Acute physiological responses of blood flow restriction between high-intensity interval repetitions in trained cyclists.

Blood flow restriction (BFR) is increasingly being used to enhance aerobic performance in endurance athletes. This study examined physiological responses to BFR applied in recovery phases within a high-intensity interval training (HIIT) session in trained cyclists. Eleven competitive road cyclists (mean ± SD, age: 28 ± 7 years, body mass: 69 ± 6 kg, peak oxygen uptake: 65 ± 9 mL · kg-1 · min-1) completed two randomised crossover conditions: HIIT with (BFR) and without (CON) BFR applied during recovery phases. HIIT consisted of six 30-s cycling bouts at an intensity equivalent to 85% of maximal 30-s power (523 ± 93 W), interspersed with 4.5-min recovery. BFR (200 mmHg, 12 cm cuff width) was applied for 2-min in the early recovery phase between each interval. Pulmonary gas exchange (V̇O2, V̇CO2, and V̇E), tissue oxygen saturation index (TSI), heart rate (HR), and serum vascular endothelial growth factor concentration (VEGF) were measured. Compared to CON, BFR increased V̇CO2 and V̇E during work bouts (both p < 0.05, dz < 0.5), but there was no effect on V̇O2, TSI, or HR (p > 0.05). In early recovery, BFR decreased TSI, V̇O2, V̇CO2, and V̇E (all p < 0.05, dz > 0.8) versus CON, with no change in HR (p > 0.05). In late recovery, when BFR was released, V̇O2, V̇CO2, V̇E, and HR increased, but TSI decreased versus CON (all p < 0.05, dz > 0.8). There was a greater increase in VEGF at 3-h post-exercise in BFR compared to CON (p < 0.05, dz > 0.8). Incorporating BFR into HIIT recovery phases altered physiological responses compared to exercise alone.

Skeletal muscle mitochondrial correlates of critical power and W' in healthy active individuals.

The asymptote (critical power; CP) and curvature constant (W') of the hyperbolic power-duration relationship can predict performance within the severe-intensity exercise domain. However, the extent to which these parameters relate to skeletal muscle mitochondrial content and respiratory function is not known. Fifteen males (peak O2 uptake, 52.2 ± 8.7 mL kg-1 min-1; peak work rate, 366 ± 40 W; and gas exchange threshold, 162 ± 41 W) performed three to five constant-load tests to task failure for the determination of CP (246 ± 44 W) and W' (18.6 ± 4.1 kJ). Skeletal muscle biopsies were obtained from the vastus lateralis to determine citrate synthase (CS) activity, as a marker of mitochondrial content, and the ADP-stimulated respiration (P) and maximal electron transfer (E) through mitochondrial complexes (C) I-IV. The CP was positively correlated with CS activity (absolute CP, r = 0.881, P < 0.001; relative CP, r = 0.751, P = 0.001). The W' was not correlated with CS activity (P > 0.05). Relative CP was positively correlated with mass-corrected CI + IIE (r = 0.659, P = 0.038), with absolute CP being inversely correlated with CS activity-corrected CIVE (r = -0.701, P = 0.024). Relative W' was positively correlated with CS activity-corrected CI + IIP (r = 0.713, P = 0.021) and the phosphorylation control ratio (r = 0.661, P = 0.038). There were no further correlations between CP or W' and mitochondrial respiratory variables. These findings support the assertion that skeletal muscle mitochondrial oxidative capacity is positively associated with CP and that this relationship is strongly determined by mitochondrial content.

Modelling human endurance: power laws vs critical power.

The power-duration relationship describes the time to exhaustion for exercise at different intensities. It is believed to be a "fundamental bioenergetic property of living systems" that this relationship is hyperbolic. Indeed, the hyperbolic (a.k.a. critical-power) model which formalises this belief is the dominant tool for describing and predicting high-intensity exercise performance, e.g. in cycling, running, rowing or swimming. However, the hyperbolic model is now the focus of a heated debate in the literature because it unrealistically represents efforts that are short (< 2 min) or long (> 15 min). We contribute to this debate by demonstrating that the power-duration relationship is more adequately represented by an alternative, power-law model. In particular, we show that the often-observed good fit of the hyperbolic model between 2 and 15 min should not be taken as proof that the power-duration relationship is hyperbolic. Rather, in this range, a hyperbolic function just happens to approximate a power law fairly well. We also prove mathematical results which suggest that the power-law model is a safer tool for pace selection than the hyperbolic model and that the former more naturally models fatigue than the latter.

Impacts of Eccentric Resistance Exercise on DNA Methylation of Candidate Genes for Inflammatory Cytokines in Skeletal Muscle and Leukocytes of Healthy Males.

Physical inactivity and a poor diet increase systemic inflammation, while chronic inflammation can be reduced through exercise and nutritional interventions. The mechanisms underlying the impacts of lifestyle interventions on inflammation remain to be fully explained; however, epigenetic modifications may be critical. The purpose of our study was to investigate the impacts of eccentric resistance exercise and fatty acid supplementation on DNA methylation and mRNA expression of TNF and IL6 in skeletal muscle and leukocytes. Eight non-resistance exercise-trained males completed three bouts of isokinetic eccentric contractions of the knee extensors. The first bout occurred at baseline, the second occurred following a three-week supplementation of either omega-3 polyunsaturated fatty acid or extra virgin olive oil and the final bout occurred after eight-weeks of eccentric resistance training and supplementation. Acute exercise decreased skeletal muscle TNF DNA methylation by 5% (p = 0.031), whereas IL6 DNA methylation increased by 3% (p = 0.01). Leukocyte DNA methylation was unchanged following exercise (p > 0.05); however, three hours post-exercise the TNF DNA methylation decreased by 2% (p = 0.004). In skeletal muscle, increased TNF and IL6 mRNA expression levels were identified immediately post-exercise (p < 0.027); however, the leukocyte mRNA expression was unchanged. Associations between DNA methylation and markers of exercise performance, inflammation and muscle damage were identified (p < 0.05). Acute eccentric resistance exercise is sufficient to induce tissue-specific DNA methylation modifications to TNF and IL6; however, neither eccentric training nor supplementation was sufficient to further modify the DNA methylation.

Calf blood flow is augmented in habitually aerobically trained versus untrained postmenopausal women in association with favorable modulation of vasculo-metabolic interactions.

INTRODUCTION: Menopause is associated with vascular dysfunction and increased risk of developing metabolic syndrome. Associations between vascular and metabolic health, and interactions with aerobic exercise training, are unknown in postmenopausal women (PMW). METHODS: In habitually aerobically trained PMW (PMWtr; n = 10; 57 ± 1 years; 40 ± 1 mL/kg/min), strain-gauge plethysmography was used to compare resting and peak calf blood flow (CBFr and CBFpk, respectively) and vascular resistance (CVRr; CVRpk) versus untrained PMW (PMWun; n = 13; 56 ± 1 years; 29 ± 1 mL/kg/min) and premenopausal women (PreM; n = 14; 26 ± 1 years; 40 ± 1 mL/kg/min). Vascular measures were taken before and 1 hour after 45 minutes of aerobic exercise (60% V̇ O2peak ), a known nitric oxide stimulus. Blood analyses included low- (LDLc) and high-density lipoprotein cholesterol (HDLc), insulin, and glucose. RESULTS: Pre-exercise, CBFr and CVRr did not differ (p > 0.05) between PMW groups, nor between PreM and PMWtr. CBFpk was highest (p < 0.05) and CVRpk was lowest (p < 0.05) in PMWtr. Blood markers were similar (p > 0.05) in PMW groups. However, in PMWtr, CBFpk was associated inversely (p < 0.05) with insulin (r = -0.725). Conversely, in PMWun, CBFpk correlated (p < 0.05) inversely with glucose (r = -0.717), positively with HDLc (r = 0.633), and CVRpk positively (p < 0.05) with LDLc (r = 0.568). Post-exercise, CBF increased and CVR decreased (p < 0.05) in all groups, yet CBFpk remained higher and CVRpk lower (p < 0.05) in PMWtr. CONCLUSION: In untrained PMW, peak CBF is associated inversely with circulating pro-atherogenic lipids and glucose. In contrast, peak CBF is associated inversely with insulin levels only in trained PMW. Habitual aerobic exercise may favorably modulate vasculo-metabolic interactions in PMW.

Critical Power, Work Capacity, and Recovery Characteristics of Team-Pursuit Cyclists.

PURPOSE: Leading a 4-km team pursuit (TP) requires high-intensity efforts above critical power (CP) that deplete riders' finite work capacity (W'), whereas riders following in the aerodynamic draft may experience some recovery due to reduced power demands. This study aimed to determine how rider ability and CP and W' measures impact TP performance and the extent to which W' can reconstitute during recovery positions in a TP race. METHODS: Three TP teams, each consisting of 4 males, completed individual performance tests to determine their CP and W'. Teams were classified based on their performance level as international (INT), national (NAT), or regional (REG). Each team performed a TP on an indoor velodrome (INT: 3:49.9; NAT: 3:56.7; and REG: 4:05.4; min:s). Ergometer-based TP simulations with an open-ended interval to exhaustion were performed to measure individual ability to reconstitute W' at 25 to 100 W below CP. RESULTS: The INT team possessed higher CP (407 [4] W) than both NAT (381 [13] W) and REG (376 [15] W) (P < .05), whereas W' was similar between teams (INT: 27.2 [2.8] kJ; NAT: 29.3 [2.4] kJ; and REG: 28.8 [1.6] kJ; P > .05). The INT team expended 104% (5%) of their initial W' during the TP and possessed faster rates of recovery than NAT and REG at 25 and 50 W below CP (P < .05). CONCLUSIONS: The CP and rate of W' reconstitution have a greater impact on TP performance than W' magnitude and can differentiate TP performance level.

Ischaemic preconditioning blunts exercise-induced mitochondrial dysfunction, speeds oxygen uptake kinetics but does not alter severe-intensity exercise capacity.

NEW FINDINGS: What is the central question of this study? Ischaemic preconditioning is a novel pre-exercise priming strategy. We asked whether ischaemic preconditioning would alter mitochondrial respiratory function and pulmonary oxygen uptake kinetics and improve severe-intensity exercise performance. What is the main finding and its importance? Ischaemic preconditioning expedited overall pulmonary oxygen uptake kinetics and appeared to prevent an increase in leak respiration, proportional to maximal electron transfer system and ADP-stimulated respiration, that was evoked by severe-intensity exercise in sham-control conditions. However, severe-intensity exercise performance was not improved. The results do not support ischaemic preconditioning as a pre-exercise strategy to improve exercise performance in recreationally active participants. ABSTRACT: We examined the effect of ischaemic preconditioning (IPC) on severe-intensity exercise performance, pulmonary oxygen uptake ( V ̇ O 2 ${\dot V_{{{\rm{O}}_{\rm{2}}}}}$ ) kinetics, skeletal muscle oxygenation (muscle tissue O2 saturation index) and mitochondrial respiration. Eight men underwent contralateral IPC (4 × 5 min at 220 mmHg) or sham-control (SHAM; 20 mmHg) before performing a cycling time-to-exhaustion test (92% maximum aerobic power). Muscle (vastus lateralis) biopsies were obtained before IPC or SHAM and ∼1.5 min postexercise. The time to exhaustion did not differ between SHAM and IPC (249 ± 37 vs. 240 ± 32 s; P = 0.62). Pre- and postexercise ADP-stimulated (P) and maximal (E) mitochondrial respiration through protein complexes (C) I, II and IV did not differ (P > 0.05). Complex I leak respiration was greater postexercise compared with baseline in SHAM, but not in IPC, when normalized to wet mass (P = 0.01 vs. P = 0.19), mitochondrial content (citrate synthase activity, P = 0.003 vs. P = 0.16; CI+IIP, P = 0.03 vs. P = 0.23) and expressed relative to P (P = 0.006 vs. P = 0.30) and E (P = 0.004 vs. P = 0.26). The V ̇ O 2 ${\dot V_{{{\rm{O}}_{\rm{2}}}}}$ mean response time was faster (51.3 ± 15.5 vs. 63.7 ± 14.5 s; P = 0.003), with a smaller slow component (270 ± 105 vs. 377 ± 188 ml min-1 ; P = 0.03), in IPC compared with SHAM. The muscle tissue O2 saturation index did not differ between trials (P > 0.05). Ischaemic preconditioning expedited V ̇ O 2 ${\dot V_{{{\rm{O}}_{\rm{2}}}}}$ kinetics and appeared to prevent an increase in leak respiration through CI, when expressed proportional to E and P evoked by severe-intensity exercise, but did not improve exercise performance.

Disturbance of desire-goal motivational dynamics during different exercise intensity domains.

PURPOSE: The desire-goal motivational conflict helps explain endurance performance; however, the physiological concomitants are unknown. The present study examined disturbances in desire to reduce effort and performance goal value across moderate, heavy, and severe exercise intensity domains, demarcated by the first (LT1) and second (LT2) lactate thresholds. In addition, the within-person relationships among blood lactate concentration, heart rate, and desire-goal conflict were examined. METHODS: Thirty participants (53% female, Mage  = 21.03 years; SD = 2.06 years) completed an incremental cycling exercise test, in which work rate was increased by 25 watts every four minutes, until voluntary exhaustion or sufficient data from the severe intensity domain had been collected. Desire to reduce effort, performance goal value, blood lactate concentration (for determination of LT1 and LT2), and heart rate were measured at the end of each stage and analyzed using multilevel models. RESULTS: The desire to reduce effort increased over the exercise test with additional shifts and accelerations after each lactate threshold. The performance goal did not show general declines, nor did it shift at LT1. However, the performance goal value shifted at LT2, and the rate of change increased at both thresholds. Within-person variation in blood lactate concentration positively correlated with the desire to reduce effort and negatively correlated with the performance goal. Within-person variation in heart rate correlated with desire to reduce effort but not the performance goal. CONCLUSION: Transitioning through both lactate thresholds is important phases for motivation during progressive exercise, particularly for the desire to reduce effort. Within-person variation in blood lactate concentration is more influential for motivation, compared with heart rate.

Lack of Predictive Power in Commonly Used Tests for Performance in Alpine Skiing.

Competitive alpine skiing is a complex sport that requires high physical and technical competence. Testing the physical status of athletes may be important to increase their ability to achieve elite sport-specific performance. This study aimed to investigate the predictive power of the national test battery of the Swedish Olympic Committee (Fysprofilen) and anthropometric variables in the prediction of competitive performance of elite alpine skiers, indicated by Fédération Internationale de Ski points. Data from fourteen Swedish elite female alpine skiers were analyzed using bivariate and multivariate statistical methods. Physiological test results and anthropometric data could not generate significant bivariate or multivariate models for prediction of competitive performance. Multivariate regression (R2) and prediction (Q2) models for Fédération Internationale de Ski Slalom and Giant Slalom rank reached R2=0.27 to 0.43, Q2=+- 0.8 to-0.17, indicating no valid models. The overall interpretation of these and previous findings are that future test batteries must be validated before implemented, and that test results should be treated with caution when it comes to prediction of future competitive results. Applying tests that are not validated against competitive performance risk misleading coaches and training advisors who aim to increase the sports-specific performance of the individual athlete.

Blood-flow-restricted exercise: Strategies for enhancing muscle adaptation and performance in the endurance-trained athlete.

NEW FINDINGS: What is the topic of this review? Blood-flow-restricted (BFR) exercise represents a potential approach to augment the adaptive response to training and improve performance in endurance-trained individuals. What advances does it highlight? When combined with low-load resistance exercise, low- and moderate-intensity endurance exercise and sprint interval exercise, BFR can provide an augmented acute stimulus for angiogenesis and mitochondrial biogenesis. These augmented acute responses can translate into enhanced capillary supply and mitochondrial function, and subsequent endurance-type performance, although this might depend on the nature of the exercise stimulus. There is a requirement to clarify whether BFR training interventions can be used by high-performance endurance athletes within their structured training programme. ABSTRACT: A key objective of the training programme for an endurance athlete is to optimize the underlying physiological determinants of performance. Training-induced adaptations are governed by physiological and metabolic stressors, which initiate transcriptional and translational signalling cascades to increase the abundance and/or function of proteins to improve physiological function. One important consideration is that training adaptations are reduced as training status increases, which is reflected at the molecular level as a blunting of the acute signalling response to exercise. This review examines blood-flow-restricted (BFR) exercise as a strategy for augmenting exercise-induced stressors and subsequent molecular signalling responses to enhance the physiological characteristics of the endurance athlete. Focus is placed on the processes of capillary growth and mitochondrial biogenesis. Recent evidence supports that BFR exercise presents an intensified training stimulus beyond that of performing the same exercise alone. We suggest that this has the potential to induce enhanced physiological adaptations, including increases in capillary supply and mitochondrial function, which can contribute to an improvement in performance of endurance exercise. There is, however, a lack of consensus regarding the potency of BFR training, which is invariably attributable to the different modes, intensities and durations of exercise and BFR methods. Further studies are needed to confirm its potential in the endurance-trained athlete.

Submaximal Eccentric Cycling in People With COPD: Acute Whole-Body Cardiopulmonary and Muscle Metabolic Responses.

BACKGROUND: Eccentric cycling (ECC) may be an attractive exercise method in COPD because of both low cardiorespiratory demand and perception of effort compared with conventional concentric cycling (CON) at matched mechanical loads. However, it is unknown whether ECC can be performed by individuals with COPD at an intensity able to cause sufficient metabolic stress to improve aerobic capacity. RESEARCH QUESTION: What are the cardiopulmonary and metabolic responses to ECC in people with COPD and healthy volunteers when compared with CON at matched mechanical loads? STUDY DESIGN AND METHODS: Thirteen people with COPD (mean ± SD age, 64 ± 9 years; FEV1, 45 ± 19% predicted; BMI, 24 ± 4 kg/m2; oxygen uptake at peak exercise [V̇O2peak], 15 ± 3 mL/kg/min) and 9 age-matched control participants (FEV1, 102 ± 13% predicted; BMI, 28 ± 5 kg/m2; V̇O2peak, 23 ± 5 mL/kg/min), performed up to six 4-min bouts of ECC and CON at matched mechanical loads of increasing intensity. In addition, 12 individuals with COPD underwent quadriceps muscle biopsies before and after 20 min of ECC and CON at 65% peak power. RESULTS: At matched mechanical loads, oxygen uptake, minute ventilation, heart rate, systolic BP, respiratory exchange ratio (all P < .001), capillary lactate, perceived breathlessness, and leg fatigue (P < .05) were lower in both groups during ECC than CON. Muscle lactate content increased (P = .008) and muscle phosphocreatine decreased (P = .012) during CON in COPD, which was not evident during ECC. INTERPRETATION: Cardiopulmonary and blood lactate responses during submaximal ECC were less compared with during CON at equivalent mechanical workloads in healthy participants and COPD patients, and this was confirmed at a muscle level in COPD patients. Submaximal ECC was well tolerated and allowed greater mechanical work at lower ventilatory cost. However, in people with COPD, a training intervention based on ECC is unlikely to stimulate cardiovascular and metabolic adaptation to the same extent as CON.

Characterising hyperinsulinemia-induced insulin resistance in human skeletal muscle cells.

Hyperinsulinaemia potentially contributes to insulin resistance in metabolic tissues, such as skeletal muscle. The purpose of these experiments was to characterise glucose uptake, insulin signalling and relevant gene expression in primary human skeletal muscle-derived cells (HMDCs), in response to prolonged insulin exposure (PIE) as a model of hyperinsulinaemia-induced insulin resistance. Differentiated HMDCs from healthy human donors were cultured with or without insulin (100 nM) for 3 days followed by an acute insulin stimulation. HMDCs exposed to PIE were characterised by impaired insulin-stimulated glucose uptake, blunted IRS-1 phosphorylation (Tyr612) and Akt (Ser473) phosphorylation in response to an acute insulin stimulation. Glucose transporter 1 (GLUT1), but not GLUT4, mRNA and protein increased following PIE. The mRNA expression of metabolic (PDK4) and inflammatory markers (TNF-α) was reduced by PIE but did not change lipid (SREBP1 and CD36) or mitochondrial (UCP3) markers. These experiments provide further characterisation of the effects of PIE as a model of hyperinsulinaemia-induced insulin resistance in HMDCs.

High-Fat Overfeeding Impairs Peripheral Glucose Metabolism and Muscle Microvascular eNOS Ser1177 Phosphorylation.

CONTEXT: The mechanisms responsible for dietary fat-induced insulin resistance of skeletal muscle and its microvasculature are only partially understood. OBJECTIVE: To determine the impact of high-fat overfeeding on postprandial glucose fluxes, muscle insulin signaling, and muscle microvascular endothelial nitric oxide synthase (eNOS) content and activation. DESIGN: Fifteen non-obese volunteers consumed a high-fat (64%) high-energy (+47%) diet for 7 days. Experiments were performed before and after the diet. Stable isotope tracers were used to determine glucose fluxes in response to carbohydrate plus protein ingestion. Muscle insulin signaling was determined as well as the content and activation state of muscle microvascular eNOS. RESULTS: High-fat overfeeding impaired postprandial glycemic control as demonstrated by higher concentrations of glucose (+11%; P = 0.004) and insulin (+19%; P = 0.035). Carbohydrate plus protein ingestion suppressed endogenous glucose production to a similar extent before and after the diet. Conversely, high-fat overfeeding reduced whole-body glucose clearance (-16%; P = 0.021) and peripheral insulin sensitivity (-26%; P = 0.006). This occurred despite only minor alterations in skeletal muscle insulin signaling. High-fat overfeeding reduced eNOS content in terminal arterioles (P = 0.017) and abolished the increase in eNOS Ser1177 phosphorylation that was seen after carbohydrate plus protein ingestion. CONCLUSION: High-fat overfeeding impaired whole-body glycemic control due to reduced glucose clearance, not elevated endogenous glucose production. The finding that high-fat overfeeding abolished insulin-mediated eNOS Ser1177 phosphorylation in the terminal arterioles suggests that impairments in the vasodilatory capacity of the skeletal muscle microvasculature may contribute to early dietary fat-induced impairments in glycemic control.

Sprinting After Having Sprinted: Prior High-Intensity Stochastic Cycling Impairs the Winning Strike for Gold.

Bunch riding in closed circuit cycling courses and some track cycling events are often typified by highly variable power output and a maximal sprint to the finish. How criterium style race demands affect final sprint performance however, is unclear. We studied the effects of 1 h variable power cycling on a subsequent maximal 30 s sprint in the laboratory. Nine well-trained male cyclists/triathletes (O2peak 4.9 ± 0.4 L⋅min-1; mean ± SD) performed two 1 h cycling trials in a randomized order with either a constant (CON) or variable (VAR) power output matched for mean power output. The VAR protocol comprised intervals of varying intensities (40-135% of maximal aerobic power) and durations (10 to 90 s). A 30 s maximal sprint was performed before and immediately after each 1 h cycling trial. When compared with CON, there was a greater reduction in peak (-5.1 ± 6.1%; mean ± 90% confidence limits) and mean (-5.9 ± 5.2%) power output during the 30 s sprint after the 1 h VAR cycle. Variable power cycling, commonly encountered during criterium and triathlon races can impair an optimal final sprint, potentially compromising race performance. Athletes, coaches, and staff should evaluate training (to improve repeat sprint-ability) and race-day strategies (minimize power variability) to optimize the final sprint.

Scalable 3D Printed Molds for Human Tissue Engineered Skeletal Muscle.

Tissue engineered skeletal muscle allows investigation of the cellular and molecular mechanisms that regulate skeletal muscle pathology. The fabricated model must resemble characteristics of in vivo tissue and incorporate cost-effective and high content primary human tissue. Current models are limited by low throughput due to the complexities associated with recruiting tissue donors, donor specific variations, as well as cellular senescence associated with passaging. This research presents a method using fused deposition modeling (FDM) and laser sintering (LS) 3D printing to generate reproducible and scalable tissue engineered primary human muscle, possessing aligned mature myotubes reminiscent of in vivo tissue. Many existing models are bespoke causing variability when translated between laboratories. To this end, a scalable model has been developed (25-500 µL construct volumes) allowing fabrication of mature primary human skeletal muscle. This research provides a strategy to overcome limited biopsy cell numbers, enabling high throughput screening of functional human tissue.

The combined effect of sprint interval training and postexercise blood flow restriction on critical power, capillary growth, and mitochondrial proteins in trained cyclists.

Sprint interval training (SIT) combined with postexercise blood flow restriction (BFR) is a novel method to increase maximal oxygen uptake (V̇o2max) in trained individuals and also provides a potent acute stimulus for angiogenesis and mitochondrial biogenesis. The efficacy to enhance endurance performance, however, has yet to be demonstrated. Trained male cyclists ( n = 21) (V̇o2max: 62.8 ± 3.7 ml·min-1·kg-1) undertook 4 wk of SIT (repeated 30-s maximal sprints) either alone (CON; n = 10) or with postexercise BFR ( n = 11). Before and after training V̇o2max, critical power (CP) and curvature constant ( W') were determined and muscle biopsies obtained for determination of skeletal muscle capillarity and mitochondrial protein content. CP increased ( P = 0.001) by a similar extent following CON (287 ± 39 W to 297 ± 43 W) and BFR (296 ± 40 W to 306 ± 36 W). V̇o2max increased following BFR by 5.9% ( P = 0.02) but was unchanged after CON ( P = 0.56). All markers of skeletal muscle capillarity and mitochondrial protein content were unchanged following either training intervention. In conclusion, 4 wk of SIT increased CP; however, this was not enhanced further with BFR. SIT was not sufficient to elicit changes in skeletal muscle capillarity and mitochondrial protein content with or without BFR. However, we further demonstrate the potency of combining BFR with SIT to enhance V̇o2max in trained individuals. NEW & NOTEWORTHY This investigation has demonstrated that 4 wk of sprint interval training (SIT) increased critical power in trained individuals; however, postexercise blood flow restriction (BFR) did not enhance this further. SIT, with or without BFR, did not induce any changes in skeletal muscle capillarity or mitochondrial protein content in our trained population. We do, however, confirm previous findings that SIT combined with BFR is a potent stimulus to enhance maximal oxygen uptake.

Aerobic Variables for Prediction of Alpine Skiing Performance - A Novel Approach.

The aim of this study was to investigate the predictive power of aerobic test results and anthropometric variables on FIS-ranking of junior elite alpine skiers. Results from twenty-three male and female adolescent elite alpine skiers from two seasons were included in the multivariate statistical models. Physical work capacity was determined by V̇O2peak, blood lactate concentration ([HLa]b), and heart rate (HR) during ergometer cycling. Anthropometric variables were body stature, body weight and calculated BMI. No significant correlation between competitive performance and aerobic work capacity or anthropometric data was observed neither in male nor female adolescent skiers. Pre-season physical tests and anthropometric data could therefore not predict end-season FIS-ranking. The best regression (R2) and prediction (Q2) models of FIS slalom (SL) and giant slalom (GS) rank reached R2=0.51 to 0.86, Q2=-0.73 to 0.18, indicating no valid models. This study could not establish V̇O2peak and other included variables as predictors of competitive performance. When combining results from commonly used tests for alpine skiers, and applying multivariate statistical models, investigated tests seems of limited used for athletes, coaches, and ski federations. Performance-specific pre-season tests must be developed and validated for prediction of performance and guidance of exercise training.

Resistance exercise stimulates mixed muscle protein synthesis in lean and obese young adults.

Obese individuals exhibit a diminished muscle protein synthesis response to nutrient stimulation when compared with their lean counterparts. However, the effect of obesity on exercise-stimulated muscle protein synthesis remains unknown. Nine lean (23.5 ± 0.6 kg/m2 ) and 8 obese (33.6 ± 1.2 kg/m2 ) physically active young adults participated in a study that determined muscle protein synthesis and intracellular signaling at rest and following an acute bout of resistance exercise. Mixed muscle protein synthesis was determined by combining stable isotope tracer ([13 C6 ]phenylalanine) infusion with serial biopsies of the vastus lateralis. A unilateral leg resistance exercise model was adopted so that resting and postexercise measurements of muscle protein synthesis could be obtained simultaneously. Obesity was associated with higher basal levels of serum insulin (P < 0.05), plasma triacylglycerol (P < 0.01), plasma cholesterol (P < 0.01), and plasma CRP (P < 0.01), as well as increased insulin resistance determined by HOMA-IR (P < 0.05). However, resting and postexercise rates of muscle protein synthesis were not significantly different between lean and obese participants (P = 0.644). Furthermore, resistance exercise stimulated muscle protein synthesis (~50% increase) in both groups (P < 0.001), with no difference between lean and obese (P = 0.809). Temporal increases in the phosphorylation of intracellular signaling proteins (AKT/4EBP1/p70S6K) were observed within the exercised leg (P < 0.05), with no differences between lean and obese. These findings suggest a normal anabolic response to muscle loading in obese young adults.

Critical power is positively related to skeletal muscle capillarity and type I muscle fibers in endurance-trained individuals.

The asymptote [critical power (CP)] and curvature constant ( W') of the hyperbolic power-duration relationship can predict performance within the severe-intensity exercise domain. However, the extent to which these parameters relate to skeletal muscle morphology is less clear, particularly in endurance-trained individuals, who, relative to their lesser-trained counterparts, possess skeletal muscles that can support high levels of oxygen transport and oxidative capacity, i.e., elevated type I fiber proportion and cross-sectional area (CSA) and capillarity. Fourteen endurance-trained men performed a maximal incremental test to determine peak oxygen uptake (V̇o2peak; 63.2 ± 4.1 ml·min-1·kg-1, mean ± SD) and maximal aerobic power (406 ± 63 W) and three to five constant-load tests to task failure for the determination of CP (303 ± 52 W) and W' (17.0 ± 3.0 kJ). Skeletal muscle biopsies were obtained from the vastus lateralis and analyzed for percent proportion of fiber types, CSA, and indexes of capillarity. CP was positively correlated with the percent proportion ( r = 0.79; P = 0.001) and CSA ( r = 0.73; P = 0.003) of type I fibers, capillary-to-fiber ratio ( r = 0.88; P < 0.001), and capillary contacts around type I fibers ( r = 0.94; P < 0.001) and type II fibers ( r = 0.68; P = 0.008). W' was not correlated with any morphological variables. These data reveal a strong positive association between CP and skeletal muscle capillarity. Our findings support the assertion that CP is an important parameter of aerobic function and offer novel insights into the physiological bases of CP. NEW & NOTEWORTHY This investigation demonstrated very strong positive correlations between critical power and skeletal muscle capillarity, particularly around type I fibers, and type I fiber composition. These correlations were demonstrated in endurance-trained individuals expected to possess well-adapted skeletal muscles, such as high levels of oxygen transport structures and high oxidative capacities, supporting the view that critical power is an important parameter of aerobic function. In contrast, the curvature constant W' was not associated with fiber type composition or capillarity.