mile time-trial in field conditions. During the treadmill test, VO2, VE, VE/VO2, heart rate, RPE and blood lactate concentrations were determined at each incremental stage of the protocol to identify blood lactate (breakpoint, [delta] 1mM, 2.5mM, 3.0mM and 4.0mM) and ventilatory [breakpoints in ventilation (ventT) and the ventilatory equivalent of oxygen (VE/VO2T)] thresholds and corresponding values. Maximal exercise time and VO2peak were also determined from the test. For the field test, soldiers were asked to complete an 8-mile course (12.8 km) in the fastest time possible.RESULTS: Mean exercise tolerance time on the treadmill test was 23:34 ± 00:38 min: sec and the mean time taken to complete the 8-mile time-trial was 1:31:45 ± 0:10:12 h:min:sec. Pearson's correlations revealed that velocity at lactate breakpoint, [delta] 1mM, 2.5mM, 3.0mM, 4.0mM and VE/VO2T were the best indicators of performance on the 8-mile time-trial (r = -0.86, -0.71, -0.79, -0.82, -0.82, -0.77 respectively). VO2 at 2.5mM threshold and velocity at ventT were moderate indicators of performance (r = 0.65 and 0.63 respectively), whereas VO2peak (r = 0.40) and percentage body fat (r = 0.01) were poor performance indicators.CONCLUSION: Blood lactate and ventilatory thresholds are useful indicators of backpack running performance in “elite” British soldiers