Live high-train low (LHTL) using hypobaric hypoxia was previously found to improve sea-level endurance performance in well-trained individuals; however, confirmatory controlled data in athletes are lacking. Here, we test the hypothesis that natural-altitude LHTL improves aerobic performance in cross-country skiers, in conjunction with expansion of total hemoglobin mass (Hb , carbon monoxide rebreathing technique) promoted by accelerated erythropoiesis. Following duplicate baseline measurements at sea level over the course of 2 weeks, nineteen Norwegian cross-country skiers (three women, sixteen men, age 20 ± 2 year, maximal oxygen uptake (VO max) 69 ± 5 mL/min/kg) were assigned to 26 consecutive nights spent at either low (1035 m, control, n = 8) or moderate altitude (2207 m, daily exposure 16.7 ± 0.5 hours, LHTL, n = 11). All athletes trained together daily at a common location ranging from 550 to 1500 m (21.2% of training time at 550 m, 44.2% at 550-800 m, 16.6% at 800-1100 m, 18.0% at 1100-1500 m). Three test sessions at sea level were performed over the first 3 weeks after intervention. Despite the demonstration of nocturnal hypoxemia at moderate altitude (pulse oximetry), LHTL had no specific effect on serum erythropoietin, reticulocytes, Hb , VO max, or 3000-m running performance. Also, LHTL had no specific effect on (a) running economy (VO assessed during steady-state submaximal exercise), (b) respiratory capacities or efficiency of the skeletal muscle (biopsy), and (c) diffusing capacity of the lung. This study, showing similar physiological responses and performance improvements in the two groups following intervention, suggests that in young cross-country skiers, improvements in sea-level aerobic performance associated with LHTL may not be due to moderate-altitude acclimatization.

Preconditioning exercise performed with WBV at 40 Hz seems to have a positive effect on cycling sprint performance in young well-trained cyclists. This suggests that athletes can incorporate body-loaded squats with WBV in preparations to specific sprint training to improve the quality of the sprint training and also to improve sprint performance in relevant competitions.

Moderate exercise increases sVCAM-1 in hyperglycemic individuals, whereas it does not affect CRP.

Background Subjects with chronic obstructive pulmonary disease (COPD) are prone to accelerated decay of muscle strength and mass with advancing age. This is believed to be driven by disease-inherent systemic pathophysiologies, which are also assumed to drive muscle cells into a state of anabolic resistance, leading to impaired abilities to adapt to resistance exercise training. Currently, this phenomenon remains largely unstudied. In this study, we aimed to investigate the assumed negative effects of COPD for health- and muscle-related responsiveness to resistance training using a healthy control-based translational approach. Methods Subjects with COPD (n = 20, GOLD II-III, FEV1predicted 57 ± 11%, age 69 ± 5) and healthy controls (Healthy, n = 58, FEV1predicted 112 ± 16%, age 67 ± 4) conducted identical whole-body resistance training interventions for 13 weeks, consisting of two weekly supervised training sessions. Leg exercises were performed unilaterally, with one leg conducting high-load training (10RM) and the contralateral leg conducting low-load training (30RM). Measurements included muscle strength (nvariables = 7), endurance performance (nvariables = 6), muscle mass (nvariables = 3), muscle quality, muscle biology (m. vastus lateralis; muscle fiber characteristics, RNA content including transcriptome) and health variables (body composition, blood). For core outcome domains, weighted combined factors were calculated from the range of singular assessments. Results COPD displayed well-known pathophysiologies at baseline, including elevated levels of systemic low-grade inflammation ([c-reactive protein]serum), reduced muscle mass and functionality, and muscle biological aberrancies. Despite this, resistance training led to improved lower-limb muscle strength (15 ± 8%), muscle mass (7 ± 5%), muscle quality (8 ± 8%) and lower-limb/whole-body endurance performance (26 ± 12%/8 ± 9%) in COPD, resembling or exceeding responses in Healthy, measured in both relative and numeric change terms. Within the COPD cluster, lower FEV1predicted was associated with larger numeric and relative increases in muscle mass and superior relative improvements in maximal muscle strength. This was accompanied by similar changes in hallmarks of muscle biology such as rRNA-content↑, muscle fiber cross-sectional area↑, type IIX proportions↓, and changes in mRNA transcriptomics. Neither of the core outcome domains were differentially affected by resistance training load. Conclusions COPD showed hitherto largely unrecognized responsiveness to resistance training, rejecting the notion of disease-related impairments and rather advocating such training as a potent measure to relieve pathophysiologies. Trial registration: ClinicalTrials.gov ID: NCT02598830. Registered November 6th 2015, https://clinicaltrials.gov/ct2/show/NCT02598830

Chronic obstructive lung disease (COPD) is associated with impaired muscle functions in addition to the impaired cardiopulmonary capacity inherent to the disease.The purpose of this study was to compare muscular performance between COPD subjects (COPD, n = 11, GOLD grade II/III; FEV 1 = 53 ± 14% predicted; 61 ± 7 years) and healthy controls (HC, n = 12, 66 ± 8 years) in three resistance exercises with different complexity: (a) one-legged knee extension (1KE), and (b) one-and (c) twolegged leg press (1LP and 2LP, respectively). For each exercise, muscular performance was defined as repetitions to exhaustion at 60% of one-repetition maximum or overall exercise volume, calculated as the sum of three exercise sets. In HC, muscular performance increased progressively with increasing physiological complexity: 1KE < 1LP < 2LP. Using 1KE as reference value, muscular performance increased by 1.9 (repetitions) or 4.6-fold (volume) in 1LP and 3.1 or 7.1-fold in 2LP. In COPD, similar increases occurred going from 1KE to 1LP (1.9 or 4.4-fold change), but not from 1LP to 2LP, where no further increase occurred. In conclusion, in COPD, performance is impaired in exercises involving larger amounts of muscle mass (>1LP), advocating utilization of one-legged resistance protocols for rehabilitation purposes. K E Y W O R D Scardiorespiratory capacity, chronic obstructive lung disease, muscular performance, resistance training, strength training, unilateral training How to cite this article: Mølmen KS, Evensen Thy E, Thallaug Dalane S, Ellefsen S, Falch GS. Muscular performance decreases with increasing complexity of resistance exercises in subjects with chronic obstructive pulmonary disease. Transl Sports Med.

Rationale. Subjects with chronic obstructive pulmonary disease (COPD) are prone to accelerated decay of muscle strength and mass with advancing age. This is mediated by systemic pathophysiologies, which are also believed to impair responses to exercise training, a notion that remains largely unstudied. Objectives. To investigate the presence of impaired training responsiveness in COPD, measured as responses to resistance training compared to healthy participants. Methods. COPD (GOLD grade II-III, n=20, age 69±5) and Healthy (n=58, age 67±4) conducted identical whole-body resistance training interventions, consisting of two weekly, supervised training sessions for 13 weeks. Leg exercises were performed unilaterally, with one leg conducting high-load training (10 repetitions maximum; RM) and the contralateral leg conducting low-load training (30RM). Measurements and Main Results. Measurements included muscle strength (n=7), endurance performance (n=6), muscle mass (n=2), muscle quality, muscle biology (vastus lateralis; muscle fiber characteristics, RNA content including transcriptome) and health-related variables (body composition, blood). For core outcome domains, weighted combined factors were calculated from the range of singular assessments. COPD showed marked improvements in lower-limb muscle strength/mass/quality and lower-limb/whole-body endurance performance, resembling or exceeding those of Healthy, measured as both relative and absolute change terms. This was accompanied by similar changes in muscle biological hallmarks (total RNA/rRNA content↑, muscle fiber cross-sectional area↑, type IIX proportions↓, changes in the mRNA transcriptome). Neither of the core outcome domains were differentially affected by resistance training load. Conclusions. COPD showed marked, unimpaired and hitherto unrecognized responsiveness to resistance training, rejecting the notion of disease-related impairments in training responsiveness.

Background Chronic obstructive pulmonary disease (COPD) is associated with skeletal muscle mitochondrial dysfunction. Resistance exercise training (RT) is a training modality with a relatively small pulmonary demand that has been suggested to increase skeletal muscle oxidative enzyme activity in COPD. Whether a shift into a more oxidative profile following RT also translates into increased mitochondrial respiratory capacity in COPD is yet to be established. Methods This study investigated the effects of 13 weeks of RT on m. vastus lateralis mitochondrial capacity in 11 persons with moderate COPD [45% females, age: 69 ± 4 years (mean ± SD), predicted forced expiratory volume in 1 s (FEV1): 56 ± 7%] and 12 healthy controls (75% females, age: 66 ± 5 years, predicted FEV1: 110 ± 16%). RT was supervised and carried out two times per week. Leg exercises included leg press, knee extension, and knee flexion and were performed unilaterally with one leg conducting high‐load training (10 repetitions maximum, 10RM) and the other leg conducting low‐load training (30 repetitions maximum, 30RM). One‐legged muscle mass, maximal muscle strength, and endurance performance were determined prior to and after the RT period, together with mitochondrial respiratory capacity using high‐resolution respirometry and citrate synthase (CS) activity (a marker for mitochondrial volume density). Transcriptome analysis of genes associated with mitochondrial function was performed. Results Resistance exercise training led to similar improvements in one‐legged muscle mass, muscle strength, and endurance performance in COPD and healthy individuals. In COPD, mitochondrial fatty acid oxidation capacity and oxidative phosphorylation increased following RT (+13 ± 22%, P = 0.033 and +9 ± 23%, P = 0.035, respectively). Marked increases were also seen in COPD for mitochondrial volume density (CS activity, +39 ± 35%, P = 0.001), which increased more than mitochondrial respiration, leading to lowered intrinsic mitochondrial function (respiration/CS activity) for complex‐1‐supported respiration (−12 ± 43%, P = 0.033), oxidative phosphorylation (−10 ± 42%, P = 0.037), and electron transfer system capacity (−6 ± 52%, P = 0.027). No differences were observed between 10RM and 30RM RT, nor were there any adaptations in mitochondrial function following RT in healthy controls. RT led to differential expression of numerous genes related to mitochondrial function in both COPD and healthy controls, with no difference being observed between groups. Conclusions Thirteen weeks of RT resulted in augmented skeletal muscle mitochondrial respiratory capacity in COPD, accompanied by alterations in the transcriptome and driven by an increase in mitochondrial quantity rather than improved mitochondrial quality.