Insufficient sleep predicts poor weight loss maintenance after 1 year.

STUDY OBJECTIVES: Insufficient sleep may attenuate weight loss, but the role of sleep in weight loss maintenance is unknown. Since weight regain after weight loss remains a major obstacle in obesity treatment, we investigated whether insufficient sleep predicts weight regain during weight loss maintenance. METHODS: In a randomized, controlled, two-by-two factorial study, 195 adults with obesity completed an 8-week low-calorie diet and were randomly assigned to 1-year weight loss maintenance with or without exercise and liraglutide 3.0 mg/day or placebo. Sleep duration and quality were measured before and after the low-calorie diet and during weight maintenance using wrist-worn accelerometers (GENEActiv) and Pittsburgh Sleep Quality Index (PSQI). To test associations between insufficient sleep and weight regain, participants were stratified at randomization into subgroups according to sleep duration (5). RESULTS: After a diet-induced 13.1 kg weight loss, participants with short sleep duration at randomization regained 5.3 kg body weight (p = .0008) and had less reduction in body fat percentage compared with participants with normal sleep duration (p = .007) during the 1-year weight maintenance phase. Participants with poor sleep quality before the weight loss regained 3.5 kg body weight compared with good quality sleepers (p = .010). During the weight maintenance phase, participants undergoing liraglutide treatment displayed increased sleep duration compared with placebo after 26 weeks (5 vs. -15 min/night) but not after 1 year. Participants undergoing exercise treatment preserved the sleep quality improvements attained from the initial weight loss. CONCLUSIONS: Short sleep duration or poor sleep quality was associated with weight regain after weight loss in adults with obesity.

High-Intensity Exercise Training Alters the Effect of N-Acetylcysteine on Exercise-Related Muscle Ionic Shifts in Men.

This study investigated whether high-intensity exercise training alters the effect of N-acetylcysteine (a precursor of antioxidant glutathione) on exercise-related muscle ionic shifts. We assigned 20 recreationally-active men to 6 weeks of high-intensity exercise training, comprising three weekly sessions of 4-10 × 20-s all-out bouts interspersed by 2 min recovery (SET, n = 10), or habitual lifestyle maintenance (n = 10). Before and after SET, we measured ionic shifts across the working muscle, using leg arteriovenous balance technique, during one-legged knee-extensor exercise to exhaustion with and without N-acetylcysteine infusion. Furthermore, we sampled vastus lateralis muscle biopsies for analyses of metabolites, mitochondrial respiratory function, and proteins regulating ion transport and antioxidant defense. SET lowered exercise-related H+, K+, lactate-, and Na+ shifts and enhanced exercise performance by ≈45%. While N-acetylcysteine did not affect exercise-related ionic shifts before SET, it lowered H+, HCO3-, and Na+ shifts after SET. SET enhanced muscle mitochondrial respiratory capacity and augmented the abundance of Na+/K+-ATPase subunits (α1 and ß1), ATP-sensitive K+ channel subunit (Kir6.2), and monocarboxylate transporter-1, as well as superoxide dismutase-2 and glutathione peroxidase-1. Collectively, these findings demonstrate that high-intensity exercise training not only induces multiple adaptations that enhance the ability to counter exercise-related ionic shifts but also potentiates the effect of N-acetylcysteine on ionic shifts during exercise.

Skeletal muscle proteins important for work capacity are altered with type 2 diabetes - Effect of 10-20-30 training.

The study examined whether men with type 2 diabetes exhibit lower expression of muscle proteins important for exercise capacity, and whether exercise training promotes adaptations in these proteins. In a cross-sectional and longitudinal study, conducted at the University of Copenhagen. Twelve men with type 2 diabetes (T2D) were compared to eleven nondiabetes counterparts (ND) matched for age and body composition (body fat percentage). T2D underwent 10 weeks of high-intensity interval exercise training (10-20-30 training). T2D had lower expression of SOD1 (-62%; p < 0.001) and ETC complex V (-34%; p = 0.003), along with higher expression of ETC complex IV (+66%; p = 0.007), MFN2 (+62%; p = 0.001), and DRP1 (+30%; p = 0.028) compared to ND. T2D had higher (p < 0.001) expression of Na+ /K+ α1 (+98%), α2 (+114%), and NHE1 (+144%) than ND. In T2D, training increased exercise capacity (+9%; p < 0.001) as well as expression of SOD2 (+44%; p = 0.029), ETC complex II (+25%; p = 0.035), III (+52%; p = 0.041), IV (+23%; p = 0.005), and V (+21%; p = 0.035), CS activity (+32%; p = 0.006) as well as Na+ /K+ α1 (+24%; p = 0.034), Kir6.2 (+36%; p = 0.029), and MCT1 (+20%; p = 0.007). Men with type 2 diabetes exhibited altered expression of a multitude of skeletal muscle proteins important for exercise capacity. Ten weeks of 10-20-30 training upregulated expression of muscle proteins regulating antioxidant defense, mitochondrial function, and ion handling while enhancing exercise capacity in men with type 2 diabetes.

Essential hypertension is associated with blunted smooth muscle cell vasodilator responsiveness and is reversed by 10-20-30 training in men.

Essential hypertension is associated with impairments in vascular function and sympathetic nerve hyperactivity; however, the extent to which the lower limbs are affected remains unclear. We examined the leg vascular responsiveness to infusion of acetylcholine (ACh), sodium nitroprusside (SNP), and phenylephrine (PEP) in 10 hypertensive men [HYP: age 59.5 ± 9.7 (means ± SD) yr; clinical and nighttime blood pressure: 142 ± 10/86 ± 10 and 141 ± 11/83 ± 6 mmHg, respectively; and body mass index (BMI): 29.2 ± 4.0 kg/m2] and 8 age-matched normotensive counterparts (NORM: age 57.9 ± 10.8 yr; clinical and nighttime blood pressure: 128 ± 9/78 ± 7 and 116 ± 3/69 ± 3 mmHg, respectively; and BMI: 26.3 ± 3.1 kg/m2). The vascular responsiveness was evaluated before and after 6 wk of 10-20-30 training, consisting of 3 × 5 × 10-s sprint followed by 30 and 20 s of low- to moderate-intensity cycling, respectively, interspersed by 3 min of rest. Before training, the vascular responsiveness to infusion of SNP was lower (P < 0.05) in HYP compared with NORM, with no difference in the responsiveness to infusion of ACh and PEP. The vascular responsiveness to infusion of SNP and ACh improved (P < 0.05) with training in HYP, with no change in NORM. With training, intra-arterial systolic blood pressure decreased (P < 0.05) by 9 mmHg in both HYP and NORM whereas diastolic blood pressure decreased (5 mmHg; P < 0.05) in HYP only. We provide here the first line of evidence in humans that smooth muscle cell vasodilator responsiveness is blunted in the lower limbs of hypertensive men. This impairment can be reversed by 10-20-30 training, which is an effective intervention to improve the responsiveness of smooth muscle cells in men with essential hypertension.

High-intensity exercise training enhances mitochondrial oxidative phosphorylation efficiency in a temperature-dependent manner in human skeletal muscle: implications for exercise performance.

The purpose of the present study was to investigate whether exercise training-induced adaptations in human skeletal muscle mitochondrial bioenergetics are magnified under thermal conditions resembling sustained intense contractile activity and whether training-induced changes in mitochondrial oxidative phosphorylation (OXPHOS) efficiency influence exercise efficiency. Twenty healthy men performed 6 wk of high-intensity exercise training [i.e., speed endurance training (SET; n = 10)], or maintained their usual lifestyle (n = 10). Before and after the intervention, mitochondrial respiratory function was determined ex vivo in permeabilized muscle fibers under experimentally-induced normothermia (35°C) and hyperthermia (40°C) mimicking in vivo muscle temperature at rest and during intense exercise, respectively. In addition, activity and content of muscle mitochondrial enzymes and proteins were quantified. Exercising muscle efficiency was determined in vivo by measurements of leg hemodynamics and blood parameters during one-legged knee-extensor exercise. SET enhanced maximal OXPHOS capacity and OXPHOS efficiency at 40°C, but not at 35°C, and attenuated hyperthermia-induced decline in OXPHOS efficiency. Furthermore, SET increased expression of markers of mitochondrial content and up-regulated content of MFN2, DRP1, and ANT1. Also, SET improved exercise efficiency and capacity. These findings indicate that muscle mitochondrial bioenergetics adapts to high-intensity exercise training in a temperature-dependent manner and that enhancements in mitochondrial OXPHOS efficiency may contribute to improving exercise performance.-Fiorenza, M., Lemminger, A. K., Marker, M., Eibye, K., Iaia, F. M., Bangsbo, J., Hostrup, M. High-intensity exercise training enhances mitochondrial oxidative phosphorylation efficiency in a temperature-dependent manner in human skeletal muscle: implications for exercise performance.

Neuromuscular Fatigue and Metabolism during High-Intensity Intermittent Exercise.

PURPOSE: To examine the degree of neuromuscular fatigue development along with changes in muscle metabolism during two work-matched high-intensity intermittent exercise protocols in trained individuals. METHODS: In a randomized, counter-balanced, crossover design, 11 endurance-trained men performed high-intensity intermittent cycle exercise protocols matched for total work and including either multiple short-duration (18 × 5 s; SS) or long-duration (6 × 20 s; LS) sprints. Neuromuscular fatigue was determined by preexercise to postexercise changes in maximal voluntary contraction force, voluntary activation level and contractile properties of the quadriceps muscle. Metabolites and pH were measured in vastus lateralis muscle biopsies taken before and after the first and last sprint of each exercise protocol. RESULTS: Peak power output (11% ± 2% vs 16% ± 8%, P < 0.01), maximal voluntary contraction (10% ± 5% vs 25% ± 6%, P < 0.05), and peak twitch force (34% ± 5% vs 67% ± 5%, P < 0.01) declined to a lesser extent in SS than LS, whereas voluntary activation level decreased similarly in SS and LS (10% ± 2% vs 11% ± 4%). Muscle [phosphocreatine] before the last sprint was 1.5-fold lower in SS than LS (P < 0.001). Preexercise to postexercise intramuscular accumulation of lactate and H was twofold and threefold lower, respectively, in SS than LS (P < 0.001), whereas muscle glycogen depletion was similar in SS and LS. Rate of muscle glycolysis was similar in SS and LS during the first sprint, but twofold higher in SS than LS during the last sprint (P < 0.05). CONCLUSIONS: These findings indicate that, in endurance-trained individuals, multiple long-sprints induce larger impairments in performance along with greater degrees of peripheral fatigue compared to work-matched multiple short-sprints, with these differences being possibly attributed to more extensive intramuscular accumulation of lactate/H and to lower rates of glycolysis during multiple long-sprint exercise.

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.

High-intensity exercise training ameliorates aberrant expression of markers of mitochondrial turnover but not oxidative damage in skeletal muscle of men with essential hypertension.

AIM: To examine whether hypertensive individuals exhibit altered muscle mitochondrial turnover and redox homeostasis compared with healthy normotensive counterparts, and whether the antihypertensive effect of high-intensity exercise training is associated with improved mitochondrial quality and enhanced anti-oxidant defence. METHODS: In a cross-sectional and longitudinal parallel design, 24 essential hypertensive (HYP) and 13 healthy normotensive (NORM) men completed 6 weeks of high-intensity interval training (HIIT). Twenty four-hour ambulatory blood pressure, body composition, cardiorespiratory fitness, exercise capacity and skeletal muscle characteristics were examined before and after HIIT. Expression of markers of mitochondrial turnover, anti-oxidant protection and oxidative damage was determined in vastus lateralis muscle biopsies. Muscle protein levels of eNOS and VEGF, and muscle capillarity were also evaluated. RESULTS: At baseline, HYP exhibited lower expression of markers of mitochondrial volume/biogenesis, mitochondrial fusion/fission and autophagy along with depressed eNOS expression compared with NORM. Expression of markers of anti-oxidant protection was similar in HYP and NORM, whereas oxidative damage was higher in HYP than in NORM. In HYP, HIIT lowered blood pressure, improved body composition, cardiorespiratory fitness and exercise capacity, up-regulated markers of mitochondrial volume/biogenesis and autophagy and increased eNOS and VEGF protein content. Furthermore, in HYP, HIIT induced divergent responses in markers of mitochondrial fusion and anti-oxidant protection, did not affect markers of mitochondrial fission, and increased apoptotic susceptibility and oxidative damage. CONCLUSION: The present results indicate aberrant muscle mitochondrial turnover and augmented oxidative damage in hypertensive individuals. High-intensity exercise training can partly reverse hypertension-related impairments in muscle mitochondrial turnover, but not redox imbalance.

Short- or long-rest intervals during repeated-sprint training in soccer?

The present study compared the effects of two repeated-sprint training (RST) programs, differing in duration of the between-sprint rest intervals, on various soccer-related exercise performances. For 5 weeks during the competitive season, twenty-nine young trained male soccer players either replaced two of their habitual fitness conditioning sessions with RST characterized by short (5-15; n = 9) or long (5-30; n = 10) rest intervals, or served as control (n = 10). The 5-15 and 5-30 protocols consisted of 6 repetitions of 30-m (~5 s) straight-line sprints interspersed with 15 s or 30 s of passive recovery, respectively. 5-15 improved 200-m sprint time (2.0±1.5%; p<0.05) and had a likely positive impact on 20-m sprint performance, whereas 5-30 lowered the 20-m sprint time (2.7±1.6%; p<0.05) but was only possibly effective for enhancing the 200-m sprint performance. The distance covered during the Yo-Yo Intermittent Recovery Test Level 2 increased following 5-15 (11.4±5.0%; p<0.05), which was possibly better than the non-significant 6.5% enhancement observed in 5-30. Improvements in the total time of a repeated-sprint ability test were possibly greater following 5-30 (3.6±0.9%; p<0.05) compared to 5-15 (2.6±1.1%; p<0.05). Both RST interventions led to similar beneficial (p<0.05) reductions in the percentage decrement score (~30%) of the repeated-sprint ability test as well as in blood lactate concentration during submaximal exercise (17-18%). No changes occurred in the control group. In soccer players, RST over a 5-week in-season period is an efficient means to simultaneously develop different components of fitness relevant to match performance, with different benefits induced by shorter compared to longer rest intervals.

Adaptations to Speed Endurance Training in Highly Trained Soccer Players.

PURPOSE: The present study examined whether a period of additional speed endurance training would improve intense intermittent exercise performance in highly trained soccer players during the season and whether the training changed aerobic metabolism and the level of oxidative enzymes in type I and type II muscle fibers. METHODS: During the last 9 wk of the season, 13 semiprofessional soccer players performed additional speed endurance training sessions consisting of two to three sets of 8-10 repetitions of 30-m sprints with 10 s of passive recovery (SET). Before and after SET, subjects completed a double-step exercise protocol that included transitions from standing to moderate-intensity running (~75% HRmax), followed by transitions from moderate- to high-intensity running (~90% HRmax) in which pulmonary oxygen uptake (V˙O2) was determined. In addition, the yo-yo intermittent recovery test level 1 was performed, and a muscle biopsy was obtained at rest. RESULTS: The yo-yo intermittent recovery test level 1 performance was 11.6% ± 6.4% (mean ± SD) better (2803 ± 330 vs 3127 ± 383 m, P < 0.05) after SET compared with before SET. In the transition from standing to moderate-intensity running, phase II pulmonary V˙O2 kinetics was 11.4% ± 16.5% faster (P < 0.05), and the running economy at this intensity was 2.3% ± 3.0% better (P < 0.05). These improvements were apparent despite the content of muscle proteins regulating oxidative metabolism (3-hydroxyacyl CoA dehydrogenase, COX IV, and OXPHOS), and capillarization was reduced (P < 0.05). The content of 3-hydroxyacyl CoA dehydrogenase and citrate synthase in type I and type II fibers did not change. CONCLUSION: In highly trained soccer players, additional speed endurance training is associated with an improved ability to perform repeated high-intensity work. To what extent the training-induced changes in V˙O2 kinetics and mechanical efficiency in type I fibers caused the improvement in performance warrants further investigation.

The Effect of Two Speed Endurance Training Regimes on Performance of Soccer Players.

In order to better understand the specificity of training adaptations, we compared the effects of two different anaerobic training regimes on various types of soccer-related exercise performances. During the last 3 weeks of the competitive season, thirteen young male professional soccer players (age 18.5±1 yr, height 179.5±6.5 cm, body mass 74.3±6.5 kg) reduced the training volume by ~20% and replaced their habitual fitness conditioning work with either speed endurance production (SEP; n = 6) or speed endurance maintenance (SEM; n = 7) training, three times per wk. SEP training consisted of 6-8 reps of 20-s all-out running bouts followed by 2 min of passive recovery, whereas SEM training was characterized by 6-8 x 20-s all-out efforts interspersed with 40 s of passive recovery. SEP training reduced (p<0.01) the total time in a repeated sprint ability test (RSAt) by 2.5%. SEM training improved the 200-m sprint performance (from 26.59±0.70 to 26.02±0.62 s, p<0.01) and had a likely beneficial impact on the percentage decrement score of the RSA test (from 4.07±1.28 to 3.55±1.01%) but induced a very likely impairment in RSAt (from 83.81±2.37 to 84.65±2.27 s). The distance covered in the Yo-Yo Intermittent Recovery test level 2 was 10.1% (p<0.001) and 3.8% (p<0.05) higher after SEP and SEM training, respectively, with possibly greater improvements following SEP compared to SEM. No differences were observed in the 20- and 40-m sprint performances. In conclusion, these two training strategies target different determinants of soccer-related physical performance. SEP improved repeated sprint and high-intensity intermittent exercise performance, whereas SEM increased muscles' ability to maximize fatigue tolerance and maintain speed development during both repeated all-out and continuous short-duration maximal exercises. These results provide new insight into the precise nature of a stimulus necessary to improve specific types of athletic performance in trained young soccer players.