Skeletal muscle generates force by either shortening (concentrically) or lengthening (eccentrically). Eccentric (ECC) exercise is characterized by a lower metabolic demand and requires less muscle activity than concentric (CON) exercise at the same level of exerted force. However, the specific effect of ECC training vs. CON training on lean and fat mass remains underexplored. The first aim of this paper was to review the available evidence regarding the effects of ECC training on whole body and segmental lean and fat mass and, when possible, compare these with the effects of CON training. The second aim was to provide some insights into the main mechanical, physiological, and metabolic adaptations of ECC training that contribute to its effects on body composition. The third aim was to determine the beneficial effects of ECC exercise on health-related parameters in overweight and obese patients. ECC training is an effective modality to improve lean mass, but when matched for load or work, the difference between ECC and CON trainings seems unclear. A few studies reported that ECC training is also efficient at reducing fat mass. By increasing post-exercise resting energy expenditure, modifying metabolic substrate, and improving both blood lipid profile and insulin resistance, ECC training is a potential exercise modality for individuals with chronic conditions such as those who are overweight and obese. Further investigations using standardized experimental conditions, examining not only segmental but also whole body composition, are required to compare ECC and CON trainings.

A characteristic feature of eccentric as compared with concentric exercise is the ability to generate greater mechanical loads for lower cardiopulmonary demands. Current evidence concurs to show that eccentric training translates into considerable gains in muscle mass and strength. Less is known, however, regarding its impact on oxygen transport and on factors to be considered for optimizing its prescription and monitoring. This article reviews the existing evidence for endurance eccentric exercise effects on the components of the oxygen transport system from systemic to mitochondria in both humans and animals. In the studies reviewed, specially designed cycle-ergometers or downhill treadmill running were used to generate eccentric contractions. Observations to date indicate that overall, the aerobic demand associated with the eccentric training load was too low to significantly increase peak maximal oxygen consumption. By extension, it can be inferred that the very high eccentric power output that would have been required to solicit a metabolic demand sufficient to enhance peak aerobic power could not be tolerated or sustained by participants. The impact of endurance eccentric training on peripheral flow distribution remains largely undocumented. Given the high damage susceptibility of eccentric exercise, the extent to which skeletal muscle oxygen utilization adaptations would be seen depends on the balance of adverse and positive signals on mitochondrial integrity. The article examines the protection provided by repeated bouts of acute eccentric exercise and reports on the impact of eccentric cycling and downhill running training programs on markers of mitochondrial function and of mitochondrial biogenesis using mostly from animal studies. The summary of findings does not reveal an impact of training on skeletal muscle mitochondrial respiration nor on selected mitochondrial messenger RNA transcripts. The implications of observations to date are discussed within future perspectives for advancing research on endurance eccentric exercise physiological impacts and using a combined eccentric and concentric exercise approach to optimize functional capacity.

As ¾ of the global population either have excess or insufficient fat, it has become increasingly critical to understand the functions and dysfunctions of adipose tissue (AT). AT serves as a key organ in energy metabolism, and recently, attention has been focused on white AT, particularly its mitochondria, as the literature evidence links their functions to adiposity. This narrative review provides an overview of mitochondrial functionality in human white AT. Firstly, it is noteworthy that the two primary AT depots, subcutaneous AT (scAT) and visceral AT (vAT), exhibit differences in mitochondrial density and activity. Notably, vAT tends to have a higher mitochondrial activity compared to scAT. Subsequently, studies have unveiled a negative correlation between mitochondrial activity and body mass index (BMI), indicating that obesity is associated with a lower mitochondrial function. While the impact of exercise on AT mitochondria remains uncertain, dietary interventions have demonstrated varying effects on AT mitochondria. This variability holds promise for the modulation of AT mitochondrial activity. In summary, AT mitochondria exert a significant influence on health outcomes and can be influenced by factors such as obesity and dietary interventions. Understanding the mechanisms underlying these responses can offer potential insights into managing conditions related to AT and overall health.

We investigated the effect of temperature increase on mitochondrial fatty acid (FA) and carbohydrate oxidation in the slow-oxidative skeletal muscles (soleus) of rats. We measured mitochondrial respiration at 35°C and 40°C with the physiological substrates pyruvate + 4 mM malate (Pyr) and palmitoyl-CoA (PCoA) + 0.5 mM malate + 2 mM carnitine in permeabilized myofibers under nonphosphorylating ([ ]) or phosphorylating ([ ]) conditions. Mitochondrial efficiency was calculated by the respiratory control ratio (RCR = [ ]/[ ]). We used guanosine triphosphate (GTP), an inhibitor of uncoupling protein (UCP), to study the mechanisms responsible for alterations of mitochondrial efficiency. We measured hydrogen peroxide (H₂O₂) production under nonphosphorylating and phosphorylating conditions at both temperatures and substrates. We studied citrate synthase (CS) and 3-hydroxyl acyl coenzyme A dehydrogenase (3-HAD) activities at both temperatures. Elevating the temperature from 35°C to 40°C increased PCoA-[ ] and decreased PCoA-RCR, corresponding to the uncoupling of oxidative phosphorylation (OXPHOS). GTP blocked the heat-induced increase of PCoA-[ ]. Rising temperature moved toward a Pyr-[ ] increase, without significance. Heat did not alter H₂O₂ production, resulting from either PCoA or Pyr oxidation. Heat induced an increase in 3-HAD but not in CS activities. In conclusion, heat induced OXPHOS uncoupling for PCoA oxidation, which was at least partially mediated by UCP and independent of oxidative stress. The classically described heat-induced glucose shift may actually be mostly due to a less efficient FA oxidation. These findings raise questions concerning the consequences of heat-induced alterations in mitochondrial efficiency of FA metabolism on thermoregulation. NEW & NOTEWORTHY Ex vivo exposure of skeletal myofibers to heat uncouples substrate oxidation from ADP phosphorylation, decreasing the efficiency of mitochondria to produce ATP. This heat effect alters fatty acids (FAs) more than carbohydrate oxidation. Alteration of FA oxidation involves uncoupling proteins without inducing oxidative stress. This alteration in lipid metabolism may underlie the preferential use of carbohydrates in the heat and could decrease aerobic endurance.

Over the last decades, a growing interest in eccentric (ECC) exercise has emerged, but mitochondrial adaptations to ECC training remain poorly documented. Using an approach for manipulating mechanical and metabolic exercise power, we positioned that for same metabolic power, training using concentric (CON) or ECC contractions would induce similar skeletal muscle mitochondrial adaptations. Sixty adult rats were randomly assigned to a control (CTRL) or three treadmill training groups running at 15m·min⁻¹ for 45min, 5days weekly for 8 weeks at targeted upward or downward slopes. Animals from the CON (+15%) and ECC30 (-30%) groups trained at iso-metabolic power while CON and ECC15 (-15%) exercised at iso-mechanical power. Assessments were made of Vastus Intermedius mitochondrial respiration (oxygraphy), enzymatic activities (spectrophotometry) and real-time qPCR for mRNA transcripts. Maximal rates of mitochondrial respiration was 14-15% higher in CON and ECC30 compared to CTRL and ECC15. Apparent K_m for ADP for trained groups was 40-66% higher than CTRL, with statistical significance reached for CON and ECC30. Complex I and citrate synthase activities were 1.6 (ECC15) to 1.8 (ECC30 and CON) times values of CTRL. Complex IV activity was higher than CTRL (p<0.05) only for CON and ECC30. mRNA transcripts analyses showed higher TFAM, SLC25A4, CKMT2 and PPID in the ECC30 compared to CTRL. Findings confirm that training-induced skeletal muscle mitochondrial function adaptations are governed by the extent of metabolic overload irrespective of exercise modality. The distinctive ECC30 mRNA transcript pattern may reflect a cytoskeleton damage-repair or ECC adaptive cycle that differs from that of biogenesis.

Mitochondrial dysfunction is widely reported in various diseases and contributes to their pathogenesis. We assessed the effect of cocoa flavanols supplementation on mitochondrial function and whole metabolism, and we explored whether the mitochondrial deacetylase sirtuin-3 (Sirt3) is involved or not. We explored the effects of 15 days of CF supplementation in wild type and Sirt3^-/- mice. Whole-body metabolism was assessed by indirect calorimetry, and an oral glucose tolerance test was performed to assess glucose metabolism. Mitochondrial respiratory function was assessed in permeabilised fibres and the pyridine nucleotides content (NAD⁺ and NADH) were quantified. In the wild type, CF supplementation significantly modified whole-body metabolism by promoting carbohydrate use and improved glucose tolerance. CF supplementation induced a significant increase of mitochondrial mass, while significant qualitative adaptation occurred to maintain H₂O₂ production and cellular oxidative stress. CF supplementation induced a significant increase in NAD⁺ and NADH content. All the effects mentioned above were blunted in Sirt3^-/- mice. Collectively, CF supplementation boosted the NAD metabolism that stimulates sirtuins metabolism and improved mitochondrial function, which likely contributed to the observed whole-body metabolism adaptation, with a greater ability to use carbohydrates, at least partially through Sirt3.