Marcas M. Bamman
University of Alabama
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Featured researches published by Marcas M. Bamman.
Sports Medicine | 2004
Gary R. Hunter; John P. McCarthy; Marcas M. Bamman
Using an integrative approach, this review highlights the benefits of resistance training toward improvements in functional status, health and quality of life among older adults. Sarcopenia (i.e. muscle atrophy) and loss of strength are known to occur with age. While its aetiology is poorly understood, the multifactorial sequelae of sarcopenia are well documented and present a major public health concern to our aging population, as both the quality of life and the likelihood of age-associated declines in health status are influenced. These age-related declines in health include decreased energy expenditure at rest and during exercise, and increased body fat and its accompanying increased dyslipidaemia and reduced insulin sensitivity. Quality of life is affected by reduced strength and endurance and increased difficulty in being physically active. Strength and muscle mass are increased following resistance training in older adults through a poorly understood series of events that appears to involve the recruitment of satellite cells to support hypertrophy of mature myofibres. Muscle quality (strength relative to muscle mass) also increases with resistance training in older adults possibly for a number of reasons, including increased ability to neurally activate motor units and increased high-energy phosphate availability. Resistance training in older adults also increases power, reduces the difficulty of performing daily tasks, enhances energy expenditure and body composition, and promotes participation in spontaneous physical activity. Impairment in strength development may result when aerobic training is added to resistance training but can be avoided with training limited to 3 days/week.
Journal of Burn Care & Research | 2012
Edward K. Merritt; James M. Cross; Marcas M. Bamman
Severe burn injuries lead to a prolonged hypercatabolic state resulting in dramatic loss of skeletal muscle mass. Postburn muscle loss is well documented but the molecular signaling cascade preceding atrophy is not. The purpose of this study is to determine the response to burn injury of signaling pathways driving muscle inflammation and protein metabolism. Muscle biopsies were collected in the early flow phase after burn injury from the vastus lateralis of a noninjured leg in patients with 20 to 60% TBSA burns and compared with uninjured, matched controls. Circulating levels of proinflammatory cytokines were also compared. Immunoblotting was performed to determine the protein levels of key signaling components for translation initiation, proteolysis, and tumor necrosis factor/nuclear factor kappa B (NF&kgr;B)and interleukin (IL)-6/STAT3 signaling. Burn subjects had significantly higher levels of circulating proinflammatory cytokines, with no difference in muscle STAT3 activity and lower NF&kgr;B activity. No differences were found in any translational signaling components. Regarding proteolytic signaling in burn, calpain-2 was 47% higher, calpastatin tended to be lower, and total ubiquitination was substantially higher. Surprisingly, a systemic proinflammatory response 3 to 10 days postburn did not lead to elevated muscle STAT3 or NF&kgr;B signaling. Signaling molecules governing translation initiation were unaffected, whereas indices of calcium-mediated proteolysis and ubiquitin-proteasome activity were upregulated. These novel findings are the first in humans to suggest that the net catabolic effect of burn injury in skeletal muscle (ie, atrophy) may be mediated, at least during the early flow phase, almost entirely by an increased proteolytic activity in the absence of suppressed protein synthesis signaling.
Journal of Burn Care & Research | 2013
Edward K. Merritt; Anna Thalacker-Mercer; James M. Cross; Samuel T. Windham; Steven J. Thomas; Marcas M. Bamman
Severe burn induces rapid skeletal muscle proteolysis after the injury, which persists for up to 1 year and results in skeletal muscle atrophy despite dietary and rehabilitative interventions. The purpose of this research was to determine acute changes in gene expression of skeletal muscle mass regulators postburn injury. Specimens were obtained for biopsy from the vastus lateralis of a nonburned leg of eight burned subjects (6M, 2F: 34.8 ± 2.7 years: 29.9 ± 3.1% TBSA burn) at 5.1 ± 1.1 days postburn injury and from matched controls. mRNA expression of cytokines and receptors in the tumor necrosis factor-&agr; (TNF-&agr;) and interleukin-6 (IL-6) families, and the ubiquitin proteasome E3 ligases, atrogin-1 and MuRF-1, was determined. TNF receptor 1A was over 3.5-fold higher in burn. Expression of TNF-like weak inducer of apoptosis and its receptor were over 1.6 and 6.0-fold higher in burn. IL-6, IL-6 receptor, and glycoprotein 130 were elevated in burned subjects with IL-6 receptor over 13-fold higher. The level of suppressor of cytokine signaling-3 was also increased nearly 6-fold in burn. Atrogin-1 and MuRF-1 were more than 4- and 3-fold higher in burn. These results demonstrate for the first time that severe burn in humans has a remarkable impact on gene expression in skeletal muscle of a nonburned limb of genes that promote inflammation and proteolysis. Because these changes likely contribute to the acute skeletal muscle atrophy in areas not directly affected by the burn, in the future it will be important to determine the responsible systemic cues.
British Journal of Sports Medicine | 2005
B R Newcomer; B Sirikul; Gary R. Hunter; E Larson-Meyer; Marcas M. Bamman
Objective:31P magnetic resonance spectroscopy (MRS) was used to document long lasting losses in muscle oxidative capacity after bouts of intense endurance exercise. Methods: The subject was a 34 year old highly fit female cyclist (Vo2max = 53.3 ml/kg/min). Over a five month period, she participated in three separate intense bouts of acute unaccustomed exercise. 31P MRS measurements were performed seven weeks after the first bout and every two weeks for 14 more weeks. In all cases, 31P MRS measurements followed three days after each bout. Results: The subject showed a decreased ability to generate ATP from oxidative phosphorylation and an increased reliance on anaerobic ATP production during the 70% and 100% maximal voluntary contractions after the exercise bouts. Increased rates of fatigue and increased indicators of exercise difficulty also accompanied these reductions in muscle oxidative capacity. Increased oxidative and anaerobic ATP production were needed to maintain the work level during a submaximal 45% maximal voluntary contraction exercise. Conclusions: Acute increases in intensity accompanied by a change in exercise mode can influence the ability of muscle to generate ATP. The muscles were less economical and required more ATP to generate force during the submaximal exercises. During the maximal exercises, the muscle’s mitochondria showed a reduced oxidative capacity. However, these reductions in oxidative capacity at the muscle level were not associated with changes in whole body maximal oxygen uptake. Finally, these reductions in muscular oxidative capacity were accompanied by increased rates of anaerobic ATP production, fatigue, and indicators of exercise difficulty.
CA: A Cancer Journal for Clinicians | 2018
Wendy Demark-Wahnefried; Kathryn H. Schmitz; Catherine M. Alfano; Jennifer R. Bail; Pamela J. Goodwin; Cynthia A. Thomson; Don W. Bradley; Kerry S. Courneya; Christie A. Befort; Crystal S. Denlinger; Jennifer A. Ligibel; William H. Dietz; Melinda R. Stolley; Melinda L. Irwin; Marcas M. Bamman; Caroline M. Apovian; Bernardine M. Pinto; Kathleen Y. Wolin; Rachel Ballard; Andrew J. Dannenberg; Elizabeth G. Eakin; Matt Longjohn; Susan D. Raffa; Lucile L. Adams-Campbell; Joanne S. Buzaglo; Sharyl J. Nass; Greta M. Massetti; Erin Balogh; Elizabeth S. Kraft; Anand K. Parekh
Mounting evidence suggests that weight management and physical activity (PA) improve overall health and well being, and reduce the risk of morbidity and mortality among cancer survivors. Although many opportunities exist to include weight management and PA in routine cancer care, several barriers remain. This review summarizes key topics addressed in a recent National Academies of Science, Engineering, and Medicine workshop entitled, “Incorporating Weight Management and Physical Activity Throughout the Cancer Care Continuum.” Discussions related to body weight and PA among cancer survivors included: 1) current knowledge and gaps related to health outcomes; 2) effective intervention approaches; 3) addressing the needs of diverse populations of cancer survivors; 4) opportunities and challenges of workforce, care coordination, and technologies for program implementation; 5) models of care; and 6) program coverage. While more discoveries are still needed for the provision of optimal weight‐management and PA programs for cancer survivors, obesity and inactivity currently jeopardize their overall health and quality of life. Actionable future directions are presented for research; practice and policy changes required to assure the availability of effective, affordable, and feasible weight management; and PA services for all cancer survivors as a part of their routine cancer care. CA Cancer J Clin 2018;68:64‐89.
Ca | 2017
Wendy Demark-Wahnefried; Kathryn H. Schmitz; Catherine M. Alfano; Jennifer R. Bail; Pamela J. Goodwin; Cynthia A. Thomson; Don W. Bradley; Kerry S. Courneya; Christie A. Befort; Crystal S. Denlinger; Jennifer A. Ligibel; William H. Dietz; Melinda R. Stolley; Melinda L. Irwin; Marcas M. Bamman; Caroline M. Apovian; Bernardine M. Pinto; Kathleen Y. Wolin; Rachel Ballard; Andrew J. Dannenberg; Elizabeth G. Eakin; Matt Longjohn; Susan D. Raffa; Lucile L. Adams-Campbell; Joanne S. Buzaglo; Sharyl J. Nass; Greta M. Massetti; Erin Balogh; E. S. Kraft; A. K. Parekh
Archive | 2015
Marcas M. Bamman; David L. Mayhew; Jeong-Su Kim; James M. Cross; Arny A. Ferrando; R. Billeter; John A. Hawley; Vladimir S. Panchev; Stephan van Vliet; Sophie L. Wardle; Kevin D. Tipton; Kenneth Smith; Karyn L. Hamilton; Donny M. Camera; Adelina V. Pancheva; Xiaonan Wang; Mary C. Vagula; J. Atherton; Benjamin F. Miller; Nicholas A. Burd; Lindsay S. Macnaughton; J Andrew
Archive | 2015
J. Hill; S. Craig Tuggle; Richard M. Allman; Marcas M. Bamman; Ronald C. Ragan; Jeong-Su Kim; James M. Cross; Marco Pahor; Todd M. Manini; Christiaan Leeuwenburgh; Thomas W. Buford; R. Gavin MacNeil; Launa G. Clough; Johannes M. Gruenwald; Katie L. Corrick; Jesse R. Trump; Jasvinder A. Singh; Arny A. Ferrando; Richard P. Evans; Michael Stec; Neil Kelly
Archive | 2015
Marcas M. Bamman; Anna Thalacker-Mercer; Michael J. Stec; Xiangqin Cui; Xiao-Ping Zhong; Troy A. Hornberger; Jae-Sung You; Hannah C. Lincoln; Chan-Ran Kim; John W. Frey; Craig A. Goodman; Johannes M. Gruenwald; Katie L. Corrick; Jesse R. Trump; Jasvinder A. Singh; Arny A. Ferrando; Richard P. Evans; Michael Stec; Neil Kelly
Archive | 2015
Marcas M. Bamman; Anna Thalacker-Mercer; Xiangqin Cui; James M. Cross; Rudolf Billeter; John A. Hawley; Vladimir S. Panchev; Stephan van Vliet; Sophie L. Wardle; Kevin D. Tipton; Kenneth Smith; Karyn L. Hamilton; Donny M. Camera; Adelina V. Pancheva; Xiaonan Wang; Mary C. Vagula; J. Atherton; Benjamin F. Miller; Nicholas A. Burd; Lindsay S. Macnaughton; J Andrew