Ameliorating effects of lifelong physical activity on healthy aging and mitochondrial function in human white adipose tissue

Growing old is patently among the most prominent risk factors for lifestyle related diseases and deterioration in physical performance. Aging in particular affects mitochondrial homeostasis and maintaining a well-functioning mitochondrial pool is imperative in order to avoid age-associated metabolic decline. White adipose tissue (WAT) is a key organ in energy balance and impaired mitochondrial function in adipocytes has been associated with increased low-grade inflammation, altered metabolism, excessive ROS production and an accelerated aging phenotype. Exercise training improves mitochondrial health but whether lifelong exercise training can sufficiently maintain WAT mitochondrial function is currently unknown. Therefore, to dissect the role and dose-dependence of lifelong exercise training on aging WAT metabolic parameters and mitochondrial function, young and older untrained, as well as moderately and highly exercise trained older male subjects were recruited and abdominal subcutaneous (s)WAT biopsies and venous blood samples were obtained to measure mitochondrial function and key metabolic factors in WAT and plasma. Mitochondrial intrinsic respiratory capacity was lower in sWAT from older than in young subjects. In spite of this, maximal mitochondrial respiration per wet weight, markers of oxidative capacity, and mitophagic capacity were increased in sWAT from lifelong highly exercise trained than all other groups. Furthermore, ROS emission was generally lower in sWAT from lifelong highly exercise trained than older untrained subjects. Taken together, aging reduces intrinsic mitochondrial respiration in human sWAT, but lifelong high volume exercise training increases oxidative capacity by increasing mitochondrial volume likely contributing to healthy aging.

The Female Athlete’s Heart: Overview and Management of Cardiovascular Diseases

The number of female athletes taking part in elite and amateur sport is ever increasing. In contrast with male athletes, few studies have focused on cardiovascular adaptations to exercise in women, the effects of lifelong exercise on heart muscle and electrical tissue, the risk of exercise-related sudden cardiac death and the management of cardiovascular disease. Women have a lower prevalence of large QRS complexes, repolarisation changes including inferior and lateral T-wave inversion, and cardiac dimensions exceeding predicted limits compared with men. The risk of exercise-related sudden cardiac death is significantly lower in women than men. Also, women who have engaged in lifelong exercise do not have a higher prevalence of AF, coronary artery calcification or myocardial fibrosis than their sedentary counterparts. Apart from providing an overview of the existing literature relating to cardiac adaptations, this review explores possible reasons for the sex differences and focuses on the management of cardiovascular disorders that affect female athletes.

Short-Term and Lifelong Exercise Training Lowers Inflammatory Mediators in Older Men

Increased basal low-grade inflammation is observed with advancing age, which is augmented by physical inactivity. However, data regarding the influence of lifelong exercise training and particularly high-intensity interval training (HIIT) on inflammatory mediators in older men are scarce. Therefore, we examined effects of 6weeks of aerobic preconditioning followed by 6weeks of HIIT on inflammatory mediators [interleukin (IL)-6, homocysteine, and high-sensitivity C-reactive protein (hsCRP)] in previously sedentary older men (SED) and masters athletes (LEX). Further, we investigated whether SED exhibited greater basal inflammatory biomarkers compared to LEX. Twenty-two men (aged 62±2years) participated in the SED group, while 17 age-matched LEX men (aged 60±5years) also participated as a positive comparison group. In SED, preconditioning (P=0.030, d=0.34) and HIIT (P=0.030, d=0.48) caused a reduction in IL-6 compared to enrollment. SED homocysteine did not change throughout (P>0.57; d<0.26), while the decrease in hsCRP after preconditioning (P=0.486, d=0.25) and after HIIT (P=0.781, d=0.23) compared to enrollment was small. HIIT did not influence IL-6 or hsCRP in LEX (all P>0.42; d<0.3). Homocysteine increased from enrollment to post-HIIT in LEX (P=0.144, d=0.83), but all other perturbations were trivial. IL-6 and hsCRP were greater in SED than LEX throughout the investigation (all P<0.029; d>0.72), but homocysteine was not different (all P >0.131; d<0.41). Results of this study suggest moderate-intensity aerobic exercise and HIIT lowers IL-6 (and possible hsCRP) in previously sedentary older men. Moreover, lifelong exercise is associated with reduced concentrations of some inflammatory biomarkers in older males, and therefore, physical activity, rather than age per se, is implicated in chronic low-grade inflammation. Moreover, physical inactivity-induced inflammation may be partly salvaged by short-term exercise training.

Effects of aging and lifelong aerobic exercise on basal and exercise-induced inflammation in women

We previously reported a positive effect of lifelong exercise on skeletal muscle inflammation in aging men. This parallel investigation in women revealed that lifelong exercise did not protect against age-related increases in circulating or muscle inflammation and that preparedness to handle loading stress was not preserved by lifelong exercise. Further investigation is necessary to understand why lifelong aerobic exercise may not confer the same anti-inflammatory benefits in women as it does in men.

Effects of aging and lifelong aerobic exercise on expression of innate immune components in human skeletal muscle

Findings from this investigation provide novel insight into the effect of aging and lifelong aerobic exercise on structural components of the innate immune system in skeletal muscle of humans. Data presented here suggest aging increases basal expression of select Toll-like receptors (TLRs), and lifelong exercise does not impact this age-related increase. Additionally, acute exercise stimulates gene expression of several TLRs, while the adaptor response is likely dysregulated with aging and maintained with lifelong exercise.

Effects of Aging, Long-Term and Lifelong Exercise on the Urinary Metabolic Footprint of Rats

Life expectancy has risen in the past decades, resulting in an increase in the number of aged individuals. Exercise remains one of the most cost-effective treatments against disease and the physical consequences of aging. The purpose of this research was to investigate the effects of aging, long-term and lifelong exercise on the rat urinary metabolome. Thirty-six male Wistar rats were divided into four equal groups: exercise from 3 to 12 months of age (A), lifelong exercise from 3 to 21 months of age (B), no exercise (C), and exercise from 12 to 21 months of age (D). Exercise consisted in swimming for 20 min/day, 5 days/week. Urine samples collection was performed at 3, 12 and 21 months of life and their analysis was conducted by liquid chromatography-mass spectrometry. Multivariate analysis of the metabolite data did not show any discrimination between groups at any of the three aforementioned ages. However, multivariate analysis discriminated the three ages clearly when the groups were treated as one. Univariate analysis showed that training increased the levels of urinary amino acids and possibly protected against sarcopenia, as evidenced by the higher levels of creatine in the exercising groups. Aging was accompanied by decreased levels of urinary amino acids and signs of increased glycolysis. Concluding, both aging and, to a lesser degree, exercise affected the rat urinary metabolome, including metabolites related to energy metabolism, with exercise showing a potential to mitigate the consequences of aging.