Effects of Six-Week Resistance Training with or without Vibration on Metabolic Markers of Bone Metabolism.

Acute and protracted effects of resistive exercise (RE) and resistive exercise with whole-body vibration (RVE) on metabolic markers of bone metabolism were investigated. Twenty-six men participated in a randomized training program including RE (n = 13; age = 23.4 ± 1.4 years) or RVE (n = 13; age = 24.3 ± 3.3 years). During the first session, acute C-terminal telopeptide of type I collagen (CTX) responses decreased by 12.9% (standard deviation, SD 13.7%) after 2 min, followed by a 15.5% (SD 36.0%) increase at 75 min after exercise (both p < 0.001). Procollagen type I amino terminal propeptide (P1NP) increased by 12.9% (SD 9.1%) at 2 min (p < 0.001) but no change occurred at 75 min. Sclerostin showed prolonged responses from 2 to 75 min post-exercise in the first session (p < 0.001). Acute responses at the first session were comparable between groups for CTX and P1NP, acute sclerostin responses were substantially greater in RE than in RVE (p = 0.003). No significant differences were noted in the resting baseline levels of CTX, P1NP, or sclerostin from the beginning to the end of the six-week progressive training. The present study therefore did not demonstrate any sizeable enhancement of bone turnover that could match the effects that have been repeatably made in response to countermeasure exercise during bed rest.

Changes in motor unit activity and respiratory oxygen uptake during 6 weeks of progressive whole-body vibration combined with progressive, high intensity resistance training.

OBJECTIVES: We hypothesized that the additional activation of motor units (MU) and the elevation of metabolic energy turnover resulting from whole-body vibration (WBV) superimposed to high intensity resistance training on a smith machine persist after 6 weeks of training with progressively increasing loads and vibration frequencies. METHODS: Two groups of healthy male subjects performed either 6 weeks of Resistive Vibration Exercise (RVE, squats and heel raises with WBV, n=13) or Resistive Exercise (RE using the same protocol, n=13). During the first (pre) and the last training session (post), we determined the oxygen uptake changes normalized to total training weight (∆V'O2/ttw) and the normalized MU activity from rectus femoris (squats) and gastrocnemius lateralis (heel raise) muscles filtered for vibration frequencies and harmonics (EMG/ttw). RESULTS: At pre measurement, RVE induced higher EMG/ttw (squats) than RE alone (group effect, P=0.006). At post measurement, EMG/ttw was reduced (time effects between P=0.087 and P<0.001 for both groups and exercises). At pre and post measurement, ∆V'O2/ttw was higher during RVE than during RE (group effects between P=0.005 and P=0.099 for both exercises). CONCLUSIONS: RVE permanently elevated metabolic energy turnover, although the initially observed additional MU activity by RVE could not be preserved in the working musculature.

Microcirculation of skeletal muscle adapts differently to a resistive exercise intervention with and without superimposed whole-body vibrations.

Whole-body vibration (WBV) training is commonly practiced and may enhance peripheral blood flow. Here, we investigated muscle morphology and acute microcirculatory responses before and after a 6-week resistive exercise training intervention without (RE) or with (RVE) simultaneous whole-body vibrations (20 Hz, 6 mm peak-to-peak amplitude) in 26 healthy men in a randomized, controlled parallel-design study. Total haemoglobin (tHb) and tissue oxygenation index (TOI) were measured in gastrocnemius muscle (GM) with near-infrared spectroscopy (NIRS). Whole-body oxygen consumption (VO2 ) was measured via spirometry, and skeletal muscle morphology was determined in soleus (SOL) muscle biopsies. Our data reveal that exercise-induced muscle deoxygenation both before and after 6 weeks training was similar in RE and RVE (P = 0.76), although VO2 was 20% higher in the RVE group (P < 0.001). The RVE group showed a 14%-point increase in reactive hyperaemia (P = 0.007) and a 27% increase in blood volume (P < 0.01) in GM after 6 weeks of training. The number of capillaries around fibres was increased by 15% after 6 weeks training in both groups (P < 0.001) with no specific effect of superimposed WBV (P = 0.61). Neither of the training regimens induced fibre hypertrophy in SOL. The present findings suggest an increased blood volume and vasodilator response in GM as an adaptation to long-term RVE, which was not observed after RE alone. We conclude that RVE training enhances vasodilation of small arterioles and possibly capillaries. This effect might be advantageous for muscle thermoregulation and the delivery of oxygen and nutrients to exercising muscle and removal of carbon dioxide and metabolites.

The relationship between exercise-induced muscle fatigue, arterial blood flow and muscle perfusion after 56 days local muscle unloading.

In the light of the dynamic nature of habitual plantar flexor activity, we utilized an incremental isokinetic exercise test (IIET) to assess the work-related power deficit (WoRPD) as a measure for exercise-induced muscle fatigue before and after prolonged calf muscle unloading and in relation to arterial blood flow and muscle perfusion. Eleven male subjects (31 ± 6 years) wore the HEPHAISTOS unloading orthosis unilaterally for 56 days. It allows habitual ambulation while greatly reducing plantar flexor activity and torque production. Endpoint measurements encompassed arterial blood flow, measured in the femoral artery using Doppler ultrasound, oxygenation of the soleus muscle assessed by near-infrared spectroscopy, lactate concentrations determined in capillary blood and muscle activity using soleus muscle surface electromyography. Furthermore, soleus muscle biopsies were taken to investigate morphological muscle changes. After the intervention, maximal isokinetic torque was reduced by 23·4 ± 8·2% (P<0·001) and soleus fibre size was reduced by 8·5 ± 13% (P = 0·016). However, WoRPD remained unaffected as indicated by an unchanged loss of relative plantar flexor power between pre- and postexperiments (P = 0·88). Blood flow, tissue oxygenation, lactate concentrations and EMG median frequency kinematics during the exercise test were comparable before and after the intervention, whereas the increase of RMS in response to IIET was less following the intervention (P = 0·03). In conclusion, following submaximal isokinetic muscle work exercise-induced muscle fatigue is unaffected after prolonged local muscle unloading. The observation that arterial blood flow was maintained may underlie the unchanged fatigability.

Whole-body vibrations do not elevate the angiogenic stimulus when applied during resistance exercise.

Knowledge about biological factors involved in exercise-induced angiogenesis is to date still scanty. The present study aimed to investigate the angiogenic stimulus of resistance exercise with and without superimposed whole-body vibrations. Responses to the exercise regimen before and after a 6-week training intervention were investigated in twenty-six healthy male subjects. Serum was collected at the initial and final exercise sessions and circulating levels of matrix metalloproteinases (MMP) -2 and -9, Vascular Endothelial Growth Factor (VEGF) and endostatin were determined via ELISA. Furthermore, we studied the proliferative effect of serum-treated human umbilical vein endothelial cells in vitro via BrdU-incorporation assay. It was found that circulating MMP-2, MMP-9, VEGF and endostatin levels were significantly elevated (P<0.001) from resting levels after both exercise interventions, with higher post-exercise VEGF concentrations in the resistance exercise (RE) group compared to the resistive vibration exercise (RVE) group. Moreover, RE provoked increased endothelial cell proliferation in vitro and higher post-exercise circulating endostatin concentrations after 6 weeks of training. These effects were elusive in the RVE group. The present findings suggest that resistance exercise leads to a transient rise in circulating angiogenic factors and superimposing vibrations to this exercise type might not further trigger a potential signaling of angiogenic stimulation in skeletal muscle.

Vascular adaptations induced by 6 weeks WBV resistance exercise training.

BACKGROUND: The impact of whole-body vibration (WBV) upon the cardiovascular system is receiving increasing attention. Despite numerous studies addressing the acute cardiovascular effects of WBV training, very little is known regarding long-term adaptations in healthy humans. METHODS: A 6-week training study, with a 70 days follow-up was designed to compare resistive exercise with or without super-imposed whole-body vibrations. Arterial diameter, intima media thickness and flow-mediated dilation (FMD) were assessed by ultrasonography in the superficial femoral artery (SFA), the brachial (BA) and the carotid arteries (CA). RESULTS: SFA resting diameter was increased from 6·22 mm (SD = 0·69 mm) at baseline to 6·52 mm (SD = 0·74 mm) at the end of the training period (P = 0·03) with no difference between groups (P = 0·48). Arterial wall thickness was significantly reduced by 4·3% (SD = 11%) in the CA only (P = 0·04). FMD was not affected by any of the interventions and in any of the investigated arteries. CONCLUSION: To the best of our knowledge, this has been the first study to show that the superposition of vibration upon conventional resistance exercise does not have a specific effect upon long-term vascular adaptation in asymptomatic humans. Our findings seem to be at variance with the findings observed in a bed-rest setting. One possible explanation could be that the independently saturable effects of flow-mediated versus acceleration-related endothelial shear stresses on arterial structure and function differ between ambulatory and bed-rest conditions.

Nesprin-2 interacts with {alpha}-catenin and regulates Wnt signaling at the nuclear envelope.

Nesprins and emerin are structural nuclear envelope proteins that tether nuclei to the cytoskeleton. In this work, we identified the cytoskeleton-associated α-N/E-catenins as novel nesprin-2-binding partners. The association involves the C termini of nesprin-2 giant and α-N/E-catenins. α-E/T/N-catenins are known primarily for their roles in cadherin-mediated cell-cell adhesion. Here, we show that, in addition, α-catenin forms complexes with nesprin-2 that include ß-catenin and emerin. We demonstrate that the depletion of nesprin-2 reduces both the amount of active ß-catenin inside the nucleus and T-cell factor/lymphoid-enhancing factor-dependent transcription. Taken together, these findings suggest novel nesprin-2 functions in cellular signaling. Moreover, we propose that, in contrast to emerin, nesprin-2 is a positive regulator of the Wnt signaling pathway.

Nesprin-2 Giant (NUANCE) maintains nuclear envelope architecture and composition in skin.

Giant isoforms, encoded by Nesprin-1 (Syne1) and Nesprin-2 (Syne2), are multifunctional actin-binding and nuclear-envelope-associated proteins belonging to the spectrin superfamily. Here, we investigate the function of Nesprin-2 Giant (NUANCE) in skin by generating mice lacking the actin-binding domain of Nesprin-2 (Nesprin-2DeltaABD). This loss results in a slight but significant thickening of the epidermis, which is a consequence of the increased epithelial nuclear size. Nonetheless, epidermal proliferation and differentiation appear normal in the knockout epidermis. Surprisingly, Nesprin-2 C-terminal-isoform expression and nuclear envelope localization were affected in certain tissues. Nuclei of primary dermal knockout fibroblasts and keratinocytes were heavily misshapen, displaying a striking similarity to nuclear deformations characteristic of laminopathies. Furthermore, emerin, the protein involved in the X-linked form of Emery-Dreifuss muscular dystrophy (EDMD), was unevenly distributed along the nuclear envelope in mutant fibroblasts, often forming aggregates in the deformed nuclear envelope areas. Thus, Nesprin-2 is an important scaffold protein implicated in the maintenance of nuclear envelope architecture. Aged knockout fibroblasts readily generated, by alternative splicing and alternative translation initiation, aberrant Nesprin-2 Giant isoforms that lacked an ABD but that were sufficient to restore nuclear shape and emerin localization; this suggests that other regions of Nesprin-2 Giant, potentially including its spectrin repeats, are crucial for these functions.