18 research outputs found
Plasma Acylcarnitines During Insulin Stimulation in Humans are Reflective of Age-Related Metabolic Dysfunction
Aerobic and Resistance Exercise Training Reverses Age-Dependent Decline in NAD + Salvage Capacity in Human skeletal muscle
© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. Aging decreases skeletal muscle mass and strength, but aerobic and resistance exercise training maintains skeletal muscle function. NAD+ is a coenzyme for ATP production and a required substrate for enzymes regulating cellular homeostasis. In skeletal muscle, NAD+ is mainly generated by the NAD+ salvage pathway in which nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting. NAMPT decreases with age in human skeletal muscle, and aerobic exercise training increases NAMPT levels in young men. However, whether distinct modes of exercise training increase NAMPT levels in both young and old people is unknown. We assessed the effects of 12 weeks of aerobic and resistance exercise training on skeletal muscle abundance of NAMPT, nicotinamide riboside kinase 2 (NRK2), and nicotinamide mononucleotide adenylyltransferase (NMNAT) 1 and 3 in young (≤35 years) and older (≥55 years) individuals. NAMPT in skeletal muscle correlated negatively with age (r2 = 0.297, P \u3c 0.001, n = 57), and VO2peak was the best predictor of NAMPT levels. Moreover, aerobic exercise training increased NAMPT abundance 12% and 28% in young and older individuals, respectively, whereas resistance exercise training increased NAMPT abundance 25% and 30% in young and in older individuals, respectively. None of the other proteins changed with exercise training. In a separate cohort of young and old people, levels of NAMPT, NRK1, and NMNAT1/2 in abdominal subcutaneous adipose tissue were not affected by either age or 6 weeks of high-intensity interval training. Collectively, exercise training reverses the age-dependent decline in skeletal muscle NAMPT abundance, and our findings highlight the value of exercise training in ameliorating age-associated deterioration of skeletal muscle function
Impact of endurance and resistance training on skeletal muscle glucose metabolism in older adults
© 2019 by the authors. Licensee MDPI, Basel, Switzerland. Aging is associated with insulin resistance and the development of type 2 diabetes. While this process is multifaceted, age-related changes to skeletal muscle are expected to contribute to impaired glucose metabolism. Some of these changes include sarcopenia, impaired insulin signaling, and imbalances in glucose utilization. Endurance and resistance exercise training have been endorsed as interventions to improve glucose tolerance and whole-body insulin sensitivity in the elderly. While both types of exercise generally increase insulin sensitivity in older adults, the metabolic pathways through which this occurs can differ and can be dependent on preexisting conditions including obesity and type 2 diabetes. In this review, we will first highlight age-related changes to skeletal muscle which can contribute to insulin resistance, followed by a comparison of endurance and resistance training adaptations to insulin-stimulated glucose metabolism in older adults
The effect of exercise type on immunofunctional and traditional growth hormone
The purpose of this study was to compare the growth hormone (GH) response, including the immunfunctional (IF) GH response, between an acute bout of aerobic and resistance exercise in the same subjects. Ten cross-trained males (24.3 ± 1.2 years) performed both 30 min of continuous cycling at 70% of V̇O2max, and intermittent free weight squatting at 70% of 1-RM, in a randomly assigned crossover design, separated by at least 1 week. Blood samples were collected at 10-min intervals for 2 h (30 min rest, 30 min exercise, 60 min recovery) and analyzed for total human and IF GH. After adjusting for the amount of work performed per minute of exercise, integrated GH AUC was significantly greater during the resistance session than the aerobic session as measured by both the total and IF GH assays (P=0.008 and P=0.014, respectively). Peak GH concentrations were significantly greater during the resistance session than the aerobic session (P=0.05). A similar overall GH pattern was observed in response to both types of exercise, with peak values occurring at the end of exercise, regardless of the GH assay used. These data demonstrate that in young, cross-trained males, intermittent resistance exercise elicits a greater response of GH, including IF GH, compared to a continuous aerobic session, when controlling for the work performed per minute, intersubject variability, relative exercise intensity and session duration. © Springer-Verlag 2007
Impact of Endurance and Resistance Training on Skeletal Muscle Glucose Metabolism in Older Adults
Perspective: Pragmatic Exercise Recommendations for Older Adults: The Case for Emphasizing Resistance Training
© Copyright © 2020 Tavoian, Russ, Consitt and Clark. Optimal health benefits from exercise are achieved by meeting both aerobic and muscle strengthening guidelines, however, most older adults (OAs) do not exercise and the majority of those who do only perform one type of exercise. A pragmatic solution to this problem may be emphasizing a single exercise strategy that maximizes health benefits. The loss of muscle mass and strength at an accelerated rate are hallmarks of aging that, without intervention, eventually lead to physical disability and loss of independence. Additionally, OAs are at risk of developing several chronic diseases. As such, participating in activities that can maintain or increase muscle mass and strength, as well as decrease chronic disease risk, is essential for healthy aging. Unfortunately, there is a widely held belief that adaptations to aerobic and resistance exercise are independent of each other, requiring the participation of both types of exercise to achieve optimal health. However, we argue that this assertion is incorrect, and we discuss crossover adaptations of both aerobic and resistance exercise. Aerobic exercise can increase muscle mass and strength, though not consistently and may be limited to exercise that overloads a particular muscle group, such as stationary bicycling. In contrast, resistance exercise is effective at maintaining muscle health with increasing age, and also has significant effects on cardiovascular disease (CVD) risk factors, type 2 diabetes (T2D), cancer, and mortality. We posit that resistance exercise is the most effective standalone exercise strategy for improving overall health in OAs and should be emphasized in future guidelines
Mice overexpressing growth hormone exhibit increased skeletal muscle myostatin and MuRF1 with attenuation of muscle mass
Abstract Background In contrast to the acute effects of growth hormone (GH) on skeletal muscle protein synthesis, long-term GH treatment appears to have negligible effects on muscle mass. Despite this knowledge, little is known regarding the chronic effects of GH on skeletal muscle protein synthesis and atrophy signaling pathways. The purpose of this study was to determine if protein synthesis pathways are attenuated and/or muscle atrophy intracellular signaling pathways are altered in the skeletal muscle of transgenic bovine GH (bGH) mice. Methods The gastrocnemius and soleus from 5-month-old male bGH mice (n = 9) and wild type (WT) controls (n = 9) were harvested and analyzed for proteins involved in the protein synthesis (Akt/mTOR), growth and proliferation (MAPK), and muscle atrophy (MuRF1 and myostatin) pathways. Results Total body mass was significantly increased in bGH mice compared to WT controls (49%, P < 0.0001). When expressed relative to total body mass, the gastrocnemius (− 28%, P < 0.0001), but not the soleus, was significantly lower in mice overexpressing GH, compared to controls. Transgenic bGH mice had elevated phosphorylation levels of protein kinase b (Akt1), 4E-binding protein 1 (4E-BP1), p70 S6 kinase, p42/44, and p38 (P < 0.05) compared to WT littermates. Mature myostatin (26 kDa), premature myostatin (52 kDa), and activin receptor type IIB (AcvR2B) protein levels were increased in bGH mice (P < 0.05), along with elevated phosphorylation levels of mothers against decapentaplegic homolog (Smad2) (59%, P < 0.0001). Mice overexpressing GH had increased MuRF1 expression (30%, P < 0.05) and insulin receptor substrate 1 (IRS1) serine phosphorylation (44%, P < 0.05) in the gastrocnemius, but not the soleus, when compared to controls. Conclusions These findings demonstrate that chronic elevations in circulating GH have a critical impact on signaling pathways involved in skeletal muscle protein synthesis and atrophy, and suggest that MuRF1, myostatin, and IRS1 serine phosphorylation may act to inhibit exaggerated glycolytic muscle growth, in environments of chronic GH/IGF-1 excess
Intramuscular Lipid Metabolism Insulin Action and Obesity
With the increasing prevalence of obesity research has focused on the molecular mechanism(s) linking obesity and skeletal muscle insulin resistance. Metabolic alterations within muscle such as changes in the cellular location of fatty acid transporter proteins decreased mitochondrial enzyme activity and defects in mitochondrial morphology likely contribute to obesity and insulin resistance. These defects are thought to play a role in the reduced skeletal muscle fatty acid oxidation (FAO) and increased intramuscular lipid (IMCL) accumulation that is apparent with obesity and other insulin resistant states such as type 2 diabetes. Intramuscular triacylglycerol (IMTG) does not appear to be a ubiquitous marker of insulin resistance although specific IMCL intermediates such as long-chain fatty acyl-CoAs (LCFA-CoAs) ceramide and diacylglycerol (DAG) may inhibit insulin signal transduction. In this review we will briefly summarize the defects in skeletal muscle lipid metabolism associated with obesity and discuss proposed mechanisms by which these defects may contribute to insulin resistance. Originally published IUBMB Life Vol. 6 No. 1 Jan 200