Low-Volume Speed Endurance Training with Reduced Volume Improves Short-Term Exercise Performance in Highly Trained Cyclists.

PURPOSE: We investigated the effects of low and high volume speed endurance training (SET), with a reduced training volume, on sprint ability, short- and long-term exercise capacity, muscle mitochondrial properties, ion transport proteins and maximal enzyme activity in highly trained athletes. METHODS: Highly-trained male cyclists (V̇O2max: 68.3 ± 5.0 mL × min-1 × kg-1, n = 24) completed six weeks of either low (SET-L; 6x30-s intervals, n = 8) or high (SET-H; 12 × 30-s intervals, n = 8) volume SET twice per week with a 30%-reduction in training volume. A control group (CON, n = 8) maintained their training. Exercise performance was evaluated by i) 6-s sprinting, ii) a 4-min time trial, iii) a 60-min preload at 60% V̇O2max followed by a 20-min time trial. A biopsy of m. vastus lateralis was collected before and after the training intervention. RESULTS: In SET-L, 4-min time trial performance was improved (P < 0.05) by 3.8%, with no change in SET-H and CON. Sprint ability, prolonged endurance exercise capacity, V̇O2max, muscle mitochondrial respiratory capacity, maximal citrate synthase activity, fiber-type specific mitochondrial proteins (complex I - V) and PFK content did not change in any of the groups. In SET-H, maximal activity of muscle PFK and abundance of Na+-K+ pump-subunit α1, α2, ß1, and phospholemman (FXYD1) were 20%, 50%, 19%, 24%, and 42 % higher (P < 0.05), respectively after compared to before the intervention, with no changes in SET-L or CON. CONCLUSIONS: Low SET volume combined with a reduced aerobic low and moderate intensity training volume does improve short duration intense exercise performance and maintain sprinting ability, V̇O2max, endurance exercise performance and muscle oxidative capacity, whereas, high volume of SET appears necessary to upregulate muscle ion transporter content and maximal PFK activity in highly trained cyclists.

Similar improvements in 5-km performance and maximal oxygen uptake with submaximal and maximal 10-20-30 training in runners, but increase in muscle oxidative phosphorylation occur only with maximal effort training.

OBJECTIVE: The aim of the present study was to examine whether 10-20-30 training (consecutive 1-min intervals consisting of 30 s at low-speed, 20 s at moderate-speed, and 10 s at high-speed), performed with submaximal effort during the 10-s high-speed runs, would lead to improved performance as well as increased maximum oxygen uptake (VO2 -max) and muscle oxidative phosphorylation (OXPHOS). In addition, to examine to what extent the effects would compare to 10-20-30 running conducted with maximal effort. DESIGN: Nineteen males were randomly assigned to 10-20-30 running performed with either submaximal (SUBMAX; n = 11) or maximal (MAX; n = 8) effort, which was conducted three times/week for 6 weeks (intervention; INT). Before and after INT, subjects completed a 5-km running test and a VO2 -max test, and a biopsy was obtained from m. vastus lateralis. RESULTS: After compared to before INT, SUBMAX and MAX improved (p < 0.05) 5-km performance by 3.0% (20.8 ± 0.4 (means±SE) vs. 21.5 ± 0.4 min) and 2.3% (21.2 ± 0.4 vs. 21.6 ± 0.4 min), respectively, and VO2 -max was ~7% higher (p < 0.01) in both SUBMAX (57.0 ± 1.3 vs. 53.5 ± 1.1 mL/min/kg) and MAX (57.8 ± 1.2 vs. 53.7 ± 0.9 mL/min/kg), with no difference in the changes between groups. In SUBMAX, muscle OXPHOS was unchanged, whereas in MAX, muscle OXPHOS subunits (I-IV) and total OXPHOS (5.5 ± 0.3 vs 4.7 ± 0.3 A.U.) were 9%-29% higher (p < 0.05) after compared to before INT. CONCLUSION: Conducting 10-20-30 training with a non-maximal effort during the 10-s high-speed runs is as efficient in improving 5-km performance and VO2 -max as maximal effort exercise, whereas increase in muscle OXPHOS occur only when the 10-s high-speed runs are performed with maximal effort.

High-Intensity Training Represses FXYD5 and Glycosylates Na,K-ATPase in Type II Muscle Fibres, Which Are Linked with Improved Muscle K+ Handling and Performance.

Na+/K+ ATPase (NKA) comprises several subunits to provide isozyme heterogeneity in a tissue-specific manner. An abundance of NKA α, ß, and FXYD1 subunits is well-described in human skeletal muscle, but not much is known about FXYD5 (dysadherin), a regulator of NKA and ß1 subunit glycosylation, especially with regard to fibre-type specificity and influence of sex and exercise training. Here, we investigated muscle fibre-type specific adaptations in FXYD5 and glycosylated NKAß1 to high-intensity interval training (HIIT), as well as sex differences in FXYD5 abundance. In nine young males (23.8 ± 2.5 years of age) (mean ± SD), 3 weekly sessions of HIIT for 6 weeks enhanced muscle endurance (220 ± 102 vs. 119 ± 99 s, p < 0.01) and lowered leg K+ release during intense knee-extensor exercise (0.5 ± 0.8 vs. 1.0 ± 0.8 mmol·min-1, p < 0.01) while also increasing cumulated leg K+ reuptake 0-3 min into recovery (2.1 ± 1.5 vs. 0.3 ± 0.9 mmol, p < 0.01). In type IIa muscle fibres, HIIT lowered FXYD5 abundance (p < 0.01) and increased the relative distribution of glycosylated NKAß1 (p < 0.05). FXYD5 abundance in type IIa muscle fibres correlated inversely with the maximal oxygen consumption (r = -0.53, p < 0.05). NKAα2 and ß1 subunit abundances did not change with HIIT. In muscle fibres from 30 trained males and females, we observed no sex (p = 0.87) or fibre type differences (p = 0.44) in FXYD5 abundance. Thus, HIIT downregulates FXYD5 and increases the distribution of glycosylated NKAß1 in type IIa muscle fibres, which is likely independent of a change in the number of NKA complexes. These adaptations may contribute to counter exercise-related K+ shifts and enhance muscle performance during intense exercise.

Effect of sample fractionation and normalization when immunoblotting for human muscle Na+/K+-ATPase subunits and glycogen synthase.

Immunoblotting is widely used in muscle physiology to determine protein regulation and abundance. However, research groups use different protocols, which may result in differential outcomes. Herein, we investigated the effect of various homogenization procedures on determination of protein abundance in human m. vastus lateralis biopsies. Furthermore, we investigated differences in abundance between young healthy males (n = 12) and type-2 diabetics (n = 4), and the effect of data normalization. Fractionated lysates had the lowest variation in total protein determination as compared to non-fractionated homogenates. Abundance of NKAα2, NKAß1, FXYD1, and glycogen synthase was higher (P < 0.05) in young healthy than in type-2 diabetics determined in both fractionated and non-fractionated samples for which normalization to the stain-free signal and/or standard curve did not affect outcomes. Precision and reliability of protein abundance determination between sample types showed a moderate to good reliability for these proteins, whereas the commonly used house-keeping protein, actin, showed poor reliability. In conclusion, fractionated and non-fractionated immunoblotting samples yield similar data for several sarcolemmal and cytosolic proteins, except for actin, which, therefore appears inappropriate for data normalization in immunoblotting of human skeletal muscle. Thus, fractionation does not seem to be a major source of bias when immunoblotting for NKA subunits and GS.

Beta2 -agonist increases skeletal muscle interleukin 6 production and release in response to resistance exercise in men.

OBJECTIVE: Several tissues produce and release interleukin-6 (IL-6) in response to beta2 -adrenergic stimulation with selective agonists (beta2 -agonists). Moreover, exercise stimulates muscle IL-6 production, but whether beta2 -agonists regulate skeletal muscle production and release of IL-6 in humans in association with exercise remains to be clarified. Thus, we investigated leg IL-6 release in response to beta2 -agonist salbutamol in lean young men at rest and in recovery from resistance exercise. DESIGN: The study employed a randomized controlled crossover design, where 12 men ingested either salbutamol (16 mg) or placebo for 4 days, followed by the last dose (24 mg) administered 1½ h before exercise. Arterial and femoral venous plasma IL-6 as well as femoral artery blood flow was measured before and ½-5 h in recovery from quadriceps muscle resistance exercise. Furthermore, vastus lateralis muscle biopsies were collected ½ and 5 h after exercise for determination of mRNA levels of IL-6 and Tumor Necrosis Factor (TNF)-α. RESULTS: Average leg IL-6 release was 1.7-fold higher (p = 0.01) for salbutamol than placebo, being 138 ± 76 and 79 ± 66 pg min-1 (mean ± SD) for salbutamol and placebo, respectively, but IL-6 release was not significantly different between treatments within specific sampling points at rest and after exercise. Muscle IL-6 mRNA was 1.5- and 1.7-fold higher (p = 0.001) for salbutamol than placebo ½ and 5 h after exercise, respectively, whereas no significant treatment differences were observed for TNF-α mRNA. CONCLUSIONS: Beta2 -adrenergic stimulation with high doses of the selective beta2 -agonist salbutamol, preceeded by 4 consecutive daily doses, induces transcription of IL-6 in skeletal muscle in response to resistance exercise, and increases muscle IL-6 release in lean individuals.

Active Relative to Passive Ischemic Preconditioning Enhances Intense Endurance Performance in Well-Trained Men.

PURPOSE: This study tested the hypothesis of whether ischemic exercise preconditioning (IPC-Ex) elicits a better intense endurance exercise performance than traditional ischemic preconditioning at rest (IPC-rest) and a SHAM procedure. METHODS: Twelve men (average V˙O2max ∼61 mL·kg-1·min-1) performed 3 trials on separate days, each consisting of either IPC-Ex (3 × 2-min cycling at ∼40 W with a bilateral-leg cuff pressure of ∼180 mm Hg), IPC-rest (4 × 5-min supine rest at 220 mm Hg), or SHAM (4 × 5-min supine rest at <10 mm Hg) followed by a standardized warm-up and a 4-minute maximal cycling performance test. Power output, blood lactate, potassium, pH, rating of perceived exertion, oxygen uptake, and gross efficiency were assessed. RESULTS: Mean power during the performance test was higher in IPC-Ex versus IPC-rest (+4%; P = .002; 95% CI, +5 to 18 W). No difference was found between IPC-rest and SHAM (-2%; P = .10; 95% CI, -12 to 1 W) or between IPC-Ex and SHAM (+2%; P = .09; 95% CI, -1 to 13 W). The rating of perceived exertion increased following the IPC-procedure in IPC-Ex versus IPC-rest and SHAM (P < .001). During warm-up, IPC-Ex elevated blood pH versus IPC-rest and SHAM (P ≤ .027), with no trial differences for blood potassium (P > .09) or cycling efficiency (P ≥ .24). Eight subjects anticipated IPC-Ex to be best for their performance. Four subjects favored SHAM. CONCLUSIONS: Performance in a 4-minute maximal test was better following IPC-Ex than IPC-rest and tended to be better than SHAM. The IPC procedures did not affect blood potassium, while pH was transiently elevated only by IPC-Ex. The performance-enhancing effect of IPC-Ex versus IPC-rest may be attributed to a placebo effect, improved pH regulation, and/or a change in the perception of effort.

Salbutamol Increases Leg Glucose Uptake and Metabolic Rate but not Muscle Glycogen Resynthesis in Recovery From Exercise.

CONTEXT: Exercise blunts the effect of beta2-agonists on peripheral glucose uptake and energy expenditure. Whether such attenuation extends into recovery is unknown. OBJECTIVE: To examine the effect of a beta2-agonist on leg glucose uptake and metabolic rate in recovery from exercise. METHODS: Using leg arteriovenous balance technique and analyses of thigh muscle biopsies, we investigated the effect of a beta2-agonist (24 mg of oral salbutamol) vs placebo on leg glucose, lactate, and oxygen exchange before and during quadriceps exercise, and 0.5 to 5 hours in recovery from quadriceps exercise, as well as on muscle glycogen resynthesis and activity in recovery. Twelve healthy, lean, young men participated. RESULTS: Before exercise, leg glucose uptake was 0.42 ±â€…0.12 and 0.20 ±â€…0.02 mmol × min-1 (mean ±â€…SD) for salbutamol and placebo (P = .06), respectively, while leg oxygen consumption was around 2-fold higher (P < .01) for salbutamol than for placebo (25 ±â€…3 vs 14 ±â€…1 mL × min-1). No treatment differences were observed in leg glucose uptake, lactate release, and oxygen consumption during exercise. But in recovery, cumulated leg glucose uptake, lactate release, and oxygen consumption was 21 mmol (95% CI 18-24, P = .018), 19 mmol (95% CI 16-23, P < .01), and 1.8 L (95% CI 1.6-2.0, P < .01) higher for salbutamol than for placebo, respectively. Muscle glycogen content was around 30% lower (P < .01) for salbutamol than for placebo in recovery, whereas no treatment differences were observed in muscle glycogen resynthesis or glycogen synthase activity. CONCLUSION: Exercise blunts the effect of beta2-agonist salbutamol on leg glucose uptake, but this attenuation diminishes in recovery. Salbutamol increases leg lactate release in recovery, which may relate to glycolytic trafficking due to excessive myocellular glucose uptake.

Aerobic High-Intensity Exercise Training Improves Cardiovascular Health in Older Post-menopausal Women.

The aim of this study was to determine the effect of a period of aerobic high intensity training on central- and peripheral cardiovascular parameters in older post-menopausal women. Eleven healthy post-menopausal (>10 years after menopause) women (mean age: 64 years; BMI: 25.3 kg m-2) completed an 8-week period of supervised, high intensity cycle training, with sessions conducted three times per week. Before and after the training period maximal oxygen uptake, body composition, popliteal artery flow mediated dilation, exercise hyperemia, arterial blood pressure, and plasma lipids were assessed. In addition, levels of estrogen related receptor α (ERRα) and vasodilator enzymes were determined in muscle biopsy samples. Training induced an 18% increase (P < 0.001) in maximal oxygen uptake. Plasma High-density lipoprotein (HDL) was higher (P < 0.05) after than before the training period. Fat mass was reduced (4.9%; P < 0.01), whereas lean body mass was unaltered. Mean arterial blood pressure was unchanged (91 vs. 88 mmHg; P = 0.058) with training. Training did not induce a change in popliteal flow mediated dilation. Exercise hyperemia at submaximal exercise was lower (P < 0.01; 11 and 4.6% at 10 and 16 W, respectively) after compared to before training. Muscle ERRα (~1.7-fold; P < 0.01) and eNOS (~1.4-fold; P < 0.05) were higher after the training intervention. The current study demonstrates that, in older post-menopausal women, a period of aerobic high intensity training effectively increases maximal oxygen uptake and improves the cardiovascular health profile, without a parallel improvement in conduit artery function.

The effect of blood-flow-restricted interval training on lactate and H+ dynamics during dynamic exercise in man.

AIM: To assess how blood-flow-restricted (BFR) interval-training affects the capacity of the leg muscles for pH regulation during dynamic exercise in physically trained men. METHODS: Ten men (age: 25 ± 4y; V˙O2max : 50 ± 5 mL∙kg-1 ∙min-1 ) completed a 6-wk interval-cycling intervention (INT) with one leg under BFR (BFR-leg; ~180 mmHg) and the other without BFR (CON-leg). Before and after INT, thigh net H+ -release (lactate-dependent, lactate-independent and sum) and blood acid/base variables were measured during knee-extensor exercise at 25% (Ex25) and 90% (Ex90) of incremental peak power output. A muscle biopsy was collected before and after Ex90 to determine pH, lactate and density of H+ -transport/buffering systems. RESULTS: After INT, net H+ release (BFR-leg: 15 ± 2; CON-leg: 13 ± 3; mmol·min-1 ; Mean ± 95% CI), net lactate-independent H+ release (BFR-leg: 8 ± 1; CON-leg: 4 ± 1; mmol·min-1 ) and net lactate-dependent H+ release (BFR-leg: 9 ± 3; CON-leg: 10 ± 3; mmol·min-1 ) were similar between legs during Ex90 (P > .05), despite a ~142% lower muscle intracellular-to-interstitial lactate gradient in BFR-leg (-3 ± 4 vs 6 ± 6 mmol·L-1 ; P < .05). In recovery from Ex90, net lactate-dependent H+ efflux decreased in BFR-leg with INT (P < .05 vs CON-leg) owing to lowered muscle lactate production (~58% vs CON-leg, P < .05). Net H+ gradient was not different between legs (~19%, P > .05; BFR-leg: 48 ± 30; CON-leg: 44 ± 23; mmol·L-1 ). In BFR-leg, NHE1 density was higher than in CON-leg (~45%; P < .05) and correlated with total-net H+ -release (r = 0.71; P = .031) and lactate-independent H+ release (r = 0.74; P = .023) after INT, where arterial [ HCO3- ] and standard base excess in Ex25 were higher in BFR-leg than CON-leg. CONCLUSION: Compared to a training control, BFR-interval training increases the capacity for pH regulation during dynamic exercise mainly via enhancement of muscle lactate-dependent H+ -transport function and blood H+ -buffering capacity.

Training with blood flow restriction increases femoral artery diameter and thigh oxygen delivery during knee-extensor exercise in recreationally trained men.

KEY POINTS: Endurance-type training with blood flow restriction (BFR) increases maximum oxygen uptake ( V̇O2max ) and exercise endurance of humans. However, the physiological mechanisms behind this phenomenon remain uncertain. In the present study, we show that BFR-interval training reduces the peripheral resistance to oxygen transport during dynamic, submaximal exercise in recreationally-trained men, mainly by increasing convective oxygen delivery to contracting muscles. Accordingly, BFR-training increased oxygen uptake by, and concomitantly reduced net lactate release from, the contracting muscles during relative-intensity-matched exercise, at the same time as invoking a similar increase in diffusional oxygen conductance compared to the training control. Only BFR-training increased resting femoral artery diameter, whereas increases in oxygen transport and uptake were dissociated from changes in the skeletal muscle content of mitochondrial electron-transport proteins. Thus, physically trained men benefit from BFR-interval training by increasing leg convective oxygen transport and reducing lactate release, thereby improving the potential for increasing the percentage of V̇O2max that can be sustained throughout exercise. ABSTRACT: In the present study, we investigated the effect of training with blood flow restriction (BFR) on thigh oxygen transport and uptake, and lactate release, during exercise. Ten recreationally-trained men (50 ± 5 mL kg-1  min-1 ) completed 6 weeks of interval cycling with one leg under BFR (BFR-leg; pressure: ∼180 mmHg) and the other leg without BFR (CON-leg). Before and after the training intervention (INT), thigh oxygen delivery, extraction, uptake, diffusion capacity and lactate release were determined during knee-extensor exercise at 25% incremental peak power output (iPPO) (Ex1), followed by exercise to exhaustion at 90% pre-training iPPO (Ex2), by measurement of femoral-artery blood flow and femoral-arterial and -venous blood sampling. A muscle biopsy was obtained from legs before and after INT to determine mitochondrial electron-transport protein content. Femoral-artery diameter was also measured. In the BFR-leg, after INT, oxygen delivery and uptake were higher, and net lactate release was lower, during Ex1 (vs. CON-leg; P < 0.05), with an 11% larger increase in workload (vs. CON-leg; P < 0.05). During Ex2, after INT, oxygen delivery was higher, and oxygen extraction was lower, in the BFR-leg compared to the CON-leg (P < 0.05), resulting in an unaltered oxygen uptake (vs. CON-leg; P > 0.05). In the CON-leg, at both intensities, oxygen delivery, extraction, uptake and lactate release remained unchanged (P > 0.05). Resting femoral artery diameter increased with INT only in the BFR-leg (∼4%; P < 0.05). Oxygen diffusion capacity was similarly raised in legs (P < 0.05). Mitochondrial protein content remained unchanged in legs (P > 0.05). Thus, BFR-interval training enhances oxygen utilization by, and lowers lactate release from, submaximally-exercising muscles of recreationally-trained men mainly by increasing leg convective oxygen transport.

Beta2 -adrenergic agonist clenbuterol increases energy expenditure and fat oxidation, and induces mTOR phosphorylation in skeletal muscle of young healthy men.

Clenbuterol is a beta2 -adrenoceptor agonist marketed as an asthma reliever but is not approved for human use in most countries due to concerns of adverse cardiac effects. Given its demonstrated hypertrophic and lipolytic actions in rodents, clenbuterol is one of the most widely abused doping substances amongt athletes and recreational body-builders seeking leanness. Herein, we examined the effect of clenbuterol ingestion on metabolic rate as well as skeletal muscle mammalian target of rapamycin (mTOR) phosphorylation and protein kinase A (PKA)-signaling in six young men. Before and 140 min after ingestion of 80 µg clenbuterol, resting metabolic rate and contractile function of the quadriceps muscle were measured, and blood samples as well as vastus lateralis muscle biopsies were collected. Clenbuterol increased resting energy expenditure by 21% (P < 0.001), and fat oxidation by 39% (P = 0.006), whereas carbohydrate oxidation was unchanged. Phosphorylation of mTORSer2448 and PKA substrates increased by 121% (P = 0.004) and 35% (P = 0.006), respectively, with clenbuterol. Maximal voluntary contraction torque decreased by 4% (P = 0.026) and the half-relaxation time shortened by 9% (P = 0.046), while voluntary activation, time to peak twitch, and peak twitch torque did not change significantly with clenbuterol. Glycogen content of the vastus lateralis muscle did not change with clenbuterol. Clenbuterol increased circulating levels of glucose (+30%; P < 0.001), lactate (+90%; P = 0.004), insulin (+130%; P = 0.009), and fatty acids (+180%; P = 0.001). Collectively, these findings indicate that clenbuterol is an efficient thermogenic substance that possibly also exerts muscle hypertrophic actions in humans. For these reasons, the restrictions imposed against clenbuterol in competitive sports seem warranted.

Blood flow-restricted training enhances thigh glucose uptake during exercise and muscle antioxidant function in humans.

This study examined the effects of blood-flow-restricted (BFR)-training on thigh glucose uptake at rest and during exercise in humans and the muscular mechanisms involved. Ten active men (~25 y; VO2max ~50 mL/kg/min) completed six weeks of training, where one leg trained with BFR (cuff pressure: ~180 mmHg) and the other leg without BFR. Before and after training, thigh glucose uptake was determined at rest and during exercise at 25% and 90% of leg incremental peak power output by sampling of femoral arterial and venous blood and measurement of femoral arterial blood flow. Furthermore, resting muscle samples were collected. After training, thigh glucose uptake during exercise was higher than before training only in the BFR-trained leg (p < 0.05) due to increased glucose extraction (p < 0.05). Further, BFR-training substantially improved time to exhaustion during exhaustive exercise (11 ±â€¯5% vs. CON-leg; p = 0.001). After but not before training, NAC infusion attenuated (~50-100%) leg net glucose uptake and extraction during exercise only in the BFR-trained leg, which coincided with an increased muscle abundance of Cu/Zn-SOD (39%), GPX-1 (29%), GLUT4 (28%), and nNOS (18%) (p < 0.05). Training did not affect Mn-SOD, catalase, and VEGF abundance in either leg (p > 0.05), although Mn-SOD was higher in BFR-leg vs. CON-leg after training (p < 0.05). The ratios of p-AMPK-Thr172/AMPK and p-ACC-Ser79/ACC, and p-ACC-Ser79, remained unchanged in both legs (p > 0.05), despite a higher p-AMPK-Thr172 in BFR-leg after training (38%; p < 0.05). In conclusion, BFR-training enhances glucose uptake by exercising muscles in humans probably due to an increase in antioxidant function, GLUT4 abundance, and/or NO availability.

N-Acetyl cysteine does not improve repeated intense endurance cycling performance of well-trained cyclists.

PURPOSE: To evaluate the effect of antioxidant supplementation on intense endurance exercise performance and the physiologic exercise response acutely and in early recovery. METHODS: Well-trained cyclists (n = 11, peak VO2: 69 ± 7 ml/min/kg) completed two identical standardized 20-min warm-up periods (WU-1 and WU-2) prior to two performance tests (PT) with a duration of ~ 4 min representing a qualifying (PT-1) and final race (PT-2) on the same day separated by 90 min. Subjects were supplemented orally with placebo (PLA) and N-acetyl cysteine (NAC; 20 mg/kg) before exercise in a double-blinded crossover design. RESULTS: Mean power during PT-1 did not differ (P = 0.39) between PLA (400 ± 44 W) and NAC (401 ± 44 W) as was the case during PT-2 with similar performance (P = 0.74) between PLA (401 ± 43 W) and NAC (400 ± 42 W). Subjective "readiness" was lowered by prior exhaustive exercise from PT-1 to PT-2 (P = 0.012) in both PLA and NAC. Plasma total antioxidant capacity was not affected by supplementation and prior exhaustive exercise (respective main effects: P = 0.83 and P = 0.19) which also was observed for peak VO2 at ~ 5 L/min (P = 0.84 and P = 0.30). In WU-1 and WU-2, both cycling economy at ~ 20% (P = 0.10 and P = 0.21) and plasma potassium at ~ 5 mmol/L (P = 0.46 and P = 0.26) were unaffected by supplementation and prior exercise. CONCLUSIONS: Athletes executing maximal efforts of a ~ 4-min duration twice daily, as seen in track cycling, appear to gain no benefit from oral NAC supplementation on acute and subsequent performance following short-term recovery. Moreover, well-trained cyclists exhibit rapid recovery from a single bout of intense endurance cycling.

Cardiac perfusion and function after high-intensity exercise training in late premenopausal and recent postmenopausal women: an MRI study.

We examined the influence of recent menopause and aerobic exercise training in women on myocardial perfusion, left ventricular (LV) dimension, and function. Two groups (n = 14 each) of healthy late premenopausal (50.2 ± 2.1 yr) and recent postmenopausal (54.2 ± 2.8 yr) women underwent cardiac magnetic resonance imaging (cMRI) at baseline and after 12 wk of high-intensity aerobic training. Measurements included LV morphology, systolic function, and myocardial perfusion at rest and during an adenosine stress test. At baseline, resting myocardial perfusion was lower in the postmenopausal than the premenopausal group (77 ± 3 vs. 89 ± 3 ml·100 g-1·min-1; P = 0.01), while adenosine-induced myocardial perfusion was not different (P = 0.81). After exercise training, resting myocardial perfusion was lower in both groups (66 ± 2; P = 0.002 vs. 81 ± 3 ml·100 g-1·min-1; P = 0.03). The adenosine-induced change in myocardial perfusion was lower in the groups combined (by 402 ± 17 ml·100 g-1·min-1; P = 0.02), and the adenosine-induced increase in heart rate was 10 ± 2 beats/min lower (P < 0.0001) in both groups after training. Normalization of myocardial perfusion using an estimate of cardiac work eliminated the differences in perfusion between the premenopausal and postmenopausal groups and the effect of training. Left ventricle mass was higher in both groups (P = 0.03; P = 0.006), whereas LV end-diastolic (P = 0.02) and stroke (P = 0.045) volumes were higher in the postmenopausal group after training. Twelve weeks of exercise training increased left ventricle mass and lowered resting and adenosine-induced myocardial perfusion, an effect that was likely related to cardiac work. The current data also suggest that the early menopausal transition has limited impact on cardiac function and structure. NEW & NOTEWORTHY This study provides for the first time estimates of myocardial perfusion in late premenopausal and recent postmenopausal women before and after a period of intense aerobic training. Resting myocardial perfusion was lower in postmenopausal than premenopausal women. Training lowered myocardial resting and stress perfusion in both groups, an effect that was likely influenced by the lower heart rate.

Cycling with blood flow restriction improves performance and muscle K+ regulation and alters the effect of anti-oxidant infusion in humans.

KEY POINTS: Training with blood flow restriction (BFR) is a well-recognized strategy for promoting muscle hypertrophy and strength. However, its potential to enhance muscle function during sustained, intense exercise remains largely unexplored. In the present study, we report that interval training with BFR augments improvements in performance and reduces net K+ release from contracting muscles during high-intensity exercise in active men. A better K+ regulation after BFR-training is associated with an elevated blood flow to exercising muscles and altered muscle anti-oxidant function, as indicated by a higher reduced to oxidized glutathione (GSH:GSSG) ratio, compared to control, as well as an increased thigh net K+ release during intense exercise with concomitant anti-oxidant infusion. Training with BFR also invoked fibre type-specific adaptations in the abundance of Na+ ,K+ -ATPase isoforms (α1 , ß1 , phospholemman/FXYD1). Thus, BFR-training enhances performance and K+ regulation during intense exercise, which may be a result of adaptations in anti-oxidant function, blood flow and Na+ ,K+ -ATPase-isoform abundance at the fibre-type level. ABSTRACT: We examined whether blood flow restriction (BFR) augments training-induced improvements in K+ regulation and performance during intense exercise in men, and also whether these adaptations are associated with an altered muscle anti-oxidant function, blood flow and/or with fibre type-dependent changes in Na+ ,K+ -ATPase-isoform abundance. Ten recreationally-active men (25 ± 4 years, 49.7 ± 5.3 mL kg-1  min-1 ) performed 6 weeks of interval cycling, where one leg trained without BFR (control; CON-leg) and the other trained with BFR (BFR-leg, pressure: ∼180 mmHg). Before and after training, femoral arterial and venous K+ concentrations and artery blood flow were measured during single-leg knee-extensor exercise at 25% (Ex1) and 90% of thigh incremental peak power (Ex2) with i.v. infusion of N-acetylcysteine (NAC) or placebo (saline) and a resting muscle biopsy was collected. After training, performance increased more in BFR-leg (23%) than in CON-leg (12%, P < 0.05), whereas K+ release during Ex2 was attenuated only from BFR-leg (P < 0.05). The muscle GSH:GSSG ratio at rest and blood flow during exercise was higher in BFR-leg than in CON-leg after training (P < 0.05). After training, NAC increased resting muscle GSH concentration and thigh net K+ release during Ex2 only in BFR-leg (P < 0.05), whereas the abundance of Na+ ,K+ -ATPase-isoform α1 in type II (51%), ß1 in type I (33%), and FXYD1 in type I (108%) and type II (60%) fibres was higher in BFR-leg than in CON-leg (P < 0.05). Thus, training with BFR elicited greater improvements in performance and reduced thigh K+ release during intense exercise, which were associated with adaptations in muscle anti-oxidant function, blood flow and Na+ ,K+ -ATPase-isoform abundance at the fibre-type level.

Inclusion of sprints in moderate intensity continuous training leads to muscle oxidative adaptations in trained individuals.

This study examined adaptations in muscle oxidative capacity and exercise performance induced by two work- and duration-matched exercise protocols eliciting different muscle metabolic perturbations in trained individuals. Thirteen male subjects ( V˙ O2 -max 53.5 ± 7.0 mL·kg-1 ·min-1 ) (means ± SD) performed 8 weeks (three sessions/week) of training consisting of 60 min of moderate intensity continuous cycling (157 ± 20 W) either without (C) or with (C+S) inclusion of 30-s sprints (473 ± 79 W) every 10 min. Total work performed during training was matched between groups. Muscle biopsies and arm venous blood were collected before as well as immediately and 2 h after exercise during the first and last training session. Plasma epinephrine and lactate concentrations after the first and last training session were 2-3-fold higher in C+S than in C. After the first and last training session, muscle phosphocreatine and pH were lower (12-25 mmol·kg d.w.-1 and 0.2-0.4 units, respectively) and muscle lactate higher (48-64 mmol·kg d.w.-1 ) in C+S than in C, whereas exercise-induced changes in muscle PGC-1α mRNA levels were similar within- and between-groups. Muscle content of cytochrome c oxidase IV and citrate synthase (CS) increased more in C+S than in C, and content of CS in type II muscle fibers increased in C+S only (9-17%), with no difference between groups. Performance during a 45-min time-trial improved by 4 ± 3 and 9 ± 3% in C+S and C, respectively, whereas peak power output at exhaustion during an incremental test increased by 3 ± 3% in C+S only, with no difference between groups. In conclusion, addition of sprints in moderate intensity continuous exercise causes muscle oxidative adaptations in trained male individuals which appear to be independent of the exercise-induced PGC-1α mRNA response. Interestingly, time-trial performance improved similarly between groups, suggesting that changes in content of mitochondrial proteins are of less importance for endurance performance in trained males.

In-season adaptations to intense intermittent training and sprint interval training in sub-elite football players.

This study investigated the in-season effect of intensified training comparing the efficacy of duration-matched intense intermittent exercise training with sprint interval training in increasing intermittent running performance, sprint ability, and muscle content of proteins related to ion handling and metabolism in football players. After the first two weeks in the season, 22 sub-elite football players completed either 10 weeks of intense intermittent training using the 10-20-30 training concept (10-20-30, n = 12) or sprint interval training (SIT, n = 10; work/rest ratio: 6-s/54-s) three times weekly, with a ~20% reduction in weekly training time. Before and after the intervention, players performed a Yo-Yo intermittent recovery test level 1 (Yo-Yo IR1) and a 30-m sprint test. Furthermore, players had a muscle biopsy taken from the vastus lateralis. Yo-Yo IR1 performance increased by 330 m (95%CI: 178-482, P ≤ 0.01) in 10-20-30, whereas no change was observed in SIT. Sprint time did not change in 10-20-30 but decreased by 0.04 second (95%CI: 0.00-0.09, P ≤ 0.05) in SIT. Muscle content of HADHA (24%, P ≤ 0.01), PDH-E1α (40%, P ≤ 0.01), complex I-V of the electron transport chain (ETC) (51%, P ≤ 0.01) and Na+ , K+ -ATPase subunits α2 (33%, P ≤ 0.05) and ß1 (27%, P ≤ 0.05) increased in 10-20-30, whereas content of DHPR (27%, P ≤ 0.01) and complex I-V of the ETC (31%, P ≤ 0.05) increased in SIT. Intense intermittent training, combining short sprints and a high aerobic load, is superior to regular sprint interval training in increasing intense intermittent running performance during a Yo-Yo IR1 test and muscle content of PDH-E1α and HADHA in sub-elite football players.

ß2-Agonist Induces Net Leg Glucose Uptake and Free Fatty Acid Release at Rest but Not During Exercise in Young Men.

Objective: The role of selective ß2-adrenergic stimulation in regulation of leg glucose uptake and free fatty acid (FFA) balance is inadequately explored in humans. The objective of this study was to investigate ß2-adrenergic effects on net leg glucose uptake and clearance, as well as FFA balance at rest and during exercise. Design: The study was a randomized, placebo-controlled crossover trial where 10 healthy men received either infusion of ß2-agonist terbutaline (0.2 to 0.4 mg) or placebo. Net leg glucose uptake and clearance and FFA balance were determined at rest and during 8 minutes of knee extensor exercise using Fick's principle. Vastus lateralis muscle biopsies were collected at rest and at cessation of exercise. The primary outcome measure was net leg glucose uptake. Results: At rest, net leg glucose uptake and clearance were 0.35 (±0.16) mmol/min and 41 (±17) mL/min (mean ± 95% CI) higher (P < 0.001) for terbutaline than placebo, corresponding to increases of 84% and 70%. During exercise, no treatment differences were observed in net leg glucose uptake, whereas clearance was 101 (±86) mL/min lower (P < 0.05) for terbutaline than placebo. At rest, terbutaline induced a net leg FFA release of 21 (±14) µmol/min, being different from placebo (P = 0.04). During exercise, net leg FFA uptake was not different between the treatments. Conclusions: These observations indicate that ß2-agonist alters net leg glucose uptake and clearance, as well as FFA balance in humans, which is associated with myocellular ß2-adrenergic and insulin-dependent signaling. Furthermore, the study shows that exercise confounds the ß2-adrenergic effect on net leg glucose uptake and FFA balance.

Training state and skeletal muscle autophagy in response to 36 h of fasting.

The present study aimed at investigating fasting-induced responses in regulators and markers of autophagy in vastus lateralis muscle from untrained and trained human subjects. Untrained and trained subjects (based on maximum oxygen uptake, muscle citrate synthase activity, and oxidative phosphorylation protein level) fasted for 36 h with vastus lateralis muscle biopsies obtained at 2, 12, 24, and 36 h after a standardized meal. Fasting reduced ( P < 0.05) skeletal muscle microtubule-associated protein-1A/1B light chain 3 (LC3)I, LC3II, and adaptor protein sequestosome 1/p62 protein content in untrained subjects only. Moreover, skeletal muscle RAC-alpha serine/threonine-protein kinase (AKT)Thr308, AMP-activated protein kinase (AMPK)Thr172, and Unc-51-like autophagy-activating kinase-1 (ULK1)Ser555 phosphorylation state, as well as Bcl-2-interacting coiled-coil protein-1 (Beclin1) and ULK1Ser757 phosphorylation, was lower ( P < 0.05) in trained than untrained subjects during fasting. In addition, the plasma concentrations of several amino acids were higher ( P < 0.05) in trained than untrained subjects, and the plasma concentration profile of several amino acids was different in untrained and trained subjects during fasting. Taken together, these findings suggest that 36-h fasting has effects on some mediators of autophagy in untrained human skeletal muscle and that training state influences the effect of fasting on autophagy signaling and on mediators of autophagy in skeletal muscle. NEW & NOTEWORTHY This study showed that skeletal muscle autophagy was only modestly affected in humans by 36 h of fasting. Hence, 36-h fasting has effects on some mediators of autophagy in untrained human skeletal muscle, and training state influences the effect of fasting on autophagy signaling and on mediators of autophagy in skeletal muscle.

Cardiovascular adaptations after 10 months of intense school-based physical training for 8- to 10-year-old children.

This study examined cardiovascular adaptations in 8- to 10-year-old schoolchildren after 10 months (a full school year) of 3 × 40 minute per week of small-sided ball games (SSG, including football, basketball, and/or floorball) or circuit strength training (CST). The study involved 291 Danish schoolchildren, 8-10 years old, cluster-randomized to SSG (n = 93, 4 schools, 5 classes), CST (n = 83, 4 schools, 4 classes), or a control group (CON, n = 115, 2 schools, 5 classes). Before and after the 10-month intervention, resting heart rate and blood pressure measurements were performed as well as comprehensive transthoracic echocardiography and peripheral arterial tonometry (PAT). Analysis of baseline-to-10-months changes showed between-group differences (P < 0.05) after both training interventions in diastolic blood pressure (delta scores: SSG -2.1 ± 6.0 mm Hg; CST -3.0 ± 7.1 mm Hg; CON 0.2 ± 5.3 mm Hg). Moreover, there were between-group differences in delta scores (P < 0.05) in interventricular septum thickness (SSG 0.17 ± 0.87 mm; CST 0.30 ± 0.94 mm; CON -0.15 ± 0.68 mm), left-atrial volume index (SSG 0.32 ± 5.13 mL/m2 ; CON 2.60 ± 5.94 mL/m2 ), and tricuspid annular plane systolic excursion (SSG -0.4 ± 3.3 mm; CON: 0.1 ± 3.6 mm). No significant between-group differences were observed for the PAT-derived reactive hyperemia index. In conclusion, 10 months of 3 × 40 minutes per week of SSG and CST in 8- to 10-year-old children decreased diastolic blood pressure and elicited discrete cardiac adaptations, suggesting that intense physical exercise in school classes can have effects on cardiovascular health in children.