Fitness altered the obesity paradox. Overweight and obese men had increased longevity only if they registered high fitness.

Evidence demonstrates that sympathetic nervous system (SNS) activation causes osteopenia via b 2 -adrenoceptor (b2-AR) signaling. Here we show that female mice with chronic sympathetic hyperactivity owing to double knockout of adrenoceptors that negatively regulate norepinephrine release, a 2A -AR and a 2C -AR (a 2A /a 2C -ARKO), present an unexpected and generalized phenotype of high bone mass with decreased bone resorption and increased formation. In a 2A /a 2C -ARKO versus wild-type (WT) mice, micro-computed tomographic (mCT) analysis showed increased, better connected, and more plate-shaped trabeculae in the femur and vertebra and increased cortical thickness in the vertebra, whereas biomechanical analysis showed increased tibial and femoral strength. Tibial mRNA expression of tartrate-resistant acid phosphatase (TRACP) and receptor activator of NF-kB (RANK), which are osteoclast-related factors, was lower in knockout (KO) mice. Plasma leptin and brain mRNA levels of cocaine amphetamine-regulated transcript (CART), which are factors that centrally affect bone turnover, and serum levels of estradiol were similar between mice strains. Tibial b 2 -AR mRNA expression also was similar in KO and WT littermates, whereas a 2A -, a 2B -and a 2C -AR mRNAs were detected in the tibia of WT mice and in osteoblast-like MC3T3-E1 cells. By immunohistochemistry, we detected a 2A -, a 2B -, a 2C -and b 2 -ARs in osteoblasts, osteoclasts, and chondrocytes of 18.5-day-old mouse fetuses and 35-day-old mice. Finally, we showed that isolated osteoclasts in culture are responsive to the selective a 2 -AR agonist clonidine and to the nonspecific a-AR antagonist phentolamine. These findings suggest that b 2 -AR is not the single adrenoceptor involved in bone turnover regulation and show that a 2 -AR signaling also may mediate the SNS actions in the skeleton. ß

It is well-established that at old age there is a significant decline in muscle strength. Reference values for muscle strength might be useful for assessment of muscle impairment and of physiological adaptations. However, it is still unclear whether gender affects the rate of decline. Therefore, the aim of this study is to investigate the effect of gender and age on handgrip strength and to establish reference values for this variable. Reviewing medical charts collected from 1994 to 2005, a convenience sample of 2,648 subjects (1,787 men and 861 women), aged between 18 and 90 years, was obtained. Our results show higher handgrip strength for men compared with women (36.8 +/- 0.20 vs. 21.0 +/- 0.18 kg; p < 0.001). The regression analysis with a quadratic model shows that aging accounts for 30% of the variance in handgrip strength (r(2) = 0.30; p < 0.001) in men and 28% (r(2) = 0.28; p < 0.001) in women. In addition, the bent linear regression with multiple regressors show that a faster decline in handgrip strength occurs at the age of 30 years for men and 50 years for women. We conclude that handgrip strength decline with age differs between genders, making useful the existence of distinct male and female normative age group data.

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The aim of the study was to assess the acute effect of whole-body vibration (WBV) exercise, with low frequency (5 Hz), on the pain level (PL), trunk flexibility, and cardiovascular responses (blood pressure [BP] and heart rate [HR]) in individuals with metabolic syndrome (MetS). Forty-four individuals were included in the study (control: 15) or in (WBV exercise: 29) groups. They were submitted to 3 bouts (1 minute each) of WBV exercise (5 Hz and peak-to-peak displacements of 2.5, 5.0, and 7.5 mm, corresponding to peak accelerations of 0.12, 0.25, and 0.35 g, respectively, sitting in a chair with the feet on the platform with knees flexed, followed by 1 minute of interset rest. The Control Group performed the same protocol, but the platform was turned off. The PL was measured through the visual analog pain scale, and the flexibility was measured through the anterior trunk flexion test. Significant improvements on PL (P = .031) and flexibility (P = .004) were found only in the WBV exercise group. The BP and HR remained at physiological levels. In conclusion, the WBV exercise would lead to physiological response decreasing PL and increasing flexibility as well as maintaining the cardiovascular responses in individuals with MetS.

Background. We tested the hypothesis that high intensity interval training (HIIT) would be more effective than moderate intensity continuous training (MIT) to improve newly emerged markers of cardiorespiratory fitness in coronary heart disease (CHD) patients, as the relationship between ventilation and carbon dioxide production (VE/VCO2 slope), oxygen uptake efficiency slope (OUES), and oxygen pulse (O2P). Methods. Seventy-one patients with optimized treatment were randomly assigned into HIIT (n = 23, age = 56 ± 12 years), MIT (n = 24, age = 62 ± 12 years), or nonexercise control group (CG) (n = 24, age = 64 ± 12 years). MIT performed 30 min of continuous aerobic exercise at 70–75% of maximal heart rate (HRmax), and HIIT performed 30 min sessions split in 2 min alternate bouts at 60%/90% HRmax (3 times/week for 16 weeks). Results. No differences among groups (before versus after) were found for VE/VCO2 slope or OUES (P > 0.05). After training the O2P slope increased in HIIT (22%, P < 0.05) but not in MIT (2%, P > 0.05), while decreased in CG (−20%, P < 0.05) becoming lower versus HIIT (P = 0.03). Conclusion. HIIT was more effective than MIT for improving O2P slope in CHD patients, while VE/VCO2 slope and OUES were similarly improved by aerobic training regimens versus controls.

Post-exercise cardiac vagal reactivation is well-investigated; however, the effect of water intake during this period has not been well studied. Therefore, our aim was to assess the influence of water intake on the cardiac vagal reactivation after 30 min of a submaximal cycling exercise. Ten healthy subjects (eight men) aged 23-35 years were evaluated. A 3-day testing cycle duration, subjects were randomly chosen to drink either 500 ml (experimental visit) or 50 ml (control visit) of water immediately after the 30-min cycling exercise at a workload representing 80% of a previously measured anaerobic threshold. A cardiac vagal index (CVI) was obtained using the 4-s exercise test measured before and after (10 and 30 min) exercise at each testing day. Data analysis (2 x 3 ANOVA for repeated measures) showed higher cardiac vagal activity at the 30-min post-exercise period when 500 ml of water was ingested. CVI values for the 500 and 50 ml trials were 1.55 +/- 0.04 vs. 1.49 +/- 0.04, P = 0.003 (mean +/- SEM), respectively. Heart rate and blood pressure values were relatively the same. In conclusion, water intake of about 500 ml immediately after 30 min of cycling exercise accelerates post-exercise cardiac vagal reactivation. These results suggest that post-exercise hydration might be beneficial not only for thermoregulation, but also for vagal reactivation.

These results indicate that maximal O(2) pulse is a significant predictor of mortality in patients with and without CPD. The addition of absolute and relative O(2) pulse data provides complementary information for risk-stratifying heterogeneous participants referred for CPX and should be routinely included in the CPX report.