Fitness, body composition and blood lipids following 3 concurrent strength and endurance training modes

The prevalence of metabolic syndrome has increased dramatically in recent years, and the cluster of metabolic abnormalities it encompasses results in increased cardiovascular morbidity and mortality. The role of abdominal (visceral) obesity and the underlying molecular and cellular mechanisms central to this association have been the subject of intensive research in recent times. The aim of this review is to correlate data in this area, highlighting the central role of excess visceral fat and its secreted adipokines, and to review existing and emerging therapies. Data were generated from a search of the PubMed database using the terms 'abdominal obesity', 'metabolic syndrome', 'insulin resistance', 'adipokines', 'interleukin-6 (IL-6)', 'adiponectin', 'tumour necrosis factor-alpha (TNF-alpha)' and 'cardiovascular disease'. Metabolic syndrome is associated with a pro-inflammatory state, and the role of visceral obesity is thought to be central to this. Visceral obesity leads to alteration of the normal physiological balance of adipokines, insulin resistance, endothelial dysfunction and a pro-atherogenic state. In association with this, the presence of conventional cardiovascular risk factors such as hypertension, dyslipidaemia and smoking results in a significantly elevated cardiovascular and metabolic (cardiometabolic) risk. Better understanding of the molecular mechanisms central to this association has led to the development of potential therapeutic agents.

The primary objective of this investigation was to identify which components of endurance training (e.g., modality, duration, frequency) are detrimental to resistance training outcomes. A meta-analysis of 21 studies was performed with a total of 422 effect sizes (ESs). Criteria for the study included were (a) compare strength training alone to strength plus endurance training (concurrent) or to compare combinations of concurrent training; (b) the outcome measures include at least one measure of strength, power, or hypertrophy; and (c) the data necessary to calculate ESs must be included or available. The mean ES for hypertrophy for strength training was 1.23; for endurance training, it was 0.27; and for concurrent training, it was 0.85, with strength and concurrent training being significantly greater than endurance training only. The mean ES for strength development for strength training was 1.76; for endurance training, it was 0.78; and for concurrent training, it was 1.44. Strength and concurrent training was significantly greater than endurance training. The mean ES for power development for strength training only was 0.91; for endurance training, it was 0.11; and for concurrent training, it was 0.55. Significant differences were found between all the 3 groups. For moderator variables, resistance training concurrently with running, but not cycling, resulted in significant decrements in both hypertrophy and strength. Correlational analysis identified significant negative relationships between frequency (-0.26 to -0.35) and duration (-0.29 to -0.75) of endurance training for hypertrophy, strength, and power. Significant relationships (p < 0.05) between ES for decreased body fat and % maximal heart rate (r = -0.60) were also found. Our results indicate that interference effects of endurance training are a factor of the modality, frequency, and duration of the endurance training selected.