BACKGROUND\nIncreased physical activity is related to reduced risk of cardiovascular disease, possibly because it leads to improvement in the lipoprotein profile. However, the amount of exercise training required for optimal benefit is unknown. In a prospective, randomized study, we investigated the effects of the amount and intensity of exercise on lipoproteins.\n\n\nMETHODS\nA total of 111 sedentary, overweight men and women with mild-to-moderate dyslipidemia were randomly assigned to participate for six months in a control group or for approximately eight months in one of three exercise groups: high-amount-high-intensity exercise, the caloric equivalent of jogging 20 mi (32.0 km) per week at 65 to 80 percent of peak oxygen consumption; low-amount-high-intensity exercise, the equivalent of jogging 12 mi (19.2 km) per week at 65 to 80 percent of peak oxygen consumption; or low-amount-moderate-intensity exercise, the equivalent of walking 12 mi per week at 40 to 55 percent of peak oxygen consumption. Subjects were encouraged to maintain their base-line body weight. The 84 subjects who complied with these guidelines served as the basis for the main analysis. Detailed lipoprotein profiling was performed by nuclear magnetic resonance spectroscopy with verification by measurement of cholesterol in lipoprotein subfractions.\n\n\nRESULTS\nThere was a beneficial effect of exercise on a variety of lipid and lipoprotein variables, seen most clearly with the high amount of high-intensity exercise. The high amount of exercise resulted in greater improvements than did the lower amounts of exercise (in 10 of 11 lipoprotein variables) and was always superior to the control condition (11 of 11 variables). Both lower-amount exercise groups always had better responses than the control group (22 of 22 comparisons).\n\n\nCONCLUSIONS\nThe highest amount of weekly exercise, with minimal weight change, had widespread beneficial effects on the lipoprotein profile. The improvements were related to the amount of activity and not to the intensity of exercise or improvement in fitness.

Effects of the amount and intensity of exercise on plasma lipoproteins: Editor's comments

Much has been published in the past 20 years on the use of measurements of arterial stiffness in animal and human research studies. This summary statement was commissioned by the American Heart Association to address issues concerning the nomenclature, methodologies, utility, limitations, and gaps in knowledge in this rapidly evolving field. The following represents an executive version of the larger online-only Data Supplement and is intended to give the reader a sense of why arterial stiffness is important, how it is measured, the situations in which it has been useful, its limitations, and questions that remain to be addressed in this field. Throughout the document, pulse-wave velocity (PWV; measured in meters per second) and variations such as carotid-femoral PWV (cfPWV; measured in meters per second) are used. PWV without modification is used in the general sense of arterial stiffness. The addition of lowercase modifiers such as “cf” is used when speaking of specific segments of the arterial circulation.

The ability to measure arterial stiffness has been present for many years, but the measurement was invasive in the early times. The improvement in technologies to enable repeated, minimal-risk, reproducible measures of this aspect of circulatory physiology led to its incorporation into longitudinal cohort studies spanning a variety of clinical populations, including those at extreme cardiovascular risk (patients on dialysis), those with comorbidities such as diabetes mellitus (DM) and hypertension, healthy elders, and general populations.

In the ≈3 decades of clinical use of PWV measures in humans, we have learned much about the importance of this parameter. PWV has proven to have independent predictive utility when evaluated in conjunction with standard risk factors for death and cardiovascular disease (CVD). However, the field of arterial stiffness investigation, which has exploded over the past 20 years, has proliferated without logistical guidance for clinical and …

Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness: A Scientific Statement From the American Heart Association

In the natural habitat of our ancestors, physical activity was not a preventive intervention but a matter of survival. In this hostile environment with scarce food and ubiquitous dangers, human genes were selected to optimize aerobic metabolic pathways and conserve energy for potential future famines.1 Cardiac and vascular functions were continuously challenged by intermittent bouts of high-intensity physical activity and adapted to meet the metabolic demands of the working skeletal muscle under these conditions.

When speaking about molecular cardiovascular effects of exercise, we should keep in mind that most of the changes from baseline are probably a return to normal values. The statistical average of physical activity in Western societies is so much below the levels normal for our genetic background that sedentary lifestyle in combination with excess food intake has surpassed smoking as the No. 1 preventable cause of death in the United States.2

Physical activity has been shown to have beneficial effects on glucose metabolism, skeletal muscle function, ventilator muscle strength, bone stability, locomotor coordination, psychological well-being, and other organ functions. However, in the context of this review, we will focus entirely on important molecular effects on the cardiovascular system. The aim of this review is to provide a bird's-eye view on what is known and unknown about the physiological and biochemical mechanisms involved in mediating exercise-induced cardiovascular effects. The resulting map is surprisingly detailed in some areas (ie, endothelial function), whereas other areas, such as direct cardiac training effects in heart failure, are still incompletely understood.

For practical purposes, we have decided to use primarily an anatomic approach to present key data on exercise effects on cardiac and vascular function. For the cardiac effects, the left ventricle and the cardiac valves will be described separately; for the vascular effects, we will follow the arterial vascular …

Cardiovascular Effects of Exercise Training Molecular Mechanisms

Endurance training decreases resting and submaximal heart rate, while maximum heart rate may decrease slightly or remain unchanged after training. The effect of endurance training on various indices of heart rate variability remains inconclusive. This may be due to the use of inconsistent analysis methodologies and different training programmes that make it difficult to compare the results of various studies and thus reach a consensus on the specific training effects on heart rate variability. Heart rate recovery after exercise involves a coordinated interaction of parasympathetic re-activation and sympathetic withdrawal. It has been shown that a delayed heart rate recovery is a strong predictor of mortality. Conversely, endurance-trained athletes have an accelerated heart rate recovery after exercise. Since the autonomic nervous system is interlinked with many other physiological systems, the responsiveness of the autonomic nervous system in maintaining homeostasis may provide useful information about the functional adaptations of the body. This review investigates the potential of using heart rate recovery as a measure of training-induced disturbances in autonomic control, which may provide useful information for training prescription.

Autonomic control of heart rate during and after exercise : measurements and implications for monitoring training status.

Epidemiological evidence indicates that regular physical activity and/or frequent structured exercise reduces the incidence of many chronic diseases in older age, including communicable diseases such as viral and bacterial infections, as well as non-communicable diseases such as cancer and chronic inflammatory disorders. Despite the apparent health benefits achieved by leading an active lifestyle, which imply that regular physical activity and frequent exercise enhance immune competency and regulation, the effect of a single bout of exercise on immune function remains a controversial topic. Indeed, to this day, it is perceived by many that vigorous exercise can temporarily suppress immune function. In the first part of this review, we deconstruct the key pillars which lay the foundation to this theory – referred to as the ‘open window’ hypothesis – and highlight that: (i) limited reliable evidence exists to support the claim that vigorous exercise heightens risk of opportunistic infections; (ii) purported changes to mucosal immunity, namely salivary IgA levels, after exercise do not signpost a period of immune suppression; and (iii) the dramatic reductions to lymphocyte numbers and function 1-2 hours after exercise reflects a transient and time-dependent redistribution of immune cells to peripheral tissues, resulting in a heightened state of immune surveillance and immune regulation, as opposed to immune suppression. In the second part of this review, we provide evidence that frequent exercise enhances – rather than suppresses – immune competency, and highlight key findings from human vaccination studies which show heightened responses to bacterial and viral antigens following bouts of exercise. Finally, in the third part of this review, we highlight that regular physical activity and frequent exercise might limit or delay ageing of the immune system, providing further evidence that exercise is beneficial for immunological health. In summary, the over-arching aim of this review is to rebalance opinion over the perceived relationships between exercise and immune function. We emphasise that it is a misconception to label any form of acute exercise as immunosuppressive, and, instead, exercise most likely improves immune competency across the lifespan.

/pdf/debunking-the-myth-of-exercise-induced-immune-suppression-19hrdk2kt9.pdf

Debunking the Myth of Exercise-induced Immune Suppression: Redefining the Impact of Exercise on Immunological Health Across the Lifespan.

Arterial stiffness is higher in strength-trained humans and lower in endurance-trained humans. However, the mechanisms underlying these different adaptations are unclear. Vascular endothelium-derived factors, such as endothelin-1 (ET-1) and nitric oxide (NO), play an important role in the regulation of vascular tonus. We hypothesized that endogenous ET-1 and NO participate in the adaptation of arterial stiffness in different types of exercise training. The purpose of this study was to investigate plasma ET-1 and NO concentrations and arterial stiffness in strength- and endurance-trained men. Young strength-trained athletes (SA; n = 11), endurance-trained athletes (EA; n = 12), and sedentary control men (C; n = 12) participated in this study. Maximal handgrip strength in SA and maximal oxygen uptake in EA were markedly greater than in C. Aortic pulse-wave velocity, which is an established index of arterial stiffness, was higher in SA and lower in EA than in C. Additionally, we measured systemic arterial compliance (SAC) using carotid artery applanation tonometry and Doppler echocardiography, because arterial stiffness is a primary determinant of the compliance. SAC was lower in SA and higher in EA compared with that in C. Plasma ET-1 concentrations were higher in SA compared with C and EA. We did not find significant differences in plasma NO concentrations (measured as the stable end product of NO, i.e., nitrite/nitrate). The relationships of plasma ET-1 concentrations to aortic pulse-wave velocity and SAC were linear. These results suggest that differences in endogenous ET-1 may partly participate in the mechanism underlying different adaptations of arterial stiffness in strength- and endurance-trained men.

Vascular endothelium-derived factors and arterial stiffness in strength- and endurance-trained men.

Fibroblast growth factor 21, a metabolic regulator, plays roles in lipolysis and glucose uptake in adipose tissues and skeletal muscles. Its expression in skeletal muscle is upregulated upon activation of the phosphatidylinositol 3‐kinase/Akt signaling pathway, which is induced by exercise and muscle contraction. We examined the increase of fibroblast growth factor 21 after acute exercise in metabolic organs, especially skeletal muscles and circulation. Participants exercised on bicycle ergometers for 60 min at 75% of their V ˙ O 2 max. Venous blood samples were taken before exercise and immediately after exercise. In an animal study, male ICR mice were divided into sedentary and exercise groups. Mice in the exercise group performed treadmill exercises at 30 m min −1 for 60 min. Shortly thereafter, blood, liver, and skeletal muscle samples were taken from mice. Acute exercise induced the increase of serum fibroblast growth factor 21 in both humans and mice, and increased fibroblast growth factor 21 expression in the skeletal muscles and the liver of mice. Acute exercise activated Akt in mice skeletal muscle. Acute exercise increases fibroblast growth factor 21 concentrations in both serum and metabolic organs. Moreover, results show that acute exercise increased the expression of fibroblast growth factor 21 in skeletal muscle, accompanied by the phosphorylation of Akt in mice.

https://physoc.onlinelibrary.wiley.com/doi/epdf/10.14814/phy2.12828

Acute exercise increases fibroblast growth factor 21 in metabolic organs and circulation.

Relationship Between Arterial Stiffness and Athletic Training Programs in Young Adult Men

Intensive physical exercise may cause muscular injury and increase oxidative stress. The purpose of this study was to examine the effect of an antioxidant, coenzyme Q10 (CoQ10), on muscular injury and oxidative stress during exercise training. Eighteen male students, all elite Japanese kendo athletes, were randomly assigned to either a CoQ10 group (n 10) or a placebo group (n 8) in a double-blind manner. Subjects in the CoQ10 group took 300 mg CoQ10 per d for 20 d, while subjects in the placebo group took the same dosage of a placebo. All subjects practised kendo 5.5 h per d for 6 d during the experimental period. Blood samples were taken 2 weeks before, during (1 d, 3 d, 5 d) and 1 week after the training. Serum creatine kinase (CK) activity and myoglobin (Mb) concentration significantly increased in both groups (at 3 d and 5 d). Serum CK (at 3 d), Mb (at 3 d) and lipid peroxide (at 3 d and 5 d) of the CoQ10 group were lower than those of the placebo group. The leucocyte counts in the placebo group significantly increased (at 3 d) and neutrophils significantly increased in both groups (at 3 d and 5 d). Serum scavenging activity against superoxide anion did not change in either group. These results indicate that CoQ10 supplementation reduced exercise-induced muscular injury in athletes.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0007114508926544

Reducing exercise-induced muscular injury in kendo athletes with supplementation of coenzyme Q10.

The left ventricle morphologically adapts to endurance exercise training (eccentric cardiac remodeling) and strength exercise training (concentric remodeling). In addition, the acceleration of vagally mediated heart rate (HR) recovery after exercise is one of the functional adaptations of the heart in endurance-trained humans. However, the effect of strength training on HR recovery is unclear.

Purpose: The purpose of this study was to investigate whether postexercise HR recovery accelerates in strength-trained athletes.

Methods: Subjects were young strength-trained athletes (ST; N = 12), endurance-trained athletes (ET; N = 12), and age-matched sedentary control men (C; N = 12). HR and oxygen uptake were measured during submaximal exercise (cycling exercise, 40% maximal oxygen uptake for 8 min) and 30 s after the exercise (the postexercise period).

Results: Left ventricular end-diastolic dimension was higher in both types of athletes compared with C, but greater in ET than in ST (C, 4.3 ± 0.1 cm; ET, 5.0 ± 0.1 cm; ST, 4.8 ± 0.1 cm). Left ventricular average wall thickness was greater in ST in comparison with ET, although it was higher in both trained men compared with C (C, 0.85 ± 0.02 cm; ET, 0.90 ± 0.02 cm; ST, 1.00 ± 0.02 cm). The time constant of postexercise HR decay, an index of vagally mediated postexercise HR recovery, was lower in ST and ET compared with C (C, 94.4 ± 9.2 s; ET, 65.9 ± 4.3 s; ST, 69.1 ± 4.0 s). Oxygen pulse was greater in ST and ET than in C (C, 9.4 ± 0.6 mL per beat; ET, 13.0 ± 0.9 mL per beat; ST, 12.8 ± 0.4 mL per beat), and it results in increased oxygen debt for both types of athletes (C, 0.257 ± 0.024 L; ET, 0.343 ± 0.030 L; ST, 0.331 ± 0.017 L). We did not find significant differences in these indices between ST and ET.

Conclusions: These results suggest that the HR recovery immediately after exercise is accelerated in both strength- and endurance-trained athletes

Yuko Tanimura

Papers

Vascular endothelium-derived factors and arterial stiffness in strength- and endurance-trained men.

Acute exercise increases fibroblast growth factor 21 in metabolic organs and circulation.

Relationship Between Arterial Stiffness and Athletic Training Programs in Young Adult Men

Reducing exercise-induced muscular injury in kendo athletes with supplementation of coenzyme Q10.

Postexercise heart rate recovery accelerates in strength-trained athletes.