Post-exercise cardiac autonomic and cardiovascular responses to heart rate-matched and work rate-matched hypoxic exercise.

PURPOSE: This study investigated the effect of performing hypoxic exercise at the same heart rate (HR) or work rate (WR) as normoxic exercise on post-exercise autonomic and cardiovascular responses. METHODS: Thirteen men performed three interval-type exercise sessions (5 × 5-min; 1-min recovery): normoxic exercise at 80% of the WR at the first ventilatory threshold (N), hypoxic exercise (FiO2 = 14.2%) at the same WR as N (H-WR) and hypoxic exercise at the same HR as N (H-HR). Autonomic and cardiovascular assessments were conducted before and after exercise, both at rest and during active squat-stand manoeuvres (SS). RESULTS: Compared to N, H-WR elicited a higher HR response (≈ 83% vs ≈ 75%HRmax, p < 0.001) and H-HR a reduced exercise WR (- 21.1 ± 9.3%, p < 0.001). Cardiac parasympathetic indices were reduced 15 min after exercise and recovered within 60 min in N and H-HR, but not after H-WR (p < 0.05). H-WR altered cardiac baroreflex sensitivity (cBRS) both at rest and during SS (specifically in the control of blood pressure fall during standing phases) in the first 60 min after the exercise bout (p < 0.05). Post-exercise hypotension (PEH) did not occur in H-HR (p > 0.05) but lasted longer in H-WR than in N (p < 0.05). CONCLUSIONS: Moderate HR-matched hypoxic exercise mimicked post-exercise autonomic responses of normoxic exercise without resulting in significant PEH. This may relate to the reduced WR and the limited associated mechanical/metabolic strain. Conversely, WR-matched hypoxic exercise impacted upon post-exercise autonomic and cardiovascular responses, delaying cardiac autonomic recovery, temporarily decreasing cBRS and evoking prolonged PEH.

Utility of lacrimal caruncle infrared thermography when monitoring alterations in autonomic activity in healthy humans.

PURPOSE: Physiological markers that estimate sympathetic activation may be used to infer pain and stress in humans. To date, effective reproducible methods are invasive and pose an undesired risk to participants. Previous work in animal models has used infrared thermography to measure the temperature of the lacrimal caruncle region and may be a promising method for measuring stress and pain non-invasively. The current study aimed to determine whether this method is useful in humans. METHODS: Sixteen young healthy participants (age: 18-35) were recruited and underwent sympathetic activation using a cold pressor test (CPT) and a muscle chemoreflex (MCR), and completed a control trial. Throughout all trials, infrared thermographic imaging of the lacrimal caruncle, heart rate, heart rate variability, mean arterial blood pressure and pulse transit time were measured. RESULTS: Heart rate (MCR: 4 ± 3 bpm, CPT: 17 ± 4 bpm p < 0.01) and mean arterial pressure increased (MCR: 6 ± 2, CPT: 5 ± 2 mmHg, p < 0.01) and pulse transit time decreased (p = 0.03) with both sympathetic activation interventions. However, lacrimal caruncle temperature did not vary under any condition remaining at 35.2 ± 0.2 °C which was similar to baseline. CONCLUSIONS: Our findings suggest infrared thermographic monitoring of eye temperature in humans does not reliably relate to sympathetic activation. This could be due to hemodynamic responses at the lacrimal caruncle that may be more complex than previously proposed with sympathetic activation. Alternatively, pulse transit time seems like a promising non-invasive measure of changes in sympathetic activation in humans.

Cardiac Autonomic and Physiological Responses to Moderate- intensity Exercise in Hypoxia.

Exercise physiological responses can be markedly affected by acute hypoxia. We investigated cardiac autonomic and physiological responses to different hypoxic training protocols. Thirteen men performed three exercise sessions (5×5-min; 1-min passive recovery): normoxic exercise at 80% of the power output (PO) at the first ventilatory threshold (N), hypoxic exercise (FiO2=14.2%) with the same PO as N (HPO) and hypoxic exercise at the same heart rate (HR) as N (HHR). PO was lower in HHR (21.1±9.3%) compared to N and HPO. Mean HR was higher in HPO (154±11 bpm, p<0.01) than N and HHR (139±10 vs. 138±9 bpm; p=0.80). SpO2 was reduced (p<0.01) to a similar extent (p>0.05) in HPO and HHR compared to N. HR recovery (HRR) and HR variability indices were similar in N and HHR (p>0.05) but reduced in HPO (p<0.05), mirroring a delayed parasympathetic reactivation. Blood lactate and ventilation were similar in N and HHR (p>0.05) and increased in HPO (p<0.001). During recovery oxygen consumption and ventilation were similar in N and HHR (p>0.05) and increased in HPO (p<0.01). Moderate HR-matched hypoxic exercise triggers similar cardiac autonomic and physiological responses to normoxic exercise with a reduced mechanical load. On the contrary, the same absolute intensity exercise in hypoxia is associated with increased exercise-induced metabolic stress and delayed cardiac autonomic recovery.

Cardiorespiratory and Autonomic Nervous System Responses to Prolonged Eccentric Cycling.

Offering large muscle benefits despite low metabolic demand, continuous eccentric exercise appears to be an interesting alternative to concentric exercise. Nevertheless, further knowledge is needed about prolonged eccentric exercise. This work sought to investigate the cardiovascular responses to prolonged constant-load eccentric compared to concentric cycling. Ten healthy males performed two 45-min exercise sessions of either concentric or eccentric cycling separated by a month and matched for heart rate during the first 5 min of exercise. Cardiorespiratory, autonomic nervous system and vascular responses were assessed at rest, and during exercise and recovery. During cycling, oxygen uptake, cardiac output and systolic blood pressure were similar but heart rate and diastolic blood pressure were greater whereas stroke volume was lower during eccentric than concentric cycling (118±21 vs. 104±10 bpm; 77±9 vs. 65±8 mmHg; 122±12 vs. 135±13 mL). Baroreflex and noradrenaline concentration were altered during eccentric cycling, and after eccentric exercise, vascular tone was greater than after concentric cycling. We observed increased cardiovascular strain and altered baroreflex activity during eccentric compared with concentric exercise, suggesting eccentric cycling triggers greater sympathetic activity.

Muscle Oxygenation Responses to Low-intensity Steady Rate Concentric and Eccentric Cycling.

Muscle deoxygenation responses provide information about the training impulse of an exercise session enabling adaptation to be predicted. Our aim was to investigate muscle oxygenation profiles during prolonged low-intensity eccentric and concentric cycling. Twelve healthy men performed two 45-min exercise sessions of concentric (CON) and eccentric (ECC) cycling, matched for the same heart rate at the start of each session. Mechanical power output during ECC was ~2.5 times that of CON (210±40 W vs. 82±16 W). Oxygen uptake, blood lactate, cardiac output and systolic arterial pressure responses did not differ between exercises. Heart rate was similar at 5 min of each exercise bout but progressively increased during ECC and was higher at 15, 30 and 45 min of ECC compared to CON (+10 bpm), with a trend for a lower stroke volume. Diastolic and mean blood pressures were higher during ECC. No significant differences were observed in muscle oxygenation profiles. Muscle oxygenation responses during prolonged low-intensity exercise were not affected by the type of muscle action at the same metabolic demand and cardiac output.

Exercise intensity modulates the appearance of circulating microvesicles with proangiogenic potential upon endothelial cells.

The effect of endurance exercise on circulating microvesicle dynamics and their impact on surrounding endothelial cells is unclear. Here we tested the hypothesis that exercise intensity modulates the time course of platelet (PMV) and endothelial-derived (EMV) microvesicle appearance in the circulation through hemodynamic and biochemical-related mechanisms, and that microvesicles formed during exercise would stimulate endothelial angiogenesis in vitro. Nine healthy young men had venous blood samples taken before, during, and throughout the recovery period after 1 h of moderate [46 ± 2% maximal oxygen uptake (V̇o2max)] or heavy (67 ± 2% V̇o2max) intensity semirecumbent cycling and a time-matched resting control trial. In vitro experiments were performed by incubating endothelial cells with rest and exercise-derived microvesicles to examine their effects on cell angiogenic capacities. PMVs (CD41+) increased from baseline only during heavy exercise (from 21 ± 1 × 103 to 55 ± 8 × 103 and 48 ± 6 × 103 PMV/µl at 30 and 60 min, respectively; P < 0.05), returning to baseline early in postexercise recovery (P > 0.05), whereas EMVs (CD62E+) were unchanged (P > 0.05). PMVs were related to brachial artery shear rate (r2 = 0.43) and plasma norepinephrine concentrations (r2 = 0.21) during exercise (P < 0.05). Exercise-derived microvesicles enhanced endothelial proliferation, migration, and tubule formation compared with rest microvesicles (P < 0.05). These results demonstrate substantial increases in circulating PMVs during heavy exercise and that exercise-derived microvesicles stimulate human endothelial cells by enhancing angiogenesis and proliferation. This involvement of microvesicles may be considered a novel mechanism through which exercise mediates vascular healing and adaptation.

Local temperature-sensitive mechanisms are important mediators of limb tissue hyperemia in the heat-stressed human at rest and during small muscle mass exercise.

Limb tissue and systemic blood flow increases with heat stress, but the underlying mechanisms remain poorly understood. Here, we tested the hypothesis that heat stress-induced increases in limb tissue perfusion are primarily mediated by local temperature-sensitive mechanisms. Leg and systemic temperatures and hemodynamics were measured at rest and during incremental single-legged knee extensor exercise in 15 males exposed to 1 h of either systemic passive heat-stress with simultaneous cooling of a single leg (n = 8) or isolated leg heating or cooling (n = 7). Systemic heat stress increased core, skin and heated leg blood temperatures (Tb), cardiac output, and heated leg blood flow (LBF; 0.6 ± 0.1 l/min; P < 0.05). In the cooled leg, however, LBF remained unchanged throughout (P > 0.05). Increased heated leg deep tissue blood flow was closely related to Tb (R(2) = 0.50; P < 0.01), which is partly attributed to increases in tissue V̇O2 (R(2) = 0.55; P < 0.01) accompanying elevations in total leg glucose uptake (P < 0.05). During isolated limb heating and cooling, LBFs were equivalent to those found during systemic heat stress (P > 0.05), despite unchanged systemic temperatures and hemodynamics. During incremental exercise, heated LBF was consistently maintained ∼ 0.6 l/min higher than that in the cooled leg (P < 0.01), with LBF and vascular conductance in both legs showing a strong correlation with their respective local Tb (R(2) = 0.85 and 0.95, P < 0.05). We conclude that local temperature-sensitive mechanisms are important mediators in limb tissue perfusion regulation both at rest and during small-muscle mass exercise in hyperthermic humans.

Restoring Akt1 activity in outgrowth endothelial cells from South Asian men rescues vascular reparative potential.

Recent data suggest reduced indices of vascular repair in South Asian men, a group at increased risk of cardiovascular events. Outgrowth endothelial cells (OEC) represent an attractive tool to study vascular repair in humans and may offer potential in cell-based repair therapies. We aimed to define and manipulate potential mechanisms of impaired vascular repair in South Asian (SA) men. In vitro and in vivo assays of vascular repair and angiogenesis were performed using OEC derived from SA men and matched European controls, prior defining potentially causal molecular mechanisms. SA OEC exhibited impaired colony formation, migration, and in vitro angiogenesis, associated with decreased expression of the proangiogenic molecules Akt1 and endothelial nitric oxide synthase (eNOS). Transfusion of European OEC into immunodeficient mice after wire-induced femoral artery injury augmented re-endothelialization, in contrast with SA OEC and vehicle; SA OEC also failed to promote angiogenesis after induction of hind limb ischemia. Expression of constitutively active Akt1 (E17KAkt), but not green fluorescent protein control, in SA OEC increased in vitro angiogenesis, which was abrogated by a NOS antagonist. Moreover, E17KAkt expressing SA OEC promoted re-endothelialization of wire-injured femoral arteries, and perfusion recovery of ischemic limbs, to a magnitude comparable with nonmanipulated European OEC. Silencing Akt1 in European OEC recapitulated the functional deficits noted in SA OEC. Reduced signaling via the Akt/eNOS axis is causally linked with impaired OEC-mediated vascular repair in South Asian men. These data prove the principle of rescuing marked reparative dysfunction in OEC derived from these men.

Moderate and heavy metabolic stress interval training improve arterial stiffness and heart rate dynamics in humans.

Traditional continuous aerobic exercise training attenuates age-related increases of arterial stiffness, however, training studies have not determined whether metabolic stress impacts these favourable effects. Twenty untrained healthy participants (n = 11 heavy metabolic stress interval training, n = 9 moderate metabolic stress interval training) completed 6 weeks of moderate or heavy intensity interval training matched for total work and exercise duration. Carotid artery stiffness, blood pressure contour analysis, and linear and non-linear heart rate variability were assessed before and following training. Overall, carotid arterial stiffness was reduced (p < 0.01), but metabolic stress-specific alterations were not apparent. There was a trend for increased absolute high-frequency (HF) power (p = 0.10) whereas both absolute low-frequency (LF) power (p = 0.05) and overall power (p = 0.02) were increased to a similar degree following both training programmes. Non-linear heart rate dynamics such as detrended fluctuation analysis [Formula: see text] also improved (p > 0.05). This study demonstrates the effectiveness of interval training at improving arterial stiffness and autonomic function, however, the metabolic stress was not a mediator of this effect. In addition, these changes were also independent of improvements in aerobic capacity, which were only induced by training that involved a high metabolic stress.

Distinct age-related brain activity patterns in the prefrontal cortex when increasing cognitive load: A functional near-infrared spectroscopy study.

Researchers have long observed distinct brain activity patterns in older adults compared with younger adults that correlate with cognitive performance. Mainly, older adults tend to show over-recruitment of bilateral brain regions during lower task loads and improved performance interpreted as compensation, but not observed at higher loads. However, there are discrepancies about whether increases in activity are compensatory and whether older adults can show compensation at higher loads. Our aim was to examine age-related differences in prefrontal cortex (PFC) activity and cognitive performance using functional near-infrared spectroscopy (fNIRS) during single and dual N-back tasks. Twenty-seven young adults (18-27 years) and 31 older adults (64-84 yrs) took part in the study. We used a robust fNIRS data methodology consisting of channel and region of interest analyses. Results showed differences in performance between task load conditions and age-related differences in reaction times but no age-group effects for accuracy. Older adults exhibited more bilateral PFC activation compared with young adults across all tasks and showed increases in brain activity in high compared to low load conditions. Our findings further support previous reports showing that older adults use compensatory recruitment of additional brain regions in PFC to maintain cognitive performance but go against the notion that such compensation is not present at higher cognitive loads. Additionally, our results indicate that fNIRS is a sensitive tool that can characterize adaptive cortical changes in healthy aging.

Cardiovascular Responses to Eccentric Cycling Based on Perceived Exertion Compared to Concentric Cycling, Effect of Pedaling Rate, and Sex.

Interest in eccentric exercises has increased over the last decades due to its efficiency in achieving moderate-high intensity muscular work with reduced metabolic demands. However, individualizing eccentric exercises in rehabilitation contexts remains challenging, as concentric exercises mainly rely on cardiovascular parameters. To overcome this, perceived exertion could serve as an individualization tool, but the knowledge about cardiovascular responses to eccentric cycling based on perceived exertion are still scarce. For this purpose, the cardiorespiratory parameters of 26 participants were assessed during two 5 min bouts of concentric cycling at 30 and 60 rpm and two bouts of eccentric cycling at 15 and 30 rpm matched for rating of perceived exertion. With this method, we hypothesized higher exercise efficiency during eccentric cycling for a same perceived exertion. The results revealed significantly elevated heart rate and cardiac index at higher pedalling rates during concentric (p < 0.001), but not during eccentric cycling (p ≈ 1). Exercise efficiency was higher during concentric cycling (64%), decreasing with pedalling rate, while eccentric cycling exhibited increased work rates (82%), and increased by over 100% with higher pedalling rate. Hence, eccentric cycling, with lower cardiorespiratory work for the same perceived exertion, facilitates higher work rates in deconditioned populations. However, further studies are needed for effective individualization.

Heavy and moderate interval exercise training alters low-flow-mediated constriction but does not increase circulating progenitor cells in healthy humans.

Moderate-intensity endurance exercise training improves vascular endothelial vasomotor function; however, the impact of high-intensity exercise training has been equivocal. Thus, the effect of the physiological stress of the exercise remains poorly understood. Furthermore, enhanced vascular repair mediated by circulating progenitor cells may also be improved. To address whether the physiological stress of exercise training is an important factor contributing to these adaptations, 20 healthy participants trained for 6 weeks. Training involved either moderate (MSIT; n = 9) or heavy metabolic stress (HSIT; n = 11) interval exercise training programmes matched for total work and duration of exercise. Before and after training, flow-mediated dilatation, low-flow-mediated constriction and total vessel reactivity were measured at the brachial artery using Doppler ultrasound. Circulating progenitor cells (CD34(+), CD133(+) and CD309/KDR(+)) were measured by flow cytometry (means ± SD). Relative (MSIT pre- 5.5 ± 3.4 versus post-training 6.6 ± 2.5%; HSIT pre- 6.6 ± 4.1 versus post-training 7.0 ± 3.4%, P = 0.33) and normalized (P = 0.16) flow-mediated dilatation did not increase with either training programme. However, low-flow-mediated constriction was greater after training in both groups (MSIT pre- -0.5 ± 3.2 versus post-training -1.9 ± 3.1%; HSIT pre- -1.0 ± 1.7 versus post-training -2.9 ± 3.0%, P = 0.04) and contributed to greater total vessel reactivity (MSIT pre- 7.4 ± 3.3 versus post-training 10.1 ± 3.7%; HSIT pre- 10.9 ± 5.9 versus post-training 12.7 ± 6.2%, P = 0.01). Peak reactive hyperaemia and the area under the shear rate curve were not different between groups, either before or after training. Although circulating progenitor cell numbers increased following heavy-intensity interval exercise training, variability was great amongst participants [MSIT pre- 16 ± 18 versus post-training 14 ± 12 cells (ml whole blood)(-1); HSIT pre- 8 ± 6 versus post-training 19 ± 23 cells (ml whole blood)(-1), P = 0.50]. Overall, vasoconstrictor function may be augmented by moderate- and heavy-intensity interval exercise training in young adults. However, circulating progenitor cell numbers were not increased, suggesting that these cells are not likely to be upregulated as a result of training.

Human exercise-induced circulating progenitor cell mobilization is nitric oxide-dependent and is blunted in South Asian men.

OBJECTIVE: Circulating progenitor cells (CPC) have emerged as potential mediators of vascular repair. In experimental models, CPC mobilization is critically dependent on nitric oxide (NO). South Asian ethnicity is associated with reduced CPC. We assessed CPC mobilization in response to exercise in Asian men and examined the role of NO in CPC mobilization per se. METHODS AND RESULTS: In 15 healthy, white European men and 15 matched South Asian men, CPC mobilization was assessed during moderate-intensity exercise. Brachial artery flow-mediated vasodilatation was used to assess NO bioavailability. To determine the role of NO in CPC mobilization, identical exercise studies were performed during intravenous separate infusions of saline, the NO synthase inhibitor L-NMMA, and norepinephrine. Flow-mediated vasodilatation (5.8%+/-0.4% vs 7.9%+/-0.5%; P=0.002) and CPC mobilization (CD34(+)/KDR(+) 53.2% vs 85.4%; P=0.001; CD133(+)/CD34(+)/KDR(+) 48.4% vs 73.9%; P=0.05; and CD34(+)/CD45(-) 49.3% vs 78.4; P=0.006) was blunted in the South Asian group. CPC mobilization correlated with flow-mediated vasodilatation and l-NMMA significantly reduced exercise-induced CPC mobilization (CD34(+)/KDR(+) -3.3% vs 68.4%; CD133(+)/CD34(+)/KDR(+) 0.7% vs 71.4%; and CD34(+)/CD45(-) -30.5% vs 77.8%; all P<0.001). CONCLUSIONS: In humans, NO is critical for CPC mobilization in response to exercise. Reduced NO bioavailability may contribute to imbalance between vascular damage and repair mechanisms in South Asian men.

Short-term unilateral leg immobilization alters peripheral but not central arterial structure and function in healthy young humans.

Short-term leg immobilization is an acute model of inactivity, which induces vascular deconditioning. The present study was conducted to determine if short-term leg immobilization induced alterations in central and peripheral conduit artery structure (diameter and compliance), function (resting blood flow and mean wall shear rate), and peripheral flow-mediated dilation. Healthy participants (n = 7 women and n = 8 men) were studied before and after 12 days of unilateral leg immobilization. Carotid artery structure and function were unaltered with immobilization indicating that the unilateral immobilization did not have a detectable effect on this representative central artery. In contrast, peripheral measures of arterial structure at the common femoral and popliteal arteries showed significant reductions in both the immobilized and non-immobilized limbs but to a greater extent in the immobilized limbs. Specifically, femoral and popliteal artery compliance and femoral artery diameter were reduced in both the immobilized and the non-immobilized limb (p < 0.05) while popliteal artery diameter was reduced only in the immobilized leg. Popliteal artery flow-mediated dilation, an indicator of peripheral artery function, was increased in the immobilized limb, which parallels reports in paralyzed limbs of spinal-cord-injured individuals. The time course of vascular alterations with inactivity likely follows a sequence of adaptations in arterial structure and function reflecting differing initial flow patterns, and arterial wall composition, and diverse hemodynamic stimuli within different blood vessels.

Post-Exercise Hypotension and Reduced Cardiac Baroreflex after Half-Marathon Run: In Men, but Not in Women.

We examined whether trained women exhibit similar cardiovascular and cardiac baroreflex alterations after a half-marathon compared to men. Thirteen women (39.1 ± 9.3 years; 165 ± 6 cm; 58.2 ± 7.5 kg; maximal aerobic speed (MAS): 13.7 ± 2.2 km·h-1) and 12 men (45.7 ± 10.5 years; 178 ± 7 cm; 75.0 ± 8.3 kg; MAS: 15.8 ± 2.2 km·h-1) ran an official half-marathon. Before and 60-min after, cardiovascular variables, parasympathetic (heart rate variability analysis) modulation and cardiac baroreflex function (transfer function and sequence analyses) were assessed during supine rest and a squat-stand test. Running performance was slower in women than in men (120 ± 19 vs. 104 ± 14 min for women and men, respectively). However, when expressed as a percentage of MAS, it was similar (78.1 ± 4.6% and 78.2 ± 5.4% of MAS for women and men, respectively). Before the run, women exhibited lower mean blood pressure (BP), cardiac output (CO) and stroke volume (SV) compared to men, together with higher parasympathetic indexes. After the race, parasympathetic indexes decreased in both sexes, but remained higher in women. Reduced SV, systolic BP and cardiac baroreflex were observed in men but not in women. Contrary to men, a competitive half-marathon did not trigger post-exercise hypotension and a reduced cardiac baroreflex in women.

Similar cardiovascular and autonomic responses in trained type 1 diabetes mellitus and healthy participants in response to half marathon.

AIMS: This field experiment examined whether trained people with type 1 diabetes mellitus (T1D) have similar cardiovascular and baroreflex alterations after a 21-km running race when compared to healthy people. METHODS: Nine T1D (39.0 ± 11.1 yr; 175.0 ± 10.2 cm; 70.8 ± 8.7 kg) were matched with 9 healthy participants (42.4 ± 5.8 yr; 175.7 ± 6.7 cm; 72.1 ± 8.5 kg) who ran an official half-marathon. Before and 1-hour after the race, cardiovascular variables, sympathetic activity (catecholamines), parasympathetic (heart rate variability analysis) modulation and cardiac baroreflex function (transfer function analysis) were assessed during supine rest and a squat stand test (forced blood pressure change). RESULTS: Performance time and weight loss [104.0 ± 13.2 and 111.0 ± 18.7 min; -2.57 ± 1.05 kg (-1.88 ± 0.88%) and -2.29 ± 1.15 kg (-1.59 ± 0.59%)] for healthy and T1D participants, respectively) were similar. Before running, no significant differences in any cardiovascular or autonomic variables were noted between the groups. After 1 h of recovery, both groups exhibited post-exercise hypotension, accompanied by increased sympathetic activity, decreased parasympathetic modulation, and reduced cardiac baroreflex sensitivity. CONCLUSIONS: Our results showed that the pattern of change in cardiovascular and autonomic nervous activity to strenuous exercise are well maintained in T1D participants with a training history of at least 5 years.

Effect of acute sprint interval exercise on central and peripheral artery distensibility in young healthy males.

Peripheral arterial distensibility is improved with sprint interval exercise training in young healthy participants (Rakobowchuk et al. in Am J Physiol Regul Integr Comp Physiol 295:R236-R242, 2008). To fully understand the mechanisms contributing to these training effects it is useful to examine the acute responses to sprint interval exercise. Following supine rest, nine healthy males completed either a single sprint interval (Wingate test) or a multiple sprint interval exercise session (4 Wingate tests each separated by 4.5 min). Following exercise, participants recovered for 60 min while central and peripheral arterial distensibility measurements were conducted at discrete time points, using applanation tonometry and ultrasound imaging and continuously, using central and peripheral pulsewave velocity (PWV). Single and multiple sprint interval exercise sessions caused similar changes in all variables. Heart rate was increased throughout recovery (p < 0.05), while central artery PWV was increased until 20 min of recovery (p < 0.05) and lower extremity PWV was decreased until ~45 min (p < 0.05). Distensibility of the superficial femoral artery showed a trend for a reduction at 2 min post-exercise (p = 0.06). These results indicate that extremely high intensity exercise transiently increases central artery stiffness, while metabolite induced vasodilation reduces peripheral stiffness in exercised limbs well into recovery.

Exercise-Derived Microvesicles: A Review of the Literature.

Initially suggested as simple cell debris, cell-derived microvesicles (MVs) have now gained acceptance as recognized players in cellular communication and physiology. Shed by most, and perhaps all, human cells, these tiny lipid-membrane vesicles carry bioactive agents, such as proteins, lipids and microRNA from their cell source, and are produced under orchestrated events in response to a myriad of stimuli. Physical exercise introduces systemic physiological challenges capable of acutely disrupting cell homeostasis and stimulating the release of MVs into the circulation. The novel and promising field of exercise-derived MVs is expanding quickly, and the following work provides a review of the influence of exercise on circulating MVs, considering both acute and chronic aspects of exercise and training. Potential effects of the MV response to exercise are highlighted and future directions suggested as exercise and sports sciences extend the realm of extracellular vesicles.

Interval exercise increases angiogenic cell function in postmenopausal women.

INTRODUCTION: Exercise can help to negate the increased cardiovascular disease risk observed in women after the menopausal transition. This study sought to determine whether interval or continuous exercise has differential effects on endothelial function and circulating angiogenic cell (CAC) number and function in postmenopausal women. METHODS: Fifteen healthy postmenopausal women completed a 30 min acute moderate-intensity continuous (CON) and interval exercise (MOD-INT) session on a cycle ergometer on separate days. Nine participants completed a further single 30 min acute heavy-intensity interval (HEAVY-INT) exercise session. Brachial artery flow-mediated dilation (FMD) was assessed pre-exercise and 15 min post-exercise session. CAC number and colony-forming capacity in vitro were assessed post exercise and compared with resting levels. RESULTS: FMD and CAC number did not change post exercise regardless of exercise type (p>0.05). However, the number (mean±SD) of colony-forming units (CFUs) increased from visit 1 (12±10 CFUs/well) to post MOD-INT (32±30 CFUs/well) and post HEAVY-INT (38±23 CFUs/well) but not post CON (13±14 CFUs/well). CONCLUSION: A single session of interval exercise is more effective than a continuous exercise session for increasing the intercellular communication of CACs, regardless of exercise intensity. The enhanced ability of CACs to form colonies may reflect an increased number and/or function of angiogenic T-cells. The repeated exertions to higher work rates during interval exercise may explain this response. Repeated exercise sessions might be required to improve FMD in postmenopausal women.