Structural Musculotendinous Parameters That Predict Failed Tendon Healing After Rotator Cuff Repair.

Background: Healing of the rotator cuff after repair constitutes a major clinical challenge with reported high failure rates. Identifying structural musculotendinous predictors for failed rotator cuff repair could enable improved diagnosis and management of patients with rotator cuff disease. Purpose: To investigate structural predictors of the musculotendinous unit for failed tendon healing after rotator cuff repair. Study Design: Cohort study; Level of evidence, 2. Methods: Included were 116 shoulders of 115 consecutive patients with supraspinatus (SSP) tear documented on magnetic resonance imaging (MRI) who were treated with an arthroscopic rotator cuff repair. Preoperative assessment included standardized clinical and imaging (MRI) examinations. Intraoperatively, biopsies of the joint capsule, the SSP tendon, and muscle were harvested for histological assessment. At 3 and 12 months postoperatively, patients were re-examined clinically and with MRI. Structural and clinical predictors of healing were evaluated using logistic and linear regression models. Results: Structural failure of tendon repair, which was significantly associated with poorer clinical outcome, was associated with older age (ß = 1.12; 95% CI, 1.03 to 1.26; P = .03), shorter SSP tendon length (ß = 0.89; 95% CI, 0.8 to 0.98; P = .02), and increased proportion of slow myosin heavy chain (MHC)-I/fast MHC-II hybrid muscle fibers (ß = 1.23; 95% CI, 1.07 to 1.42; P = .004). Primary clinical outcome (12-month postoperative Constant score) was significantly less favorable for shoulders with fatty infiltration of the infraspinatus muscle (ß = -4.71; 95% CI, -9.30 to -0.12; P = .044). Conversely, a high content of fast MHC-II muscle fibers (ß = 0.24; 95% CI, 0.026 to 0.44; P = .028) was associated with better clinical outcome. Conclusion: Both decreased tendon length and increased hybrid muscle fiber type were independent predictors for retear. Clinical outcome was compromised by tendon retearing and increased fatty infiltration of the infraspinatus muscle. A high content of fast MHC-II SSP muscle fibers was associated with a better clinical outcome. Registration: NCT02123784 (ClinicalTrials.govidentifier).

Resistance training preserves high-intensity interval training induced improvements in skeletal muscle capillarization of healthy old men: a randomized controlled trial.

Skeletal muscle capillarization is a determining factor in gas and metabolite exchange, while its impairments may contribute to the development of sarcopenia. Studies on the potential of resistance training (RT) to induce angiogenesis in older muscles have been inconclusive, and effects of sequential endurance training (ET) and RT on capillarization are unknown. Healthy older men (66.5 ± 3.8 years) were engaged in either 12 weeks of habitual course observation (HC) followed by 12 weeks of RT (n = 8), or 12 weeks of high-intensity interval training (HIIT) followed by 12 weeks of RT (n = 9). At baseline, following 12 and 24 weeks, m. vastus lateralis biopsies were obtained. (Immuno-)histochemistry was used to assess indices of muscle fiber capillarization, muscle fiber morphology and succinate dehydrogenase (SDH) activity. Single periods of RT and HIIT resulted in similar improvements in capillarization and SDH activity. During RT following HIIT, improved capillarization and SDH activity, as well as muscle fiber morphology remained unchanged. The applied RT and HIIT protocols were thus similarly effective in enhancing capillarization and oxidative enzyme activity and RT effectively preserved HIIT-induced adaptations of these parameters. Hence, both, RT and HIIT, are valid training modalities for older men to improve skeletal muscle vascularization.

Satellite cell content in Huntington's disease patients in response to endurance training.

BACKGROUND: Skeletal muscle wasting is a hallmark of Huntington's disease (HD). However, data on myocellular characteristics and myofiber remodeling in HD patients are scarce. We aimed at gaining insights into myocellular characteristics of HD patients as compared to healthy controls at rest and after a period of increased skeletal muscle turnover. METHODS: Myosin heavy chain (MyHC)-specific cross-sectional area, satellite cell content, myonuclear number, myonuclear domain, and muscle fiber type distribution were determined from vastus lateralis muscle biopsies at rest and after 26 weeks of endurance training in HD patients and healthy controls. RESULTS: At the beginning of the study, there were no differences in myocellular characteristics between HD patients and healthy controls. Satellite cell content per MyHC-1 fiber (P = 0.014) and per MyHC-1 myonucleus (P = 0.006) increased significantly in healthy controls during the endurance training intervention, whereas it remained constant in HD patients (P = 0.804 and P = 0.975 for satellite cell content per MyHC-1 fiber and myonucleus, respectively). All further variables were not altered during the training intervention in HD patients and healthy controls. CONCLUSIONS: Similar skeletal muscle characteristics between HD patients and healthy controls at baseline suggested similar potential for myofiber remodeling in response to exercise. However, the missing satellite cell response in MyHC-1 myofibers following endurance training in HD patients points to a potential dysregulation in the exercise-induced activation and/or proliferation of satellite cells. In the longer-term, impaired myonuclear turnover might be associated with the clinical observation of skeletal muscle wasting.

Greater blood volume and Hb mass in obese women quantified by the carbon monoxide-rebreathing method affects interpretation of iron biomarkers and iron requirements.

BACKGROUND/OBJECTIVE: Iron deficiency (ID) is common in overweight and obese individuals (OW/OB) but the mechanism is uncertain. Greater blood volume (BV) in OW/OB may increase hemoglobin (Hb) mass and iron requirements, and confound iron biomarkers by hemodilution. Quantification of BV/PV changes in OW/OB is challenging and a formula to estimate BV/PV based on anthropometric indices would be valuable. In normal weight (NW) and OW/OB women, we aimed at: (1) measure BV and assess whether differences in BV affect concentrations and total circulating mass of Hb and iron biomarkers; (2) develop an algorithm describing BV in OW/OB. SUBJECTS/METHODS: In a cross-sectional study, we measured BV in NW, OW, and OB non-anemic women (n = 62) by using the carbon monoxide-rebreathing method, body composition by dual energy X-ray absorptiometry, and iron and inflammatory status. RESULTS: OW and OB women had 11 and 16% higher mean BV and PV compared to NW (P < 0.05), respectively. In OW/OB compared to NW, total circulating masses of IL-6, hepcidin, Hb, and sTfR were higher, while total mass of serum iron was lower (for all, P < 0.05). An equation including height, body mass and lean mass to estimate BV in all BMI groups (R2 = 0.76). CONCLUSION: An equation based on anthropometric indices provides a good estimate of increased BV in OW/OB women. In OW/OB women, there is an increase in Hb mass that likely increases iron requirements for erythropoiesis and circulating TfR mass. At the same time, higher hepcidin concentrations may lower serum iron mass. Both these mechanisms may increase risk for ID in OW/OB women.

Effects of endurance training on skeletal muscle mitochondrial function in Huntington disease patients.

BACKGROUND: Mitochondrial dysfunction may represent a pathogenic factor in Huntington disease (HD). Physical exercise leads to enhanced mitochondrial function in healthy participants. However, data on effects of physical exercise on HD skeletal muscle remains scarce. We aimed at investigating adaptations of the skeletal muscle mitochondria to endurance training in HD patients. METHODS: Thirteen HD patients and 11 healthy controls completed 26 weeks of endurance training. Before and after the training phase muscle biopsies were obtained from M. vastus lateralis. Mitochondrial respiratory chain complex activities, mitochondrial respiratory capacity, capillarization, and muscle fiber type distribution were determined from muscle samples. RESULTS: Citrate synthase activity increased during the training intervention in the whole cohort (P = 0.006). There was no group x time interaction for citrate synthase activity during the training intervention (P = 0.522). Complex III (P = 0.008), Complex V (P = 0.043), and succinate cytochrome c reductase (P = 0.008) activities increased in HD patients and controls by endurance training. An increase in mass-specific mitochondrial respiratory capacity was present in HD patients during the endurance training intervention. Overall capillary-to-fiber ratio increased in HD patients by 8.4% and in healthy controls by 6.4% during the endurance training intervention. CONCLUSIONS: Skeletal muscle mitochondria of HD patients are equally responsive to an endurance-training stimulus as in healthy controls. Endurance training is a safe and feasible option to enhance indices of energy metabolism in skeletal muscle of HD patients and may represent a potential therapeutic approach to delay the onset and/or progression of muscular dysfunction. TRIAL REGISTRATION: ClinicalTrials.gov NCT01879267 . Registered May 24, 2012.

Robot-assisted assessment of muscle strength.

Impairment of neuromuscular function in neurological disorders leads to reductions in muscle force, which may lower quality of life. Rehabilitation robots that are equipped with sensors are able to quantify the extent of muscle force impairment and to monitor a patient during the process of neurorehabilitation with sensitive and objective assessment methods. In this article, we provide an overview of fundamental aspects of muscle function and how the corresponding variables can be quantified by means of meaningful robotic assessments that are primarily oriented towards upper limb neurorehabilitation. We discuss new concepts for the assessment of muscle function, and present an overview of the currently available systems for upper limb measurements. These considerations culminate in practical recommendations and caveats for the rational quantification of force magnitude, force direction, moment of a force, impulse, critical force (neuromuscular fatigue threshold) and state and trait levels of fatigue.

T/T homozygosity of the tenascin-C gene polymorphism rs2104772 negatively influences exercise-induced angiogenesis.

BACKGROUND: Mechanical stress, including blood pressure related factors, up-regulate expression of the pro-angiogenic extracellular matrix protein tenascin-C in skeletal muscle. We hypothesized that increased capillarization of skeletal muscle with the repeated augmentation in perfusion during endurance training is associated with blood vessel-related expression of tenascin-C and would be affected by the single-nucleotide polymorphism (SNP) rs2104772, which characterizes the non-synonymous exchange of thymidine (T)-to-adenosine (A) in the amino acid codon 1677 of tenascin-C. METHODS: Sixty-one healthy, untrained, male white participants of Swiss descent performed thirty 30-min bouts of endurance exercise on consecutive weekdays using a cycling ergometer. Genotype and training interactions were called significant at Bonferroni-corrected p-value of 5% (repeated measures ANOVA). RESULTS: Endurance training increased capillary-to-fiber-ratio (+11%), capillary density (+7%), and mitochondrial volume density (+30%) in m. vastus lateralis. Tenascin-C protein expression in this muscle was confined to arterioles and venules (80% of cases) and increased after training in A-allele carriers. Prior to training, volume densities of subsarcolemmal and myofibrillar mitochondria in m. vastus lateralis muscle were 49% and 18%, respectively, higher in A/A homozygotes relative to T-nucleotide carriers (A/T and T/T). Training specifically increased capillary-to-fiber ratio in A-nucleotide carriers but not in T/T homozygotes. Genotype specific regulation of angiogenesis was reflected by the expression response of 8 angiogenesis-associated transcripts after exercise, and confirmed by training-induced alterations of the shear stress related factors, vimentin and VEGF A. CONCLUSION: Our findings provide evidence for a negative influence of T/T homozygosity in rs2104772 on capillary remodeling with endurance exercise.

Exercise effects in Huntington disease.

Huntington disease (HD) is a relentlessly progressive neurodegenerative disorder with symptoms across a wide range of neurological domains, including cognitive and motor dysfunction. There is still no causative treatment for HD but environmental factors such as passive lifestyle may modulate disease onset and progression. In humans, multidisciplinary rehabilitation has a positive impact on cognitive functions. However, a specific role for exercise as a component of an environmental enrichment effect has been difficult to demonstrate. We aimed at investigating whether endurance training (ET) stabilizes the progression of motor and cognitive dysfunction and ameliorates cardiovascular function in HD patients. Twelve male HD patients (mean ± SD, 54.8 ± 7.1 years) and twelve male controls (49.1 ± 6.8 years) completed 26 weeks of endurance training. Before and after the training intervention, clinical assessments, exercise physiological tests, and a body composition measurement were conducted and a muscle biopsy was taken from M. vastus lateralis. To examine the natural course of the disease, HD patients were additionally assessed 6 months prior to ET. During the ET period, there was a motor deficit stabilization as indicated by the Unified Huntington's Disease Rating Scale motor section score in HD patients (baseline: 18.6 ± 9.2, pre-training: 26.0 ± 13.7, post-training: 26.8 ± 16.4). Peak oxygen uptake ([Formula: see text]) significantly increased in HD patients (∆[Formula: see text] = +0.33 ± 0.28 l) and controls (∆[Formula: see text] = +0.29 ± 0.41 l). No adverse effects of the training intervention were reported. Our results confirm that HD patients are amenable to a specific exercise-induced therapeutic strategy indicated by an increased cardiovascular function and a stabilization of motor function.

The Angiotensin Converting Enzyme Insertion/Deletion Polymorphism Modifies Exercise-Induced Muscle Metabolism.

OBJECTIVE: A silencer region (I-allele) within intron 16 of the gene for the regulator of vascular perfusion, angiotensin-converting enzyme (ACE), is implicated in phenotypic variation of aerobic fitness and the development of type II diabetes. We hypothesised that the reportedly lower aerobic performance in non-carriers compared to carriers of the ACE I-allele, i.e. ACE-DD vs. ACE-ID/ACE-II genotype, is associated with alterations in activity-induced glucose metabolism and capillarisation in exercise muscle. METHODS: Fifty-three, not-specifically trained Caucasian men carried out a one-legged bout of cycling exercise to exhaustion and/or participated in a marathon, the aim being to identify and validate genotype effects on exercise metabolism. Respiratory exchange ratio (RER), serum glucose and lipid concentration, glycogen, and metabolite content in vastus lateralis muscle based on ultra-performance lipid chromatography-mass spectrometry (UPLC-MS), were assessed before and after the cycling exercise in thirty-three participants. Serum metabolites were measured in forty subjects that completed the marathon. Genotype effects were assessed post-hoc. RESULTS: Cycling exercise reduced muscle glycogen concentration and this tended to be affected by the ACE I-allele (p = 0.09). The ACE-DD genotype showed a lower maximal RER and a selective increase in serum glucose concentration after exercise compared to ACE-ID and ACE-II genotypes (+24% vs. +2% and -3%, respectively). Major metabolites of mitochondrial metabolism (i.e. phosphoenol pyruvate, nicotinamide adenine dinucleotide phosphate, L-Aspartic acid, glutathione) were selectively affected in vastus lateralis muscle by exercise in the ACE-DD genotype. Capillary-to-fibre ratio was 24%-lower in the ACE-DD genotype. Individuals with the ACE-DD genotype demonstrated an abnormal increase in serum glucose to 7.7 mM after the marathon. CONCLUSION: The observations imply a genetically modulated role for ACE in control of glucose import and oxidation in working skeletal muscle. ACE-DD genotypes thereby transit into a pre-diabetic state with exhaustive exercise, which relates to a lowered muscle capillarisation, and deregulation of mitochondria-associated metabolism.

One bout of vibration exercise with vascular occlusion activates satellite cells.

NEW FINDINGS: What is the central question of this study? Acute skeletal muscle satellite cell (SC) activation is associated with skeletal muscle hypertrophy. Although the quantity of SCs has been reported to increase following a single bout of resistance exercise, data on muscle fibre type-specific SC quantity and/or activation status after a single bout of vibration is presently lacking. What is the main finding and its importance? By determining SCs from muscle biopsies of the vastus lateralis using immunohistochemistry, we conclude that modification of vibration exercise by superimposition of occlusion induced activation and differentiation of SCs in young men, which had not been observed with whole-body vibration or blood flow restriction alone. We tested the hypothesis that whole-body vibration (WBV) is insufficient to expand satellite cell numbers 24 h postexercise, whereas WBV in combination with blood flow restriction (BFR) is sufficient. Twenty-five young men were randomly assigned to one of the following three groups: WBV, BFR exercise or WBVBFR. Satellite cell numbers were determined from muscle biopsies of the vastus lateralis muscle using immunohistochemistry. Satellite cell quantity and frequency (+99.4%, P = 0.012 and +77.1%, P = 0.010, respectively) increased only in the WBVBFR group. Similar results were obtained for the quantity and frequency of myogenin-positive myonuclei (+139.0%, P < 0.001 and +148.4%, P < 0.001, respectively). We conclude that modification of WBV by superimposition of BFR induced activation and differentiation of satellite cells in young men, which had not been observed with WBV or BFR alone. These data suggest that WBVBFR might represent a novel viable anabolic stimulus.

Long-Term Endurance Exercise in Humans Stimulates Cell Fusion of Myoblasts along with Fusogenic Endogenous Retroviral Genes In Vivo.

Myogenesis is defined as growth, differentiation and repair of muscles where cell fusion of myoblasts to multinucleated myofibers is one major characteristic. Other cell fusion events in humans are found with bone resorbing osteoclasts and placental syncytiotrophoblasts. No unifying gene regulation for natural cell fusions has been found. We analyzed skeletal muscle biopsies of competitive cyclists for muscle-specific attributes and expression of human endogenous retrovirus (ERV) envelope genes due to their involvement in cell fusion of osteoclasts and syncytiotrophoblasts. Comparing muscle biopsies from post- with the pre-competitive seasons a significant 2.25-fold increase of myonuclei/mm fiber, a 2.38-fold decrease of fiber area/nucleus and a 3.1-fold decrease of satellite cells (SCs) occurred. We propose that during the pre-competitive season SC proliferation occurred following with increased cell fusion during the competitive season. Expression of twenty-two envelope genes of muscle biopsies demonstrated a significant increase of putative muscle-cell fusogenic genes Syncytin-1 and Syncytin-3, but also for the non-fusogenic erv3. Immunohistochemistry analyses showed that Syncytin-1 mainly localized to the sarcolemma of myofibers positive for myosin heavy-chain isotypes. Cellular receptors SLC1A4 and SLC1A5 of Syncytin-1 showed significant decrease of expression in post-competitive muscles compared with the pre-competitive season, but only SLC1A4 protein expression localized throughout the myofiber. Erv3 protein was strongly expressed throughout the myofiber, whereas envK1-7 localized to SC nuclei and myonuclei. Syncytin-1 transcription factors, PPARγ and RXRα, showed no protein expression in the myofiber, whereas the pCREB-Ser133 activator of Syncytin-1 was enriched to SC nuclei and myonuclei. Syncytin-1, Syncytin-3, SLC1A4 and PAX7 gene regulations along with MyoD1 and myogenin were verified during proliferating or actively-fusing human primary myoblast cell cultures, resembling muscle biopsies of cyclists. Myoblast treatment with anti-Synycytin-1 abrogated cell fusion in vitro. Our findings support functional roles for ERV envelope proteins, especially Syncytin-1, contributing to cell fusion of myotubes.

Reduced Bone Strength and Muscle Force in Women 27 Years After Anorexia Nervosa.

CONTEXT: A substantial body of research findings indicate that muscle mass and bone mass are reduced in populations of anorexic females, even in such populations whose anorexia nervosa had been in remission for longer periods. OBJECTIVE: This study aimed to investigate whether the bone of an anorexia nervosa recovery cohort is adapted to maximal muscle forces and whether there are alterations in the structure of the tibia in this population, as compared with a control group. DESIGN, SETTING, AND PARTICIPANTS: This was a cross-sectional study of 22 women in Switzerland who have remained in stable recovery from anorexia nervosa for an average of 27 years. The measurements were compared with those of an age- and gender-matched control group (n = 73). INTERVENTIONS: There were no interventions. MAIN OUTCOME MEASURES: Bone characteristics of the tibia and maximal voluntary ground reaction force (Fm1LH) were measured. RESULTS: The variability in volumetric bone mineral content (vBMC) at the 14% site was explained by 54.7% on the grounds of Fm1LH (P < .001). Formerly anorexic women had an 11.6% lower Fm1LH (P = .001), a significantly lower vBMC at 4% and 14% of tibia length, and an 11.9% (P = .001) lower body mass than the age- and gender-matched control population. Present body mass of the anorexia group correlated positively with vBMC at the 14% site (P < .001). CONCLUSIONS: Despite the fact that findings reflected an adaptation of bone to the acting forces, most results indicated that the test cohort generally suffered from a secondary bone defect. In addition, maximal muscle force was also impaired in the formerly anorexic women.

The muscle-bone interaction in Turner syndrome.

OBJECTIVES: Turner syndrome (TS) is associated with an increased fracture rate due to reduced bone strength, which is mainly determined by skeletal muscle force. This study aimed to assess the muscle force-bone strength relationship in TS and to compare it with that of healthy controls. METHODS: This study included 39 girls with TS and 67 healthy control girls. Maximum muscle force (Fmax) was assessed through multiple one-legged hopping with jumping mechanography. Peripheral quantitative computerized tomography assessed the bone strength index at the tibial metaphysis (BSI 4) and the polar strength-strain index at the diaphysis (SSI polar 66). The effect of TS on the muscle-bone unit was tested using multiple linear regression. RESULTS: TS had no impact on Fmax (p=0.14); however, a negative effect on bone strength (p<0.001 for BSI 4 and p<0.01 for SSI polar 66) was observed compared with healthy controls. Bone strength was lower in the TS group (by 18%, p<0.01, for BSI 4 and by 7%, p=0.027, for SSI polar 66), even after correcting for Fmax. CONCLUSIONS: Similar muscle force induces lower bone strength in TS compared with healthy controls, which suggests altered bone-loading sensitivity in TS.

Alterations in bone mineral density and lower extremity lean mass after hip arthroscopy in a professional female Ironman triathlete: a case study.

INTRODUCTION: Femoroacetabular impingement is a pathomechanical condition of the hip, which is often treated through arthroscopic techniques. The ensuing immobilization period is associated with decreases in muscle mass and bone mass. To date, minimal knowledge is present about the development of tissue mass during the considerably short rehabilitation period before returning to competition in elite endurance athletes. CASE DESCRIPTION: Before and after surgery, a professional female Ironman triathlete underwent dual-energy X-ray absorptiometry and peripheral quantitative computed tomography measurements. DISCUSSION AND EVALUATION: Areal bone mineral density (aBMD) of the proximal femur and lower extremity lean mass decreased in the surgically treated lower extremity during the two-month period of immobilization after the hip arthroscopy. These losses were compensated for after only six weeks of rehabilitation. A similar progression of aBMD values was observed in the lumbar spine. The adaptational pattern in volumetric BMD (vBMD) and volumetric bone mineral content (vBMC) of the tibiae were more complex, but attained pre-immobilization values for most variables also after six weeks of rehabilitation. All other variables attained pre-immobilization values no later than nine months after the surgical intervention. CONCLUSIONS: The athlete showed a high plasticity of bone and lean tissue with an optimal short- and midterm outcome. Following a two months immobilization period after a hip arthroscopy, aBMD, vBMD and vBMC achieved pre-surgical levels after four months of rehabilitation in a female Ironman triathlete. A nine-month follow-up measurement confirmed the safety of the fast return to sport.

High-intensity interval training with vibration as rest intervals attenuates fiber atrophy and prevents decreases in anaerobic performance.

UNLABELLED: Aerobic high-intensity interval training (HIT) improves cardiovascular capacity but may reduce the finite work capacity above critical power (W') and lead to atrophy of myosin heavy chain (MyHC)-2 fibers. Since whole-body vibration may enhance indices of anaerobic performance, we examined whether side-alternating whole-body vibration as a replacement for the active rest intervals during a 4 x 4 min HIT prevents decreases in anaerobic performance and capacity without compromising gains in aerobic function. Thirty-three young recreationally active men were randomly assigned to conduct either conventional 4 x 4 min HIT, HIT with 3 min of WBV at 18 Hz (HIT+VIB18) or 30 Hz (HIT+VIB30) in lieu of conventional rest intervals, or WBV at 30 Hz (VIB30). Pre and post training, critical power (CP), W', cellular muscle characteristics, as well as cardiovascular and neuromuscular variables were determined. W' (-14.3%, P = 0.013), maximal voluntary torque (-8.6%, P = 0.001), rate of force development (-10.5%, P = 0.018), maximal jumping power (-6.3%, P = 0.007) and cross-sectional areas of MyHC-2A fibers (-6.4%, P = 0.044) were reduced only after conventional HIT. CP, V̇O2peak, peak cardiac output, and overall capillary-to-fiber ratio were increased after HIT, HIT+VIB18, and HIT+VIB30 without differences between groups. HIT-specific reductions in anaerobic performance and capacity were prevented by replacing active rest intervals with side-alternating whole-body vibration, notably without compromising aerobic adaptations. Therefore, competitive cyclists (and potentially other endurance-oriented athletes) may benefit from replacing the active rest intervals during aerobic HIT with side-alternating whole-body vibration. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT01875146.

An Ironman triathlon reduces neuromuscular performance due to impaired force transmission and reduced leg stiffness.

PURPOSE: An Ironman triathlon is associated with changes in body composition as well as decreases in neuromuscular function. While the changes in body composition occurring during an Ironman are well investigated, comprehensive data on the changes in neuromuscular performance are scarce. In the present study, we investigated the mechanical alterations underlying reported reductions in maximal muscular force and power after an Ironman race in men. METHODS: Before and directly after an Ironman, countermovement jump (CMJ), squat jump (SJ), and multiple one-legged hopping (m1LH) maneuvers were performed to assess fatigue-related alterations in mechanical variables in thirteen male non-professional triathletes. RESULTS: During CMJ, peak power (P = 0.003), peak velocity (P < 0.001), jump height (P = 0.007), and rate of force development (P = 0.042) decreased during the Ironman. Total (P < 0.001) and positive (P = 0.003) impulses during a CMJ were reduced after the triathlon, while both negative impulses did not differ pre to post Ironman. Absolute peak force remained constant during CMJ (P = 0.200) and SJ (P = 0.764). Maximal voluntary ground reaction force (F m1LH, P < 0.001) and peak stiffness (P = 0.003) during m1LH were decreased after the Ironman. CONCLUSIONS: The reduced CMJ height was a result of the lower positive impulse. Therefore, the neuromuscular deficit after the Ironman race was due to impairments in force transmission, resulting in a lower average positive force during CMJ, because of a slower rate of force development. The decreased F m1LH could be partly explained by reduced leg stiffness.

Physiological alterations after a marathon in the first 90-year-old male finisher: case study.

INTRODUCTION: Endurance performance decreases during ageing due to alterations in physiological characteristics, energy stores, and psychological factors. To investigate alterations in physiological characteristics and body composition of elderly master athletes in response to an extreme endurance event, we present the case of the first ninety-year-old official male marathon finisher. CASE DESCRIPTION: Before and directly after the marathon, a treadmill incremental test, dual-energy X-ray absorptiometry, peripheral quantitative computed tomography, mechanography, and dynamometry measurements were conducted. The athlete finished the marathon in 6 h 48 min 55 s, which corresponds to an average competition speed of 6.19 km h(-1). DISCUSSION AND EVALUATION: Before the marathon, [Formula: see text] was 31.5 ml min(-1) kg(-1) body mass and peak heart rate was 140 beats min(-1). Total fat mass increased in the final preparation phase (+3.4%), while leg fat mass and leg lean mass were slightly reduced after the marathon (-3.7 and -1.6%, respectively). Countermovement jump (CMJ) peak power and peak velocity decreased after the marathon (-16.5 and -14.7%, respectively). Total impulse during CMJ and energy cost of running were not altered by the marathon. In the left leg, maximal voluntary ground reaction force (F m1LH) and maximal isometric voluntary torque (MIVT) were impaired after the marathon (-12.2 and -14.5%, respectively). CONCLUSIONS: Side differences in F m1LH and MIVT could be attributed to the distinct non-symmetrical running pattern of the athlete. Similarities in alterations in leg composition and CMJ performance existed between the nonagenarian athlete and young marathon runners. In contrast, alterations in total body composition and m1LH performance were markedly different in the nonagenarian athlete when compared to his younger counterparts.

Hypoxic training: effect on mitochondrial function and aerobic performance in hypoxia.

PURPOSE: The effects of hypoxic training on exercise performance remain controversial. Here, we tested the hypotheses that i) hypoxic training possesses ergogenic effects at sea level and altitude and ii) the benefits are primarily mediated by improved mitochondrial function of the skeletal muscle. METHODS: We determined aerobic performance (incremental test to exhaustion and time trial for a set amount of work) in moderately trained subjects undergoing 6 wk of endurance training (3-4 times per week, 60 min per session) in normoxia (placebo, n = 8) or normobaric hypoxia (FIO2 = 0.15, n = 9) using a double-blind and randomized design. Exercise tests were performed in normoxia and acute hypoxia (FIO2 = 0.15). Skeletal muscle mitochondrial respiratory capacities and electron coupling efficiencies were measured via high-resolution respirometry. Total hemoglobin mass was assessed by carbon monoxide rebreathing. RESULTS: Skeletal muscle respiratory capacity was not altered by training or hypoxia; however, electron coupling control respective to fat oxidation slightly diminished with hypoxic training. Hypoxic training did increase total hemoglobin mass more than the placebo (8.4% vs 3.3%, P = 0.02). In normoxia, hypoxic training had no additive effect on maximal measures of oxygen uptake or time trial performance. In acute hypoxia, hypoxic training conferred no advantage on maximal oxygen uptake but tended to enhance time trial performance more than normoxic training (52% vs 32%, P = 0.09). CONCLUSIONS: Our data suggest that, in moderately trained subjects, 6 wk of hypoxic training possesses no ergogenic effect at sea level. It is not excluded that hypoxic training might facilitate endurance capacity at moderate altitude; however, this issue is still open and needs to be further examined.