Atrophy/hypertrophy cell signaling in muscles of young athletes trained with vibrational-proprioceptive stimulation.

Neurol Res. 2011 Dec;33(10):998-1009. Atrophy/hypertrophy cell signaling in muscles of young athletes trained with vibrational-proprioceptive stimulation. Kern H, Pelosi L, Coletto L, Musar\uf2 A, Sandri M, Vogelauer M, Trimmel L, Cvecka J, Hamar D, Kovarik J, L\uf6fler S, Sarabon N, Protasi F, Adami N, Biral D, Zampieri S, Carraro U. Source Wilhelminenspital, Wien, Austria. Abstract OBJECTIVE: To compare the effects of isokinetic (ISO-K) and vibrational-proprioceptive (VIB) trainings on muscle mass and strength. METHODS: In 29 ISO-K- or VIB-trained young athletes we evaluated: force, muscle fiber morphometry, and gene expression of muscle atrophy/hypertrophy cell signaling. RESULTS: VIB training increased the maximal isometric unilateral leg extension force by 48\ub71%. ISO-K training improved the force by 24\ub78%. Both improvements were statistically significant (P\u2a7f0\ub701). The more functional effectiveness of the VIB training in comparison with the ISO-K training was shown by the statistical significance changes only in VIB group in: rate of force development in time segment 0-50 ms (P<0\ub7001), squat jump (P<0\ub705) and 30-m acceleration running test (P<0\ub705). VIB training induced a highly significant increase of mean diameter of fast fiber (+9%, P<0\ub7001), but not of slow muscle fibers (-3%, not significant). No neural cell adhesion molecule-positive (N-CAM(+)) and embryonic myosin heavy chain-positive (MHC-emb(+)) myofibers were detected. VIB induced a significant twofold increase (P<0\ub705) of the skeletal muscle isoform insulin-like growth factor-1 (IGF-1) Ec mRNA. Atrogin-1 and muscle ring finger-1 (MuRF-1) did not change, but myostatin was strongly downregulated after VIB training (P<0\ub7001). Peroxisome proliferator-activated receptor \u3b3 coactivator-1\u3b1 (PGC-1\u3b1) expression increased in post-training groups, but only in VIB reached statistical significance (+228%, P<0\ub705). DISCUSSION: We demonstrated that both trainings are effective and do not induce muscle damage. Only VIB-trained group showed statistical significance increase of hypertrophy cell signaling pathways (IGF-1Ec and PGC-1\u3b1 upregulation, and myostatin downregulation) leading to hypertrophy of fast twitch muscle fibers. PMID: 22196751 [PubMed - in process

Aerobic-Strength Exercise Improves Metabolism and Clinical State in Parkinson's Disease Patients

Regular exercise ameliorates motor symptoms in Parkinson's disease (PD). Here, we aimed to provide evidence that exercise brings additional benefits to the whole-body metabolism and skeletal muscle molecular and functional characteristics, which might help to explain exercise-induced improvements in the clinical state. 3-months supervised endurance/strength training was performed in early/mid-stage PD patients and age/gender-matched individuals (n = 11/11). The effects of exercise on resting energy expenditure (REE), glucose metabolism, adiposity, and muscle energy metabolism (31P-MRS) were evaluated and compared to non-exercising PD patients. Two muscle biopsies were taken to determine intervention-induced changes in fiber type, mitochondrial content, and expression of genes related to muscle energy metabolism, as well as proliferative and regenerative capacity. Exercise improved the clinical disability score (MDS-UPDRS), bradykinesia, balance, walking speed, REE, and glucose metabolism and increased muscle expression of energy sensors (AMPK). However, the exercise-induced increase in muscle mass/strength, mitochondrial content, type II fiber size, and postexercise phosphocreatine (PCr) recovery (31P-MRS) were found only in controls. Nevertheless, MDS-UPDRS was associated with muscle AMPK and mechano-growth factor (MGF) expression. Improvements in fasting glycemia were positively associated with muscle function and the expression of Sirt1 and Cox7a1, and the parameters of fitness/strength were positively associated with the expression of MyHC2, MyHC7, and MGF. Moreover, reduced bradykinesia was associated with better muscle metabolism (maximal oxidative capacity and postexercise PCr recovery; 31P-MRS). Exercise training improved the clinical state in early/mid-stage Parkinson's disease patients, including motor functions and whole-body metabolism. Although the adaptive response to exercise in PD was different from that of controls, exercise-induced improvements in the PD clinical state were associated with specific adaptive changes in muscle functional, metabolic, and molecular characteristics.www.ClinicalTrials.gov, identifier NCT02253732

Electrical stimulation (ES) counteracts muscle decline in seniors

none19The loss in muscle mass coupled with a decrease in specific force and shift in fiber composition arehallmarks of aging. Training and regular exercise attenuate the signs of sarcopenia. However,pathologic conditions limit the ability to perform physical exercise.We addressed whether electrical stimulation (ES) is an alternative intervention to improve musclerecovery and defined the molecular mechanism associated with improvement in muscle structure andfunction.We analyzed, at functional, structural, and molecular level, the effects of ES training on healthyseniors with normal life style, without routine sport activity.ES was able to improve muscle torque and functional performances of seniors and increased the sizeof fast muscle fibers. At molecular level, ES induced up-regulation of IGF-1 and modulation ofMuRF1, a muscle-specific atrophy-related gene. ES also induced up-regulation of relevant markersof differentiating satellite cells and of extracellular matrix remodeling, which might guarantee shapeand mechanical forces of trained skeletal muscle as well as maintenance of satellite cell function,reducing fibrosis.Our data provide evidence that ES is a safe method to counteract muscle decline associated withaging.© 2014 Kern, Barberi, Loefler, Sbardella, Burgraff, Fruhmann, Carraro, Mosole, Sarabon, Vogelauer, Mayer, Krenn, Cvecka, Romanello, Pietrangelo, Protasi, Sandri, Zampieri and Musarò.noneKern H.; Barberi L.; Lofler S.; Sbardella S.; Burggraf S.; Fruhmann H.; Carraro U.; Mosole S.; Sarabon N.; Vogelauer M.; Mayer W.; Krenn M.; Cvecka J.; Romanello V.; Pietrangelo L.; Protasi F.; Sandri M.; Zampieri S.; Musaro A.Kern, H.; Barberi, L.; Lofler, S.; Sbardella, S.; Burggraf, S.; Fruhmann, H.; Carraro, U.; Mosole, S.; Sarabon, N.; Vogelauer, M.; Mayer, W.; Krenn, M.; Cvecka, J.; Romanello, V.; Pietrangelo, L.; Protasi, F.; Sandri, M.; Zampieri, S.; Musaro, A

Long-term high-level exercise promotes muscle reinnervation with age.

he histologic features of aging muscle suggest that denervation contributes to atrophy, that immobility accelerates the process, and that routine exercise may protect against loss of motor units and muscle tissue. Here, we compared muscle biopsies from sedentary and physically active seniors and found that seniors with a long history of high-level recreational activity up to the time of muscle biopsy had 1) lower loss of muscle strength versus young men (32% loss in physically active vs 51% loss in sedentary seniors); 2) fewer small angulated (denervated) myofibers; 3) a higher percentage of fiber-type groups (reinnervated muscle fibers) that were almost exclusive of the slow type; and 4) sparse normal-size muscle fibers coexpressing fast and slow myosin heavy chains, which is not compatible with exercise-driven muscle-type transformation. The biopsies from the old physically active seniors varied from sparse fiber-type groupings to almost fully transformed muscle, suggesting that coexpressing fibers appear to fill gaps. Altogether, the data show that long-term physical activity promotes reinnervation of muscle fibers and suggest that decades of high-level exercise allow the body to adapt to age-related denervation by saving otherwise lost muscle fibers through selective recruitment to slow motor units. These effects on size and structure of myofibers may delay functional decline in late aging.Trial registration: ClinicalTrials.gov (NCT01679977)

Long-term high-level exercise promotes muscle reinnervation with age.

The histologic features of aging muscle suggest that denervation contributes to atrophy, that immobility accelerates the process, and that routine exercise may protect against loss of motor units and muscle tissue. Here, we compared muscle biopsies from sedentary and physically active seniors and found that seniors with a long history of high-level recreational activity up to the time of muscle biopsy had 1) lower loss of muscle strength versus young men (32% loss in physically active vs 51% loss in sedentary seniors); 2) fewer small angulated (denervated) myofibers; 3) a higher percentage of fiber-type groups (reinnervated muscle fibers) that were almost exclusive of the slow type; and 4) sparse normal-size muscle fibers coexpressing fast and slow myosin heavy chains, which is not compatible with exercise-driven muscle-type transformation. The biopsies from the old physically active seniors varied from sparse fiber-type groupings to almost fully transformed muscle, suggesting that coexpressing fibers appear to fill gaps. Altogether, the data show that long-term physical activity promotes reinnervation of muscle fibers and suggest that decades of high-level exercise allow the body to adapt to age-related denervation by saving otherwise lost muscle fibers through selective recruitment to slow motor units. These effects on size and structure of myofibers may delay functional decline in late aging. Trial registration: ClinicalTrials.gov (NCT01679977)

Lifelong Physical Exercise Delays Age-Associated Skeletal Muscle Decline

Aging is usually accompanied by a significant reduction in muscle mass and force. To determine the relative contribution of inactivity and aging per se to this decay, we compared muscle function and structure in (a) male participants belonging to a group of well-trained seniors (average of 70 years) who exercised regularly in their previous 30 years and (b) age-matched healthy sedentary seniors with (c) active young men (average of 27 years). The results collected show that relative to their sedentary cohorts, muscle from senior sportsmen have: (a) greater maximal isometric force and function, (b) better preserved fiber morphology and ultrastructure of intracellular organelles involved in Ca2+ handling and ATP production, (c) preserved muscle fibers size resulting from fiber rescue by reinnervation, and (d) lowered expression of genes related to autophagy and reactive oxygen species detoxification. All together, our results indicate that: (a) skeletal muscle of senior sportsmen is actually more similar to that of adults than to that of age-matched sedentaries and (b) signaling pathways controlling muscle mass and metabolism are differently modulated in senior sportsmen to guarantee maintenance of skeletal muscle structure, function, bioenergetic characteristics, and phenotype. Thus, regular physical activity is a good strategy to attenuate age-related general decay of muscle structure and function (ClinicalTrials.gov: NCT01679977)

Lifelong physical exercise delays age-associated skeletal muscle decline.

none23siAging is usually accompanied by a significant reduction in muscle mass and force. To determine the relative contribution of inactivity and aging per se to this decay, we compared muscle function and structure in (a) male participants belonging to a group of well-trained seniors (average of 70 years) who exercised regularly in their previous 30 years and (b) age-matched healthy sedentary seniors with (c) active young men (average of 27 years). The results collected show that relative to their sedentary cohorts, muscle from senior sportsmen have: (a) greater maximal isometric force and function, (b) better preserved fiber morphology and ultrastructure of intracellular organelles involved in Ca(2+) handling and ATP production, (c) preserved muscle fibers size resulting from fiber rescue by reinnervation, and (d) lowered expression of genes related to autophagy and reactive oxygen species detoxification. All together, our results indicate that: (a) skeletal muscle of senior sportsmen is actually more similar to that of adults than to that of age-matched sedentaries and (b) signaling pathways controlling muscle mass and metabolism are differently modulated in senior sportsmen to guarantee maintenance of skeletal muscle structure, function, bioenergetic characteristics, and phenotype. Thus, regular physical activity is a good strategy to attenuate age-related general decay of muscle structure and functionnoneZampieri, S; Pietrangelo, L; Loefler, S; Fruhmann, H; Vogelauer, M; Burggraf, S; Pond, A; Grim-Stieger, M; Cvecka, J; Sedliak, M; Tirpáková, V; Mayr, W; Sarabon, N; Rossini, K; Barberi, L; De Rossi, M; Romanello, V; Boncompagni, S; Musarò, A; Sandri, M; Protasi, F; Carraro, U; Kern, H.Zampieri, Sandra; Pietrangelo, L; Loefler, S; Fruhmann, H; Vogelauer, M; Burggraf, S; Pond, A; Grim Stieger, M; Cvecka, J; Sedliak, M; Tirpáková, V; Mayr, W; Sarabon, N; Rossini, Katia; Barberi, L; De Rossi, M; Romanello, Vanina; Boncompagni, S; Musaro', Antonio; Sandri, Marco; Protasi, F; Carraro, Ugo; Kern, H