Larger improvements in fatigue resistance and mitochondrial function with high‐ than with low‐intensity contractions during interval training of mouse skeletal muscle

2021 ◽  
Vol 35 (11) ◽  
Author(s):  
Takashi Yamada ◽  
Iori Kimura ◽  
Yuki Ashida ◽  
Katsuyuki Tamai ◽  
Hiroyori Fusagawa ◽  
...  
2013 ◽  
Vol 45 (6) ◽  
pp. 1051-1059 ◽  
Author(s):  
JAMES N. MCKEEHEN ◽  
SUSAN A. NOVOTNY ◽  
KRISTEN A. BALTGALVIS ◽  
JARROD A. CALL ◽  
DAVID J. NUCKLEY ◽  
...  

2011 ◽  
pp. P3-441-P3-441
Author(s):  
Christian Roy ◽  
Sabina Paglialunga ◽  
Joris Hoeks ◽  
Katherine Cianflone ◽  
Patrick Schrauwen

2020 ◽  
Vol 319 (3) ◽  
pp. R296-R314
Author(s):  
Cameron Hill ◽  
Rob S. James ◽  
Val. M. Cox ◽  
Frank Seebacher ◽  
Jason Tallis

The present study aimed to simultaneously examine the age-related, muscle-specific, sex-specific, and contractile mode-specific changes in isolated mouse skeletal muscle function and morphology across multiple ages. Measurements of mammalian muscle morphology, isometric force and stress (force/cross-sectional area), absolute and normalized (power/muscle mass) work-loop power across a range of contractile velocities, fatigue resistance, and myosin heavy chain (MHC) isoform concentration were measured in 232 isolated mouse (CD-1) soleus, extensor digitorum longus (EDL), and diaphragm from male and female animals aged 3, 10, 30, 52, and 78 wk. Aging resulted in increased body mass and increased soleus and EDL muscle mass, with atrophy only present for female EDL by 78 wk despite no change in MHC isoform concentration. Absolute force and power output increased up to 52 wk and to a higher level for males. A 23–36% loss of isometric stress exceeded the 14–27% loss of power normalized to muscle mass between 10 wk and 52 wk, although the loss of normalized power between 52 and 78 wk continued without further changes in stress ( P > 0.23). Males had lower power normalized to muscle mass than females by 78 wk, with the greatest decline observed for male soleus. Aging did not cause a shift toward slower contractile characteristics, with reduced fatigue resistance observed in male EDL and female diaphragm. Our findings show that the loss of muscle quality precedes the loss of absolute performance as CD-1 mice age, with the greatest effect seen in male soleus, and in most instances without muscle atrophy or an alteration in MHC isoforms.


2019 ◽  
Vol 126 (2) ◽  
pp. 454-461 ◽  
Author(s):  
C. P. Hedges ◽  
J. S. T. Woodhead ◽  
H. W. Wang ◽  
C. J. Mitchell ◽  
D. Cameron-Smith ◽  
...  

Measurement of skeletal muscle mitochondrial respiration requires invasive biopsy to obtain a muscle sample. Peripheral blood mononuclear cell (PBMC) mitochondrial protein content appears to reflect training status in young men; however, no studies have investigated whether there are training-induced changes in PBMC mitochondrial respiration. Therefore, we determined whether PBMC mitochondrial respiration could be used as a marker of skeletal muscle mitochondrial respiration in young healthy men and whether PBMC mitochondrial respiration responds to short-term training. Skeletal muscle and PBMC samples from 10 healthy young (18–35 yr) male participants were taken before and after a 2-wk high-intensity interval training protocol. High-resolution respirometry was used to determine mitochondrial respiration from muscle and PBMCs, and Western blotting and quantitative PCR were used to assess mitochondrial biogenesis in PBMCs. PBMC mitochondrial respiration was not correlated with muscle mitochondrial respiration at baseline ( R2 = 0.012–0.364, P > 0.05). While muscle mitochondrial respiration increased in response to training (32.1–61.5%, P < 0.05), PBMC respiration was not affected by training. Consequently, PBMCs did not predict training effect on muscle mitochondrial respiration ( R2 = 0.024–0.283, P > 0.05). Similarly, gene and protein markers of mitochondrial biogenesis did not increase in PBMCs following training. This suggests PBMC mitochondrial function does not reflect that of skeletal muscle and does not increase following short-term high-intensity training. PBMCs are therefore not a suitable biomarker for muscle mitochondrial function in young healthy men. It may be useful to study PBMC mitochondrial function as a biomarker of muscle mitochondrial function in pathological populations with different respiration capacities. NEW & NOTEWORTHY Research in primates has suggested that peripheral blood mononuclear cells (PBMCs) may provide a less-invasive alternative to a muscle biopsy for measuring muscle mitochondrial function. Furthermore, trained individuals appear to have greater mitochondrial content in PBMCs. Here we show that in healthy young men, PBMCs do not reflect skeletal muscle mitochondrial function and do not adapt in response to a training intervention that increases muscle mitochondrial function, suggesting PBMCs are a poor marker of muscle mitochondrial function in humans.


2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Lise K. Hansen ◽  
Henrik D. Schrøder ◽  
Lars Lund ◽  
Karthikeyan Rajagopal ◽  
Vrisha Maduri ◽  
...  

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Chien-Te Lin ◽  
Kelsey H. Fisher-Wellman ◽  
Christopher G.R. Perry ◽  
Rachel Kozy ◽  
Daniel S. Lark ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document