Exercise training increases skeletal muscle mitochondrial volume density by enlargement of existing mitochondria and not de novo biogenesis

2017 ◽  
Vol 222 (1) ◽  
pp. e12905 ◽  
Author(s):  
A.-K. Meinild Lundby ◽  
R. A. Jacobs ◽  
S. Gehrig ◽  
J. de Leur ◽  
M. Hauser ◽  
...  
2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 127-127
Author(s):  
Chloey P Guy ◽  
Lauren T Wesolowski ◽  
Audrey L Earnhardt ◽  
Dustin Law ◽  
Don A Neuendorff ◽  
...  

Abstract Temperament impacts skeletal muscle mitochondria in Brahman heifers, but this has not been investigated in steers or between cattle breeds. We hypothesized mitochondrial measures would be greater in Angus than Brahman, temperamental than calm steers, and the trapezius (TRAP) than the longissimus thoracis (LT) muscle. Samples from calm (n = 13 per breed), intermediate (n = 12 per breed), and temperamental (n=13 per breed) Angus and Brahman steers (mean±SD 10.0±0.8 mo) were evaluated for mitochondrial enzyme activities via colorimetry. Calm and temperamental LT samples were evaluated for oxidative phosphorylation (P) and electron transfer (E) capacities by high-resolution respirometry. Data were analyzed using linear models with fixed effects of breed, muscle, temperament, and all interactions. Brahman tended to have greater mitochondrial volume density (citrate synthase activity; CS) than Angus (P = 0.08), while intrinsic (relative to CS) mitochondrial function (cytochrome c oxidase activity) was greater in Angus than Brahman (P = 0.001) and greater in TRAP than LT (P = 0.008). Angus exhibited greater integrative (per mg tissue) and intrinsic P with complex I (PCI), P with complexes I+II (PCI+II), maximum noncoupled E, and E with complex II (ECII; P ≤ 0.04) and tended to have greater intrinsic leak (P = 0.1) than Brahman. Contribution of PCI to total E was greater in Angus than Brahman (P = 0.01), while contribution of ECII to total E was greater in Brahman than Angus (P = 0.05). A trend for the interaction of breed and temperament (P = 0.07) indicated calm Angus had the greatest intrinsic ECII (P ≤ 0.03) while intrinsic ECII was similar between temperamental Angus and calm and temperamental Brahman. Integrative PCI+II and ECII, and the contribution of PCI and PCI+II to overall E tended to be greater in temperamental than calm steers (P ≤ 0.09), while intrinsic ECII tended to be greater in calm than temperamental steers (P = 0.07). The impact of these mitochondrial differences on meat quality measures remains to be determined.


1985 ◽  
Vol 248 (4) ◽  
pp. R415-R421 ◽  
Author(s):  
P. L. Else ◽  
A. J. Hulbert

Body composition, mitochondrial volume density, and mitochondrial membrane surface area were measured in six species of mammals representing a 100-fold weight range (18-2,067 g). The mammals examined included three eutherian species, two marsupial, and one monotreme species. The tissues examined were liver, kidney, brain, lung, heart, and skeletal muscle (gastrocnemius). Allometric equations were derived for tissue weight, and the allometric exponents ranged from 0.69 (brain) to 1.01 (skeletal muscle). Allometric relationships for mitochondrial membrane surface area were also determined both per milliliter tissue and per total tissue. Small mammals had a higher mitochondrial membrane surface area per milliliter tissue than large mammals in all tissues examined. These differences were significant in liver, kidney, brain, and heart. Total mitochondrial membrane surface area per tissue had allometric exponents ranging from 0.55 (kidney) to 0.78 (skeletal muscle). When total mitochondrial membrane surface area was summated for the major internal organs examined (liver, kidney, heart, and brain), the allometric equation was mitochondrial membrane surface area (m2) = 3.04 body wt0.59 (g). This was similar to the exponent of standard metabolic rate against body weight in the species examined (i.e., 0.62). The inclusion of skeletal muscle and lung into the summated mitochondrial membrane surface area increased the exponent to 0.76. This is compared with the relationship between maximal O2 consumption and body size in mammals.


1988 ◽  
Vol 64 (3) ◽  
pp. 1179-1185 ◽  
Author(s):  
R. J. Tomanek ◽  
C. V. Gisolfi ◽  
C. A. Bauer ◽  
P. J. Palmer

To test the hypothesis that exercise training can reverse the decrements in coronary reserve, capillary density, and mitochondrial volume density evident during established hypertension, we trained spontaneously hypertensive (SHR) and normotensive (WKY) rats on a treadmill over a 3-mo period. At 7 mo of age we used microspheres to evaluate myocardial perfusion in conscious rats. Exercise training did not alter hypertension or left ventricular hypertrophy but did increase maximal O2 consumption in both SHR and WKY. A decrement in left and right ventricular coronary reserve in SHR, compared with WKY, was indicated by 1) a smaller increment in myocardial perfusion during maximal vasodilation with dipyridamole and 2) a higher minimal coronary vascular resistance per unit mass. Exercise training had no significant effect on any index of myocardial perfusion in SHR or WKY. A 12% decrement in capillary numerical density in the endomyocardium of SHR was not reversed by exercise training. We estimated the volume densities of mitochondria, myofibrils, and sarcoplasm using electron microscopy and point-counting stereology on perfusion-fixed hearts. None of the parameters in either SHR or WKY was changed by exercise training. It is concluded that exercise training does not reverse the decrements in coronary reserve and capillary numerical density associated with hypertension in adult rats. Moreover the previously observed enhancement of mitochondrial volume density due to exercise in young hypertensive rats was not observed in adult SHR.


2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 204-205
Author(s):  
Lauren T Wesolowski ◽  
Chloey P Guy ◽  
Edith J Mayorga ◽  
Tori E Rudolph ◽  
Alyssa D Freestone ◽  
...  

Abstract Heat stress can negatively impact pig health and performance but the effects of heat stress on skeletal muscle mitochondrial function are largely unknown. We hypothesized that mitochondrial function and capacity would be impaired in heat stressed (HS) compared to thermoneutral (TN) pigs but mitochondrially-targeted coenzyme Q (MitoQ) supplementation would rescue the impairment. Oxidative portions of the semitendinosus muscle were evaluated from TN and HS gilts receiving no supplementation (CON) or MitoQ for 2 d prior to and during the 24h environmental heat treatment (n = 8 per group). Mitochondrial oxidative phosphorylation (P) and electron transfer (E) capacities were determined via high resolution respirometry and mitochondrial volume density and function were quantified by citrate synthase (CS) and cytochrome c oxidase activities, respectively. Data were analyzed using linear models in SAS v9.4 with fixed effects of heat, MitoQ treatment (trt), and heat×trt interaction. There were trends for the interaction of trt and heat (P≤0.1) on integrative (per mg tissue) and intrinsic (relative to CS) P with complexes I and II (PCI+II), maximum noncoupled E (ECI+II), and E with complex II only (ECII), in which all measures were greater in HS-MitoQ than TN-MitoQ (P≤0.03), but measures did not differ due to HS in CON pigs. The contribution of leak to total E (flux control ratio, FCRLeak) was lesser in HS-MitoQ than HS-CON, TN-CON, and TN-MitoQ (P≤0.02). The FCRPCI was greater (P≤0.05) while the FCRPCI+II was lesser (P=0.01) in TN compared to HS pigs. Finally, the FCRPCI+II was greater (P=0.02) while the FCRECII tended to be lesser (P=0.09) for CON than MitoQ pigs. Neither mitochondrial volume density nor function were affected by HS or MitoQ supplementation. In total, these data indicate improved mitochondrial capacities following heat stress in pigs receiving MitoQ but no difference in mitochondrial capacities in unsupplemented, HS pigs.


2015 ◽  
Vol 594 (5) ◽  
pp. 1151-1166 ◽  
Author(s):  
Robert A. Jacobs ◽  
Anne-Kristine Meinild Lundby ◽  
Simone Fenk ◽  
Saskia Gehrig ◽  
Christoph Siebenmann ◽  
...  

2018 ◽  
Vol 103 (6) ◽  
pp. 851-859 ◽  
Author(s):  
David Montero ◽  
Klavs Madsen ◽  
Anne-Kristine Meinild-Lundby ◽  
Fredrik Edin ◽  
Carsten Lundby

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