SUMMARY Hypertension (HTN), one of the most common medical disorders, is associated with an increased incidence of all-cause and cardiovascular disease (CVD) mortality. Lifestyle modifications are advocated for the prevention, treatment, and control of HTN, with exercise being an integral component. Exercise programs that primarily involve endurance activity prevent the development of HTN and lower blood pressure (BP) in adults with normal BP and those with HTN. The BP lowering effects of exercise are most pronounced in people with HTN who engage in endurance exercise with BP decreasing approximately 5–7 mm Hg after an isolated exercise session (acute) or following exercise training (chronic). Moreover, BP is reduced for up to 22 h after an endurance exercise bout (e.g., postexercise hypotension), with the greatest decreases among those with the highest baseline BP. The proposed mechanisms for the BP lowering effects of exercise include neurohumoral, vascular, and structural adaptations. Decreases in catecholamines and total peripheral resistance, improved insulin sensitivity, and alterations in vasodilators and vasoconstrictors are some of the postulated explanations for the antihypertensive effects of exercise. Emerging data suggest genetic links to the BP reductions associated with acute and chronic endurance exercise. Nonetheless, definitive conclusions regarding the mechanisms for the BP reductions following endurance exercise cannot be made at this time. Individuals with controlled HTN and no CVD or renal complications may participate in an exercise program or competitive athletics, but should be evaluated, treated, and monitored closely. Preliminary peak or symptom-limited exercise testing may be warranted, especially for men over 45 and women over 55 yr planning a vigorous exercise program (i.e., 60% u VO2R, oxygen uptake reserve). In the interim, while formal evaluation and management are taking place, it is reasonable for the majority of patients to begin moderate intensity exercise training (40 –60% u VO2R) such as walking. When pharmacologic therapy is indicated in physically active people it should, ideally: a) lower BP at rest and during exertion; b) decrease total peripheral resistance; and, c) not adversely affect exercise capacity. For these reasons, angiotensin converting enzyme (ACE) inhibitors (or angiotensin II receptor blockers in case of ACE inhibitor intolerance) and calcium channel blockers are currently the drugs of choice for recreational exercisers and athletes who have HTN. Exercise remains a cornerstone therapy for the primary prevention, treatment, and control of HTN. The optimal training frequency, intensity, time, and type (FITT) need to be better defined to optimize the BP lowering capacities of exercise, particularly in children, women, older adults, and

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Exercise and Hypertension

Purpose Physical activity has been associated with reduced blood pressure in observational epidemiologic studies and individual clinical trials. This meta-analysis of randomized, controlled trials was conducted to determine the effect of aerobic exercise on blood pressure. Data sources English-language articles published before September 2001. Study selection 54 randomized, controlled trials (2419 participants) whose intervention and control groups differed only in aerobic exercise. Data extraction Using a standardized protocol and data extraction form, three of the investigators independently abstracted data on study design, sample size, participant characteristics, type of intervention, follow-up duration, and treatment outcomes. Data synthesis In a random-effects model, data from each trial were pooled and weighted by the inverse of the total variance. Aerobic exercise was associated with a significant reduction in mean systolic and diastolic blood pressure (-3.84 mm Hg [95% CI, -4.97 to -2.72 mm Hg] and -2.58 mm Hg [CI, -3.35 to -1.81 mm Hg], respectively). A reduction in blood pressure was associated with aerobic exercise in hypertensive participants and normotensive participants and in overweight participants and normal-weight participants. Conclusions Aerobic exercise reduces blood pressure in both hypertensive and normotensive persons. An increase in aerobic physical activity should be considered an important component of lifestyle modification for prevention and treatment of high blood pressure.

Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials.

Stress-induced immunological reactions to exercise have stimulated much research into stress immunology and neuroimmunology. It is suggested that exercise can be employed as a model of temporary immunosuppression that occurs after severe physical stress. The exercise-stress model can be easily manipulated experimentally and allows for the study of interactions between the nervous, the endocrine, and the immune systems. This review focuses on mechanisms underlying exercise-induced immune changes such as neuroendocrinological factors including catecholamines, growth hormone, cortisol, β-endorphin, and sex steroids. The contribution of a metabolic link between skeletal muscles and the lymphoid system is also reviewed. The mechanisms of exercise-associated muscle damage and the initiation of the inflammatory cytokine cascade are discussed. Given that exercise modulates the immune system in healthy individuals, considerations of the clinical ramifications of exercise in the prevention of diseases for which the...

Exercise and the Immune System: Regulation, Integration, and Adaptation

Exercise reduces blood pressure in both hypertensive and normotensive persons. An increase in aerobic physical activity should be considered an important component of lifestyle modification for pre...

Effect of Aerobic Exercise on Blood Pressure

Considerable knowledge has accumulated in recent decades concerning the significance of physical activity in the treatment of a number of diseases, including diseases that do not primarily manifest as disorders of the locomotive apparatus. In this review we present the evidence for prescribing exercise therapy in the treatment of metabolic syndrome-related disorders (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, obesity), heart and pulmonary diseases (chronic obstructive pulmonary disease, coronary heart disease, chronic heart failure, intermittent claudication), muscle, bone and joint diseases (osteoarthritis, rheumatoid arthritis, osteoporosis, fibromyalgia, chronic fatigue syndrome) and cancer, depression, asthma and type 1 diabetes. For each disease, we review the effect of exercise therapy on disease pathogenesis, on symptoms specific to the diagnosis, on physical fitness or strength and on quality of life. The possible mechanisms of action are briefly examined and the principles for prescribing exercise therapy are discussed, focusing on the type and amount of exercise and possible contraindications.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-0838.2006.00520.x

Evidence for prescribing exercise as therapy in chronic disease.

Sleep loss is common in patients with respiratory disorders. To determine whether sleep loss affects respiratory muscle function, we compared respiratory muscle and pulmonary functions after normal sleep with those measured after a 30-h sleepless period in 30 normal male subjects. The respiratory muscle strength was estimated by the maximal static inspiratory and expiratory pressures. Inspiratory muscle endurance was determined by the product of pressure load and the sustained time, i.e., pressure-time index, while the subject breathed against an inspiratory pressure load on a modified Nickerson-Keens device. We found that inspiratory muscle endurance was decremented from 871 ± 61 to 638 ± 69 cm H2O·min after sleep deprivation. Twelve-second maximal voluntary ventilation was also significantly reduced after sleep loss. Nevertheless, the respiratory muscle strength, FEV1 and FVC were unaltered. We therefore conclude that inspiratory muscle endurance may deteriorate after a 30-h sleep loss.

Sleep loss impairs inspiratory muscle endurance.

Wang, Jong-Shyan, Chauying J. Jen, and Hsiun-Ing Chen.Effects of chronic exercise and deconditioning on platelet function in women. J. Appl. Physiol.83(6): 2080–2085, 1997.—To investigate the effec...

Effects of chronic exercise and deconditioning on platelet function in women

To investigate the effects of inspiratory muscle resistive loading training (IMT) on exercise performance in chronic obstructive pulmonary disease (COPD), 13 patients undergoing standard pulmonary rehabilitation were divided into control (n = 6) and experimental (n = 7) groups. Prior to training, we measured inspiratory muscle strength and endurance, resting pulmonary function, and exercise performance on a bicycle ergometer (a progressive test and an endurance test at two thirds of maximal work load). We then determined their resistive loads for training by measuring their 10-min maximal sustainable resistance. Training by patients in the experimental group involved inspiring against a predetermined resistive load. The control subjects breathed through a sham training tube, so that studies were performed in double-blind fashion. The training consisted of 15-min sessions twice daily for 4 wk. The IMT dramatically improved inspiratory muscle endurance--represented as either sustainable inspiratory pressure (SIP) or endurance time at 60% of maximal inspiratory mouth pressure (Pimmax) at functional residual capacity. The SIP of the trained group increased from 29 +/- 11 to 46 +/- 11% of Pimmax (p less than 0.005). Training slightly increased inspiratory muscle strength (p less than 0.05), as determined by Pimmax. In contrast, resting pulmonary function and performance of both progressive and constant-load exercise remained unchanged. We conclude that 4-wk IMT in a pulmonary rehabilitation setting improves inspiratory muscle endurance in patients with COPD without changing pulmonary function or exercise performance.

Inspiratory muscle training in patients with chronic obstructive pulmonary disease.

Although increased ventilation is one of the most readily observed physiological responses to exercise, it is uncertain how severely this hyperpnea stresses the ventilatory muscles. As one approach to this question, we compared short-term maximal running performance in nine subjects with and without prior ventilatory work designed to reduce ventilatory muscle endurance. This work consisted of 150 min of sustained maximum ventilation performed isocapnically while the subjects were seated. Both the level of sustained expired minute ventilation and the O2 uptake associated with it slowly declined with time during this 150-min period. On the average, subjects were able to maintain two-thirds of their 12-s maximum voluntary ventilation (MVV) during this long-term breathing test. The test had no effect on subsequently measured vital capacity, forced expiratory volume in 1 s, or the MVV. However, in short-term maximal running, at constant speed upgrades increased 1% each minute until volitional exhaustion, performance after prior breathing work was reduced as compared with control (6.5 vs. 7.6 min; P less than 0.01). Subjects ceased work at significantly lower ventilation (117 vs. 124 1.min-1 BTPS; P less than 0.05) and heart rate (179 vs. 187 beats.min-1; P less than 0.01) and reached significantly lower peak O2 uptake (3.07 vs. 3.24 1.min-1 STPD; P less than 0.05) during maximal running after ventilatory work. We conclude that reduced ventilatory muscle endurance alone is sufficient to decrease short-term maximal running performance.

Exercise performance after ventilatory work

To determine whether sleep is necessary for the peripheral sympathetic nervous system response to exercise, we compared eight subjects' sympathoadrenal responses to treadmill walking at a constant exercise rate eliciting a heart rate around 160 beats X min-1 after normal sleep with those measured after a 50-h sleepless period. We found that sleeplessness left the sympathetic response to exercise intact. After 12 min of exercise, heart rate and plasma norepinephrine, epinephrine, and dopamine levels were similar in both situations. In addition, we could find no other alterations in the physiological response to exercise after sleep loss, and minute ventilation, oxygen uptake, blood lactate levels, and rectal and skin temperatures were identical in the two conditions. Nevertheless, despite both unaltered physiological responses to exercise and doubled monetary incentives to perform, sleep loss reduced time to exhaustion by 20% (P less than 0.01). We concluded that sleep loss does not diminish the peripheral sympathetic nervous system response to exercise, although it reduces exercise tolerance through mechanisms that are unexplained as yet.

Hsiun-Ing Chen

Papers

Sleep loss impairs inspiratory muscle endurance.

Effects of chronic exercise and deconditioning on platelet function in women

Inspiratory muscle training in patients with chronic obstructive pulmonary disease.

Exercise performance after ventilatory work

Sleep loss and the sympathoadrenal response to exercise.