ORCID Profile
0000-0002-9999-8020
Current Organisation
Universidade de São Paulo
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Publisher: Springer Science and Business Media LLC
Date: 2010
Publisher: Wiley
Date: 18-01-2022
DOI: 10.1111/APHA.13782
Abstract: The mechanisms underlying the immunometabolic disturbances during skeletal muscle atrophy caused by a plethora of circumstances ranging from hospitalization to spaceflight missions remain unknown. Here, we outline the possible pathways that might be dysregulated in such conditions and assess the potential of physical exercise to mitigate and promote the recovery of muscle morphology, metabolism and function after intervals of disuse. Studies applying exercise to attenuate disuse-induced muscle atrophy have shown a pivotal role of circulating myokines in the activation of anabolic signalling pathways. These muscle-derived factors induce accretion of contractile proteins in the myofibers, and at the same time decrease protein breakdown and loss. Regular exercise plays a crucial role in re-establishing adequate immunometabolism and increasing the migration and presence in the muscle of macrophages with an anti-inflammatory phenotype (M2) and T regulatory cells (Tregs) after disease-induced muscle loss. Additionally, the switch in metabolic pathways (glycolysis to oxidative phosphorylation [OXPHOS]) is important for achieving rapid metabolic homeostasis during muscle regeneration. In this review, we discuss the molecular aspects of the immunometabolic response elicited by exercise during skeletal muscle regeneration. There is not, nevertheless, consensus on a single optimal intensity of exercise required to improve muscle strength, mass and functional capacity owing to the wide range of exercise protocols studied so far. Despite the absence of agreement on the specific strategy, physical exercise appears as a powerful complementary strategy to attenuate the harmful effects of muscle disuse in different scenarios.
Publisher: Wiley
Date: 09-06-2010
DOI: 10.1111/J.1365-2362.2010.02316.X
Abstract: This study examined the effects of acute supramaximal exercise (approximately 115% VO(2max)) on the blood lipid profile for three different carbohydrate (CHO) storage levels (control, low and high). Six male subjects were randomly ided into three different groups: control, low CHO and high CHO. These groups differed in the diet to which the subjects were submitted before each exercise session. The lipid profile [triglycerides (TG), very low-density lipoprotein (VLDL), high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, TG/HDL-C ratio and total cholesterol) was determined at rest, immediately after exercise and 1 h after exercise bouts. The time to exhaustion was lower in the low CHO condition compared with the control and high CHO condition (3.59 +/- 0.72 2.91 +/- 0.56 and 4.26 +/- 0.69 min P < 0.05). The energy expenditure (control: 251.1 +/- 56.0 kJ low CHO: 215.2 +/- 28.6 kJ and high CHO: 310.4 +/- 64.9 kJ) was significantly different between the low and high CHO conditions (P < 0.05). There were no significant changes in the lipid profile for any of the experimental conditions (control, low and high P 0.05). These results indicate that a supramaximal exercise session has no significant effects on lipid metabolism.
Publisher: Springer Science and Business Media LLC
Date: 06-07-2010
DOI: 10.1007/S00726-010-0678-0
Abstract: Amino acids such as leucine and its metabolite α-ketoisocaproate (KIC), are returning to be the focus of studies, mainly because of their anti-catabolic properties, through inhibition of muscle proteolysis and enhancement of protein synthesis. It is clear that these effects may counteract catabolic conditions, as well as enhance skeletal muscle mass and strength in athletes. Moreover, beta-hydroxy-beta-methylbutyrate (HMB) has been shown to produce an important effect in reducing muscle damage induced by mechanical stimuli of skeletal muscle. This review aims to describe the general scientific evidence of KIC and HMB supplementation clinical relevance, as well as their effects (e.g., increases in skeletal muscle mass and/or strength), associated with resistance training or other sports. Moreover, the possible mechanisms of cell signaling regulation leading to increases and/or sparing (during catabolic conditions) of skeletal muscle mass are discussed in detail based on the recent literature.
Publisher: Springer Science and Business Media LLC
Date: 24-06-2009
DOI: 10.1007/S00421-009-1115-5
Abstract: A reduction in LDL cholesterol and an increase in HDL cholesterol levels are clinically relevant parameters for the treatment of dyslipidaemia, and exercise is often recommended as an intervention. This study aimed to examine the effects of acute, high-intensity exercise ( approximately 90% VO(2max)) and varying carbohydrate levels (control, low and high) on the blood lipid profile. Six male subjects were distributed randomly into exercise groups, based on the carbohydrate diets (control, low and high) to which the subjects were restricted before each exercise session. The lipid profile (triglycerides, VLDL, HDL cholesterol, LDL cholesterol and total cholesterol) was determined at rest, and immediately and 1 h after exercise bouts. There were no changes in the time exhaustion (8.00 +/- 1.83 7.82 +/- 2.66 and 9.09 +/- 3.51 min) and energy expenditure (496.0 +/- 224.8 411.5 +/- 223.1 and 592.1 +/- 369.9 kJ) parameters with the three varying carbohydrate intake (control, low and high). Glucose and insulin levels did not show time-dependent changes under the different conditions (P > 0.05). Total cholesterol and LDL cholesterol were reduced after the exhaustion and 1 h recovery periods when compared with rest periods only in the control carbohydrate intake group (P < 0.05), although this relation failed when the diet was manipulated. These results indicate that acute, high-intensity exercise with low energy expenditure induces changes in the cholesterol profile, and that influences of carbohydrate level corresponding to these modifications fail when carbohydrate (low and high) intake is manipulated.
Publisher: Springer Science and Business Media LLC
Date: 22-01-2010
No related grants have been discovered for Marilia Seelaender.