Homocysteine-lowering exercise effect is greater in hyperhomocysteinemic people living with HIV: a randomized clinical trial.

Elevated concentration of homocysteine has been identified as an independent risk factor for the development of cardiovascular disease and is frequently associated with oxidative stress. Moreover, studies have shown that people living with human immunodeficiency virus (PLHIV) present elevated concentration of homocysteine and oxidative stress compared with people without HIV. Our purpose was to describe blood homocysteine and oxidative stress markers in PLHIV and those without HIV infection, and to examine the effects of a 16-week combined training exercise program (CTE) on oxidative stress and homocysteine concentrations of PLHIV. We included 49 PLHIV (21 men, 28 women) and 33 people without HIV infection (13 men, 20 women). After baseline evaluations, 30 PLHIV were randomized to either CTE (trained group, n = 18) or the control group (n = 12); CTE consisted of aerobic and strength exercise sessions during 16 weeks, 3 times a week. Plasma homocysteine, oxidative damage markers, folate, and vitamin B12 were assessed pre- and post-training and by hyperhomocysteinemia (homocysteine ≥ 15 µmol/L) status. At baseline, PLHIV had higher levels of homocysteine and malondialdehyde, as well as reduced circulating folate when compared with people without HIV infection. CTE resulted in a 32% reduction (p < 0.05) in homocysteine concentration and a reduction in lipid hydroperoxide in PLHIV with hyperhomocysteinemia, which was not observed in those without hyperhomocysteinemia. Hyperhomocysteinemic participants experienced a 5.6 ± 3.2 µmol/L reduction in homocysteine after CTE. In summary, 16 weeks of CTE was able to decrease elevated homocysteine concentration and enhance redox balance of PLHIV with hyperhomocysteinemia, which could improve their cardiovascular risk.

Influence of exercise amount and intensity on long-term weight loss maintenance and skeletal muscle mitochondrial ROS production in humans.

Sustaining a weight loss after a lifestyle intervention is challenging. The objective of the present study was to investigate if mitochondrial function is associated with the ability to maintain a weight loss. Sixty-eight former participants in an 11-12-week lifestyle intervention were recruited into 2 groups; weight loss maintenance (WLM; body mass index (BMI): 32 ± 1 kg/m2) and weight regain (WR; BMI: 43 ± 2 kg/m2) based on weight loss measured at a follow-up visit (WLM: 4.8 ± 0.4; WR: 7.6 ± 0.8 years after lifestyle intervention). Maximal oxygen consumption rate, physical activity level, and blood and muscle samples were obtained at the follow-up experiment. Mitochondrial respiratory capacity and reactive oxygen species (ROS) production were measured. Fasting blood samples were used to calculate glucose homeostasis index. WR had impaired glucose homeostasis and decreased maximal oxygen uptake and physical activity level compared with WLM. The decreased physical activity in WR was due to a lower activity level at vigorous and moderate intensities. Mitochondrial respiratory capacity and citrate synthase (CS) activity was higher in WLM, but intrinsic mitochondrial respiratory capacity (mitochondrial respiratory capacity corrected for mitochondrial content (CS activity)) was similar. ROS production was higher in WR compared with WLM, which was accompanied by a decreased content of antioxidant proteins in WR. Intrinsic mitochondrial respiratory capacity in skeletal muscle is not associated with the ability to maintain a long-term weight loss. WLM had a higher maximal oxygen uptake, physical activity level, mitochondrial respiratory capacity and CS activity compared with WR. The reduced glucose tolerance was concurrent with increased ROS production per mitochondria in WR, and could also be associated with the lower physical activity level in this group.