Andrew Maiorana

Effect of exercise training on endothelium‐derived nitric oxide function in humans

Vascular endothelial function is essential for maintenance of health of the vessel wall and for vasomotor control in both conduit and resistance vessels. These functions are due to the production of numerous autacoids, of which nitric oxide (NO) has been the most widely studied. Exercise training has been shown, in many animal and human studies, to augment endothelial, NO‐dependent vasodilatation in both large and small vessels. The extent of the improvement in humans depends upon the muscle mass subjected to training; with forearm exercise, changes are restricted to the forearm vessels while lower body training can induce generalized benefit. Increased NO bioactivity with exercise training has been readily and consistently demonstrated in subjects with cardiovascular disease and risk factors, in whom antecedent endothelial dysfunction exists. These conditions may all be associated with increased oxygen free radicals which impact on NO synthase activity and with which NO reacts; repeated exercise and shear stress stimulation of NO bioactivity redresses this radical imbalance, hence leading to greater potential for autacoid bioavailability. Recent human studies also indicate that exercise training may improve endothelial function by up‐regulating eNOS protein expression and phosphorylation. While improvement in NO vasodilator function has been less frequently found in healthy subjects, a higher level of training may lead to improvement. Regarding time course, studies indicate that short‐term training increases NO bioactivity, which acts to homeostatically regulate the shear stress associated with exercise. Whilst the increase in NO bioactivity dissipates within weeks of training cessation, studies also indicate that if exercise is maintained, the short‐term functional adaptation is succeeded by NO‐dependent structural changes, leading to arterial remodelling and structural normalization of shear. Given the strong prognostic links between vascular structure, function and cardiovascular events, the implications of these findings are obvious, yet many unanswered questions remain, not only concerning the mechanisms responsible for NO bioactivity, the nature of the cellular effect and relevance of other autacoids, but also such practical questions as the optimal intensity, modality and volume of exercise training required in different populations.

Impact of inactivity and exercise on the vasculature in humans

The effects of inactivity and exercise training on established and novel cardiovascular risk factors are relatively modest and do not account for the impact of inactivity and exercise on vascular risk. We examine evidence that inactivity and exercise have direct effects on both vasculature function and structure in humans. Physical deconditioning is associated with enhanced vasoconstrictor tone and has profound and rapid effects on arterial remodelling in both large and smaller arteries. Evidence for an effect of deconditioning on vasodilator function is less consistent. Studies of the impact of exercise training suggest that both functional and structural remodelling adaptations occur and that the magnitude and time-course of these changes depends upon training duration and intensity and the vessel beds involved. Inactivity and exercise have direct “vascular deconditioning and conditioning” effects which likely modify cardiovascular risk.

Exercise training, vascular function, and functional capacity in middle-aged subjects

PURPOSE The aim of this study was to investigate the effect of 8 wk of exercise training on functional capacity, muscular strength, body composition, and vascular function in sedentary but healthy subjects by using a randomized, crossover protocol. METHODS After familiarization sessions, 19 subjects aged 47 +/- 2 yr (mean +/- SE) undertook a randomized, crossover design study of the effect of 8 wk of supervised circuit training consisting of combined aerobic and resistance exercise. Peak oxygen uptake (.VO(2peak)), sum of 7 maximal voluntary contractions and the sum of 8 skinfolds and 5 segment girths were determined at entry, crossover, and 16 wk. Endothelium-dependent and -independent vascular function were determined by forearm strain-gauge plethysmography and intrabrachial infusions of acetylcholine (ACh) and sodium nitroprusside (SNP) in 16 subjects. RESULTS Training did not alter ACh or SNP responses. .VO(2peak), (28.6 +/- 1.1 to 32.6 +/- 1.3 mL.kg(-1).min(-1), P < 0.001), exercise test duration (17.4 +/- 1.1 to 22.1 +/- 1.2 min, P < 0.001), and muscular strength (465 +/- 27 to 535 +/- 27 kg, P < 0.001) significantly increased after the exercise program, whereas skinfolds decreased (144 +/- 10 vs 134 +/- 9 mm, P < 0.001). CONCLUSION These results suggest that moderate intensity circuit training designed to minimize the involvement of the arms improves functional capacity, body composition, and strength in healthy, middle-aged subjects without significantly influencing upper limb vascular function. This finding contrasts with previous studies in subjects with type 2 diabetes and heart failure that employed an identical training program.

The Impact of Exercise Training on Conduit Artery Wall Thickness and Remodeling in Chronic Heart Failure Patients

Exercise training is an important adjunct to medical therapy in chronic heart failure, but the extent to which exercise impacts on conduit artery remodeling is unknown. The aim of this study was to evaluate the impact of aerobic and resistance exercise training modalities on arterial remodeling in patients with chronic heart failure. We randomized 36 untrained subjects with chronic heart failure to resistance training (58.8±3.5 years), aerobic training (61.3±2.8 years), or an untrained control group (64.4±2.4 years). Peak oxygen consumption during cycle ergometry increased after 12 weeks in both the resistance and aerobic training (P<0.001) groups, but not in controls, whereas leg strength only increased after resistance training (P<0.05). Brachial artery wall thickness decreased in the resistance training group (475±10 versus 443±13 &mgr;m; P<0.01), whereas no changes were apparent in the aerobic or control groups. Brachial diameter increased by ≈6% and ≈5% in the aerobic training and resistance training groups (P<0.01), with no change evident in the control group. The wall:lumen ratio consequently declined in the resistance training group at 12 weeks (0.121±0.004 versus 0.107±0.004; P<0.01) and increased in the control group (0.111±0.006 versus 0.121±0.009; P<0.05). No wall:lumen change was evident in the aerobic training group. Our findings suggest that exercise has a systemic impact on remodeling of conduit arteries in humans and that resistance exercise training may be advantageous in subjects with chronic heart failure in this regard.

The Effects of Two Modes of Exercise on Aerobic Fitness and Fat Mass in an Overweight Population

We examined the effects of an 8-week exercise intervention on aerobic fitness, android and gynoid fat mass, and blood lipids in overweight and obese participants. Twenty-four sedentary participants (average BMI = 30 ± 2 kg/m2; 18 females, 6 males) were randomized into either interval training and diet education (INT group), continuous aerobic exercise and diet education (CON group), or diet education only (DIET group). Durations of exercise sessions were similar (∼30 minutes), with both exercise groups completing the same amount of work. The INT and CON groups demonstrated significant improvements over time for (p < 0.01 and p < 0.05, ES = 1.1 and 1.2, respectively) and time to exhaustion on a graded exercise test (p < 0.01 and ES = 0.8 for both groups). Further, a large effect size (0.7) was recorded for the loss in android fat mass over time in the INT group only.

A CONTROLLED TRIAL OF CIRCUIT WEIGHT TRAINING ON AEROBIC CAPACITY AND MYOCARDIAL OXYGEN DEMAND IN MEN AFTER CORONARY ARTERY BYPASS SURGERY

BACKGROUND Cardiovascular benefits of resistance training in cardiac patients have been suggested but not studied in a randomized, controlled trial of circuit weight training (CWT) without an aerobic exercise component. The purpose of the current study was to examine the effects of 10 weeks of CWT on muscular strength, peak oxygen consumption (peak VO2), and myocardial oxygen demand (mVO2) in men after coronary artery bypass surgery. METHODS Twenty-six, post-coronary bypass male subjects (mean 19 months after bypass), aged 60 +/- 8.5 years, were randomly allocated to 10 weeks of CWT at 40 to 60% of maximum voluntary contraction (n = 12) or to a control group (n = 14). Muscular strength was assessed using a modified one repetition maximum technique. Peak VO2 was recorded during symptom-limited treadmill exercise. Rate pressure product, as an indirect measure of mVO2, was measured during isometric, isodynamic, and dynamic exercise. RESULTS No ischemic symptoms nor electrocardiographic changes were recorded during testing or training. Strength increased by 18% (P < 0.005) in five out of seven exercises in the training group, but was unchanged in the control group. Training did not improve peak VO2. Rate pressure product during isometric and isodynamic exercise decreased from pre- to post-testing (P < 0.05) but was equivalent to that seen in the control group. CONCLUSIONS Moderate intensity CWT is safe and can improve strength in selected low-risk patients after coronary artery bypass surgery. However, it does not significantly increase peak VO2 nor reduce mVO2 during isometric, isodynamic, and dynamic exercise.

Point:Counterpoint: Exercise training does/does not induce vascular adaptations beyond the active muscle beds

A few years ago we published a series of studies that investigated the impact of exercise training on vascular function in humans ([20][1]–[22][2], [26][3]–[29][4]). All of these studies involved a similar exercise training intervention, a combination of resistance and aerobic exercise,

Exercise & Sports Science Australia Position Statement on exercise training and chronic heart failure

Chronic heart failure (CHF) is a complex syndrome characterised by progressive decline in left ventricular function, low exercise tolerance and raised mortality and morbidity. Regular exercise participation has been shown to be a safe and effective treatment modality in the majority of CHF patients, partially reversing some of the maladaptations evident in myocardial and skeletal muscle function, and resulting in improvements in physical fitness and quality of life, and perhaps reduced mortality. The volume and intensity of exercise that is recommended depends on the syndrome severity, however in most patients it should consist of a combination of low-to-moderate intensity aerobic (endurance) exercise on most days of the week and individually prescribed low-to-moderate intensity resistance (strength) training at least twice per week. Additionally, all patients should be closely monitored prior to and during exercise for contraindications by an appropriately trained health professional. The purpose of this statement is to inform and guide exercise practitioners and health professionals in the safe and effective prescription and supervision of exercise for patients with CHF.

Exercise training and artery function in humans: nonresponse and its relationship to cardiovascular risk factors

The objectives of our study were to examine 1) the proportion of responders and nonresponders to exercise training in terms of vascular function; 2) a priori factors related to exercise training-induced changes in conduit artery function, and 3) the contribution of traditional cardiovascular risk factors to exercise-induced changes in artery function. We pooled data from our laboratories involving 182 subjects who underwent supervised, large-muscle group, endurance-type exercise training interventions with pre-/posttraining measures of flow-mediated dilation (FMD%) to assess artery function. All studies adopted an identical FMD protocol (5-min ischemia, distal cuff inflation), contemporary echo-Doppler methodology, and observer-independent automated analysis. Linear regression analysis was used to identify factors contributing to changes in FMD%. We found that cardiopulmonary fitness improved, and weight, body mass index (BMI), cholesterol, and mean arterial pressure (MAP) decreased after training, while FMD% increased in 76% of subjects (P < 0.001). Training-induced increase in FMD% was predicted by lower body weight (β = -0.212), lower baseline FMD% (β = -0.469), lower training frequency (β = -0.256), and longer training duration (β = 0.367) (combined: P < 0.001, r = 0.63). With the exception of a modest correlation with total cholesterol (r = -0.243, P < 0.01), changes in traditional cardiovascular risk factors were not significantly related to changes in FMD% (P > 0.05). In conclusion, we found that, while some subjects do not demonstrate increases following exercise training, improvement in FMD% is present in those with lower pretraining body weight and endothelial function. Moreover, exercise training-induced change in FMD% did not correlate with changes in traditional cardiovascular risk factors, indicating that some cardioprotective effects of exercise training are independent of improvement in risk factors.

Achieving coordinated secondary prevention of coronary heart disease for all in need (SPAN)

Effective disease management after an acute coronary event is essential, but infrequently implemented, due to challenges around the research evidence and its translation. Policy-makers, health professionals and researchers are confronted by the need for increased services, to improve access and equity, but often with finite and reducing resources. There is a clear need to develop innovative ways of delivering ongoing preventative care to the vast and increasing population with coronary disease. However, translation into clinical practice is becoming increasingly difficult while the volume of trial and review evidence of disparate models of delivery expands. Indeed, the prevention literature has evolved into a complex web of differing models offered to diverse patient populations in an array of settings. We describe a united organisation of care that aims to facilitate coordinated secondary prevention for all in need (SPAN). SPAN is inherently flexible yet provides a minimum level of health service standardisation. It can be delivered across any area health service regardless of a patients age, gender, ethnicity, geographical location, or socioeconomic status. Importantly, the setting, communication technologies and components of each patients care are governed and woven into continuing care provided by the family physician in concert with a cardiac care facilitator.