The Effect of Monophasic Oral Contraceptives on Muscle Strength and Markers of Recovery After Exercise-Induced Muscle Damage: A Systematic Review.

CONTEXT: Oral contraceptives (OCs) manipulate hormonal fluctuations of the menstrual cycle and affect physical performance. Most investigations on the effect of OCs on physical performance did not discriminate between different types of OCs. Thus, the effects of monophasic OCs (MOCs) - the most common type of OCs - on muscle strength and recovery from exercise are largely unknown. OBJECTIVE: To examine the effect of MOC use on muscle strength and markers of recovery after exercise-induced muscle damage (EIMD) in premenopausal women. DATA SOURCES: Electronic databases Embase, PubMed, SportDiscus, and Web of Science were searched for studies examining the effect of MOCs on acute muscle strength and recovery. STUDY SELECTION: Keywords applied for the study selection were oral contraceptive* AND muscle strength or oral contraceptive* AND muscle damage. STUDY DESIGN: Systematic review. LEVEL OF EVIDENCE: Lowest quality assessed for an included study in this review was serious risk of bias using ROBINS-I tool made from Cochrane for nonrandomized studies. DATA EXTRACTION: A total of 104 studies on muscle strength were identified, of which 11 met the inclusion criteria. Concerning recovery, 51 studies were identified, of which 4 met the inclusion criteria. RESULTS: Of the 11 studies included, 10 showed no effect of MOCs on acute muscle strength. Of the 4 studies on recovery, 2 found a greater decrease in muscle strength, and 3 found higher creatine kinase (CK) levels after EIMD in MOC users than in nonusers. The included studies were all rated with moderate-to-serious risk of bias. CONCLUSION: These findings suggest that MOCs may impair recovery from EIMD as indicated by lowered muscle strength and elevated CK levels. There is insufficient evidence to conclude whether MOCs acutely affect muscle strength. Moderate-to-serious risk of bias in studies makes interpretation challenging.

Effects of Follicular and Luteal Phase-Based Menstrual Cycle Resistance Training on Muscle Strength and Mass.

There is an increasing interest in female athletic performance-especially concerning the impact of the female menstrual cycle on training response. Indeed, fluctuations in female sex hormones, estrogen and progesterone, during the menstrual cycle regulate protein metabolism and recovery processes in skeletal muscle and may thus impact exercise training-related outcomes. Studies demonstrate that anaerobic capacity and muscle strength are greatest during the follicular phase of the menstrual cycle, when estrogen levels peak. In addition, studies indicate that resistance training conducted in the follicular phase of the menstrual cycle (follicular phase-based resistance training) may be superior to luteal phase-based training in terms of enhancing muscle strength and mass. This raises the possibility that the physiological capabilities of skeletal muscle to adapt to exercise training are dependent on the menstrual cycle and can be important for female athletes in optimizing their training. In this paper, we critically review the current state of the art concerning the impact of menstrual cycle phase-based resistance training and highlight why follicular phase-based resistance training possibly is superior to luteal phase-based training in enhancing resistance training outcomes. Finally, we identify directions for further research.

Effect of High-Intensity Interval Training and Intermittent Fasting on Body Composition and Physical Performance in Active Women.

Nutritional strategies may have an effect on body composition and physical performance. Intermittent fasting (IF) is an eating pattern that cycles between periods of eating and fasting in specified time periods. Moreover, it is a common strategy among members of the athlete population that are looking for weight loss. However, this strategy may negatively affect physical performance, as compared to other weight loss strategies. The main purpose of this research was to use a cross-over design to study the effects of HIIT, with or without intermittent fasting, on muscular and anaerobic performance in 14 active women (27 ± 6 y). To assess performance, body composition (anthropometry), hand-grip strength, and counter-movement jump (CMJ) height was measured, and a 30 s Wingate test was completed assessed. HIIT + IF reduced fat mass (1 kg, p < 0.05, d = 1.1; 1.5%, p < 0.01, d = 1.0) and increased CMJ height (6.2 cm, p < 0.001, d = 1.8). In addition, the change in CMJ height in HIIT + IF was higher over HIIT (5.2 cm, p < 0.001, d = 1.9). In conclusion, intermittent fasting could be a nutritional strategy to decrease fat mass and increase jumping performance. However, longer duration programs would be necessary to determine whether other parameters of muscle performance could be positively affected by IF.

Validation and Practical Applications of Performance in a 6-Min Rowing Test in the Danish Armed Forces.

Personnel of the Danish Armed Forces must complete a yearly basic physical fitness test consisting of a Cooper's 12-min run test (CRT) and four strength-related bodyweight exercises. However, there is no validated alternative to the CRT allowing injured or sailing personnel to conduct the yearly basic physical fitness test. Therefore, the aim of this study was to validate performance in a 6-min rowing ergometer test (6MRT) against CRT performance. Thirty-one individuals (M/F: 20/11, age: 34 ± 12 years) employed at the Danish Armed Forces completed testing on two independent days; (I) the CRT on an outdoor track and (II) a 6MRT with pulmonary measurements of breath-by-breath oxygen uptake. In addition, 5 participants (M/F: 4/1, age: 40 ± 10 years) completed re-testing of the 6MRT. No difference was observed between VO2max estimated from the CRT and measured during the 6MRT. Absolute VO2max correlated strongly (r = 0.95; p < 0.001) to performance in the 6MRT, and moderately (r = 0.80; p < 0.001) to performance in the CRT. Bodyweight (BW) and fat free mass (FFM) correlated stronger to performance in the 6MRT compared to the CRT. 6MRT re-testing yielded similar performance results. The 6MRT is a valid and reliable alternative to the CRT, allowing injured or sailing personnel of the Danish Armed Forces to complete the basic physical fitness test as required, albeit 6MRT performance demands must be made relative to bodyweight.

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.

Hypertension is associated with blunted NO-mediated leg vasodilator responsiveness that is reversed by high-intensity training in postmenopausal women.

The menopausal transition is associated with increased prevalence of hypertension, and in time, postmenopausal women (PMW) will exhibit a cardiovascular disease risk score similar to male counterparts. Hypertension is associated with vascular dysfunction, but whether hypertensive (HYP) PMW have blunted nitric oxide (NO)-mediated leg vasodilator responsiveness and whether this is reversible by high-intensity training (HIT) is unknown. To address these questions, we examined the leg vascular conductance (LVC) in response to femoral infusion of acetylcholine (ACh) and sodium nitroprusside (SNP) and skeletal muscle markers of oxidative stress and NO bioavailability before and after HIT in PMW [12.9 ± 6.0 (means ± SD) years since last menstrual cycle]. We hypothesized that ACh- and SNP-induced LVC responsiveness was reduced in hypertensive compared with normotensive (NORM) PMW and that 10 wk of HIT would reverse the blunted LVC response and decrease blood pressure (BP). Nine hypertensive (HYP (clinical systolic/diastolic BP, 149 ± 11/91 ± 83 mmHg) and eight normotensive (NORM (122 ± 13/75 ± 8 mmHg) PMW completed 10 wk of biweekly small-sided floorball training (4-5 × 3-5 min interspersed by 1-3-min rest periods). Before training, the SNP-induced change in LVC was lower (P < 0.05) in HYP compared with in NORM. With training, the ACh- and SNP-induced change in LVC at maximal infusion rates, i.e., 100 and 6 µg·min-1·kg leg mass-1, respectively, improved (P < 0.05) in HYP only. Furthermore, training decreased (P < 0.05) clinical systolic/diastolic BP (-15 ± 11/-9 ± 7 mmHg) in HYP and systolic BP (-10 ± 9 mmHg) in NORM. Thus, the SNP-mediated LVC responsiveness was blunted in HYP PMW and reversed by a period of HIT that was associated with a marked decrease in clinical BP.

Increased prostacyclin formation after high-intensity interval training in late postmenopausal women.

PURPOSE: Aging impairs vascular function in women, with the largest detrimental effects occurring during the menopausal transition. Deficiency in the nitric oxide system has been suggested to be responsible for impairment in vascular function with aging, but recent observations suggest that the prostacyclin system, acting in redundancy with the nitric oxide system, may be of importance too. Improvement in vascular function is a hallmark of exercise training and we hypothesize that leg vascular function is improved by exercise training in late postmenopausal women, and that the underlying mechanism is increased endothelial formation of prostacyclin and responsiveness to prostacyclin by the vascular smooth muscle cells. METHOD: Femoral-arterial infusion of acetylcholine and epoprostenol was used to assess vascular function and prostacyclin release in ten late postmenopausal women (62 ± 7 years) before and after 10 weeks of high-intensity interval training (floorball conducted as small-sided games). RESULT: The training intervention increased fitness level (V̇O2max) by 7 ± 7% and reduced systolic and diastolic blood pressure by 10 ± 10 and 5 ± 6 mmHg, respectively. Leg vascular responsiveness to during acetylcholine and epoprostenol infusion was unchanged with training, whereas the release of prostacyclin during acetylcholine infusion increased by 125%. CONCLUSIONS: In late postmenopausal women, vascular function assessed by femoral-arterial infusion of acetylcholine was not improved after 10 weeks of floorball training, but acetylcholine-induced prostacyclin formation and blood pressure were substantially improved. It is possible that a longer training period could lead to improvements in vascular function and that the observed increase in prostacyclin formation is one of the initial underlying changes.

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.

Efficacy of 10-20-30 training versus moderate-intensity continuous training on HbA1c, body composition and maximum oxygen uptake in male patients with type 2 diabetes: A randomized controlled trial.

AIM: To compare the efficacy of 10-20-30 training versus moderate-intensity continuous training (MICT) on HbA1c, body composition and maximum oxygen uptake (V˙O2 max) in male patients with type 2 diabetes (T2D). MATERIALS AND METHODS: Fifty-one male participants with T2D were randomly assigned (1:1) to a 10-20-30 (N = 26) and a MICT (N = 25) training group. Interventions consisted of supervised cycling three times weekly for 10 weeks, lasting 29 minutes (10-20-30) and 50 minutes (MICT) in a local non-clinical setting. The primary outcome was change in HbA1c from baseline to 10-week follow-up. RESULTS: Of 51 participants enrolled, 44 (mean age 61.0 ± 6.8 [mean ± SD] years, diagnosed 7.5 ± 5.8 years, baseline HbA1c 7.4% ± 1.3%) were included in the analysis. Training compliance was 84% and 86% in 10-20-30 and MICT, respectively. No adverse events occurred during the intervention. HbA1c decreased (P <0.001) by 0.5 (95% CI -0.72 to -0.21) percentage points with training in 10-20-30, with no change in MICT. The change in 10-20-30 was greater (P <0.05) than in MICT. Visceral fat mass decreased (P <0.05) only with 10-20-30 training, whereas total fat mass decreased (P <0.01) and V˙O2 max increased (P <0.01) with training in both groups. CONCLUSIONS: Ten weeks of 10-20-30 training was superior to MICT in lowering HbA1c, and only 10-20-30 training decreased visceral fat mass in patients with T2D. Furthermore, 10-20-30 training was as effective as MICT in reducing total fat mass and increasing V˙O2 max, despite a 42% lower training time commitment.

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.

Abundance of ClC-1 chloride channel in human skeletal muscle: fiber type specific differences and effect of training.

Cl- channel protein 1 (ClC-1) may be important for excitability and contractility in skeletal muscle, but ClC-1 abundance has not been examined in human muscle. The aim of the present study was to examine ClC-1 abundance in human skeletal muscle, including fiber type specific differences and the effect of exercise training. A commercially available antibody was tested with positive and negative control tissue, and it recognized specifically ClC-1 in the range from 100 to 150 kDa. Abundance of ClC-1 was 38% higher ( P < 0.01) in fast twitch Type IIa muscle fibers than in slow twitch Type I. Muscle ClC-1 abundance did not change with 4 wk of training consisting of 30 min cycling at 85% of maximal heart rate (HRmax) and 3 × 30-s all out sprints or during a 7-wk training period with 10-12 × 30 s uphill cycling and 4-5 × ~4 min cycling at 90%-95% of HRmax. ClC-1 abundance correlated negatively ( P < 0.01) with maximal oxygen consumption ( r = -0.552) and incremental exercise performance ( r = -0.546). In addition, trained cyclists had lower ( P < 0.01) ClC-1 abundance than lesser trained individuals. The present observations indicate that a low abundance of muscle ClC-1 may be beneficial for exercise performance, but the role of abundance and regulation of ClC-1 in skeletal muscle of humans with respect to exercise performance and trainability need to be elucidated. NEW & NOTEWORTHY Abundance of the Cl- channel protein 1 (ClC-1) chloride channel may be important for excitability and contractility in human skeletal muscle and may therefore have implications for fatigue development. In this study, we confirmed ClC-1 specificity for a commercially available antibody, and this study is first to our knowledge to determine ClC-1 protein abundance in human muscle by Western blotting. We observed that abundance of ClC-1 was higher in fast compared with slow twitch fibers and lower in trained individuals than in recreationally active.

Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle.

Moderately trained male subjects (mean age 25 years; range 19-33 years) completed an 8-week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30-sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts.

Impact of adrenaline and metabolic stress on exercise-induced intracellular signaling and PGC-1α mRNA response in human skeletal muscle.

This study tested the hypothesis that elevated plasma adrenaline or metabolic stress enhances exercise-induced PGC-1α mRNA and intracellular signaling in human muscle. Trained (VO2-max: 53.8 ± 1.8 mL min(-1) kg(-1)) male subjects completed four different exercise protocols (work load of the legs was matched): C - cycling at 171 ± 6 W for 60 min (control); A - cycling at 171 ± 6 W for 60 min, with addition of intermittent arm exercise (98 ± 4 W). DS - cycling at 171 ± 6 W interspersed by 30 sec sprints (513 ± 19 W) every 10 min (distributed sprints); and CS - cycling at 171 ± 6 W for 40 min followed by 20 min of six 30 sec sprints (clustered sprints). Sprints were followed by 3:24 min:sec at 111 ± 4 W. A biopsy was obtained from m. vastus lateralis at rest and immediately, and 2 and 5 h after exercise. Muscle PGC-1α mRNA content was elevated (P < 0.05) three- to sixfold 2 h after exercise relative to rest in C, A, and DS, with no differences between protocols. AMPK and p38 phosphorylation was higher (P < 0.05) immediately after exercise than at rest in all protocols, and 1.3- to 2-fold higher (P < 0.05) in CS than in the other protocols. CREB phosphorylation was higher (P < 0.05) 2 and 5 h after exercise than at rest in all protocols, and higher (P < 0.05) in DS than CS 2 h after exercise. This suggests that neither plasma adrenaline nor muscle metabolic stress determines the magnitude of PGC-1α mRNA response in human muscle. Furthermore, higher exercise-induced changes in AMPK, p38, and CREB phosphorylation are not associated with differences in the PGC-1α mRNA response.

Effect of speed endurance and strength training on performance, running economy and muscular adaptations in endurance-trained runners.

PURPOSE: To investigate the effects of combined strength and speed endurance (SE) training along with a reduced training volume on performance, running economy and muscular adaptations in endurance-trained runners. METHODS: Sixteen male endurance runners (VO2-max: ~60 ml kg(-1) min(-1)) were randomly assigned to either a combined strength and SE training (CSS; n = 9) or a control (CON; n = 7) group. For 8 weeks, CSS replaced their normal moderate-intensity training (~63 km week(-1)) with SE (2 × week(-1)) and strength training (2 × week(-1)) as well as aerobic high (1 × week(-1)) and moderate (1 × week(-1)) intensity training with a reduction in total volume of ~58 %, whereas CON continued their training (~45 km week(-1)). RESULTS: In CSS, 400-m and Yo-Yo intermittent recovery test performance was improved by 5 % (P < 0.01) and 19 % (P < 0.001), respectively, during the intervention period. Maximal aerobic speed was 0.6 km h(-1) higher (P < 0.05), and maximal activity of lactate dehydrogenase subunits 1 and 2 was 17 % (P < 0.05) higher after compared to before the intervention period. Time to exhaustion and peak blood lactate during an incremental treadmill test was 9 % (P < 0.05) and 32 % (P < 0.01), respectively, higher and expression of Na(+)-K(+) pump ß1 subunit was 15 % higher (P < 0.05) after compared to before the intervention period. 10-K performance, maximum oxygen uptake and running economy were unchanged. In CON, no changes were observed. CONCLUSIONS: Adding strength and speed endurance training, along with a reduced training volume, can improve short-term exercise capacity and induce muscular adaptations related to anaerobic capacity in endurance-trained runners.

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.

Intensive training and reduced volume increases muscle FXYD1 expression and phosphorylation at rest and during exercise in athletes.

The present study examined the effect of intensive training in combination with marked reduction in training volume on phospholemman (FXYD1) expression and phosphorylation at rest and during exercise. Eight well-trained cyclists replaced their regular training with speed-endurance training (10-12 × âˆ¼30-s sprints) two or three times per week and aerobic high-intensity training (4-5 × 3-4 min at 90-95% of peak aerobic power output) 1-2 times per week for 7 wk and reduced the training volume by 70%. Muscle biopsies were obtained before and during a repeated high-intensity exercise protocol, and protein expression and phosphorylation were determined by Western blot analysis. Expression of FXYD1 (30%), actin (40%), mammalian target of rapamycin (mTOR) (12%), phospholamban (PLN) (16%), and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) γ/δ (25%) was higher (P < 0.05) than before the training intervention. In addition, after the intervention, nonspecific FXYD1 phosphorylation was higher (P < 0.05) at rest and during exercise, mainly achieved by an increased FXYD1 Ser-68 phosphorylation, compared with before the intervention. CaMKII, Thr-287, and eukaryotic elongation factor 2 Thr-56 phosphorylation at rest and during exercise, overall PKCα/ß, Thr-638/641, and mTOR Ser-2448 phosphorylation during repeated intense exercise as well as resting PLN Thr-17 phosphorylation were also higher (P < 0.05) compared with before the intervention period. Thus, a period of high-intensity training with reduced training volume increases expression and phosphorylation levels of FXYD1, which may affect Na(+)/K(+) pump activity and muscle K(+) homeostasis during intense exercise. Furthermore, higher expression of CaMKII and PLN, as well as increased phosphorylation of CaMKII Thr-287 may have improved intracellular Ca(2+) handling.