Effect of aerobic and resistance training; the skeletal muscle mitochondrial function in the spirit study cohort

The aim of this investigation was to examine the effect of aerobic and resistance training on the skeletal muscle mitochondrial function. Wellington Hospital New Zealand, Massey University, Wellington Campus New Zealand. Sep 2008- Sep 2011. There was a very large effect [6.7 +/- 1.2] in the AER group for BHAD activity whereas in the PRT group a large effect [2.7 +/- 1.2] for BHAD activity was observed. There was an increase in CS activity in both groups [PRT; p = 0.007, AER; p=0.03] however, the activity increase was more in the PRT group [effect size = 1.8 +/- 1.3]. COX activity was raised in both groups as well though the effect size in the PRT group was 2.3 +/- 1.2 meaning a very large change with PRT exercise compared to a moderate effect [1.0 +/- 1.2] with AER exercise. Overall these findings suggest that both PRT and AER exercise can be effective therapeutic modalities for the induction of changes at the cellular level in muscle of people with T2DM

Effect of eccentric training on mitochondrial function and oxidative stress in the skeletal muscle of rats

The objective of the present study was to investigate the effects of eccentric training on the activity of mitochondrial respiratory chain enzymes, oxidative stress, muscle damage, and inflammation of skeletal muscle. Eighteen male mice (CF1) weighing 30-35 g were randomly divided into 3 groups (N = 6): untrained, trained eccentric running (16°; TER), and trained running (0°) (TR), and were submitted to an 8-week training program. TER increased muscle oxidative capacity (succinate dehydrogenase and complexes I and II) in a manner similar to TR, and TER did not decrease oxidative damage (xylenol and creatine phosphate) but increased antioxidant enzyme activity (superoxide dismutase and catalase) similar to TR. Muscle damage (creatine kinase) and inflammation (myeloperoxidase) were not reduced by TER. In conclusion, we suggest that TER improves mitochondrial function but does not reduce oxidative stress, muscle damage, or inflammation induced by eccentric contractions.

Skeletal muscle mitochondrial dysfunction & diabetes.

Skeletal muscle insulin resistance is a key contributor to the pathophysiology of type 2 diabetes. Recent studies have shown that insulin resistance in a variety of conditions including type 2 diabetes, ageing and in offspring of type 2 diabetes is associated with muscle mitochondrial dysfunction. The important question is whether insulin resistance results from muscle mitochondrial dysfunction or vise versa. Gene array studies from muscle biopsy samples showed that transcript levels of several genes, especially OXPHOS genes are altered in type 2 diabetic patients during poor glycaemic control but many of these alterations are normalized by insulin treatment suggesting that reduced insulin action is a factor involved in muscle mitochondrial dysfunction. Moreover, insulin infusion while maintaining glucose and amino acid levels results in increase in muscle mitochondrial gene transcript levels and ATP production indicating that insulin is a key regulator of muscle mitochondrial biogenesis. At a similar post-absorptive insulin levels both type 2 diabetic patients and non diabetic controls have similar muscle mitochondrial ATP production but increasing insulin from low to high levels stimulate ATP production only in non diabetic people but not in the diabetic people. The lack of muscle mitochondrial response to insulin in type 2 diabetic patients is likely to be related to insulin resistance and reduced substrate utilization.

Physiological constraints in the aerobic performance of hummingbirds

Hovering flight has been described as the most energetically expensive form of locomotion. Among the vertebrates, hummingbirds weighing only 1.5-20 g are the elite practitioners of this aerial art. Their flight muscles are, therefore, the most oxygen demanding locomotor muscles per unit tissue mass of all vertebrates. Tissue level functional and structural adaptations for oxygen transport are compared between hummingbirds and mammals in this paper. Hummingbirds present extreme structural adaptations in their flight muscles. Mitochondrial densities greater than 30 per cent are observed in their pectoral muscles, and the surface area of the inner membrane of their mitochondria is tvace that of mammals. This doubling of their mitochondrial oxidative capacity is accompanied by a proportional increase in the specific activity (per g tissue) of the mitochondrial manganese superoxide dismutase (SOD-Mn) in their flight muscles, thus indicating that oxygen toxicity is not a constraint in the aerobic performance of hummingbirds during hovering flight. Finally, the liver appears to play a major role in providing the necessary substrates for their high aerobic performance, and also in eliminating the oxygen free radicals formed during oxidative phosphorylation.

Oxidative metabolism and body weight: inactive, active, and mitochondrial volumes

In homeotherms, the standardized (basal) metabolic rate should not be expressed per kilogram of body weight (specific metabolic rate), nor per unit of body surface (square meters of body-ambient interface), since both mitochondrial thermogenesis and heat-loss mechanisms (radiation, conduction, convection, evaporation) are not uniform processes. On the contrary, each organism is an heterogeneous bioreactor, which is composed at least of two compartments: 1) a metabolically active volume (aV), where oxidative phosphorylation takes place; and 2) a metabolically inactive volume (iV), where oxygen consumption is negligible. The ratio (aV/iV) is not invariant, since iV increases disproportionately with the scaling up of body size, and as shown by us, when the three main components of iV, i.e., skeleton, fat deposits, and blood volume, are added together, a similar disproportionality is found. The aV was determined by subtracting the iV from the total volume (V) of an organism, or by estimating the volume occupied by all mitochondria, or mitochondrial volume (mtV). For this purpose two procedures are discussed: 1) the stereological or morphometric method; and 2) the oxygen consumption per unit time or physiometric method. The latter procedure is based on the equivalence between an VO2 = 3 ml O2.min-1 and a mtV of 1 ml, whose oxidative phosphorylation yields an approximate power output of 1 watt. The correspondence between oxygen consumption, heat production, and electron flux at the respiratory chain of the mitochondrial cristae, is discussed. From a physical point of view, the metabolic rate is a ®power® function (P = M L2T-3), where M = mass, L = length, and T = time. The dimensional analysis and the statistical treatment of the corresponding numerical values of more than 200 allometric equations yields the 3/4 power, law established by Kleiber (1961), for the relationship between basal metabolism and body weight. Instead of expressing the metabolic rate per unit body weight (kg-1) or per unit body surface (m-2) structural and functional criteria should be taken into account as, for instance, the distinction between iV and aV, and particularly by emphasizing the paramount importance of the mtV where oxidative phosphorylation takes place. An allometric equation relating mtV and body weight (W) could be tentatively established for interspecies comparisons