Quantitative assessment of cardiorespiratory fitness, skeletal muscle function, and body composition in adults with primary malignant glioma

e13002 Background: The neuropsychological impact of malignant glioma is well documented; the physiological and functional effects are not known. We conducted a pilot study to quantitatively assess cardiorespiratiory fitness, skeletal muscle function, and body composition of patients with primary malignant glioma. Methods: Using a cross-sectional design, patients with clinically stable postsurgical (10 ± 7 days post surgery) high-grade glioma (HGG; n=25) and low-grade glioma (LGG) were studied. Participants performed a cardiopulmonary exercise test (CPET) with expired gas analysis to assess peak exercise capacity (VO2peak) and other parameters of cardiovascular function. Other physiological outcomes included skeletal muscle cross-sectional area (CSA; magnetic resonance imaging), isokinetic muscle strength (isokinetic dynamometer), and body composition (air displacement plethysmography). QOL was assessed by the Functional Assessment of Cancer Therapy-Brain scale (FACT-BR). Results: CPET was a feasible and safe procedure for malignant glioma patients with no serious adverse events. Peak VO2 indexed to total body weight and lean body mass for both groups was 13.0 mL.min-1 and 19 mL.min-1; the equivalent to 59% and 38% below age and sex-predicted normative values, respectively. Skeletal muscle isokinetic strength was significantly lower in HGG relative to LGG patients (83 vs. 125 Nm, p=.025) and predicted peak VO2 (r = 0.44, p<0.05). In patients with HGG, only self-reported exercise behavior was correlated with QOL (r = 0.42; p=.046) while sex (male) (r = 0.44; p=.037), lean mass (r = -0.41; p=.049), and VO2peak (r = -0.40; p=.052) were associated with fatigue. Conclusions: CPET is a safe and feasible tool to evaluate physical functioning in select patients with malignant glioma. Postsurgical glioma patients have markedly reduced exercise capacity, isokinetic strength and CSA. Muscle strength is an important contributor to poor VO2peak in this population. Prospective studies are now required to determine whether such abnormalities influence prognosis as well as test the effect of appropriately selected interventions to prevent and/or mitigate dysfunction. No significant financial relationships to disclose.

Download Full-text

Quantitative assessment of cardiorespiratory fitness, skeletal muscle function, and body composition in adults with primary malignant glioma

Cancer ◽

10.1002/cncr.24808 ◽

2010 ◽

Vol 116 (3) ◽

pp. 695-704 ◽

Cited By ~ 27

Author(s):

Lee W. Jones ◽

Allan H. Friedman ◽

Miranda J. West ◽

Stephanie K. Mabe ◽

Jennifer Fraser ◽

...

Keyword(s):

Skeletal Muscle ◽

Body Composition ◽

Malignant Glioma ◽

Cardiorespiratory Fitness ◽

Muscle Function ◽

Quantitative Assessment ◽

Skeletal Muscle Function

Download Full-text

Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice

Scientific Reports ◽

10.1038/s41598-021-90565-0 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

C. Homer-Bouthiette ◽

L. Xiao ◽

Marja M. Hurley

Keyword(s):

Skeletal Muscle ◽

Growth Factor ◽

Muscle Strength ◽

Fibroblast Growth Factor ◽

Muscle Function ◽

Fibroblast Growth Factor 2 ◽

Fibroblast Growth ◽

Skeletal Muscle Function ◽

Age Related ◽

Gait Disturbances

AbstractFibroblast growth factor 2 (FGF2) is important in musculoskeletal homeostasis, therefore the impact of reduction or Fgf2 knockout on skeletal muscle function and phenotype was determined. Gait analysis as well as muscle strength testing in young and old WT and Fgf2KO demonstrated age-related gait disturbances and reduction in muscle strength that were exacerbated in the KO condition. Fgf2 mRNA and protein were significantly decreased in skeletal muscle of old WT compared with young WT. Muscle fiber cross-sectional area was significantly reduced with increased fibrosis and inflammatory infiltrates in old WT and Fgf2KO vs. young WT. Inflammatory cells were further significantly increased in old Fgf2KO compared with old WT. Lipid-related genes and intramuscular fat was increased in old WT and old Fgf2KO with a further increase in fibro-adipocytes in old Fgf2KO compared with old WT. Impaired FGF signaling including Increased β-Klotho, Fgf21 mRNA, FGF21 protein, phosphorylated FGF receptors 1 and 3, was observed in old WT and old Fgf2KO. MAPK/ ERK1/2 was significantly increased in young and old Fgf2KO. We conclude that Fgf2KO, age-related decreased FGF2 in WT mice, and increased FGF21 in the setting of impaired Fgf2 expression likely contribute to impaired skeletal muscle function and sarcopenia in mice.

Download Full-text

GPR30 ACTIVATION IMPROVES EXERCISE CAPACITY AND SKELETAL MUSCLE FUNCTION IN SENESCENT FEMALE F344BN RATS

The Gerontologist ◽

10.1093/geront/gnv502.15 ◽

2015 ◽

Vol 55 (Suppl_2) ◽

pp. 105-105

Keyword(s):

Skeletal Muscle ◽

Exercise Capacity ◽

Muscle Function ◽

Skeletal Muscle Function

Download Full-text

The Effects of Aging and Training on Skeletal Muscle

The American Journal of Sports Medicine ◽

10.1177/03635465980260042401 ◽

1998 ◽

Vol 26 (4) ◽

pp. 598-602 ◽

Cited By ~ 130

Author(s):

Donald T. Kirkendall ◽

William E. Garrett

Keyword(s):

Skeletal Muscle ◽

Muscle Mass ◽

Muscle Function ◽

Cellular Level ◽

Type I ◽

Loss Of Function ◽

Skeletal Muscle Function ◽

Cross Sectional ◽

Age Related ◽

General Slowing

Aging results in a gradual loss of muscle function, and there are predictable age-related alterations in skeletal muscle function. The typical adult will lose muscle mass with age; the loss varies according to sex and the level of muscle activity. At the cellular level, muscles loose both cross-sectional area and fiber numbers, with type II muscle fibers being the most affected by aging. Some denervation of fibers may occur. The combination of these factors leads to an increased percentage of type I fibers in older adults. Metabolically, the glycolytic enzymes seem to be little affected by aging, but the aerobic enzymes appear to decline with age. Aged skeletal muscle produces less force and there is a general “slowing” of the mechanical characteristics of muscle. However, neither reduced muscle demand nor the subsequent loss of function is inevitable with aging. These losses can be minimized or even reversed with training. Endurance training can improve the aerobic capacity of muscle, and resistance training can improve central nervous system recruitment of muscle and increase muscle mass. Therefore, physical activity throughout life is encouraged to prevent much of the age-related impact on skeletal muscle.

Download Full-text

Heat therapy improves body composition and muscle function, but does not affect capillary or collateral growth in a model of obesity and hindlimb ischemia

Journal of Applied Physiology ◽

10.1152/japplphysiol.00535.2020 ◽

2020 ◽

Author(s):

Kyoungrae Kim ◽

Bohyun Ro ◽

Frederick W. Damen ◽

Daniel P. Gramling ◽

Trevor D. Lehr ◽

...

Keyword(s):

Skeletal Muscle ◽

Body Composition ◽

Body Mass ◽

Muscle Function ◽

Exercise Intolerance ◽

Contractile Dysfunction ◽

Skeletal Muscle Function ◽

Positive Effects ◽

Collateral Growth ◽

Heat Therapy

Heat therapy (HT) has emerged as a potential adjunctive therapy to alleviate the symptoms of peripheral artery disease (PAD), but the mechanisms underlying the positive effects of this treatment modality remain undefined. Using a model of diet-induced obesity (DIO) and ischemia-induced muscle damage, we tested the hypothesis that HT would alter body composition, promote vascular growth and mitochondrial biogenesis, and improve skeletal muscle function. Male DIO C57Bl/6J mice underwent bilateral ligation of the femoral artery and were randomly allocated to receive HT or a control intervention for 30 min daily over 3 weeks. When compared to a group of lean, sham-operated animals, ligated DIO mice exhibited increases in body and fat masses, exercise intolerance and contractile dysfunction of the isolated soleus (SOL) and extensor digitorum longus (EDL) muscles. Repeated HT averted an increase in body mass induced by high-fat feeding due to reduced fat accrual. Fat mass was ~25% and 29% lower in the HT group relative to controls after 2 and 3 weeks of treatment, respectively. Muscle mass relative to body mass and maximal absolute force of the EDL, but not SOL, were higher in animals exposed to HT. There were no group differences in skeletal muscle capillarization, the expression of angiogenic factors, mitochondrial content and the diameter of the gracilis arteries. These findings indicate that HT reduces diet-induced fat accumulation and rescues skeletal muscle contractile dysfunction. This practical treatment may prove useful for diabetic and obese PAD patients who are unable to undergo conventional exercise regimens.

Download Full-text

Corticosteroids and skeletal muscle function in cystic fibrosis

Journal of Applied Physiology ◽

10.1152/japplphysiol.00506.2002 ◽

2003 ◽

Vol 95 (4) ◽

pp. 1379-1384 ◽

Cited By ~ 49

Author(s):

Sinead C. Barry ◽

Charles G. Gallagher

Keyword(s):

Skeletal Muscle ◽

Cystic Fibrosis ◽

Muscle Strength ◽

Muscle Weakness ◽

Muscle Function ◽

Knee Extensor ◽

Skeletal Muscle Function ◽

Peripheral Muscle ◽

Causative Effect ◽

Concomitant Medications

Patients with cystic fibrosis (CF) have reduced peripheral muscle strength. We tested the hypothesis that steroid treatment contributes to muscle weakness in adults with CF. Twenty-three stable CF patients were studied. Measurements included knee extensor (KE), knee flexor (KF), elbow flexor (EF), handgrip (HG), expiratory (Pemax), and inspiratory (Pimax) muscle strengths. Spirometry, body mass index (BMI), and days spent in hospital over the preceding 12 mo (DH) were also measured. Average daily dose of prednisolone over the preceding 12 mo (ADD) was 5.1 mg/day. Pearson's correlation analysis revealed that ADD correlated significantly with skeletal muscle strengths (KF%, r = -0.63, P < 0.01) with the exception of HG%. These findings are independent of age, BMI, pulmonary function, and DH. Multiple-regression analysis revealed that ADD was the most significant predictor of all measures of skeletal muscle function except HG%. It was independently responsible for 54% of the variance in Pimax%, for 46% of the variance in Pemax%, for 45% of the variance in KE%, for 39% of the variance in KF%, and for 41% of the variance in EF%. Concomitant medications (e.g., theophylline) were shown to have no causative effect. Corticosteroids contribute to the skeletal muscle weakness seen in CF patients. The correlation of proximal muscle strength, but not HG strength, with steroid dosage further supports a cause-effect relationship.

Download Full-text

Exercise Capacity Is Limited In Diabetic Mice Due To The Impairment Of Skeletal Muscle Function

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000274412.07192.96 ◽

2007 ◽

Vol 39 (Supplement) ◽

pp. S360

Author(s):

Takashi Yokota ◽

Shintaro Kinugawa ◽

Syoji Matsushima ◽

Naoki Inoue ◽

Yukihiro Ohta ◽

...

Keyword(s):

Skeletal Muscle ◽

Exercise Capacity ◽

Muscle Function ◽

Diabetic Mice ◽

Skeletal Muscle Function

Download Full-text

Role of TRPC1 channel in skeletal muscle function

AJP Cell Physiology ◽

10.1152/ajpcell.00241.2009 ◽

2010 ◽

Vol 298 (1) ◽

pp. C149-C162 ◽

Cited By ~ 81

Author(s):

Nadège Zanou ◽

Georges Shapovalov ◽

Magali Louis ◽

Nicolas Tajeddine ◽

Chiara Gallo ◽

...

Keyword(s):

Skeletal Muscle ◽

Muscle Function ◽

Transient Receptor Potential ◽

Force Production ◽

Receptor Potential ◽

Cross Sectional Area ◽

Sectional Area ◽

Skeletal Muscle Function ◽

Cross Sectional

Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu , excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1−/−mice. The influx of Ca2+through TRPC1 channels represents a minor part of the entry of Ca2+into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+concentration ([Ca2+]i) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1−/−mice stimulated repeatedly progressively display lower [Ca2+]itransients than those observed in TRPC1+/+fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1−/−mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1−/−mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca2+during repeated contractions and help muscles to maintain their force during sustained repeated contractions.

Download Full-text