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Limb immobilization causes local vasculature to experience detrimental adaptations. Simple strategies to increase blood flow (heating, fidgeting) successfully prevent acute (≤ 1 day) impairments; however, none have leveraged the hyperemic response over prolonged periods (weeks) mirroring injury rehabilitation. Throughout a 14-day unilateral limb immobilization, we sought to preserve vascular structure and responsiveness by repeatedly activating a reactive hyperemic response via blood flow restriction (BFR) and amplifying this stimulus by combining BFR with electric muscle stimulation (EMS). Young healthy adults (M:F = 14:17, age = 22.4 ± 3.7 years) were randomly assigned to control, BFR, or BFR + EMS groups. BFR and BFR + EMS groups were treated for 30 min twice daily (3 × 10 min ischemia–reperfusion cycles; 15% maximal voluntary contraction EMS), 5 days/week (20 total sessions). Before and after immobilization, artery diameter, flow-mediated dilation (FMD) and blood flow measures were collected in the superficial femoral artery (SFA). Following immobilization, there was less retrograde blood velocity (+ 1.8 ± 3.6 cm s−1, P = 0.01), but not retrograde shear (P = 0.097). All groups displayed reduced baseline and peak SFA diameter following immobilization (− 0.46 ± 0.41 mm and − 0.43 ± 0.39 mm, P

This study aimed to investigate the effects of blood flow restriction (BFR) combined with electrical muscle stimulation (EMS) on skeletal muscle mass and strength during a period of limb disuse.Thirty healthy participants (22 ± 3 yr; 23 ± 3 kg·m-2) were randomly assigned to control (CON; n = 10), BFR alone (BFR; n = 10), or BFR combined with EMS (BFR + EMS; n = 10). All participants completed unloading of a single leg for 14 d, with no treatment (CON), or while treated with either BFR or BFR + EMS (twice daily, 5 d·wk-1). BFR treatment involved arterial three cycles of 5-min occlusion using suprasystolic pressure, each separated by 5 min of reperfusion. EMS (6 s on, 15 s off; 200 μs; 60 Hz; 15% maximal voluntary contraction [MVC]) was applied continuously throughout the three BFR cycles. Quadriceps muscle mass (whole-thigh lean mass via dual-energy x-ray absorptiometry and vastus lateralis [VL] muscle thickness via ultrasound) and strength (via knee extension MVC) were assessed before and after the 14-d unloading period.After limb unloading, whole-thigh lean mass decreased in the control group (-4% ± 1%, P0.001) and BFR group (-3% ± 2%, P = 0.001), but not in the BFR + EMS group (-0.3% ± 3%, P = 0.8). VL muscle thickness decreased in the control group (-4% ± 4%, P = 0.005) and was trending toward a decrease in the BFR group (-8% ± 11%, P = 0.07) and increase in the BFR + EMS group (+5% ± 10%, P = 0.07). Knee extension MVC decreased over time (P0.005) in the control group (-18% ± 15%), BFR group (-10% ± 13%), and BFR + EMS group (-18% ± 15%), with no difference between groups (P0.5).Unlike BFR performed in isolation, BFR + EMS represents an effective interventional strategy to attenuate the loss of muscle mass during limb disuse, but it does not demonstrate preservation of strength.

PURPOSE Ultraendurance exercise is steadily growing in popularity; however, the effect of increasingly prolonged durations of exercise on the vascular endothelium is unknown. The aim of this study was to characterize the effect of various ultramarathon running distances on vascular form and function. METHODS We evaluated vascular endothelial function via flow-mediated dilation (FMD) in the superficial femoral artery, as well as microvascular function, inflammatory factors, and central artery stiffness, before and after participants completed 25-km (7M:2F), 50-km (11M:10F), 80-km (9M:4F), or 160-km (9M:2F) trail races all run on the same day and course. RESULTS Completion required 149 ± 20, 386 ± 111, 704 ± 130, and 1470 ± 235 min, with corresponding average paces of 6.0 ± 0.8, 7.7 ± 2.2, 8.6 ± 1.3, and 9.6 ± 1.3 min·km-1, respectively. At baseline, there were no differences in participant characteristics across race distance groups. Shear rate stimulus trended toward an increase after the race (P = 0.07), but resting postrace artery diameter (P < 0.001) was elevated to a similar extent in all conditions. There was a reduction in FMD after the 50-km race (Δ -1.9% ± 2.2%, P < 0.01), but not the 25-km (Δ +0.3% ± 2.9%, P = 0.8), the 80-km (Δ -1.5% ± 3.2%, P = 0.1), or the 160-km (Δ +0.5% ± 2.5%, P = 0.5) race. Inflammatory markers increased most after 160 km, but arterial stiffness and microvascular function were not differently affected by race distance. CONCLUSIONS Although the superficial femoral artery baseline diameter was larger postexercise regardless of race distance, only the 50-km race reduced FMD, whereas a short-duration higher-intensity race (25 km) and longer-duration lower-intensity races (160 km) did not. Therefore, a 50-km ultramarathon may represent the intersection between higher-intensity exercise over a prolonged duration, causing reduced endothelial function not seen in shorter or longer distances.

To use repeated control trials to measure within-subject variability and assess the existence of responders to ischemic preconditioning (IPC). Secondly, to determine whether repeated IPC can evoke a dosed ergogenic response.Twelve aerobically fit individuals each completed three control and three IPC 5-km cycling time trials. IPC trials included: (i) IPC 15-min preceding the trial (traditional IPC), (ii) IPC 24-h and 15-min preceding (IPC × 2), (iii) IPC 48-h, 24-h, and 15-min preceding (IPC × 3). IPC consisted of 3 × 5-min cycles of occlusion and reperfusion at the upper thighs. To assess the existence of a true response to IPC, individual performance following traditional IPC was compared to each individual's own 5-km TT coefficient of variation. In individuals who responded to IPC, all three IPC conditions were compared to the mean of the three control trials (CON9 of 12 (75%) participants improved 5-km time (-1.8 ± 1.7%) following traditional IPC, however, only 7 of 12 (58%) improved greater than their own variability between repeated controls (true responders). In true responders only, we observed a significant mean improvement in 5-km TT completion following traditional IPC (478 ± 50 s), IPC × 2 (481 ± 51 s), and IPC × 3 (480.5 ± 49 s) compared to mean CONA majority of participants responded to IPC, providing support for a meaningful IPC-mediated performance benefit. However, repeated bouts of IPC on consecutive days do not enhance the ergogenic effect of a single bout of IPC.

To examine if repeated exposure to IPC treatment prior to training sessions improves oxygen uptake and 1-km running performance in highly trained middle-distance runners. Fourteen highly trained endurance runners (11 male/3 female, 19 ± 2 years, 64 ± 5 ml kg−1 min−1) completed a baseline maximal oxygen consumption ( $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ ) test and 1-km running performance test before random assignment to an IPC or control group. Both groups were prescribed identical endurance training over an 8-week varsity season; however, the IPC group performed an IPC protocol (5 min ischemia, repeated 3 times, each separated by 5 min reperfusion) before every training session. After 8 weeks of training, participants completed a follow-up $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ test and 1-km time trial. $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ did not increase from baseline in either group following the 8-week training bout (P = 0.2), and neither group varied more than the other ( $$\Delta \dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ = IPC 0.6 ± 2 ml kg−1 min−1; control 1.5 ± 2 ml kg−1 min−1, P = 0.6) or beyond typical measurement error. The IPC decreased 1-km time trial time by 0.4% (0.5 ± 2 s), while the control group decreased by 1% (1.5 ± 3 s), but neither change was significant compared to baseline (P = 0.2). There was also no difference in time trial improvement between IPC and control (P = 0.6). However, there was a trend towards IPC significantly improving running economy at low intensity (P = 0.057). Our data suggest that over a normal 8-week season in a population of highly trained middle-distance runners there is no benefit of undergoing chronic, repeated IPC treatments before training for augmenting maximal aerobic power or 1-km performance time.

Walking exercise is the most effective noninvasive therapy that improves walking ability in peripheral artery disease (PAD). Biologic mechanisms by which exercise improves walking in PAD are unclear. This review summarizes evidence regarding effects of walking exercise on lower extremity skeletal muscle in PAD. In older people without PAD, aerobic exercise improves mitochondrial activity, muscle mass, capillary density, and insulin sensitivity in skeletal muscle. However, walking exercise increases lower extremity ischemia in people with PAD, and therefore, mechanisms by which this exercise improves walking may differ between people with and without PAD. Compared with people without PAD, gastrocnemius muscle in people with PAD has greater mitochondrial impairment, increased reactive oxygen species, and increased fibrosis. In multiple small trials, walking exercise therapy did not consistently improve mitochondrial activity in people with PAD. In one 12-week randomized trial of people with PAD randomized to supervised exercise or control, supervised treadmill exercise increased treadmill walking time from 9.3 to 15.1 minutes, but simultaneously increased the proportion of angular muscle fibers, consistent with muscle denervation (from 7.6% to 15.6%), while angular myofibers did not change in the control group (from 9.1% to 9.1%). These findings suggest an adaptive response to exercise in PAD that includes denervation and reinnervation, an adaptive process observed in skeletal muscle of people without PAD during aging. Small studies have not shown significant effects of exercise on increased capillary density in lower extremity skeletal muscle of participants with PAD, and there are no data showing that exercise improves microcirculatory delivery of oxygen and nutrients in patients with PAD. However, the effects of supervised exercise on increased plasma nitrite abundance after a treadmill walking test in people with PAD may be associated with improved lower extremity skeletal muscle perfusion and may contribute to improved walking performance in response to exercise in people with PAD. Randomized trials with serial, comprehensive measures of muscle biology, and physiology are needed to clarify mechanisms by which walking exercise interventions improve mobility in PAD.

This study investigated cross-sectional associations of peripheral artery disease (PAD) severity (defined by the ankle–brachial index (ABI)) and amounts of daily sustained physical activity (PA) (defined as > 100 activity counts per minute lasting 5 consecutive minutes or more). This study also investigated associations of amounts of daily sustained PA with 6-minute walk (6MW) distance and the Short Form-36 physical functioning domain (SF-36 PF) score in cross-sectional analyses and with serious adverse events (SAEs) in longitudinal analyses of people with PAD. PA was measured continuously for 10 days using a tri-axial accelerometer at baseline in 277 participants with PAD randomized to the LITE clinical trial. In regression analyses, each 0.15 lower ABI value was associated with a 5.67% decrease in the number of daily bouts of sustained PA (95% CI: 3.85–6.54; p < 0.001). Every additional bout of sustained PA per day was associated with a 4.56-meter greater 6MW distance (95% CI: 2.67–6.46; p < 0.0001), and a 0.81-point improvement in SF-36 PF score (95% CI: 0.34–1.28; p < 0.001). Participants with values of daily bouts of sustained PA below the median had higher rates of SAEs during follow-up, compared to participants above the median (41% vs 24%; p = 0.002). In conclusion, among participants with PAD, lower ABI values were associated with fewer bouts of daily sustained PA. A greater number of bouts of daily sustained PA were associated with better 6MW performance and SF-36 PF score, and, in longitudinal analyses, lower rates of SAEs. Clinicaltrials.gov ID: NCT02538900.

Cardiac function has been shown to transiently decrease following prolonged exercise, with greater durations related to increased impairment. However, the prospective assessment of exercise duration on cardiac performance is rare, and the influence of relative exercise intensity is typically not assessed in relation to these changes. The aim of this study was to determine whether progressively longer running distances over the same course would elicit greater cardiac impairment. The present investigation examined cardiac alterations in 49 athletes, following trail-running races of 25, 50, 80, and 160 km, performed on the same course on the same day. Echocardiography, including conventional and speckle tracking imaging, was performed with legs-raised to 60° to mitigate alterations in preload both pre- and post-race. Race-intensities were monitored via heart rate (HR). Following the races, mean arterial pressure (Δ−11 ± 7 mmHg, P < 0.0001), and HR (Δ19 ± 14 bpm, P < 0.0001) were altered independent of race distance. Both left and right ventricular (LV and RV) diastolic function were reduced (ΔLV E/A −0.54 ± 0.49, P < 0.0001; ΔRV A’ + 0.02 ± 0.04 m/s, P = 0.01) and RV systolic function decreased (ΔTAPSE −0.25 ± 0.9 cm, P = 0.01), independent of race distance. Cardiac impairment was not apparent using speckle tracking analysis with cubic spline interpolation. While race duration was unrelated to cardiac alterations, increased racing HR was related to greater RV base dilation (r = −0.37, P = 0.03). Increased time spent at higher exercise intensities was related to reduced LV ejection fraction following 25 km (r = −0.81, P = 0.03), LV systolic strain rate following 50 km (r = 0.59, P = 0.04), and TAPSE (r = −0.81, P = 0.03) following 80 km races. Increased running duration did not affect the extent of exercise-induced cardiac fatigue, however, intensity may be a greater driver of cardiac alterations.

The influence of muscle sympathetic nerve activity (MSNA) responses on local vascular conductance during exercise are not well established. Variations in exercise mode and active muscle mass can produce divergent MSNA responses. Therefore, we sought to examine the effects of small- versus large-muscle mass dynamic exercise on vascular conductance and MSNA responses in the inactive limb. Thirty-five participants completed two study visits in a randomized order. During visit 1, superficial femoral artery (SFA) blood flow (Doppler ultrasound) was assessed at rest and during steady-state rhythmic handgrip (RHG; 1:1 duty cycle, 40% maximal voluntary contraction), one-leg cycling (17 ± 3% peak power output), and concurrent exercise at the same intensities. During visit 2, MSNA (contralateral fibular nerve microneurography) was acquired successfully in 12/35 participants during the same exercise modes. SFA blood flow increased during RHG ( P < 0.0001) and concurrent exercise ( P = 0.03) but not cycling ( P = 0.91). SFA vascular conductance was unchanged during RHG ( P = 0.88) but reduced similarly during concurrent and cycling exercise (both P < 0.003). RHG increased MSNA burst frequency ( P = 0.04) without altering burst amplitude ( P = 0.69) or total MSNA ( P = 0.26). In contrast, cycling and concurrent exercise had no effects on MSNA burst frequency (both P ≥ 0.10) but increased burst amplitude (both P ≤ 0.001) and total MSNA (both P ≤ 0.007). Across all exercise modes, the changes in MSNA burst amplitude and SFA vascular conductance were correlated negatively ( r = −0.43, P = 0.02). In summary, the functional vascular consequences of alterations in sympathetic outflow to skeletal muscle are most closely associated with changes in MSNA burst amplitude, but not frequency, during low-intensity dynamic exercise. NEW & NOTEWORTHY Low-intensity small- versus large-muscle mass exercise can elicit divergent effects on muscle sympathetic nerve activity (MSNA). We examined the relationships between changes in MSNA (burst frequency and amplitude) and superficial femoral artery (SFA) vascular conductance during rhythmic handgrip, one-leg cycling, and concurrent exercise in the inactive leg. Only changes in MSNA burst amplitude were inversely associated with SFA vascular conductance responses. This result highlights the functional importance of measuring MSNA burst amplitude during exercise.

Purpose: Ischemic preconditioning (IPC) through purposeful circulatory occlusion may enhance exercise performance. The value of IPC for improving performance is controversial owing to challenges with employing effective placebo controls. This study examines the efficacy of IPC versus a deceptive sham protocol for improving performance to determine whether benefits of IPC are attributable to true physiological effects. It was hypothesized that IPC would favorably alter performance more than a sham treatment and that physiological responses to exercise would be affected only after IPC treatment. Methods: In a randomized order, 16 participants performed incremental exercise to exhaustion on a cycle ergometer in control conditions and after sham and IPC treatments. Participants rated their belief as to the efficacy of each treatment compared with control. Results: Time to exhaustion was greatest after IPC (control = 1331 [270] s, IPC = 1429 [300] s, sham = 1343 [255] s, P = .02), despite negative performance expectations after IPC and positive expectation after sham. Maximal aerobic power remained unchanged after both SHAM and IPC (control = 42.0 [5.2], IPC = 41.7 [5.5], sham = 41.6 [5.5] mL·kg−1·min−1, P = .7), as did submaximal lactate concentration (control = 8.9 [2.6], sham = 8.0 [1.9], IPC = 7.7 [2.1] mmol, P = .1) and oxygen uptake (control = 37.8 [4.8], sham = 37.5 [5.3], IPC = 37.5 [5.5] mL·kg−1·min−1, P = .6). Conclusions: IPC before cycling exercise provides an ergogenic benefit that is not attributable to a placebo effect from positive expectation and that was not explained by traditionally suggested mechanisms.

The aim of this study was to comprehensively assess the effects of rhythmic handgrip (RHG), one-leg cycling, and concurrent arm and leg exercise on muscle sympathetic nerve activity (MSNA) and vasc...

Objectives To systematically search and assess studies that have combined blood flow restriction (BFR) with exercise, and to perform meta-analysis of the reported results to quantify the effectiveness of BFR exercise on muscle strength and hypertrophy. Design A systematic review. Methods A computer assisted database search was conducted for articles investigating the effect of exercise combined with BFR on muscle hypertrophy and strength. A total of 916 hits were screened in order based on title, abstract, and full article, resulting in 47 articles that fit the review criteria. Results A total of 400 participants were included from 19 different studies measuring muscle strength increases when exercise is combined with BFR. Exercise was separated into aerobic and resistance exercise. Resulting from BFR aerobic exercise, there was a mean strength improvement of 0.4Nm between the experimental group and control group, while BFR resistance exercise resulted in a mean improvement of 0.3kg. A total of 377 participants were included in 19 studies measuring muscle size increase (cross sectional area) when exercise was combined with BFR. The mean difference in muscle size between the experimental group and control group was 0.4cm 2 . Conclusion Current evidence suggests that the addition of BFR to dynamic exercise training is effective for augmenting changes in both muscle strength and size. This effect was consistent for both resistance training and aerobically-based exercise, although the effect sizes varied. The magnitude of observed changes are noteworthy, particularly considering the relatively short duration of the average intervention.

Purpose: To identify the combined effect of increasing tissue level oxygen consumption and metabolite accumulation on the ergogenic efficacy of ischemic preconditioning (IPC) during both maximal aerobic and maximal anaerobic exercise. Methods: Twelve healthy males (22 ± 2 years, 179 ± 2 cm, 80 ± 10 kg, 48 ± 4 ml.kg-1.min-1) underwent four experimental conditions: (i) no IPC control, (ii) traditional IPC, (iii) IPC with EMS, and (iv) IPC with treadmill walking. IPC involved bilateral leg occlusion at 220 mmHg for 5 min, repeated three times, separated by 5 min of reperfusion. Within 10 min following the IPC procedures, a 30 s Wingate test and subsequent (after 25 min rest) incremental maximal aerobic test were performed on a cycle ergometer. Results: There was no statistical difference in anaerobic peak power between the no IPC control (1211 ± 290 W), traditional IPC (1209 ± 300 W), IPC + EMS (1206 ± 311 W), and IPC + Walk (1220 ± 288 W; P = 0.7); nor did VO2max change between no IPC control (48 ± 2 ml.kg-1.min-1), traditional IPC (48 ± 6 ml.kg-1.min-1), IPC + EMS (49 ± 4 ml.kg-1.min-1) and IPC + Walk (48 ± 6 ml.kg-1.min-1; P = 0.3). However, the maximal watts during the VO2max increased when IPC was combined with both EMS (304 ± 38 W) and walking (308 ± 40 W) compared to traditional IPC (296 ± 39 W) and no IPC control (293 ± 48 W; P = 0.02). Conclusion: This study shows that in a group of participants for whom a traditional IPC stimulus was not effective, the magnification of the IPC stress through muscle contractions while under occlusion led to a subsequent exercise performance response. These findings support that amplification of the ischemic preconditioning stimulus augments the effect for exercise capacity.

The contribution of central command to the peripheral vasoconstrictor response during exercise has been investigated using primarily handgrip exercise. The purpose of the present study was to compare muscle sympathetic nerve activity (MSNA) responses during passive (involuntary) and active (voluntary) zero-load cycling to gain insights into the effects of central command on sympathetic outflow during dynamic exercise. Hemodynamic measurements and contralateral leg MSNA (microneurography) data were collected in 18 young healthy participants at rest and during 2 min of passive and active zero-load one-legged cycling. Arterial baroreflex control of MSNA burst occurrence and burst area were calculated separately in the time domain. Blood pressure and stroke volume increased during exercise ( P < 0.0001) but were not different between passive and active cycling ( P > 0.05). In contrast, heart rate, cardiac output, and total vascular conductance were greater during the first and second minute of active cycling ( P < 0.001). MSNA burst frequency and incidence decreased during passive and active cycling ( P < 0.0001), but no differences were detected between exercise modes ( P > 0.05). Reductions in total MSNA were attenuated during the first ( P < 0.0001) and second ( P = 0.0004) minute of active compared with passive cycling, in concert with increased MSNA burst amplitude ( P = 0.02 and P = 0.005, respectively). The sensitivity of arterial baroreflex control of MSNA burst occurrence was lower during active than passive cycling ( P = 0.01), while control of MSNA burst strength was unchanged ( P > 0.05). These results suggest that central feedforward mechanisms are involved primarily in modulating the strength, but not the occurrence, of a sympathetic burst during low-intensity dynamic leg exercise. NEW & NOTEWORTHY Muscle sympathetic nerve activity burst frequency decreased equally during passive and active cycling, but reductions in total muscle sympathetic nerve activity were attenuated during active cycling. These results suggest that central command primarily regulates the strength, not the occurrence, of a muscle sympathetic burst during low-intensity dynamic leg exercise.

Context: The combined effect of neuromuscular electrical stimulation (NMES) and blood flow restriction (BFR) on muscle mass and strength has not been thoroughly investigated. Objective: To examine the effects of combined and independent BFR and a low-intensity NMES on skeletal muscle adaptation. Design: Exploratory study. Setting: Laboratory. Participants: Twenty recreationally active subjects. Main Outcome Measures: Subjects had each leg randomly allocated to 1 of 4 possible intervention groups: (1) cyclic BFR alone, (2) NMES alone, (3) BFR + NMES, or (4) control. Each leg was stimulated in its respective intervention group for 32 minutes, 4 days per week for 6 weeks. Mean differences in size (in grams) and isometric strength (in kilograms), between week 0 and week 6, were calculated for each group. Results: Leg strength increased 32 (19) kg in the BFR + NMES group, which differed from the 3 (11) kg change in the control group (P = .03). The isolated NMES and BFR groups revealed increases of 16 (28) kg and 18 (17) kg, respectively, but these did not statistically differ from the control, or one another. No alterations were statistically significant for leg size. Conclusion: Compared with a control that received no treatment, the novel combination of BFR and NMES led to increasing muscular strength of the knee extensors, but not muscle mass which had a large interindividual variability in response.

Background Ice hockey is a popular sport comprised of high-intensity repeated bouts of activity. Light activity, as opposed to passive rest, has been shown to improve power output in repeated sprinting and could potentially help to offset venous pooling, poor perfusion, and the risk of an ischemic event. The objective of our study was, thus, to examine the efficacy of low-intensity lower body activity following a simulated hockey shift for altering hemodynamic function. Methods In a cross-over design, 15 healthy hockey players (23 ± 1 years, 54 ± 3 mL/kg/min) performed two simulated hockey shifts. In both conditions, players skated up to 85 % of age-predicted heart rate maximum, followed by either passive recovery or active recovery while hemodynamic measures were tracked for up to 180 s of rest. Results Light active recovery within the confines of an ice hockey bench, while wearing skates and protective gear, was effective for augmenting cardiac output (an average of 2.5 ± 0.2 L/min, p = 0.03) at 45, 50, and 120 s. These alterations were driven by a sustained elevation in heart rate (12 bpm, p = 0.05) combined with a physiological relevant but non-significant (11.6 mL, p = 0.06) increase in stroke volume. Conclusions Standing and pacing between shifts offers a realistic in-game solution to help slow the precipitous drop in cardiac output (heart rate and stroke volume) that typically occurs with passive rest. Prolonging the duration of an elevated cardiac output further into recovery may be beneficial for promoting recovery of the working skeletal muscles and also avoiding venous pooling and reduced myocardial perfusion. Key Points Evidence that light activity in the form of standing/pacing is effective for maintaining cardiac output, and thus venous return Increased cardiac output and venous return may help reduce the chances of poor perfusion (ischemia) and could also promote recovery for performance This is a simple, low-risk, intervention demonstrated for the first time to work within the confines of a player’s bench while wearing hockey gear