The present study investigated whether football has favorable effects in the treatment of mild-to-moderate arterial hypertension in untrained middle-aged men. Twenty-five untrained males aged 31-54 year with mild-to-moderate hypertension were randomized to a football training group (FTG, two 1-h sessions per week) and a control group receiving physician-guided traditional recommendations on cardiovascular risk factor modification (doctoral advice group, DAG). After 3 months, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were lowered (P<0.05) by 12 +/- 3 and 7 +/- 1 mmHg in FTG, respectively, whereas no significant changes were observed for DAG, with the 3 months values being lower (P<0.05) in FTG than DAG (SBP: 138 +/- 2 vs 148 +/- 2 mmHg; DBP: 84 +/- 2 vs 92 +/- 2 mmHg). The resting heart rate was lowered (P<0.05) by 12 +/- 2 b.p.m. in FTG after 3 months (67 +/- 3 vs 79 +/- 3 b.p.m.), whereas no change was observed for DAG. After 3 months, FTG had higher (P<0.05) VO(2max) (8 +/- 2%; 35.0 +/- 1.6 vs 32.5 +/- 1.3 mL/min/kg) and lower (P<0.05) fat mass (1.7 +/- 0.6 kg), whereas no change was observed for DAG. In conclusion, football training is an attractive non-pharmacological supplement to the treatment of mild-to-moderate arterial hypertension in untrained middle-aged men.

Endurance training increases peak fat oxidation (PFO) during exercise, but whether this is independent of changes in body weight is not known. The aim of the present study was to investigate the effects of endurance training with or without weight loss or a diet-induced weight loss on PFO and on key skeletal muscle mitochondrial proteins involved in fat oxidation. Sixty moderately overweight, sedentary but otherwise healthy men were randomized to 12 wk of training (T), diet (D), training and increased caloric intake (T-iD), or continuous sedentary control (C). Isoenergetic deficits corresponding to 600 kcal/day were comprised of endurance exercise for T and caloric restriction for D. T-iD completed similar training but was not in 600 kcal deficit because of dietary replacement. PFO and the exercise intensity at which this occurred (FatMax) were measured by a submaximal exercise test and calculated by polynomial regression. As intended by study design, a similar weight loss was observed in T (-5.9 ± 0.7 kg) and D (-5.2 ± 0.8 kg), whereas T-iD (-1.0 ± 0.5 kg) and C (0.1 ± 0.6 kg) remained weight stable. PFO increased to a similar extent with 42% in T [0.16 g/min; 95% confidence intervals (CI): 0.02; 0.30, P = 0.02] and 41% in T-iD (0.16 g/min; 95% CI: 0.01; 0.30, P = 0.04) compared with C, but did not increase in D (P = 0.96). In addition, the analysis of covariance showed that changes in both PFO (0.10 g/min; 95% CI: 0.03; 0.17, P = 0.03) and FatMax (6.3% V̇o2max; 95% CI: 1.4; 11.3, P < 0.01) were independently explained by endurance training. In conclusion, endurance training per se increases PFO in moderately overweight men.

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