Acute partial sleep deprivation attenuates blood pressure responses to cycling exercise.

Exaggerated blood pressure (BP) responses during exercise are independently associated with future development of hypertension. Partial sleep deprivation (PSD) can increase 24-hour ambulatory BP, but the effects on exercise BP are unclear. We hypothesized that acute PSD would augment the BP response to constant load cycling exercise and a 20-minute time trial. Twenty-two, healthy adults (22±3 years; 13 males; V̇O2peak: 43.6±8.2 ml.kg-1.min-1) completed a randomized crossover trial whereby they slept normally (normal sleep-wake schedule for each participant), or sleep was partially deprived (early awakening, 40% of normal sleep duration). Each participant completed a 12-minute warm-up consisting of two 6-minute steps (step 1: 62±25 W; step 2: 137±60 W) followed by a 20-minute time trial on a cycle ergometer. PSD did not alter power output during the 20-minute time trial ([control vs. PSD] 170±68 vs. 168±68 W, P=0.65). Systolic BP did not differ during step 1 of the warm-up (141±15 vs. 137±12 mmHg, P=0.39) but was lower following PSD during step 2 (165±21 vs. 159±22 mmHg, P=0.004) and the 20-minute time trial (171±20 vs. 164±23 mmHg, P<0.001). These results were maintained when V̇O2peak was included as a covariate. Systolic BP responses were modulated by sex (time x visit x sex interaction P=0.03), with attenuated systolic BP during the warm-up and the 20-minute time trial in males but not females. In contrast to our hypothesis, acute PSD attenuates systolic BP responses during constant load and 20-minute time trial cycling exercise, though these observations appear to be primarily driven by changes in males.

The addition of blood flow restriction during resistance exercise does not increase prolonged low-frequency force depression.

At a given exercise intensity, blood flow restriction (BFR) reduces the volume of exercise required to impair post-exercise neuromuscular function. Compared to traditional exercise, the time course of recovery is less clear. After strenuous exercise, force output assessed with electrical muscle stimulation is impaired to a greater extent at low versus high stimulation frequencies, a condition known as prolonged low-frequency force depression (PLFFD). It is unclear if BFR increases PLFFD after exercise. This study tested if BFR during exercise increases PLFFD and slows recovery of neuromuscular function compared to regular exercise. Fifteen physically active participants performed six low-load sets of knee-extensions across four conditions: resistance exercise to task failure (RETF), resistance exercise to task failure with BFR applied continuously (BFRCONT) or intermittently (BFRINT), and resistance exercise matched to the lowest exercise volume condition (REVM). Maximal voluntary contraction (MVC) force output, voluntary activation and a force-frequency (1-100 Hz) curve were measured before and 0, 1, 2, 3, 4 and 24 h after exercise. Exercise to task failure caused similar reductions at 0 h for voluntary activation (RETF = 81.0 ± 14.2%, BFRINT = 80.9 ± 12.4% and BFRCONT = 78.6 ± 10.7%) and MVC force output (RETF = 482 ± 168 N, BFRINT = 432 ± 174 N, and BFRCONT = 443 ± 196 N), which recovered to baseline values between 4 and 24 h. PLFFD occurred only after RETF at 1 h supported by a higher frequency to evoke 50% of the force production at 100 Hz (1 h: 17.5 ± 4.4 vs. baseline: 15 ± 4.1 Hz, P = 0.0023), BFRINT (15.5 ± 4.0 Hz; P = 0.03), and REVM (14.9 ± 3.1 Hz; P = 0.002), with a trend versus BFRCONT (15.7 ± 3.5 Hz; P = 0.063). These findings indicate that, in physically active individuals, using BFR during exercise does not impair the recovery of neuromuscular function by 24 h post-exercise.

Altered carbohydrate oxidation during exercise in overreached endurance athletes is applicable to training monitoring with continuous glucose monitors.

PURPOSE: The purpose of the study was to investigate whether carbohydrate utilization is altered during exercise in overreached endurance athletes and examine the utility of continuous glucose monitors (CGM) to detect overreaching status. METHODS: Eleven endurance athletes (M:8, F:3) completed a 5-week training block consisting of 1 week of reduced training (PRE), 3 weeks of high-intensity overload training (POST), and 1 week of recovery training (REC). Participants completed a Lamberts and Lambert Submaximal Cycling Test (LSCT) and 5 km time-trial at PRE, POST, and REC time points, 15 min following the ingestion of a 50 g glucose beverage with glucose recorded each minute via CGM. RESULTS: Performance in the 5 km time-trial was reduced at POST (∆-7 ± 10 W, p = 0.04, η p 2 = 0.35) and improved at REC (∆12 ± 9 W from PRE, p = 0.01, η p 2 = 0.66), with reductions in peak lactate (∆-3.0 ± 2.0 mmol/L, p = 0.001, η p 2 = 0.71), peak HR (∆-6 ± 3 bpm, p < 0.001, η p 2 = 0.86), and Hooper-Mackinnon well-being scores (∆10 ± 5 a.u., p < 0.001, η p 2 = 0.79), indicating athletes were functionally overreached. The respiratory exchange ratio was suppressed at POST relative to REC during the 60% (POST: 0.80 ± 0.05, REC: 0.87 ± 0.05, p < 0.001, η p 2 = 0.74), and 80% (POST: 0.93 ± 0.05, REC: 1.00 ± 0.05, p = 0.003, η p 2 = 0.68) of HR-matched submaximal stages of the LSCT. CGM glucose was reduced during HR-matched submaximal exercise in the LSCT at POST (p = 0.047, η p 2 = 0.36), but not the 5 km time-trial (p = 0.07, η p 2 = 0.28) in overreached athletes. CONCLUSION: This preliminary investigation demonstrates a reduction in CGM-derived glucose and carbohydrate oxidation during submaximal exercise in overreached athletes. The use of CGM during submaximal exercise following standardized nutrition could be employed as a monitoring tool to detect overreaching in endurance athletes.

Assessing Leg Blood Flow and Cardiac Output During Running Using Thermodilution.

Cardiac output (Q̇C) and leg blood flow (Q̇LEG) can be measured simultaneously with high accuracy using transpulmonary and femoral vein thermodilution with a single-bolus injection. The invasive measure has offered important insight into leg hemodynamics and blood flow distribution during exercise. Despite being the natural modality of exercise in humans, there has been no direct measure of Q̇LEG while running in humans. We sought to determine the feasibility of the thermodilution technique for measuring Q̇LEG and conductance during high-intensity running, in an exploratory case study. A trained runner (30 years male) completed two maximal incremental tests on a cycle ergometer and motorized treadmill. Q̇LEG and Q̇C were determined using the single-bolus thermodilution technique. Arterial and venous blood were sampled throughout exercise, with continuous monitoring of metabolism, intra-arterial and venous pressure, and temperature. The participant reached a greater peak oxygen uptake (V̇O2peak) during running relative to cycling (74 vs. 68 mL/kg/min) with comparable Q̇LEG (19.0 vs. 19.5 L/min) and Q̇C (27.4 vs. 26.2 L/min). Leg vascular conductance was greater during high-intensity running relative to cycling (82 vs. 70 mL/min/mmHg @ ~80% V̇O2peak). The "beat phenomenon" was apparent in femoral flow while running, producing large gradients in conductance (62-90 mL/min/mmHg @ 70% V̇O2peak). In summary, we present the first direct measure of Q̇LEG and conductance in a running human. Our findings corroborate several assumptions about Q̇LEG during running compared with cycling. Importantly, we demonstrate that using thermodilution in running exercise can be completed effectively and safely.

Effect of blood flow restriction and electrical muscle stimulation on human glycemic response to a glucose challenge.

PURPOSE: To determine whether reduced tissue oxygen availability through blood flow restriction (BFR) alone, or in combination with electrically induced muscle contractions, can improve glucose clearance after an acute glucose challenge. METHODS: In a randomized crossover design, 21 young participants (females: 12) were allocated to perform 1) electrical muscle stimulation (EMS), 2) BFR, 3) EMS + BFR or 4) no treatment (control). Participants completed each condition immediately preceding a 2 h oral glucose tolerance test (100 g). Primary analyses were performed on the glucose area under the curve (AUC) at time points 0-30, 30-120, and 0-120 min. Secondary analyses were performed on glycemic responses based on biological sex and estimated muscle phenotype. RESULTS: Compared to the control (322±25 mM∙min), the 0-30 min AUC was reduced following EMS (293±22 mM∙min, p = 0.0004), and EMS + BFR (298±36 mM∙min., p = 0.006), whereas BFR in isolation did not differ (306±30 mM∙min, p = 0.1). The 30-120 and 0-120 min glucose AUCs were similar across conditions. Based on effect size from the control conditions, our secondary analysis suggests different 0-30 min glycemic responses after EMS + BFR between females (dz = 0.206) vs. males (dz = 1.461) and/or slow (dz = 0.426) vs. fast (dz = 1.075) muscle phenotype. CONCLUSION: Reducing tissue oxygen availability with BFR did not augment the effects of EMS in the overall group; however, we provide preliminary data to suggest possible sex and/or muscle phenotypic responses in glycemic regulation with these modalities.

Ergogenic effect of ischemic preconditioning is not directly conferred to isolated skeletal muscle via blood.

PURPOSE: Ischemic preconditioning (IPC) in humans has been demonstrated to confer ergogenic benefit to aerobic exercise performance, with an improvement in the response rate when the IPC stimulus is combined with concurrent exercise. Despite potential performance improvements, the nature of the neuronal and humoral mechanisms of conferral and their respective contributions to ergogenic benefit remain unclear. We sought to examine the effects of the humoral component of ischemic preconditioning on skeletal muscle tissue using preconditioned human serum and isolated mouse soleus. METHODS: Isolated mouse soleus was electrically stimulated to contract while in human serum preconditioned with either traditional (IPC) or augmented (AUG) ischemic preconditioning compared to control (CON) and exercise (ERG) preconditioning. Force frequency (FF) curves, twitch responses, and a fatigue-recovery protocol were performed on muscles before and after the addition of serum. After preconditioning, human participants performed a 4 km cycling time trial in order to identify responders and non-responders to IPC. RESULTS: No differences in indices of contractile function, fatiguability, nor recovery were observed between conditions in mouse soleus muscles. Further, no human participants improved performance in a 4-km cycling time trial in response to traditional nor augmented ischemic preconditioning compared to control or exercise conditions (CON 407.7 ± 41.1 s, IPC 411.6 ± 41.9 s, ERG 408.8 ± 41.4 s, AUG 414.1 ± 41.9 s). CONCLUSIONS: Our findings do not support the conferral of ergogenic benefit via a humoral component of IPC at the intracellular level. Ischemic preconditioning may not manifest prominently at submaximal exercise intensities, and augmented ischemic preconditioning may have a hormetic relationship with performance improvements.

Cardiac Remodeling in Elite Aquatic Sport Athletes.

OBJECTIVE: To characterize and compare the sport-specific cardiac structure of elite swimmers (SW), water polo players (WP), and artistic swimmers (AS). DESIGN: A cross-sectional assessment of elite aquatic athletes' hearts. SETTING: The athletes' village at the 2019 FINA World Championships. PARTICIPANTS: Ninety athletes from swimming (SW) (20 M/17 F), water polo (WP) (21 M/9 F), and artistic swimming (AS) (23 F). ASSESSMENT AND MAIN OUTCOME MEASURES: An echocardiographic assessment of cardiac structure was performed on noncompetition days. RESULTS: Male SW displayed primarily eccentric volume-driven remodeling, whereas male WP had a greater incidence of pressure-driven concentric geometry (SW = 5%, WP = 25%) with elevated relative wall-thickness (RWT) (SW = 0.35 ± 0.04, WP = 0.44 ± 0.08, P < 0.001). Female SW and WP hearts were similar with primarily eccentric-remodeling, but SW and WP had greater concentricity index than artistic swimmers (SW = 6.74 ± 1.45 g/(mL)2/3, WP = 6.80 ± 1.24 g/(mL)2/3, AS = 5.52 ± 1.08 g/(mL)2/3, P = 0.007). AS had normal geometry, but with increased posterior-wall specific RWT (SW = 0.32 ± 0.05, AS = 0.42 ± 0.11, P = 0.004) and greater left atrial area than SW (SW = 9.7 ± 0.9 cm2/m2, AS = 11.0 ± 1.1 cm2/m2, P = 0.003). All females had greater incidence of left ventricular (LV) posterior/septal wall-thickness ≥11 mm than typically reported (SW = 24%, WP = 11%, AS = 17%). CONCLUSIONS: Male athletes presented classic sport-specific differentiation, with SW demonstrating primarily volume-driven eccentric remodelling, and WP with greater concentric geometry indicative of pressure-driven remodeling. Female SW and WP did not display this divergence, likely because of sex-differences in adaptation. AS had unique LV-specific adaptations suggesting elevated pressure under low-volume conditions. The overall incidence of elevated wall-thickness in female athletes may point to an aquatic specific pressure-stress.

Off-Ice Resisted Sprints Best Predict All-Out Skating Performance in Varsity Hockey Players.

ABSTRACT: Thompson, KM, Safadie, A, Ford, J, and Burr, JF. Off-ice resisted sprints best predict all-out skating performance in varsity hockey players. J Strength Cond Res 36(9): 2597-2601, 2022-Off-ice fitness testing is commonly used to predict the physiological abilities of ice-hockey players. Although there is a notable association between certain off-ice tests of jump power and anaerobic capacity with on-ice skating acceleration ( r = 0.3-0.7), it is likely that off-ice tests which more closely resemble the demands of skating will have better predictive ability of this skill. The aim of the current study was to compare the suitability of common off-ice fitness tests and off-ice resisted sprints for predicting 15-m on-ice skate time. Male and female varsity-level hockey players performed a battery of common off-ice fitness tests, resisted sprints, and on-ice 15-m sprints over 3 testing days. At least moderate correlations between off-ice tests and on-ice sprints were observed for all common fitness tests (all p ≤ 0.002): Wingate peak power ( r = -0.65), Wingate fatigue rate ( r = -0.53), vertical jump ( r = -0.52), and broad jump ( r = -0.61), with resisted sprint tests showing the strongest associations (off-ice 15-kg resisted sprint ( r = 0.79) and off-ice 30-kg resisted sprint ( r = 0.74)). In multivariate analysis, stepwise regression revealed the 15-kg resisted sprint as the sole meaningful predictor of on-ice sprint time ( R = 0.79, R2 = 0.62; p ≤ 0.001). We conclude that resisted off-ice sprints have better predictive ability of on-ice skate time compared with commonly used off-ice tests. Resisted sprinting can be used by strength and conditioning staff as an indicator of on-ice acceleration ability during periods of limited access to on-ice facilities or as a component of fitness testing.

Exercise alters cardiac function independent of acute systemic inflammation in healthy men.

Acute elevations in inflammatory cytokines have been demonstrated to increase aortic and left ventricular stiffness and reduce endothelial function in healthy subjects. As vascular and cardiac functions are often transiently reduced following prolonged exercise, it is possible that cytokines released during exercise may contribute to these alterations. The a priori aims of this study were to determine whether vaccine-induced increases in inflammatory cytokines would reduce vascular and left ventricular function, whether vascular alterations would drive cardiac impairments, and whether this would be potentiated by moderate exercise. In a randomized crossover fashion, 16 male participants were tested under control (CON) and inflammatory (INF) conditions, wherein INF testing occurred 8 h following administration of an influenza vaccine. On both days, participants underwent measures of echocardiography performed during light cycling (stress-echocardiography), carotid-femoral pulse wave velocity (cf-PWV), and superficial femoral flow-mediated dilation (FMD) before and after cycling for 90 min at ∼85% of their first ventilatory threshold. IL-6 increased significantly (Δ1.9 ± 1.3 pg/mL, P < 0.001), whereas TNFα was nonsignificantly augmented (Δ0.05 ± 0.11 pg/mL, P = 0.09), 8 h following vaccination. Vascular function was unaltered following cycling or inflammation (all P > 0.05). The use of echocardiography during light cycling revealed cardiac alterations traditionally expected to occur only with greater exercise loads, with reduced systolic (e.g., longitudinal strain CON: Δ3.3 ± 4.4%, INF: Δ1.7 ± 2.7%, P = 0.002) and diastolic function (e.g., E/A ratio CON: Δ-0.32 ± 0.34 a.u., INF:Δ-0.25 ± 0.27 a.u., P = 0.002) following cycling, independent of inflammation. The vaccine reduced stroke volume (SV) (main effect of condition P = 0.009) before-and-after cycling. These findings indicate that reduced cardiac function following exercise occurs largely independent of additional inflammatory load.NEW & NOTEWORHTHY This experimental investigation sought to determine the role of inflammation on the occurrence of cardiovascular alterations following exercise. Despite successfully stimulating systemic inflammation via vaccination, vascular and cardiac functions were largely unaltered. Prolonged exercise itself reduced cardiac function assessed via echocardiography performed during light exercise stress. This demonstrates a potential advantage to using stress-echocardiography for measuring exercise-induced cardiac fatigue, as typical resting measures following similar exercise exposures commonly suggest no effect.

Cardiac autonomic recovery following traditional and augmented remote ischemic preconditioning.

PURPOSE: While the possible ergogenic benefits of remote ischemic preconditioning (RIPC) make it an attractive training modality, the mechanisms of action remain unclear. Alterations in neural tone have been demonstrated in conjunction with circulatory occlusion, yet investigation of the autonomic nervous system following RIPC treatment has received little attention. We sought to characterize alterations in autonomic balance to both RIPC and augmented RIPC (RIPCaug) performed while cycling, using acute and sustained autonomic indices. METHODS: Thirteen participants (8M:5F) recorded baseline waking heart rate variability (HRV) for 5 days prior to treatment. Participants then completed control exercise (CON), RIPC, and RIPCaug interventions in a randomized cross-over design. Cardiovascular measurements were recorded immediately before and after each intervention at rest, and during an orthostatic challenge. Waking HRV was repeated the morning after each intervention. RESULTS: RIPC resulted in acutely reduced resting heart rates (HR) (∆ - 4 ± 6 bpm, P = 0.02) and suppressed HR 30 s following the orthostatic challenge compared to CON (64 ± 10 vs 74 ± 9 bpm, P = 0.003). RIPCaug yielded elevated HRs compared to CON and RIPC prior to (P = 0.003) and during the orthostatic challenge (P = 0.002). RIPCaug reduced LnSDNN (Baseline 4.39 ± 0.27; CON 4.44 ± 0.39; RIPC 4.41 ± 0.34; RIPCaug 4.22 ± 0.29, P = 0.02) and LnHfa power (Baseline 7.82 ± 0.54; CON 7.73 ± 1.11; RIPC 7.89 ± 0.78; RIPCaug 7.23 ± 0.87, P = 0.04) the morning after treatment compared to all other conditions. CONCLUSIONS: Our data suggest that RIPC may influence HR acutely, possibly through a reduction in cardiac sympathetic activity, and that RIPCaug reduces HRV through cardiac vagal withdrawal or increased cardiac sympathetic modulation, with alterations persisting until the following morning. These findings imply a dose-response relationship with potential for optimization of performance.

Examining the relationship between arterial stiffness and swim-training volume in elite aquatic athletes.

PURPOSE: Factors such as prone body position, hydrostatic pressure, and intermittent breath-holding subject aquatic athletes to unique physical and environmental stressors during swimming exercise. The relationship between exposure to aquatic exercise and both arterial stiffness and wave reflection properties is not well-understood. This study assessed central artery stiffness and wave reflection properties in elite pool-swimmers (SW), long-distance open-water swimmers (OW), and water polo players (WP) to examine the relationship between these variables and aquatic exercise. METHODS: Athletes competing in SW, OW and WP events at the FINA World Championships were recruited. Carotid-femoral pulse wave velocity, and pulse wave analysis were used to quantify arterial stiffness, and central wave reflection properties. RESULTS: Athletes undertook differing amounts of weekly swimming distance in training according to their discipline (SW: 40.2 ± 21.1 km, OW: 59.7 ± 28.4 km, WP: 11.4 ± 6.3 km; all p < 0.05). Pulse wave velocity (Males [SW: 6.0 ± 0.6 m/s, OW: 6.5 ± 0.8 m/s, WP: 6.7 ± 0.9 m/s], Females [SW: 5.4 ± 0.6 m/s, OW: 5.3 ± 0.5 m/s, WP: 5.2 ± 0.8 m/s; p = 0.4]) was similar across disciplines for females but was greater in male WP compared to male SW (p = 0.005). Augmentation index (Males [SW: - 3.4 ± 11%, OW: - 9.6 ± 6.4%, WP: 1.7 ± 10.9%], Females [SW: 3.5 ± 13.5%, OW: - 13.2 ± 10.7%, WP: - 2.8 ± 10.7%]) was lower in male OW compared to WP (p = 0.03), and higher in female SW compared to OW (p = 0.002). Augmentation index normalized to a heart rate of 75 bpm was inversely related to weekly swim distance in training (r = - 0.27, p = 0.004). CONCLUSIONS: This study provides evidence that the central vasculature of elite aquatic athletes differs by discipline, and this is associated with training load.

Blood flow restriction in the presence or absence of muscle contractions does not preserve vasculature structure and function following 14-days of limb immobilization.

PURPOSE: 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). METHODS: 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). RESULTS: 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 < 0.01); however, there were no differences by group or across time for FMD (% diameter change, shear-corrected, or allometrically scaled) nor microvascular function assessed by peak flow capacity. CONCLUSION: Following immobilization, our results reveal (1) neither BFR nor BFR + EMS mitigate artery structure impairments, (2) intervention-induced shear stress did not affect vascular function assessed by FMD, and (3) retrograde blood velocity is reduced at rest offering potential insight to mechanisms of flow regulation. In conclusion, BFR appears insufficient as a treatment strategy for preventing macrovascular dysfunction during limb immobilization.

A Review of Nonpharmacological Strategies in the Treatment of Relative Energy Deficiency in Sport.

Relative energy deficiency in sport (RED-S) can result in negative health and performance outcomes in both male and female athletes. The underlying etiology of RED-S is low energy availability (LEA), which occurs when there is insufficient dietary energy intake to meet exercise energy expenditure, corrected for fat-free mass, leaving inadequate energy available to ensure homeostasis and adequate energy turnover (optimize normal bodily functions to positively impact health), but also optimizing recovery, training adaptations, and performance. As such, treatment of RED-S involves increasing energy intake and/or decreasing exercise energy expenditure to address the underlying LEA. Clinically, however, the time burden and methodological errors associated with the quantification of energy intake, exercise energy expenditure, and fat-free mass to assess energy availability in free-living conditions make it difficult for the practitioner to implement in everyday practice. Furthermore, interpretation is complicated by the lack of validated energy availability thresholds, which can result in compromised health and performance outcomes in male and female athletes across various stages of maturation, ethnic races, and different types of sports. This narrative review focuses on pragmatic nonpharmacological strategies in the treatment of RED-S, featuring factors such as low carbohydrate availability, within-day prolonged periods of LEA, insufficient intake of bone-building nutrients, lack of mechanical bone stress, and/or psychogenic stress. This includes the implementation of strategies that address exacerbating factors of LEA, as well as novel treatment methods and underlying mechanisms of action, while highlighting areas of further research.

Moderate Load Resisted Sprints Do Not Improve Subsequent Sprint Performance in Varsity-Level Sprinters.

ABSTRACT: Thompson, K, Whinton, AK, Ferth, S, Spriet, LL, and Burr, JF. Moderate load resisted sprints do not improve subsequent sprint performance in varsity-level sprinters. J Strength Cond Res 35(1): 72-77, 2021-Resisted sprint training (RST) is commonly used for performance enhancement in athletics and team sports to develop acceleration ability. Evidence suggests that RST may be effective as a short-term intervention to improve successive sprints. Although these improvements have been measured in team sport athletes, limited research has considered the acute effects of RST training in sprint-trained athletes. Therefore, the aim of the current study was to determine whether performing RST with varsity-level sprinters using sled-equivalent resistive loads of ∼45% body mass results in a potentiation effect, leading to improvements in subsequent maximal sprint performance over 0-5 m and 0-20 m. Competitive sprinters (n = 20) were randomly assigned to perform a pre/post maximal 20-m sprint separated by either 3 resisted (RST group) or unresisted (URS group) sprints. The RST or URS protocol was performed on 4 occasions separated by at least 7 days. No significant differences were observed between the RST and URS groups comparing changes in sprint times over 0-5 m (URS Δ <0.01 ± 0.03 seconds, RST Δ <0.01 ± 0.03 seconds) and 0-20 m (URS Δ 0.013 ± 0.04 seconds, RST Δ <0.01 ± 0.04 seconds). We conclude that resisted sprints using sled-equivalent loads of 45% body mass are ineffective at inducing a potentiating effect on subsequent sprint performance in varsity-level sprinters. In this population of trained athletes, greater loads may be necessary to induce a potentiating effect.

Repetition Failure Occurs Earlier During Low-Load Resistance Exercise With High But Not Low Blood Flow Restriction Pressures: A Systematic Review and Meta-analysis.

ABSTRACT: Cerqueira, MS, Lira, M, Mendonça Barboza, JA, Burr, JF, Wanderley e Lima, TB, Maciel, DG, and De Brito Vieira, WH. Repetition failure occurs earlier during low-load resistance exercise with high but not low blood flow restriction pressures: a systematic review and meta-analysis. J Strength Cond Res XX(X): 000-000, 2021-High-load and low-load resistance training (LL-RT) performed to failure are considered effective for improving muscle mass and strength. Alternatively, LL-RT with blood flow restriction (LL-BFR) may accelerate repetition failure and has been suggested to be more time efficient than LL-RT. This study explores the evidence for the effects of LL-BFR vs. LL-RT on repetition failure. A systematic literature search was conducted in the PubMed, CINAHL, Web of Science, CENTRAL, Scopus, SPORTDiscus, and PEDro databases. Meta-analyses of mean differences and 95% confidence intervals (CIs) were performed using a random-effects model. Subgroup analyses were conducted for both the high and low blood flow restriction pressures. The search identified n = 10 articles that met the inclusion criteria. The meta-analysis comprised a total of 218 healthy subjects. Low-load resistance training with blood flow restriction with high pressures (≥50% arterial occlusion pressure [AOP]) precipitate repetition failure in ∼14.5 fewer repetitions (95% CI -19.53 to -9.38) compared with LL-RT, whereas the use of low pressures (<50% AOP) stimulated repetition failure with ∼1.4 fewer repetitions (95% CI -3.11 to 0.37); however, this difference was not statistically significant. Repetition failure has been demonstrated to be an important normalizing variable when comparing the hypertrophic and strength effects resulting from resistance training and occurs earlier during low-load resistance exercise with high but not low blood flow restriction pressures.

In vitro ketone-supported mitochondrial respiration is minimal when other substrates are readily available in cardiac and skeletal muscle.

KEY POINTS: Ketone bodies are proposed to represent an alternative fuel source driving energy production, particularly during exercise. Biologically, the extent to which mitochondria utilize ketone bodies compared to other substrates remains unknown. We demonstrate in vitro that maximal mitochondrial respiration supported by ketone bodies is low when compared to carbohydrate-derived substrates in the left ventricle and red gastrocnemius muscle from rodents, and in human skeletal muscle. When considering intramuscular concentrations of ketone bodies and the presence of other carbohydrate and lipid substrates, biological rates of mitochondrial respiration supported by ketone bodies are predicted to be minimal. At the mitochondrial level, it is therefore unlikely that ketone bodies are an important source for energy production in cardiac and skeletal muscle, particularly when other substrates are readily available. ABSTRACT: Ketone bodies (KB) have recently gained popularity as an alternative fuel source to support mitochondrial oxidative phosphorylation and enhance exercise performance. However, given the low activity of ketolytic enzymes and potential inhibition from carbohydrate oxidation, it remains unknown if KBs can contribute to energy production. We therefore determined the ability of KBs (sodium dl-ß-hydroxybutyrate, ß-HB; lithium acetoacetate, AcAc) to stimulate in vitro mitochondrial respiration in the left ventricle (LV) and red gastrocnemius (RG) of rats, and in human vastus lateralis. Compared to pyruvate, the ability of KBs to maximally drive respiration was low in isolated mitochondria and permeabilized fibres (PmFb) from the LV (∼30-35% of pyruvate), RG (∼10-30%), and human vastus lateralis (∼2-10%). In PmFb, the concentration of KBs required to half-maximally drive respiration (LV: 889 µm ß-HB, 801 µm AcAc; RG: 782 µm ß-HB, 267 µm AcAc) were greater than KB content representative of the muscle microenvironment (∼100 µm). This would predict low rates (∼1-4% of pyruvate) of biological KB-supported respiration in the LV (8-14 pmol s-1 mg-1 ) and RG (3-6 pmol s-1 mg-1 ) at rest and following exercise. Moreover, KBs did not increase respiration in the presence of saturating pyruvate, submaximal pyruvate (100 µm) reduced the ability of physiological ß-HB to drive respiration, and addition of other intracellular substrates (succinate + palmitoylcarnitine) decreased maximal KB-supported respiration. As a result, product inhibition is likely to limit KB oxidation. Altogether, the ability of KBs to drive mitochondrial respiration is minimal and they are likely to be outcompeted by other substrates, compromising their use as an important energy source.

Low-load resistance training to task failure with and without blood flow restriction: muscular functional and structural adaptations.

The application of blood flow restriction (BFR) during resistance exercise is increasingly recognized for its ability to improve rehabilitation and for its effectiveness in increasing muscle hypertrophy and strength among healthy populations. However, direct comparison of the skeletal muscle adaptations to low-load resistance exercise (LL-RE) and low-load BFR resistance exercise (LL-BFR) performed to task failure is lacking. Using a within-subject design, we examined whole muscle group and skeletal muscle adaptations to 6 wk of LL-RE and LL-BFR training to repetition failure. Muscle strength and size outcomes were similar for both types of training, despite ~33% lower total exercise volume (load × repetition) with LL-BFR than LL-RE (28,544 ± 1,771 vs. 18,949 ± 1,541 kg, P = 0.004). After training, only LL-BFR improved the average power output throughout the midportion of a voluntary muscle endurance task. Specifically, LL-BFR training sustained an 18% greater power output from baseline and resulted in a greater change from baseline than LL-RE (19 ± 3 vs. 3 ± 4 W, P = 0.008). This improvement occurred despite histological analysis revealing similar increases in capillary content of type I muscle fibers following LL-RE and LL-BFR training, which was primarily driven by increased capillary contacts (4.53 ± 0.23 before training vs. 5.33 ± 0.27 and 5.17 ± 0.25 after LL-RE and LL-BFR, respectively, both P < 0.05). Moreover, maximally supported mitochondrial respiratory capacity increased only in the LL-RE leg by 30% from baseline (P = 0.006). Overall, low-load resistance training increased indexes of muscle oxidative capacity and strength, which were not further augmented with the application of BFR. However, performance on a muscle endurance test was improved following BFR training.

The Effect of a Stretch-Shortening Cycle on Muscle Activation and Muscle Oxygen Consumption: A Study of History-Dependence.

Caron, KE, Burr, JF, and Power, GA.. The effect of a stretch-shortening cycle on muscle activation and muscle oxygen consumption: a study of history-dependence. J Strength Cond Res 34(11): 3139-3148, 2020-Stretch-shortening cycles (SSCs) are observed in a variety of human movements and are associated with increases in performance. Few studies have considered the effects of stretch-induced residual force enhancement (rFE) and shortening-induced residual force depression (rFD) during an SSC, and none have considered these properties during voluntary contractions. With force matched via a robotically resisted Smith machine, we hypothesized that in the isometric steady-state following an SSC (a) muscle activation (electromyography) of the knee and hip extensors would be greater and (b) muscle oxygen consumption be higher than the reference isometric condition (ISO), but less than the rFD condition. Subjects (n = 20, male, 24.9 ± 3.9 year) performed a squat exercise over 100-140° knee angle and a matched ISO at the top and bottom of the squat. After active shortening, the vastus medialis (VM), vastus lateralis (VL), and gluteus maximus (GM) showed activation increase in the rFD-state compared with ISO (∼15%, ∼11%, and ∼25% respectively). During the isometric steady-state following the SSC, there was no difference in activation as compared with ISO for VM, VL, but GM showed an activation increase of ∼15%. VM and VL showed an activation increase in the rFD-state compared with the isometric steady-state following SSC (∼16 and ∼10% respectively). Muscle oxygen consumption (tissue saturation index) was not different during the isometric steady-states following rFD and SSC compared with ISO. During a voluntary SSC exercise, the activation increase expected in the FD-state was attenuated, with no change in muscle oxygen consumption. The concomitant role of rFE and rFD during a voluntary position-matched SSC seems to counteract shortening-induced activation increase and may optimize movement economy.

Repeated Application of a Novel Creatine Cream Improves Muscular Peak and Average Power in Male Subjects.

Whinton, AK, Donahoe, K, Gao, R, Thompson, KMA, Aubry, R, Saunders, TJ, Johnston, A, Chilibeck, PD, and Burr, JF. Repeated application of a novel creatine cream improves muscular peak and average power in male subjects. J Strength Cond Res 34(9): 2482-2491, 2020-Using a multicenter, randomized controlled trial, (N = 123, age 23 ± 4 years) we sought to determine whether administration of a novel, topical creatine supplement could improve muscular performance after acute and repeated (7-day) exposure. To study the acute performance enhancing effects of the supplement, subjects completed 5 sets of 15 maximal concentric single-leg knee extensions with and without the application of a low- (low dose [LD]-3.5 ml) or high-dose (high dose [HD]-7 ml) topical creatine cream. After a wash-out period, subjects had one leg randomized to receive either the creatine or placebo cream, with further randomization into an oral creatine or placebo supplement group. Subjects completed 5 sets of 15 maximal concentric single leg knee extensions before and after the supplementation protocol. After acute application, no significant differences in peak power (LD: 252 ± 93 W, HD: 261 ± 100 W, p = 0.21), average power (LD: 172 ± 65 W, HD: 177 ± 69 W, p = 0.78), or fatigue index (LD: 13.4 ± 10.6%, HD: 14 ± 11.9%, p = 0.79) were observed between experimental and placebo creams (peak power: LD: 244 ± 76 W, HD: 267 ± 109 W; average power: LD: 168 ± 57 W, HD: 177 ± 67 W; fatigue index: LD: 12.4 ± 9.6%, HD: 12.8 ± 10.6%) or when controlling for sex. After the 7-day supplementation protocol, a significant increase in average power (creatine: 203 ± 61-220 ± 65 W, placebo: 224 ± 61-214 ± 61 W) and peak power (creatine: 264 ± 73-281 ± 80 W, placebo: 286 ± 79-271 ± 73 W) in the leg receiving creatine cream was observed in male subjects. No differences were observed in female subjects. The topical creatine cream did not enhance measures of muscle performance after acute application, but was able to improve peak and average power in male subjects after 7 consecutive days of application.

Blood flow restricted resistance exercise and reductions in oxygen tension attenuate mitochondrial H2 O2 emission rates in human skeletal muscle.

KEY POINTS: Blood flow restricted resistance exercise (BFR-RE) is capable of inducing comparable adaptations to traditional resistance exercise (RE), despite a lower total exercise volume. It has been suggested that an increase in reactive oxygen species (ROS) production may be involved in this response; however, oxygen partial pressure ( PO2 ) is reduced during BFR-RE, and the influence of PO2 on mitochondrial redox balance remains poorly understood. In human skeletal muscle tissue, we demonstrate that both maximal and submaximal mitochondrial ROS emission rates are acutely decreased 2 h following BFR-RE, but not RE, occurring along with a reduction in tissue oxygenation during BFR-RE. We further suggest that PO2 is involved in this response because an in vitro analysis revealed that reducing PO2 dramatically decreased mitochondrial ROS emissions and electron leak to ROS. Altogether, these data indicate that mitochondrial ROS emission rates are attenuated following BFR-RE, and such a response is likely influenced by reductions in PO2 . ABSTRACT: Low-load blood flow restricted resistance exercise (BFR-RE) training has been proposed to induce comparable adaptations to traditional resistance exercise (RE) training, however, the acute signalling events remain unknown. Although a suggested mechanism of BFR-RE is an increase in reactive oxygen species (ROS) production, oxygen partial pressure ( PO2 ) is reduced during BFR-RE, and the influence of O2 tension on mitochondrial redox balance remains ambiguous. We therefore aimed to determine whether skeletal muscle mitochondrial bioenergetics were altered following an acute bout of BFR-RE or RE, and to further examine the role of PO2 in this response. Accordingly, muscle biopsies were obtained from 10 males at rest and 2 h after performing three sets of single-leg squats (RE or BFR-RE) to failure at 30% one-repetition maximum. We determined that mitochondrial respiratory capacity and ADP sensitivity were not altered in response to RE or BFR-RE. Although maximal (succinate) and submaximal (non-saturating ADP) mitochondrial ROS emission rates were unchanged following RE, BFR-RE attenuated these responses by ∼30% compared to pre-exercise, occurring along with a reduction in skeletal muscle tissue oxygenation during BFR-RE (P < 0.01 vs. RE). In a separate cohort of participants, evaluation of mitochondrial bioenergetics in vitro revealed that mild O2 restriction (50 µm) dramatically attenuated maximal (∼4-fold) and submaximal (∼50-fold) mitochondrial ROS emission rates and the fraction of electron leak to ROS compared to room air (200 µm). Combined, these data demonstrate that mitochondrial ROS emissions are attenuated following BFR-RE, a response which may be mediated by a reduction in skeletal muscle PO2 .