Effects of isometric leg training on ambulatory blood pressure and morning blood pressure surge in young normotensive men and women.

Despite the reported association between diurnal variations in ambulatory blood pressure (BP) and elevated cardiovascular disease risk, little is known regarding the effects of isometric resistance training (IRT), a practical BP-lowering intervention, on ambulatory BP and morning BP surge (MBPS). Thus, we investigated whether (i) IRT causes reductions in ambulatory BP and MBPS, in young normotensives, and (ii) if there are any sex differences in these changes. Twenty normotensive individuals (mean 24-h SBP = 121 ± 7, DBP = 67 ± 6 mmHg) undertook 10-weeks of bilateral-leg IRT (4 × 2-min/2-min rest, at 20% maximum voluntary contraction (MVC) 3 days/week). Ambulatory BP and MBPS (mean systolic BP (SBP) 2 h after waking minus the lowest sleeping 1 h mean SBP) was measures pre- and post-training. There were significant reductions in 24-h ambulatory SBP in men (- 4 ± 2 mmHg, P = 0.0001) and women (- 4 ± 2 mmHg, P = 0.0001) following IRT. Significant reductions were also observed in MBPS (- 6 ± 8 mmHg, p = 0.044; - 6 ± 7 mmHg, P = 0.019), yet there were no significant differences between men and women in these changes, and 24-h ambulatory diastolic BP remained unchanged. Furthermore, a significant correlation was identified between the magnitude of the change in MBPS and the magnitude of changes in the mean 2-h SBP after waking for both men and women (men, r = 0.89, P = 0.001; women, r = 0.74, P = 0.014). These findings add further support to the idea that IRT, as practical lifestyle intervention, is effective in significantly lowering ambulatory SBP and MBPS and might reduce the incidence of adverse cardiovascular events that often occur in the morning.

Getting the best GRIP on blood pressure control: Investigating a cost-effective isometric handgrip alternative.

OBJECTIVES: The World Health Organization emphasises the need for cost-effective alternative methods to lower blood pressure (BP). Endorsed nationally in HTN guidelines, isometric handgrip (IHG) training is an alternative method of BP control. The purpose of this study was to compare the BP, heart rate (HR) and rates of perceived exertion (RPE) responses between a bout of IHG training performed using the traditional computerized device and a more affordable, inflatable stress ball. METHODS: Twenty healthy adults performed one bout (4, 2-min isometric contractions, with 1-min rests between each contraction at 30% maximal voluntary contraction) of IHG training using the traditional computerized device, and one bout with the inflatable stress ball. BP, HR, and RPE were recorded. RESULTS: No statistically significant differences between devices were observed with HR, BP, and RPE (p < 0.05). However, average RPE for both devices ranged between 5 and 6 indicating that participants were rating 30% of their MVC, consistent with previous work. DISCUSSION: The similar cardiovascular and psychophysical responses provide support for the potential use of this low individual- and provider-burden, cost-efficient IHG device, and lay the foundation for a future training study to test the hypothesis of benefit.

Adiponectin-Consideration for its Role in Skeletal Muscle Health.

Adiponectin regulates metabolism through blood glucose control and fatty acid oxidation, partly mediated by downstream effects of adiponectin signaling in skeletal muscle. More recently, skeletal muscle has been identified as a source of adiponectin expression, fueling interest in the role of adiponectin as both a circulating adipokine and a locally expressed paracrine/autocrine factor. In addition to being metabolically responsive, skeletal muscle functional capacity, calcium handling, growth and maintenance, regenerative capacity, and susceptibility to chronic inflammation are all strongly influenced by adiponectin stimulation. Furthermore, physical exercise has clear links to adiponectin expression and circulating concentrations in healthy and diseased populations. Greater physical activity is generally related to higher adiponectin expression while lower adiponectin levels are found in inactive obese, pre-diabetic, and diabetic populations. Exercise training typically restores plasma adiponectin and is associated with improved insulin sensitivity. Thus, the role of adiponectin signaling in skeletal muscle has expanded beyond that of a metabolic regulator to include several aspects of skeletal muscle function and maintenance critical to muscle health, many of which are responsive to, and mediated by, physical exercise.

Physical literacy improves with the Run Jump Throw Wheel program among students in grades 4-6 in southwestern Ontario.

The purpose of this study was to determine whether the introduction of a fundamental movement skills (FMS) program to grade 4-6 physical education (PE) classes could improve students' physical literacy (PL) and influence the amount of effort exerted in PE class. Athletics Canada's grassroots Run Jump Throw Wheel (RJTW) Program was delivered for 10 weeks during PE classes (2 schools: four grade 4, four grade 5, two grade 6, one split grade 5-6 class, and one split grade 6-7 class, totalling 310 students). Participants completed the Canadian Assessment of Physical Literacy (CAPL) and wore heart rate monitors and pre- and postintervention. The CAPL score increased 3.3 (±8.8) points from the pretest to the post-test (t = 6.47, p < 0.001). Improvements were not significantly different by grade or gender, but those in the suburban-area school improved more so than those attending the rural-area school (F[1,294] = 4.82, p < 0.004). Among those participants that increased their PL (n = 186), the CAPL scores increased by 8.6 (±5.9) points versus those that decreased (n = 110; -5.6 ± 4.8 points), F[1,294] = 452.11, p < 0.001. No significant differences in time spent in physical activity were observed between the pre- and post-test (i.e., 17.0 ± 7.0 min and 19.3 ± 7.0 min, respectively, t = 1.70, p = 0.091). The RJTW program increased participants' overall FMS, as well as their knowledge and understanding regarding these FMS, both key components of PL.

Acute Response to a 2-Minute Isometric Exercise Test Predicts the Blood Pressure-Lowering Efficacy of Isometric Resistance Training in Young Adults.

BACKGROUND: This work aimed to explore whether different forms of a simple isometric exercise test could be used to predict the blood pressure (BP)-lowering efficacy of different types of isometric resistance training (IRT) in healthy young adults. In light of the emphasis on primary prevention of hypertension, identifying those with normal BP who will respond to IRT is important. Also, heightened BP reactivity increases hypertension risk, and as IRT reduces BP reactivity in patients with hypertension, it warrants further investigation in a healthy population. METHODS: Forty-six young men and women (24 ± 5 years; 116 ± 10/ 68 ± 8 mm Hg) were recruited from 2 study sites: Windsor, Canada (n = 26; 13 women), and Northampton, United Kingdom (n = 20; 10 women). Resting BP and BP reactivity to an isometric exercise test were assessed prior to and following 10 weeks of thrice weekly IRT. Canadian participants trained on a handgrip dynamometer (isometric handgrip, IHG), while participants in the UK trained on an isometric leg extension dynamometer (ILE). RESULTS: Men and women enrolled in both interventions demonstrated significant reductions in systolic BP (P < 0.001) and pulse pressure (P < 0.05). Additionally, test-induced systolic BP changes to IHG and ILE tests were associated with IHG and ILE training-induced reductions in systolic BP after 10 weeks of training, respectively (r = 0.58 and r = 0.77; for IHG and ILE; P < 0.05). CONCLUSIONS: The acute BP response to an isometric exercise test appears to be a viable tool to identify individuals who may respond to traditional IRT prescription.

The effects of recreational sport on VO2peak, VO2 kinetics and submaximal exercise performance in males and females.

The purpose of the present study was to examine changes in VO(2peak), VO(2) kinetics and steady-state exercise performance following 4 weeks of participation in recreational sport. Subjects (male n = 8, female n = 9) participated in recreational sport (basketball, floor hockey and soccer) four times per week for 4 weeks. Both before and after training, VO(2peak) was measured on a cycle ergometer, VO(2) kinetics was determined as the average of three transitions to 80 W, and heart rate (HR) and respiratory exchange ratio (RER) were measured during 60 min at a work rate corresponding to 50 % of pre-training VO(2peak). HR was also monitored during all training sessions. After training, VO(2peak) was increased in females, but not males, while VO(2) kinetics (τVO(2)) were sped in both males and females. HR during constant load exercise was reduced in both males and females, but exercise RER was only reduced in females. Mean HR during participation in sport was higher in males than females and higher during basketball than both floor hockey and soccer. These results demonstrate that training adaptations traditionally associated with endurance exercise can also be obtained through regular participation in recreational sport.

Sex and life expectancy.

BACKGROUND: A sexual dimorphism in human life expectancy has existed in almost every country for as long as records have been kept. Although human life expectancy has increased each year, females still live longer, on average, than males. Undoubtedly, the reasons for the sex gap in life expectancy are multifaceted, and it has been discussed from both sociological and biological perspectives. However, even if biological factors make up only a small percentage of the determinants of the sex difference in this phenomenon, parity in average life expectancy should not be anticipated. OBJECTIVE: The aim of this review is to highlight biological mechanisms that may underlie the sexual dimorphism in life expectancy. METHODS: Using PubMed, ISI Web of Knowledge, and Google Scholar, as well as cited and citing reference histories of articles through August 2012, English-language articles were identified, read, and synthesized into categories that could account for biological sex differences in human life expectancy. RESULTS: The examination of biological mechanisms accounting for the female-based advantage in human life expectancy has been an active area of inquiry; however, it is still difficult to prove the relative importance of any 1 factor. Nonetheless, biological differences between the sexes do exist and include differences in genetic and physiological factors such as progressive skewing of X chromosome inactivation, telomere attrition, mitochondrial inheritance, hormonal and cellular responses to stress, immune function, and metabolic substrate handling among others. These factors may account for at least a part of the female advantage in human life expectancy. CONCLUSIONS: Despite noted gaps in sex equality, higher body fat percentages and lower physical activity levels globally at all ages, a sex-based gap in life expectancy exists in nearly every country for which data exist. There are several biological mechanisms that may contribute to explaining why females live longer than men on average, but the complexity of the human life experience makes research examining the contribution of any single factor for the female advantage difficult. However, this information may still prove important to the development of strategies for healthy aging in both sexes.

Core temperature is a greater influence than endogenous 17ß-estradiol on the exercise-induced accumulation of myocardial heat shock protein mRNA.

Female rats typically do not show significant increases in myocardial Hsp70 after exercise unless trained (exercise over days or weeks). 17ß-Estradiol (E2) has been linked to this inhibition, but it varies considerably over the rodent estrus cycle. Consequently, we examined whether the inhibitory effects of endogenously produced E2 (measured immediately pre-exercise) were acute in exercised female Sprague-Dawley rats (60 min treadmill running at 30 m·min(-1)). Myocardial hsp70-1 and hsp70-2 mRNA were measured 30 min post-exercise, and their expression was inversely correlated with pre-exercise plasma Ε2 ( hsp70-1 mRNA, r(2) = 0.308, p = 0.011; hsp70-2 mRNA, r(2) = 0.238, p = 0.029). However, hsp70-1 and hsp70-2 mRNA exhibited much stronger correlations with core temperature achieved during exercise (r(2) = 0.812, p = 0.000; and r(2) = 0.738, p = 0.000, respectively). Consequently, although endogenous Ε2 in gonadally intact female rats may attenuate myocardial hsp70 mRNA accumulation, suggesting a reason why training maximizes this response in females, core temperature during exercise is still a greater stimulus to this response.

Myocardial Hsp70 phosphorylation and PKC-mediated cardioprotection following exercise.

Both protein kinase C (PKC) activation and Hsp70 expression have been shown to be key components for exercise-mediated myocardial protection during ischemia-reperfusion injury. Given that Hsp70 has been shown to undergo inducible phosphorylation in striated muscle and liver, we hypothesized that PKC may regulate myocardial Hsp70 function and subsequent exercise-conferred cardioprotection through this phosphorylation. Hence, acute exercise of male Sprague-Dawley rats (30 m/min for 60 min at 2% grade) was employed to assess the role of PKC and its selected isoforms in phosphorylation of Hsp70 and protection of the myocardium during ischemia-reperfusion injury. It was observed that administration of the PKC inhibitor chelerythrine chloride (5 mg/kg) suppressed the activation of three exercise-induced PKC isoforms (PKCalpha, PKCdelta, and PKCepsilon) and attenuated the exercise-mediated reduction of myocardial infarct size during ischemia-reperfusion injury. While this study also demonstrated that exercise led to an alteration in the phosphorylation status of Hsp70, this posttranslational modification appeared to be dissociated from PKC activation, as exercise-induced phosphorylation of Hsp70 was unchanged following inhibition of PKC. Taken together, these results indicate that selected isoforms of PKC play an important role in exercise-mediated protection of the myocardium during ischemia-reperfusion injury. However, exercise-induced phosphorylation of Hsp70 does not appear to be a mechanism by which PKC induces this cardioprotective effect.

Heat shock proteins and exercise: a primer.

Heat shock proteins (HSPs) are, in general, prosurvival molecules within the cellular environment, and the overexpression of even just 1 family of HSPs can lead to protection against and improvements after a variety of stressors. Not surprisingly, a fertile area of study has grown out of efforts to exploit the innate biologic behaviour of HSPs. Exercise, because of the inherent physiologic stresses associated with it, is but 1 stimulus that can result in a robust increase in various HSPs in several tissues, not the least of which happen to be the heart and skeletal muscle. The purpose of this review is to introduce the reader to the major HSP families, the control of their expression, and some of their biologic functions, specifically with respect to the influence of exercise. Moreover, as the first in a series of reviews from a common symposium, we will briefly introduce the concepts presented by the other authors, which include the effects of different exercise paradigms on skeletal muscle HSPs in the adult and aged systems, HSPs as regulators of inflammation, and the ion channel stabilizing effects of HSPs.

Response of the myocardium to exercise: sex-specific regulation of hsp70.

Sex is a potent modifier of the cardiovascular system because males and females differ in several aspects of the heart's biology and physiology. Epidemiologically, premenopausal women possess a distinct advantage over men in the occurrence of cardiovascular heart disease; however, this advantage shifts to men once a negative cardiac event has occurred. The reasons for these differences are not completely understood and are likely attributable to many factors. Nonetheless, the sex hormones seem to be important regulators of myocardial health. Of particular note, the sex hormones influence the molecular and physiological responses of the heart to the stress of exercise including the expression of several vital proteins such as the cardioprotective 70-kDa heat-shock protein, Hsp70. This review will focus on the exercise-induced expression of Hsp70 and how it is modified by sex. A better understanding of how sex, the sex hormones in particular, modifies the exercise stress response has important implications in the prescription of exercise to males and females, young or old.

Exercise-mediated regulation of Hsp70 expression following aerobic exercise training.

An issue central to understanding the biological benefits associated with regular exercise training is to elucidate the intracellular mechanisms governing exercise-conferred cardioprotection. Heat shock proteins (HSPs), most notably the inducible 70-kDa HSP family member Hsp70, are believed to participate in the protection of the myocardium during cardiovascular stress. Following acute exercise, activation of PKA mediates the suppression of an intermediary protein kinase, ERK1/2, which phosphorylates and suppresses the activation of the heat shock transcription factor 1 (HSF1). However, following exercise training, ERK1/2 has been reported to regulate the transcriptional activation of several genes involved in cell growth and proliferation and has been shown to be associated with training-mediated myocardial hypertrophy. The present project examined the transcriptional activation of hsp70 gene expression in acutely exercised (60 min at 30 m/min) naïve sedentary and aerobically trained (8 wk, low intensity) male Sprague-Dawley rats. Following acute exercise stress, no significant differences were demonstrated in the expression of myocardial Hsp70 mRNA and activation of PKA between sedentary and trained animals. However, trained animals elicited expression of the hsp70 gene (P < 0.05) in the presence of elevated ERK1/2 activation. Given the association of ERK1/2 and the suppression of hsp70 gene expression following acute exercise in naïve sedentary rats, these results suggest that training results in adaptations that allow for the simultaneous initiation of both proliferative and protective responses. While it is unclear what factors are associated with this training-related shift, increases in HSF1 DNA binding affinity (P < 0.05) and posttranscriptional modifications of the Hsp70 transcript are suggested.

Exercise training improves myocardial tolerance to ischemia in male but not in female rats.

Acute exercise increases myocardial tolerance to ischemia-reperfusion (I-R) injury in male but not in female rat hearts, possibly due to a decreased heat shock protein 70 (Hsp70) response in the female hearts. This study examined whether repetitive exercise training would increase Hsp70 and myocardial tolerance to I-R injury in female rat hearts. Adaptations in myocardial manganese superoxide dismutase (MnSOD) and endothelial nitric oxide synthase (eNOS) were also assessed. Ten-week old male (M) and female (F) Sprague-Dawley rats (n = 40 total) exercise-trained for 14 wk; the last 8 wk consisted of running 1 h at 30 m/min (2% incline), 5 days/wk. Following training, left ventricle mechanical function (LVMF) was monitored for 30 min of reperfusion following 30 min of global ischemia (Langendorff procedure). Myocardial Hsp70 content was not different in M and F control groups, while increases were observed in both trained groups (M greater than F; P < 0.05). Although MnSOD content did not differ between groups, endothelial nitric oxide synthase (eNOS) levels were decreased in F, with no change in M, following training (P < 0.05). Hearts from control F demonstrated a greater recuperation of all indices of LVMF following I-R compared with control M hearts (P < 0.05). Hearts of trained M exhibited improved recovery of LVMF (left ventricular diastolic pressure, left ventricular end-diastolic pressure, +dP/dt, -dP/dt) during reperfusion compared with control M hearts (P < 0.05). In contrast, hearts of trained F did not show any change in recovery from I-R. Hence, exercise training is more beneficial to M than F in improving myocardial function following I-R injury.

Neuropeptide Y bioavailability is suppressed in the hindlimb of female Sprague-Dawley rats.

We recently reported that male, but not female, rats exhibit basal endogenous neuropeptide Y Y(1)-receptor modulation of hindlimb vasculature. The lack of baseline endo-genous Y(1)-receptor control in females was evident despite the expression of Y(1)-receptors and neuropeptide Y in hindlimb skeletal muscle tissue. The following study addressed the hypothesis that neuropeptide Y bioavailability is blunted in female rats under baseline conditions. It was further hypothesized that enhanced prejunctional autoinhibitory neuropeptide Y Y(2)-receptor expression and/or proteolytic processing of released neuropeptide Y may persist in female rats. Using western blot analysis, it was observed that females had greater overall neuropeptide Y Y(2)-receptor expression in skeletal muscle compared to males (P < 0.05). To address the prevalence/impact of baseline endogenous Y(2)-receptor activation on neuropeptide Y release in hindlimb vasculature, an arterial infusion of BIIE0246 (specific non-peptide Y(2)-receptor antagonist; 170 microg kg(-1)) was carried out on female and male rats. Y(2)-receptor blockade resulted in a decrease in hindlimb vascular conductance in females and males (P < 0.05). However, the BIIE0246-induced decrease in vascular conductance was Y(1)-receptor dependent in females, but not males (P < 0.05). In addition, compared to baseline, BIIE0246 infusion resulted in increased plasma neuropeptide Y concentration in females (P < 0.05), while there was no observable change in males. In a final experiment, systemic inhibition of proteolytic enzymes dipeptidylpeptidase IV (via 500 nM diprotin A) and aminopeptidase P (via 180 nM 2-mercaptoethanol) elicited a Y(1)-receptor-dependent decrease in hindlimb vascular conductance in females (P < 0.05). It was concluded that our previously reported lack of basal endogenous Y(1)-receptor activation in female hindlimb vasculature was (at least partially) due to prejunctional Y(2)-receptor autoinhibition and proteolytic processing of neuropeptide Y.

Gender-modulated endogenous baseline neuropeptide Y Y1-receptor activation in the hindlimb of Sprague-Dawley rats.

This study examined the effect of neuropeptide Y Y(1)-receptor blockade both alone, and in interaction with alpha(1)-adrenoceptor antagonism, on basal hindlimb vascular conductance in male and female Sprague-Dawley rats. Hindlimb vascular conductance was measured during infusion of BIBP3226 (Y(1)-receptor antagonist; 100 microg kg(-1)), prazosin (alpha(1)-receptor antagonist; 20 microg kg(-1)), and combined blockade. In males, vascular conductance increased 1.1 +/- 0.3 microl min(-1) mmHg(-1) above baseline with BIBP3226, and 2.4 +/- 0.4 microl min(-1) mmHg(-1) above baseline with prazosin (both P < 0.05). The increase in vascular conductance during combined blockade (5.1 +/- 0.7 microl min(-1) mmHg(-1)) was greater than the sum of the independent BIBP3226 and prazosin responses (P < 0.05). In females, basal hindlimb vascular conductance was unaffected by Y(1)-receptor blockade. However, alpha(1)-receptor blockade resulted in a 3.5 +/- 0.6 microl min(-1) mmHg(-1) increase in vascular conductance above baseline, which was not different than the combined blockade condition. Males had greater skeletal muscle neuropeptide Y concentration (P < 0.05; ELISA) than females. Furthermore, compared with females, male skeletal muscle contained greater Y(1)-receptor expression (P < 0.05; Western blot). It was concluded that, under baseline conditions, agonist and receptor-based mechanisms for Y(1)-receptor dependent control of vascular conductance in skeletal muscle was greater in male versus female rats.

Exercise-induced elevation of HSP70 is intensity dependent.

Exercise induces expression of the protective heat shock protein, HSP70, in striated muscle. To characterize the relationship between induction of this protein and exercise intensity in muscles exhibiting different recruitment patterns, male Sprague-Dawley rats were assigned to a sedentary control or one of seven exercise groups for which treadmill running speed varied between 15 and 33 m/min (n = 8/group). Twenty-four hours after a single 60-min exercise bout, hearts, red and white portions of the vastus (RV and WV, respectively) muscles, and soleus (Sol) muscles were harvested and analyzed for both relative and absolute HSP70 content. Cardiac HSP70 was significantly elevated only when animals were exercised at 24 m/min and beyond. Similarly, HSP70 was elevated in RV at running speeds above 24 m/min but did not increase in WV until 27 m/min. In contrast, HSP70 content was initially elevated in the Sol but subsequently declined at the highest running speeds. The observed patterns of HSP70 expression in skeletal muscle were in general accordance with known muscle recruitment patterns and suggest that alterations in muscle loading, resulting from changes in exercise intensity, are an important component of exercise-induced increases in HSP70 content.