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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.

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.

Background/objectives: A number of recent studies dealing with the relationship between the effects of high body mass (BM) and fat mass (FM) on bone mass and strength exhibit a range of contrasting variations in their findings. These diverse findings have led to an ongoing controversy as to whether high BM and FM positively or negatively affect bone mass and strength. Excessive FM and the associated low-grade inflammation might overturn the higher mechanical stimulus arising from a higher BM. Therefore, we aimed at quantifying the functional muscle-bone unit in premenopausal women with markedly diverging body composition., Subjects/methods: Sixty-four young women with BMs ranging from 50 to 113 kg and body fat percentages between 20.7% and 51.8% underwent jumping mechanography and peripheral quantitative computed tomography measurements. Maximum voluntary ground reaction force during multiple one-legged hopping (F m1LH ), as well as bone characteristics at 4, 14 and 38% of tibia length, were determined. Body composition was assessed by dual-energy X-ray absorptiometry, and serum inflammatory markers were analyzed from blood samples., Results: F m1LH predicted volumetric bone mineral content at the 14% site by 48.7%. Women with high body fat percentage had significantly higher F m1LH , significantly lower relative bone mass, relative bone strength and relative bone area, as well as higher serum inflammatory markers in comparison to women with lower body fat percentage., Conclusions: In conclusion, high body fat percentage was associated with lower relative bone mass and strength despite normal habitual muscle force in premenopausal women, indicating that high body fat percentage compromised the functional muscle-bone unit in these individuals.

Background: Mitochondrial myopathy severely affects skeletal muscle structure and function resulting in defective oxidative phosphorylation. However, the major pathomechanisms and therewith effective treatment approaches remain elusive. Therefore, the aim of the present study was to investigate disease-related impairments in skeletal muscle properties in patients with mitochondrial myopathy. Accordingly, skeletal muscle biopsies were obtained from six patients with moleculargenetically diagnosed mitochondrial myopathy (one male and five females, 53 ± 9 years) and eight age- and gender-matched healthy controls (two males and six females, 58 ± 14 years) to determine mitochondrial respiratory capacity of complex I-V, mitochondrial volume density and fiber type distribution., Results: Mitochondrial volume density (4.0 ± 0.5 vs. 5.1 ± 0.8 %) as well as respiratory capacity of complex I-V were lower (P < 0.05) in mitochondrial myopathy and associated with a higher (P < 0.001) proportion of type II fibers (65.2 ± 3.6 vs. 44.3 ± 5.9 %). Additionally, mitochondrial volume density and maximal oxidative phosphorylation capacity correlated positively (P < 0.05) to peak oxygen uptake., Conclusion: Mitochondrial myopathy leads to impaired mitochondrial quantity and quality and a shift towards a more glycolytic skeletal muscle phenotype.

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.