A low dose of alcohol does not impact skeletal muscle performance after exercise-induced muscle damage

2010 ◽  
Vol 111 (4) ◽  
pp. 725-729 ◽  
Author(s):  
Matthew J. Barnes ◽  
Toby Mündel ◽  
Stephen R. Stannard
2009 ◽  
Vol 107 (3) ◽  
pp. 853-858 ◽  
Author(s):  
Christina M. Dieli-Conwright ◽  
Tanya M. Spektor ◽  
Judd C. Rice ◽  
E. Todd Schroeder

Hormone therapy (HT) is a potential treatment to relieve symptoms of menopause and prevent the onset of disease such as osteoporosis in postmenopausal women. We evaluated changes in markers of exercise-induced skeletal muscle damage and inflammation [serum creatine kinase (CK), serum lactate dehydrogenase (LDH), and skeletal muscle mRNA expression of IL-6, IL-8, IL-15, and TNF-α] in postmenopausal women after a high-intensity resistance exercise bout. Fourteen postmenopausal women were divided into two groups: women not using HT (control; n = 6, 59 ± 4 yr, 63 ± 17 kg) and women using traditional HT (HT; n = 8, 59 ± 4 yr, 89 ± 24 kg). Both groups performed 10 sets of 10 maximal eccentric repetitions of single-leg extension on the Cybex dynamometer at 60°/s with 20-s rest periods between sets. Muscle biopsies of the vastus lateralis were obtained from the exercised leg at baseline and 4 h after the exercise bout. Gene expression was determined by RT-PCR for IL-6, IL-8, IL-15, and TNF-α. Blood draws were performed at baseline and 3 days after exercise to measure CK and LDH. Independent t-tests were performed to test group differences (control vs. HT). A probability level of P ≤ 0.05 was used to determine statistical significance. We observed significantly greater changes in mRNA expression of IL-6, IL-8, IL-15, and TNF-α ( P ≤ 0.01) in the control group compared with the HT group after the exercise bout. CK and LDH levels were significantly greater after exercise ( P ≤ 0.01) in the control group. Postmenopausal women not using HT experienced greater muscle damage after maximal eccentric exercise, indicating a possible protective effect of HT against exercise-induced skeletal muscle damage.


1978 ◽  
Vol 378 (2) ◽  
pp. 149-154 ◽  
Author(s):  
N. A. Berdina ◽  
J. M. Kots ◽  
I. M. Rodionov ◽  
V. I. Tkhorevsky ◽  
O. L. Vinogradova ◽  
...  

1995 ◽  
Vol 27 (Supplement) ◽  
pp. S37 ◽  
Author(s):  
J. Komulainen ◽  
X. Han ◽  
W. Wang ◽  
S. Koskinen ◽  
V. Kovanen ◽  
...  

2011 ◽  
Vol 29 (13) ◽  
pp. 1425-1434 ◽  
Author(s):  
David C. Hughes ◽  
Stephen H. Day ◽  
Ildus I. Ahmetov ◽  
Alun G. Williams

2019 ◽  
Vol 126 (1) ◽  
pp. 30-43 ◽  
Author(s):  
Henning Wackerhage ◽  
Brad J. Schoenfeld ◽  
D. Lee Hamilton ◽  
Maarit Lehti ◽  
Juha J. Hulmi

One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as “hypertrophy stimulus,” and the sensor of such a signal as “hypertrophy sensor.” In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.


2019 ◽  
Vol 60 (3) ◽  
pp. 515-528 ◽  
Author(s):  
Penghui Li ◽  
Ailing Liu ◽  
Wei Xiong ◽  
Haiyan Lin ◽  
Wenjun Xiao ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 744 ◽  
Author(s):  
Eduard Isenmann ◽  
Franziska Blume ◽  
Daniel Bizjak ◽  
Vera Hundsdörfer ◽  
Sarah Pagano ◽  
...  

Physical performance and regeneration after exercise is enhanced by the ingestion of proteins and carbohydrates. These nutrients are generally consumed by athletes via whey protein and glucose-based shakes. In this study, effects of protein and carbohydrate on skeletal muscle regeneration, given either by shake or by a meal, were compared. 35 subjects performed a 10 km run. After exercise, they ingested nothing (control), a protein/glucose shake (shake) or a combination of white bread and sour milk cheese (food) in a randomized cross over design. Serum glucose (n = 35), serum insulin (n = 35), serum creatine kinase (n = 15) and myoglobin (n = 15), hematologic parameters, cortisol (n = 35), inflammation markers (n = 27) and leg strength (n = 15) as a functional marker were measured. Insulin secretion was significantly stimulated by shake and food. In contrast, only shake resulted in an increase of blood glucose. Food resulted in a decrease of pro, and stimulation of anti-inflammatory serum markers. The exercise induced skeletal muscle damage, indicated by serum creatine kinase and myoglobin, and exercise induced loss of leg strength was decreased by shake and food. Our data indicate that uptake of protein and carbohydrate by shake or food reduces exercise induced skeletal muscle damage and has pro-regenerative effects.


Sign in / Sign up

Export Citation Format

Share Document