Role of muscle mass in the association between handgrip strength and blood pressure in children and adolescents.

Studies have reported conflicting results on the association between handgrip strength (HGS) and blood pressure during childhood and adolescence. High multicollinearity involving somatic components that influence both HGS and blood pressure might be an important source of bias. This study sought to investigate the independent effects of HGS and muscle mass on blood pressure levels in children and adolescents. Muscle mass and fat mass (Multifrequency Electrical Bioimpedance) and systolic (SBP) and diastolic (DBP) blood pressure (Automatic oscillometric device) were assessed in 833 volunteers aged 6-18 years, of both sexes. Handgrip strength-for-age quartiles were calculated and participants were assigned to groups by HGS quartiles. Analysis of covariance was conducted to address the linear association between HGS and SBP adjusted for height, muscle mass, and fat mass. To test for linear trend, contrast analysis was conducted. Partial eta-squared was used to confirm or rule out a small significant effect of the independent variables on SBP. The effect size of HGS on SBP was not significant in both sexes. In girls, 1.7% of the between-groups variance in SBP was accounted for by muscle mass (P = 0.016). In boys, 2.3% and 1.8% of the between-groups variance in SBP was accounted for by muscle mass (P = 0.001) and height (P = 0.005), respectively. In conclusion, children with a more advanced physical maturity for their age, that is, who are taller, stronger, and have greater fat-free mass, may be nearly reaching the physiological parameters of adulthood, and consequently have higher systolic blood pressure.

Testosterone deficiency impairs cardiac interfibrillar mitochondrial function and myocardial contractility while inducing oxidative stress.

Introduction: Clinical studies have shown that low levels of endogenous testosterone are associated with cardiovascular diseases. Considering the intimate connection between oxidative metabolism and myocardial contractility, we determined the effects of testosterone deficiency on the two spatially distinct subpopulations of cardiac mitochondria, subsarcolemmal (SSM) and interfibrillar (IFM). Methods: We assessed cardiac function and cardiac mitochondria structure of SSM and IFM after 12 weeks of testosterone deficiency in male Wistar rats. Results and Discussion: Results show that low testosterone reduced myocardial contractility. Orchidectomy increased total left ventricular mitochondrial protein in the SSM, but not in IFM. The membrane potential, size and internal complexity in the IFM after orchidectomy were higher compared to the SHAM group. However, the rate of oxidative phosphorylation with all substrates in the IFM after orchidectomy was lower compared to the SHAM group. Testosterone replacement restored these changes. In the testosterone-deficient SSM group, oxidative phosphorylation was decreased with palmitoyl-L-carnitine as substrate; however, the mitochondrial calcium retention capacity in IFM was increased. There was no difference in swelling of the mitochondria in either group. These changes in IFM were followed by a reduction in phosphorylated form of AMP-activated protein kinase (p-AMPK-α), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) translocation to mitochondria and decreased mitochondrial transcription factor A (TFAM). Testosterone deficiency increased NADPH oxidase (NOX), angiotensin converting enzyme (ACE) protein expression and reduced mitochondrial antioxidant proteins such as manganese superoxide dismutase (Mn-SOD) and catalase in the IFM. Treatment with apocynin (1.5 mM in drinking water) normalized myocardial contractility and interfibrillar mitochondrial function in the testosterone depleted animals. In conclusion, our findings demonstrate that testosterone deficiency leads to reduced myocardial contractility and impaired cardiac interfibrillar mitochondrial function. Our data suggest the involvement of reactive oxygen species, with a possibility of NOX as an enzymatic source.

Endurance training restores spatially distinct cardiac mitochondrial function and myocardial contractility in ovariectomized rats.

We previously demonstrated that the loss of female hormones induces cardiac and mitochondrial dysfunction in the female heart. Here, we show the impact of endurance training for twelve weeks, a nonpharmacological therapy against cardiovascular disease caused by ovariectomy and its contribution to cardiac contractility, mitochondrial quality control, bioenergetics and oxidative damage. We found that ovariectomy induced cardiac hypertrophy and dysfunction by decreasing SERCA2 and increasing phospholamban protein expression. Endurance training restored myocardial contractility, SERCA2 levels, increased calcium transient in ovariectomized rats but did not change phospholamban protein expression or cardiac hypertrophy. Additionally, ovariectomy decreased the amount of intermyofibrillar mitochondria and induced mitochondrial fragmentation that were accompanied by decreased levels of mitofusin 1, PGC-1α, NRF-1, total AMPK-α and mitochondrial Tfam. Endurance training prevented all these features except for mitofusin 1. Ovariectomy reduced O2 consumption, elevated O2.- release and increased Ca2+-induced mitochondrial permeability transition pore opening in both mitochondrial subpopulations. Ovariectomy also increased NOX-4 protein expression in the heart, reduced mitochondrial Mn-SOD, catalase protein expression and increased protein carbonylation in both mitochondrial subpopulations, which were prevented by endurance training. Taken together, our findings show that endurance training prevented cardiac contractile dysfunction and mitochondrial quality control in ovariectomized rats.

Estrogen regulates spatially distinct cardiac mitochondrial subpopulations.

Increased susceptibility to permeability transition pore (mPTP) is a significant concern to decreased cardiac performance in postmenopausal females. The goal of this study was to assess the effects of estrogen deficiency on the two spatially distinct mitochondrial subpopulations from left ventricle: subsarcolemmal mitochondria (SSM) and intermyofibrillar mitochondria (IFM) based on: morphology, membrane potential, oxidative phosphorylation, mPTP and reactive oxygen species production. Female rats (8weeks old) that underwent bilateral ovariectomy were randomly assigned to receive daily treatment with placebo (OVX), estrogen replacement (OVX+E2) and Sham for 60days. The yield for IFM was found higher in the OVX group and lower in the SSM. SSM internal complexity and size were higher in the OVX group, although membrane potential was not different. The maximal rate of mitochondrial respiration, states 3 and 4, using glutamate+malate as substrate, were higher in IFM and SSM from the OVX group. The respiratory control ratio (RCR - state3/state 4), was not different in both SSM and IFM with glutamate+malate. The ADP:O ratio was found lower in IFM and SSM from OVX compared to Sham. When pyruvate was used, state 3 was found unchanged in both IFM and SSM, state 4 was greater in IFM from OVX rats compared to Sham and the ADP/O ratio was decreased. The RCR was unchanged in both subpopulations. The IFM from OVX rats presented a lower Ca2+retention capacity compared to Sham, however, the SSM remained unchanged. Hydrogen peroxide formation was found increased in the IFM from OVX animals with glutamate+malate and rotenone+succinate as substrates. The SSM showed increased ROS production only with rotenone+succinate. Western blot analyzes showed decreased levels of PGC-1α and NRF-1 in the OVX group. Estrogen replacement was able to restore most of the alterations induced by ovariectomy. In conclusion, our data shows that estrogen deficiency has distinct effects on the two spatially distinct mitochondrial subpopulations in oxidative phosphorylation, morphology, calcium retention capacity and ROS production.

Sex differences in the regulation of spatially distinct cardiac mitochondrial subpopulations.

Spatially distinct mitochondrial subpopulation may mediate myocardial pathology through permeability transition pore opening (MPTP). The goal of this study was to assess sex differences on the two spatially distinct mitochondrial subpopulations: subsarcolemmal mitochondria (SSM) and intermyofibrillar mitochondria (IFM) based on morphology, membrane potential, mitochondrial function, oxidative phosphorylation, and MPTP. Aged matched Wistar rats were used to study SSM and IFM. Mitochondrial size was larger in SSM than in IFM in both genders. However, SSM internal complexity, yield, and membrane potential were higher in male than in female. The maximal rate of mitochondrial respiration, states 3 and 4, using glutamate + malate as substrate, were higher in IFM and SSM in the male group compared to female. The respiratory control ratio (RCR-state3/state 4), was not different in both SSM and IFM with glutamate + malate. The ADP:O ratio was found higher in IFM and SSM from female compared to males. When pyruvate was used, state 3 was found unchanged in both IFM and SSM, state 4 was also greater in male IFM compared to female. The RCR increased in the SSM while IFM remained the same. State 4 was higher in male SSM while in the IFM remained the same. The IFM presented a higher Ca(2+) retention capacity compared with SSM, however, there was a greater sensitivity to Ca(2+)-induced MPTP in SSM and IFM in the male group compared to female. In conclusion, our data show that spatially distinct mitochondrial subpopulations have sex-based differences in oxidative phosphorylation, morphology, and calcium retention capacity.

Heart rate at 4 s after the onset of exercise in endurance-trained men.

It has been suggested that the increase in heart rate (HR) at the onset of exercise is caused by vagal withdrawal. In fact, endurance runners show a lower HR in maximum aerobic tests. However, it is still unknown whether endurance runners have a lower HR at 4 s after the onset of exercise (4th-sec-HR). We sought to measure the HR at the onset of the 4 s exercise test (4-sET), clarifying its relationship to heart rate variability (HRV), spectral indices, and cardiac vagal index (CVI) in endurance runners (ER) and healthy untrained controls (CON). HR at 4th-sec-HR, CVI, and percent HR increase during exercise were analyzed in the 4-sET. High frequency spectrum (HF-nu), low frequency spectrum (LF-nu), and low frequency/high frequency band ratio (LF/HF) were analyzed from the HRV. ER showed a significantly higher HF, and both a lower LF and LF/HF ratio compared with the CON. ER presented a significantly lower 4th-sec-HR, although neither CVI nor HR increases during exercise were statistically different from the CON. In conclusion, ER presented a lower 4th-sec-HR secondary to increased vagal influence over the sinus node. CVI seems to be too weak to use for discriminating individuals with respect to the magnitude of HR vagal control.

Comparação da resposta autonômica cardiovascular de praticantes de musculação, corredores de longa distância e não praticantes de exercício / Comparison of cardiovascular autonomic response among body builders, long distance runners and non-trained

Objetivou-se comparar a resposta autonômica cardiovascular (RAC) de praticantes de musculação, corredores de longa distância e não praticantes de exercício. Homens, 21 a 55 anos, foram agrupados em: Praticantes Musculação (PM, n = 31); Praticantes Corrida (PC, n = 28); Controle (C, n = 35). Foram selecionadas quatro técnicas para avaliação da RAC: Frequência cardíaca de repouso (FCR), Teste pressórico do frio (TPF), Variabilidade da FC (VFC) e recuperação da FC pós-teste máximo em esteira. A FCR foi menor no grupo PC (PC = 54 ± 2; PM= 62 ± 2; C = 65 ± 2 bpm; média ± EPM). A recuperação da FC aos 60 s pós-teste de esforço foi maior no grupo PC (PC = 34 ± 3; PM = 23 ± 1; C = 24 ± 2; bpm). Quanto aos parâmetros espectrais de alta (HF) e baixa (LF) frequência da VFC, o grupo PC apresentou maior HF (55,1 ± 4,0 n.u) e menor LF (43,1 ± 4,0 n.u) comparado ao grupo C (HF = 40,7 ± 3,3; LF = 56,7 ± 3,5 n.u). O grupo PM não apresentou qualquer diferença de RAC em comparação ao grupo C. Conclui-se que prática contínua em musculação por longo prazo, diferentemente da prática de corrida de longa distância, não é capaz de alterar significativamente a RAC.

The aim of the study was to compare the cardiovascular autonomic response (CAR) of recreational weight trainers, long distance runners and non-exercised subjects. Men, 21 to 55 years old, were grouped in: recreational weight trainers (W, n = 31), long distance runners (R, n = 28) and non-exercised (C, n = 35). Four strategies of evaluation of the CAR were selected: Resting heart rate (RHR), cold pressor test (CPT), heart rate variability (HRV) and heart rate recovery (HHR) following maximal exercise test. The RHR was lower (R = 54 ± 2; W = 62 ± 2; C= 65 ± 2 bpm; mean ± SE) and the HHR 60s post exercise was larger in the R group (R = 34 ± 3; W = 23 ± 1; C = 24 ± 2 bpm). The R group presented larger high-frequency (HF; 55.1 ± 4.0 n.u) and smaller low-frequency (LF; 43.1 ± 4.0 n.u) components of HRV than C group (HF = 40.7 ± 3.3; LF = 56.7 ± 3.5 n.u.). The W group did not show any differences compared to C group. The study's conclusion was that long-term weight-training program, unlike of long-term running training, it is not able to alter significantly the regulatory pattern of CAR.

Spectral analysis of heart rate variability with the autoregressive method: what model order to choose?

This work assessed the influence of the autoregressive model order (ARMO) on the spectral analysis of the heart rate variability (HRV). A sample of 68 R-R series obtained from digital ECG records of young healthy adults in the supine position was used. Normalized spectral indexes for each ARMO were compared by Friedman test followed by the Dunn's procedure and statistical significance was set at P<0.05. The results showed that the AR method using orders from 9 to 25 produces normalized spectral parameters statistically similar and, hence, the algorithms commonly employed to estimate optimum order are not mandatory in this case.