scholarly journals Increased Reliance on Carbohydrates for Aerobic Exercise in Highland Andean Leaf-Eared Mice, but Not in Highland Lima Leaf-Eared Mice

Metabolites ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 750
Author(s):  
Marie-Pierre Schippers ◽  
Oswaldo Ramirez ◽  
Margarita Arana ◽  
Grant B. McClelland
Keyword(s):  
Exercise Performance ◽  
Metabolic Regulation ◽  
Gastrocnemius Muscle ◽  
Deer Mouse ◽  
Maximal Oxygen Consumption ◽  
Submaximal Exercise ◽  
Carbohydrate Oxidation ◽  
Hypoxia Tolerance ◽  
Exercise Induced ◽  
Common Laboratory

Exercise is an important performance trait in mammals and variation in aerobic capacity and/or substrate allocation during submaximal exercise may be important for survival at high altitude. Comparisons between lowland and highland populations is a fruitful approach to understanding the mechanisms for altitude differences in exercise performance. However, it has only been applied in very few highland species. The leaf-eared mice (LEM, genus Phyllotis) of South America are a promising taxon to uncover the pervasiveness of hypoxia tolerance mechanisms. Here we use lowland and highland populations of Andean and Lima LEM (P. andium and P. limatus), acclimated to common laboratory conditions, to determine exercise-induced maximal oxygen consumption (V˙O2max), and submaximal exercise metabolism. Lowland and highland populations of both species showed no difference in V˙O2max running in either normoxia or hypoxia. When run at 75% of V˙O2max, highland Andean LEM had a greater reliance on carbohydrate oxidation to power exercise. In contrast, highland Lima LEM showed no difference in exercise fuel use compared to their lowland counterparts. The higher carbohydrate oxidation seen in highland Andean LEM was not explained by maximal activities of glycolytic enzymes in the gastrocnemius muscle, which were equivalent to lowlanders. This result is consistent with data on highland deer mouse populations and suggests changes in metabolic regulation may explain altitude differences in exercise performance.

Adipose triacylglycerol lipase deletion alters whole body energy metabolism and impairs exercise performance in mice

2009 ◽  
Vol 297 (2) ◽  
pp. E505-E513 ◽  
Author(s):  
Elisabeth Huijsman ◽  
Caro van de Par ◽  
Catherine Economou ◽  
Chris van der Poel ◽  
Gordon S. Lynch ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Exercise Performance ◽  
Liver Glycogen ◽  
Carbohydrate Oxidation ◽  
Hormone Sensitive Lipase ◽  
Whole Body ◽  
Endurance Capacity ◽  
Triacylglycerol Lipase ◽  
Plasma Ffa ◽  
Exercise Induced

Adipose triacylglycerol lipase (ATGL) and hormone-sensitive lipase (HSL) are essential for efficient lipolysis in adipose tissue and skeletal muscle. Herein, we utilized whole body knockout mice to address the importance of ATGL and HSL for metabolic function and exercise performance. ATGL deletion severely disrupts whole-body substrate partitioning at rest; reducing plasma free fatty acid (FFA) availability (WT: 0.49 ± 0.06 vs. ATGL−/− 0.34 ± 0.03 mM), which in turn enhances carbohydrate oxidation during fasting (mean RER, WT: 0.86 ± 0.02, ATGL−/− 0.90 ± 0.01) and is associated with depleted muscle and liver glycogen stores. While plasma FFA was modestly reduced (23%) and whole body carbohydrate metabolism increased in HSL−/− mice, resting glycogen storage was not compromised. Studies in isolated muscles revealed that the capacity of ATGL and HSL−/− muscle to transport exogenous fatty acids is not compromised and the capacity to oxidize fatty acids is actually increased (3.7- and 1.3-fold above WT for ATGL and HSL). The exercise-induced increase in plasma FFA and glycerol was blunted with ATGL or HSL deletion, demonstrating an impaired capacity for exercise-induced lipolysis in these mice. Carbohydrate oxidation was increased concomitantly during exercise in ATGL−/− and HSL−/− mice, resulting in more muscle and liver glycogen depletion. Maximal running velocity and endurance capacity were reduced by 42% and 46% in ATGL−/− mice, but not in HSL−/− mice. The reduction in performance in ATGL−/− mice was not due to defective muscle contractile performance. These results demonstrate an essential role for both ATGL and HSL in maintaining adequate FFA supply to sustain normal substrate metabolism at rest and during exercise.

Role of AMPK and PPARγ1 in exercise-induced lipoprotein lipase in skeletal muscle

2014 ◽  
Vol 306 (9) ◽  
pp. E1085-E1092 ◽  
Author(s):  
Takashi Sasaki ◽  
Rieko Nakata ◽  
Hiroyasu Inoue ◽  
Makoto Shimizu ◽  
Jun Inoue ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Lipoprotein Lipase ◽  
Metabolic Regulation ◽  
Gastrocnemius Muscle ◽  
Critical Role ◽  
Mrna Levels ◽  
Compound C ◽  
Lpl Gene ◽  
Exercise Induced

Exercise can effectively ameliorate type 2 diabetes and insulin resistance. Here we show that the mRNA levels of one of peroxisome proliferator-activated receptor (PPAR) family members, PPARγ1, and genes related to energy metabolism, including PPARγ coactivator-1 protein-1α (PGC-1α) and lipoprotein lipase (LPL), increased in the gastrocnemius muscle of habitual exercise-trained mice. When mice were intraperitoneally administered an AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), the mRNA levels of the aforementioned three genes increased in gastrocnemius muscle. AICAR treatment to C2C12 differentiated myotubes also increased PPARγ1 mRNA levels, but not PPARα and -δ mRNA levels, concomitant with increased PGC-1α mRNA levels. An AMPK inhibitor, compound C, blocked these AICAR effects. AICAR treatment increased the half-life of PPARγ1 mRNA nearly threefold (4–12 h) by activating AMPK. When C2C12 myoblast cells infected with a PPARγ1 expression lentivirus were differentiated into myotubes, PPARγ1 overexpression dramatically increased LPL mRNA levels more than 40-fold. In contrast, when PPARγ1 expression was suppressed in C2C12 myotubes, LPL mRNA levels were significantly reduced, and the effect of AICAR on increased LPL gene expression was almost completely blocked. These results indicated that PPARγ1 was intimately involved in LPL gene expression in skeletal muscle and the AMPK-PPARγ1 pathway may play a role in exercise-induced LPL expression. Thus, we identified a novel critical role for PPARγ1 in response to AMPK activation for controlling the expression of a subset of genes associated with metabolic regulation in skeletal muscle.

Cardiovascular, Respiratory and Metabolic Effects of Nebivolol During Maximal and Submaximal Exercise Performance

1991 ◽  
Vol 3 (S1) ◽  
pp. 33-39 ◽  
Author(s):  
E. W. Derman ◽  
M. Haus ◽  
F. Dunbar ◽  
T. D. Noakes
Keyword(s):  
Exercise Performance ◽  
Submaximal Exercise ◽  
Metabolic Effects

Effects of growth hormone transgenesis on metabolic rate, exercise performance and hypoxia tolerance in tilapia hybrids

2003 ◽  
Vol 63 (2) ◽  
pp. 398-409 ◽  
Author(s):  
D. J. McKenzie ◽  
R. Martínez ◽  
A. Morales ◽  
J. Acosta ◽  
R. Morales ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Metabolic Rate ◽  
Exercise Performance ◽  
Hypoxia Tolerance

scholarly journals SOD Derived from Bacillus amyloliquefaciens GF423 Has Protection Against Exercise-Induced Oxidative Stress in Healthy Subjects

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 764-764
Author(s):  
Yea-eun Nam ◽  
Yunsoo Kim ◽  
Yeni Lim ◽  
Hye Jin Kim ◽  
Oran Kwon
Keyword(s):  
Oxidative Stress ◽  
Healthy Subjects ◽  
Antioxidant Defense ◽  
Maximal Oxygen Consumption ◽  
Intervention Group ◽  
Lipid Peroxides ◽  
Experimental Period ◽  
Cellular Damage ◽  
Double Blind ◽  
Exercise Induced

Abstract Objectives Excessive reactive oxygen species (ROS) can cause cellular damage, causing a variety of degenerative diseases such as atherosclerosis, ischemic heart disease, and cancer. SOD is thought to play a central role in scavenging ROS generated in cells by enhancing the antioxidant defense system, including catalase and glutathione peroxidase. This study aims to test the hypothesis that exogenous SOD administration can help to protect against oxidative stress encountered at very early stages in the daily life of healthy subjects. Methods A total of 80 healthy adults were assigned to either an intervention group consuming B. amyloliquefaciens GF423 SOD (250 IU/capsule) daily for 8 weeks or a placebo in a randomized, double-blind and parallel design. Aerobic exercise by a treadmill for 30 minutes at an intensity of 60% of the maximal oxygen consumption (VO2max) of each subject was used to induce oxidative stress at the beginning and end of the experimental period. Blood and urine samples were collected immediately after and 30 min after the exercise challenge to measure biochemical markers related to oxidative stress and inflammation. Results A single administration of exogenous SOD induced a marked decrease in urinary lipid peroxides and plasma pro-inflammatory cytokines as compared to placebo administration. Furthermore, repeated administration of exogenous SOD for eight weeks resulted in a significant improvement of erythrocyte redox balance. Conclusions These findings suggest that the supply of exogenous SOD may be useful to enhance the antioxidant defense capacity and anti-inflammatory response in response to exercise-induced oxidative stress. Funding Sources This work was supported by the Bio-Synergy Research Project (NRF-2012M3A9C4048761) from the Ministry of Science, ICT, and Future Planning, and the BK21PLUS (Brain Korea 21 plus) program (22a20130012143) from the Ministry of Education and the GenoFocus Inc, Republic of Korea.

Sign in / Sign up

Export Citation Format

Share Document