Various Factors May Modulate the Effect of Exercise on Testosterone Levels in Men

Exercise has been proposed to increase serum testosterone concentrations. The analysis of existing literature demonstrates a large degree of variability in hormonal changes during exercise. In our manuscript, we summarized and reviewed the literature, and concluded that this variability can be explained by the effect of numerous factors, such as (a) the use of different types of exercise (e.g., endurance vs. resistance); (b) training intensity and/or duration of resting periods; (c) study populations (e.g., young vs. elderly; lean vs. obese; sedentary vs. athletes); and (d) the time point when serum testosterone was measured (e.g., during or immediately after vs. several minutes or hours after the exercise). Although exercise increases plasma testosterone concentrations, this effect depends on many factors, including the aforementioned ones. Future studies should focus on clarifying the metabolic and molecular mechanisms whereby exercise may affect serum testosterone concentrations in the short and long-terms, and furthermore, how this affects downstream mechanisms

Mitochondrial respiratory capacity and coupling control decline with age in human skeletal muscle

Mitochondrial health is critical to physiological function, particularly in tissues with high ATP turnover, such as striated muscle. It has been postulated that derangements in skeletal muscle mitochondrial function contribute to impaired physical function in older adults. Here, we determined mitochondrial respiratory capacity and coupling control in skeletal muscle biopsies obtained from young and older adults. Twenty-four young (28 ± 7 yr) and thirty-one older (62 ± 8 yr) adults were studied. Mitochondrial respiration was determined in permeabilized myofibers from the vastus lateralis after the addition of substrates oligomycin and CCCP. Thereafter, mitochondrial coupling control was calculated. Maximal coupled respiration (respiration linked to ATP production) was lower in muscle from older vs. young subjects (P < 0.01), as was maximal uncoupled respiration (P = 0.06). Coupling control in response to the ATP synthase inhibitor oligomycin was lower in older adults (P < 0.05), as was the mitochondria flux control ratio, coupled respiration normalized to maximal uncoupled respiration (P < 0.05). Calculation of respiratory function revealed lower respiration linked to ATP production (P < 0.001) and greater reserve respiration (P < 0.01); i.e., respiratory capacity not used for phosphorylation in muscle from older adults. We conclude that skeletal muscle mitochondrial respiratory capacity and coupling control decline with age. Lower respiratory capacity and coupling efficiency result in a reduced capacity for ATP production in skeletal muscle of older adults

Quantification of muscle triglyceride synthesis rate requires an adjustment for total triglyceride content

Intramyocellular triglyceride (imTG) in skeletal muscle plays a significant role in metabolic health, and an infusion of [13C16]palmitate can be used to quantitate the in vivo fractional synthesis rate (FSR) and absolute synthesis rate (ASR) of imTGs. However, the extramyocellular TG (emTG) pool, unless precisely excised, contaminates the imTG pool, diluting the imTG-bound tracer enrichment and leading to underestimation of FSR. Because of the difficulty of excising the emTGs precisely, it would be advantageous to be able to calculate the imTG synthesis rate without dissecting the emTGs from each sample. Here, we tested the hypothesis that the ASR of total TGs (tTGs), a combination of imTGs and emTGs, calculated as "FSR × tTG pool," reasonably represents the imTG synthesis. Muscle lipid parameters were measured in nine healthy women at 90 and 170 min after the start of [13C16]palmitate infusion. While the measurements of tTG content, enrichment, and FSR did not correlate (P &gt; 0.05), those of the tTG ASR were significantly correlated (r = 0.947, P &lt; 0.05). These results demonstrate that when imTGs and emTGs are pooled, the resulting underestimation of imTG FSR is balanced by the overestimation of the imTG content. We conclude that imTG metabolism is reflected by the measurement of the tTG ASR

Palmitoyl-carnitine production by blood cells associates with the concentration of circulating acyl-carnitines in healthy overweight women

BackgroundCirculating acyl-carnitines (acyl-CNTs) are associated with insulin resistance (IR) and type 2 diabetes (T2D) in both rodents and humans. However, the mechanisms whereby circulating acyl-CNTs are increased in these conditions and their role in whole-body metabolism remains unknown. The purpose of this study was to determine if, in humans, blood cells contribute in production of circulating acyl-CNTs and associate with whole-body fat metabolism.Methods and resultsEight non-diabetic healthy women (age: 47&nbsp;±&nbsp;19&nbsp;y; BMI: 26&nbsp;±&nbsp;1&nbsp;kg·m-2) underwent stable isotope tracer infusion and hyperinsulinemic-euglycemic clamp study to determine in&nbsp;vivo whole-body fatty acid flux and insulin sensitivity. Blood samples collected at baseline (0&nbsp;min) and after 3&nbsp;h of clamp were used to determine the synthesis rate of palmitoyl-carnitine (palmitoyl-CNT) in&nbsp;vitro. The fractional synthesis rate of palmitoyl-CNT was significantly higher during hyperinsulinemia (0.788&nbsp;±&nbsp;0.084 vs. 0.318&nbsp;±&nbsp;0.012%·hr-1, p&nbsp;=&nbsp;0.001); however, the absolute synthesis rate (ASR) did not differ between the periods (p&nbsp;=&nbsp;0.809) due to ∼30% decrease in blood palmitoyl-CNT concentration (p&nbsp;=&nbsp;0.189) during hyperinsulinemia. The ASR of palmitoyl-CNT significantly correlated with the concentration of acyl-CNTs in basal (r&nbsp;=&nbsp;0.992, p&nbsp;&lt;&nbsp;0.001) and insulin (r&nbsp;=&nbsp;0.919, p&nbsp;=&nbsp;0.001) periods; and the basal ASR significantly correlated with plasma palmitate oxidation (r&nbsp;=&nbsp;0.764, p&nbsp;=&nbsp;0.027).ConclusionIn women, blood cells contribute to plasma acyl-CNT levels and the acyl-CNT production is linked to plasma palmitate oxidation, a marker of whole-body fat metabolism. Future studies are needed to confirm the role of blood cells in acyl-CNT and lipid metabolism under different physiological (i.e., in response to meal) and pathological (i.e., hyperlipidemia, IR and T2D) conditions