Influence of complete spinal cord injury on skeletal muscle within 6 mo of injury. Impact of Very Early Physical Therapy During Septic Shock on Skeletal Muscle: A Randomized Controlled Trial Neuromuscular electrical stimulation attenuates thigh skeletal muscles atrophy but not trunk muscles after spinal cord injury. Neuromuscular electrical stimulation prevents muscle wasting in critically ill comatose patients. Vastus Medialis Obliquus Atrophy Effects of systemic hypoxia on human muscular adaptations to resistance exercise training Single muscle fiber adaptations to resistance training in old (>80 yr) men: evidence for limited skeletal muscle plasticity. The effects of three different training modalities on the cross-sectional area of the paravertebral muscles. Protein Supplementation Does Not Further Increase Latissimus Dorsi Muscle Fiber Hypertrophy after Eight Weeks of Resistance Training in Novice Subjects, but Partially Counteracts the Fast-to-Slow Muscle Fiber Transition Resistance Training Alters Cytokine Gene Expression in Skeletal Muscle of Adults with Type 2 Diabetes Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training.
This study examined the influence of  spinal cord injury ( SCI )  on affected skeletal muscle . The right vastus lateralis muscle was biopsied in 12 patients as soon as they were clinical ly stable ( average 6 wk after SCI ) , and 11 and 24 wk after injury . Sample s were also taken from nine able-bodied controls at two time points 18 wk apart . Surface electrical stimulation ( ES ) was applied to the left quadriceps femoris muscle to assess fatigue at these same time intervals . Biopsies were analyzed for fiber type percent and cross-sectional area ( CSA ) , fiber type-specific succinic dehydrogenase ( SDH ) and alpha-glycerophosphate dehydrogenase ( GPDH ) activities , and myosin heavy chain percent . Controls showed no change in any variable over time . Patients showed 27 - 56 % atrophy ( P = 0.000 ) of type I , IIa , and IIax+IIx fibers from 6 to 24 wk after injury , result ing in fiber CSA approximately one-third that of controls . Their fiber type specific SDH and GPDH activities increased ( P < /= 0.001 ) from 32 to 90 % over the 18 wk , thereby approaching or surpassing control values . The relative CSA of type I fibers and percentage of myosin heavy chain type I did not change . There was apparent conversion among type II fiber subtypes ; type IIa decreased and type IIax+IIx increased ( P < /= 0.012 ) . Force loss during ES did not change over time for either group but was greater ( P = 0.000 ) for SCI patients than for controls overall ( 27 vs. 9 % ) . The results indicate that vastus lateralis muscle shows marked fiber atrophy , no change in the proportion of type I fibers , and a relative independence of metabolic enzyme levels from activation during the first 24 wk after clinical ly complete SCI . Over this time , quadriceps femoris muscle showed moderately greater force loss during ES in patients than in controls . It is suggested that the predominant response of mixed human skeletal muscle within 6 mo of SCI is loss of contractile protein . Therapeutic interventions could take advantage of this to increase muscle mass Objectives : As the catabolic state induced by septic shock together with the physical inactivity of patients lead to the rapid loss of muscle mass and impaired function , the purpose of this study was to test whether an early physical therapy during the onset of septic shock regulates catabolic signals and preserves skeletal muscle mass . Design : R and omized controlled trial . Setting : Tertiary mixed ICU . Patients : Adult patients admitted for septic shock within the first 72 hours . Interventions : Patients were assigned r and omly into two groups . The control group benefited from manual mobilization once a day . The intervention group had twice daily sessions of both manual mobilization and 30-minute passive/active cycling therapy . Measurements and Main Results : Skeletal muscle biopsies and electrophysiology testing were performed at day 1 and day 7 . Muscle biopsies were analyzed for histology and molecular components of signaling pathways regulating protein synthesis and degradation as well as inflammation markers . Hemodynamic values and patient perception were collected during each session . Twenty-one patients were included . Three died before the second muscle biopsy . Ten patients in the control and eight in the intervention group were analyzed . Markers of the catabolic ubiquitin-proteasome pathway , muscle atrophy F-box and muscle ring finger-1 messenger RNA , were reduced at day 7 only in the intervention group , but without difference between groups ( muscle atrophy F-box : –7.3 % ± 138.4 % in control vs –56.4 % ± 37.4 % in intervention group ; p = 0.23 and muscle ring finger-1 : –30.8 % ± 66.9 % in control vs –62.7 % ± 45.5 % in intervention group ; p = 0.15 ) . Muscle fiber cross-sectional area ( µm2 ) was preserved by exercise ( –25.8 % ± 21.6 % in control vs 12.4 % ± 22.5 % in intervention group ; p = 0.005 ) . Molecular regulations suggest that the excessive activation of autophagy due to septic shock was lower in the intervention group , without being suppressed . Markers of anabolism and inflammation were not modified by the intervention , which was well tolerated by the patients . Conclusions : Early physical therapy during the first week of septic shock is safe and preserves muscle fiber cross-sectional area The current study examined the effects of 12weeks of surface neuromuscular electrical stimulation ( NMES ) and ankle weights on the cross-sectional areas ( CSAs ) of three thigh [ Gracilis ( Gra ) , Sartorious ( Sar ) and Adductor ( Add ) ] as well as two trunk [ hip flexor ( HF ) and back extensor ( BE ) ] muscle groups in men with spinal cord injury ( SCI ) . Seven individuals with chronic motor complete SCI were r and omly assigned into a resistance training + diet ( RT+diet ; n=4 ) or diet control ( n=3 ) groups . The RT+diet group underwent twice weekly training with surface NMES and ankle weights for 12weeks . Training composed of four sets of 10 repetitions of leg extension exercise while sitting in their wheelchairs . Both groups were asked to monitor their dietary intake . Magnetic resonance images were captured before and after 12weeks of interventions . Gra muscle CSA showed no change before and after interventions . A significant interaction ( P=0.001 ) was noted between both groups as result of 9 % increase and 10 % decrease in the Gra muscle CSA of the RT+diet and diet groups , respectively . Sar muscle CSA increased [ 1.7±0.4 - 2.5±0.5cm(2 ) ; P=0.029 ] in the RT+diet group with no change [ 2.9±1.4 - 2.6±1.3cm(2 ) ] in the diet group ; with interaction noted between both groups ( P=0.002 ) . Analysis of covariance indicated that Add muscle CSA was 38 % greater in the RT+diet compared to the diet group ( P=0.025 ) after 12weeks ; a trend of interaction was also noted between both groups ( P=0.06 ) . HF and BE muscle groups showed no apparent changes in CSA in both groups . The results suggested that surface NMES can delay the process of progressive skeletal muscle atrophy after chronic SCI . However , the effects are localized to the trained thigh muscles and do not extend to the proximal trunk muscles Fully se date d patients , being treated in the intensive care unit ( ICU ) , experience substantial skeletal muscle loss . Consequently , survival rate is reduced and full recovery after awakening is compromised . Neuromuscular electrical stimulation ( NMES ) represents an effective method to stimulate muscle protein synthesis and alleviate muscle disuse atrophy in healthy subjects . We investigated the efficacy of twice-daily NMES to alleviate muscle loss in six fully se date d ICU patients admitted for acute critical illness [ n=3 males , n=3 females ; age 63 ± 6 y ; APACHE II ( Acute Physiology and Chronic Health Evaluation II ) disease-severity-score : 29 ± 2 ] . One leg was subjected to twice-daily NMES of the quadriceps muscle for a period of 7 ± 1 day whereas the other leg acted as a non-stimulated control ( CON ) . Directly before the first and on the morning after the final NMES session , quadriceps muscle biopsies were collected from both legs to assess muscle fibre-type-specific cross-sectional area ( CSA ) . Furthermore , phosphorylation status of the key proteins involved in the regulation of muscle protein synthesis was assessed and mRNA expression of selected genes was measured . In the CON leg , type 1 and type 2 muscle-fibre-CSA decreased by 16 ± 9 % and 24 ± 7 % respectively ( P<0.05 ) . No muscle atrophy was observed in the stimulated leg . NMES increased mammalian target of rapamycin ( mTOR ) phosphorylation by 19 ± 5 % when compared with baseline ( P<0.05 ) , with no changes in the CON leg . Furthermore , mRNA expression of key genes involved in muscle protein breakdown either declined [ forkhead box protein O1 ( FOXO1 ) ; P<0.05 ] or remained unchanged [ muscle atrophy F-box ( MAFBx ) and muscle RING-finger protein-1 ( MuRF1 ) ] , with no differences between the legs . In conclusion , NMES represents an effective and feasible interventional strategy to prevent skeletal muscle atrophy in critically ill comatose patients Background : Quadriceps atrophy and in particular atrophy of the vastus medialis obliquus ( VMO ) muscle have been frequently related with patellofemoral pain syndrome ( PFPS ) , despite very little objective evidence . Hypothesis : Patients with PFPS exhibit atrophy of the VMO in comparison with healthy controls . Study Design : Case-control study ; Level of evidence , 3 . Methods : Forty-six patients with PFPS and 30 healthy control persons with similar age , gender , body mass index , and activity index distributions underwent magnetic resonance imaging ( MRI ) of the quadriceps .  The muscle size was determined by calculating the cross-sectional area of the total quadriceps and its components . Results : The cross-sectional area ( CSA ) of the VMO was significantly smaller in the PFPS group than in the control group ( 16.67 ± 4.97 cm2 vs 18.36 ± 5.25 cm2 ) ( P = .040 ) . A tendency was noted for a smaller total quadriceps CSA for the PFPS patients at midthigh level ( 66.99 ± 15.06 cm2 vs 70.83 ± 15.30 cm2 ) ( P = .074 ) . Conclusion : This is the first study to examine VMO size in PFPS patients by MRI . Patients with patellofemoral problems exhibited atrophy of the VMO . Although it is not clear whether this atrophy is a result or a cause of PFPS , the results of this study do show that atrophy of the VMO is a contributing factor in PFPS . Longitudinal , prospect i ve studies are needed to establish the cause-effect relation of VMO atrophy and PFPS Abstract Hypoxia is an important modulator of endurance exercise‐induced oxidative adaptations in skeletal muscle . However , whether hypoxia affects resistance exercise‐induced muscle adaptations remains unknown . Here , we determined the effect of resistance exercise training under systemic hypoxia on muscular adaptations known to occur following both resistance and endurance exercise training , including muscle cross‐sectional area ( CSA ) , one‐repetition maximum ( 1RM ) , muscular endurance , and makers of mitochondrial biogenesis and angiogenesis , such as peroxisome proliferator‐activated receptor‐γ coactivator‐1α ( PGC‐1α ) , citrate synthase ( CS ) activity , nitric oxide synthase ( NOS ) , vascular endothelial growth factor ( VEGF ) , hypoxia‐inducible factor‐1 ( HIF‐1 ) , and capillary‐to‐fiber ratio . Sixteen healthy male subjects were r and omly assigned to either a normoxic resistance training group ( NRT , n = 7 ) or a hypoxic ( 14.4 % oxygen ) resistance training group ( HRT , n = 9 ) and performed 8 weeks of resistance training .  Blood and muscle biopsy sample s were obtained before and after training . After training muscle CSA of the femoral region , 1RM for bench‐press and leg‐press , muscular endurance , and skeletal muscle VEGF protein levels significantly increased in both groups . The increase in muscular endurance was significantly higher in the HRT  group . Plasma VEGF concentration and skeletal muscle capillary‐to‐fiber ratio were significantly higher in the HRT group than the NRT group following training . Our results suggest that , in addition to increases in muscle size and strength , HRT may also lead to increased muscular endurance and the promotion of angiogenesis in skeletal muscle The purpose of this study was to investigate whole muscle and single muscle fiber adaptations in very old men in response to progressive resistance training ( PRT ) .  Six healthy independently living old men ( 82 + /- 1 yr ; range 80 - 86 yr , 74 + /- 4 kg )  resistance-trained the knee extensors ( 3 sets , 10 repetitions ) at approximately 70 % one repetition maximum 3 days/wk for 12 wk . Whole thigh muscle cross-sectional area ( CSA ) was assessed before and after PRT using computed tomography ( CT ) . Muscle biopsies were obtained from the vastus lateralis before and after the PRT program . Isolated myosin heavy chain ( MHC ) I and IIa single muscle fibers ( n = 267 ; 142 pre ; 125 post ) were studied for diameter , peak tension , shortening velocity , and power . An additional set of isolated single muscle fibers ( n = 2,215 ; 1,202 pre ; 1,013 post ) was used to identify MHC distribution . One repetition maximum knee extensor strength increased ( P < 0.05 ) 23 + /- 4 kg ( 56 + /- 4 to 79 + /- 7 kg ; 41 % ) . Muscle CSA increased ( P < 0.05 ) 3 + /- 1 cm2 ( 120 + /- 7 to 123 + /- 7 cm2 ; 2.5 % ) . Single muscle fiber contractile function and MHC distribution were unaltered with PRT . These data indicate limited muscle plasticity at the single-muscle fiber level with a resistance-training program among the very old . The minor increases in whole muscle CSA coupled with the static nature of the myocellular profile indicate that the strength gains were primarily neurological . These data contrast typical muscle responses to resistance training in young ( approximately 20 yr ) and old ( approximately 70 yr ) humans and indicate that the physiological regulation of muscle remodeling is adversely modified in the oldest old The purpose of this study was to determine the effect of different training schedules on the cross-sectional area ( CSA ) of the paravertebral muscles ( PA ) in chronic low back pain ( CLBP ) patients . To achieve this goal 59 patients were r and omly assigned to three different 10-week rehabilitation programs : stabilization training ( group 1 , n=19 ) , stabilization training combined with dynamic resistance training ( group 2 , n=20 ) and stabilization training combined with dynamic-static resistance training ( group 3 , n=20 ) . The CSA of the PA was derived from st and ard computerized tomography ( CT ) images at three different levels . The CSA of the PA was found to increase statistically in group 2 ( upper end-plate of L4 ) and group 3 ( upper end-plate of L3 and lower end-plate of L4 ) . In contrast , no statistical differences over time were found in group 1 . Since stabilization exercises have no effect on the CSA of the PA , intensive lumbar resistance training seems to be necessary to restore the size of the PA in CLBP patients with atrophied back muscles . No systematic difference in hypertrophy between dynamic and dynamic-static strengthening training modes was found The response to resistance training and protein supplementation in the latissimus dorsi muscle ( LDM ) has never been investigated . We investigated the effects of resistance training ( RT ) and protein supplementation on muscle mass , strength , and fiber characteristics of the LDM . Eighteen healthy young subjects were r and omly assigned to a progressive eight-week RT program with a normal protein diet ( NP ) or high protein diet ( HP ) ( NP 0.85 vs. HP 1.8 g of protein·kg−1·day−1 ) . One repetition maximum tests , magnetic resonance imaging for cross-sectional muscle area ( CSA ) , body composition , and single muscle fibers mechanical and phenotype characteristics were measured . RT induced a significant gain in strength ( + 17 % , p < 0.0001 ) , whole muscle CSA ( p = 0.024 ) , and single muscle fibers CSA ( p < 0.05 ) of LDM in all subjects . Fiber isometric force increased in proportion to CSA ( + 22 % , p < 0.005 ) and thus no change in specific tension occurred . A significant transition from 2X to 2A myosin expression was induced by training . The protein supplementation showed no significant effects on all measured outcomes except for a smaller reduction of 2X myosin expression . Our results suggest that in LDM protein supplementation does not further enhance RT-induced muscle fiber hypertrophy nor influence mechanic muscle fiber characteristics but partially counteracts the fast-to-slow fiber shift Resistance training results in muscle hypertrophy and improves glycemic control in patients with type 2 diabetes . Whether resistance training modulates inflammation in muscles of diabetic patients remains unknown . We examined the expression of genes encoding the cytokines , tumor necrosis factor-α ( TNF-α ) , interleukin-1β ( IL-lβ ) and transforming growth factor-β , ( TGF-β , ) as well as the pan-leukocyte marker CD18 . Thirty men and women ( 67 ± 7 years ) were r and omized to either 16 weeks of resistance training and usual diabetes care ( EX ) or to usual diabetes care only ( CON ) . Muscle biopsies were obtained from the vastus lateralis muscle prior to the 16-week intervention , and 72 h following the maximal strength test post-intervention . Fiber cross-sectional area ( CSA ) was determined following ATPase staining . Cytokine and CD18 transcript levels were assessed by real-time PCR . Resistance training increased CSA of type I and II fibers ( both P < 0.05 ) and IL-1β transcript levels ( P = 0.05 ) . TNF-α ( P < 0.05 ) and TGF-β1 transcripts ( P < 0.05 ) increased over time in the EX group , but these increases did not differ from those in the CON group . In both groups , the increase in CD18 transcripts remained minimal . The two groups differ by the relationship between changes in CD18 and changes in cytokine transcripts , suggesting that resistance training affects the source of cytokines in muscle . Our studies establish that resistance training in older adults with type 2 diabetes results in muscle fiber hypertrophy , despite a greater accumulation of inflammatory cytokine transcripts in muscle Twelve male subjects with recreational resistance training background s completed 12 wk of intensified resistance training ( 3 sessions/wk ; 8 exercises/session ; 3 sets/exercise ; 10 repetitions maximum/set ) . All major muscle groups were trained , with four exercises emphasizing the forearm flexors . After training , strength ( 1-repetition maximum preacher curl ) increased by 25 % ( P < 0.05 ) . Magnetic resonance imaging scans revealed an increase in the biceps brachii muscle cross-sectional area ( CSA ) ( from 11.8 + /- 2.7 to 13.3 + /- 2.6 cm2 ; n = 8 ; P < 0.05 ) . Muscle biopsies of the biceps brachii revealed increases ( P < 0.05 ) in fiber areas for type I ( from 4,196 + /- 859 to 4,617 + /- 1,116 microns2 ; n = 11 ) and II fibers ( from 6,378 + /- 1,552 to 7,474 + /- 2,017 microns2 ; n = 11 ) . Fiber number estimated from the above measurements did not change after training ( 293.2 + /- 61.5 x 10(3 ) pretraining ; 297.5 + /- 69.5 x 10(3 ) posttraining ; n = 8) . However , the magnitude of muscle fiber hypertrophy may influence this response because those subjects with less relative muscle fiber hypertrophy , but similar increases in muscle CSA , showed evidence of an increase in fiber number . Capillaries per fiber increased significantly ( P < 0.05 ) for both type I ( from 4.9 + /- 0.6 to 5.5 + /- 0.7 ; n = 10 ) and II fibers ( from 5.1 + /- 0.8 to 6.2 + /- 0.7 ; n = 10 ) . No changes occurred in capillaries per fiber area or muscle area . In conclusion , resistance training result ed in hypertrophy of the total muscle CSA and fiber areas with no change in estimated fiber number , whereas capillary changes were proportional to muscle fiber growth
Our meta analysis of a homogeneous set of studies is the first to provide valuable LLNs for fiber CSA according to fiber type and gender .
Skeletal muscle atrophy is a major systemic impairment in chronic diseases .
Yet its determinants have been hard to identify because a clear research definition has not been agreed upon .
The reduction in muscle fiber cross-sectional area ( CSA ) is a widely acknowledged marker of muscle atrophy , but no reference values for the muscle fiber CSA at the age of the onset of chronic disease have ever been published .