effects of detraining on cardiovascular responses to exercise: role of blood volume edward f. coyle,...

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Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol. 60(l): 95-99, 1986. Large decline in SV during upright exercise after only 12 days of inactivity and little further decline in SV occurs after 3 mo of inactivity. VO 2 max was determined, and cardiac output was measured during upright cycling at 50-60% VO 2 max in eight endurance-trained men before and after 2-4 wk of inactivity. Detraining produced a 9% decline in blood volume (5,177 to 4,692). SV was reduced by 12% (P < 0.05) and VO 2 max declined 6% (P < 0.01); heart rate (HR) and total peripheral resistance (TPR) during submaximal exercise were increased 11% (P < 0.01) and 8% (P < 0.05). When blood volume was expanded to a similar absolute level (5,500 ± 200 ml) by 6% dextran in saline, the effects of detraining on cardiovascular response were reversed. SV and VO 2 max were increased (P < 0.05) by PV expansion in the detrained state

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Page 1: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Effects of detraining on cardiovascular responses to exercise: role of blood volumeEDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGANJ. Appl. Physiol. 60(l): 95-99, 1986.

Large decline in SV during upright exercise after only 12 days of inactivity and little further

decline in SV occurs after 3 mo of inactivity. VO2 max was determined, and cardiac output was

measured during upright cycling at 50-60% VO2 max in eight endurance-trained men before and

after 2-4 wk of inactivity. Detraining produced a 9% decline in blood volume (5,177 to 4,692). SV

was reduced by 12% (P < 0.05) and VO2 max declined 6% (P < 0.01); heart rate (HR) and total

peripheral resistance (TPR) during submaximal exercise were increased 11% (P < 0.01) and 8% (P

< 0.05). When blood volume was expanded to a similar absolute level (5,500 ± 200 ml) by 6%

dextran in saline, the effects of detraining on cardiovascular response were reversed. SV and

VO2 max were increased (P < 0.05) by PV expansion in the detrained state to within 2-4% of

trained values. Additionally, HR and TPR during submaximal exercise were lowered to near

trained values. These findings indicate that the decline in cardiovascular function following a

few weeks of detraining is largely due to a reduction in blood volume, which appears to

limit ventricular filling during upright exercise.

Page 2: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Effect of Aerobic Exercise on Blood Pressure: A Meta-Analysis of Randomized, Controlled TrialsSeamus P. Whelton; Ashley Chin, MPH, MA; Xue Xin, MD, MS; and Jiang He, MD, PhDAnn Intern Med. 2002;136:493-503.

Page 3: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

This meta-analysis is a comprehensive examination of the effect of aerobic exercise on blood

pressure and is based on randomized, controlled clinical trials. Our meta-analysis included 54

clinical trials that involved 2419 participants and were conducted in a wide range of geographic

regions and ethnic populations. Our study showed that aerobic exercise has an impressive blood

pressure–lowering effect: 3.84 mm Hg for systolic blood pressure and 2.58 mm Hg for diastolic

blood pressure. It is important to distinguish between the individual and public health

implications of our findings. The blood pressure reduction that we observed may be of

moderate interest to practitioners treating individual patients. However, a small decrease in the

population’s average blood pressure level should dramatically reduce incidence of and death

from cardiovascular disease in communities. All forms of exercise seem to be effective in

reducing blood pressure. Aerobic exercise reduces insulin resistance and insulin levels in

hypertensive patients. Change in blood pressure during exercise is strongly associated with

reduction in serum concentrations of total cholesterol and insulin resistance.

Page 4: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Effects of Aging, Sex, and Physical Training on Cardiovascular Responses to ExerciseTakeshi Ogawa, MD; Robert J. Spina, PhD; Wade H. Martin III, MD; Wendy M. Kohrt, PhD;Kenneth B. Schechtman, PhD; John O. Holloszy, MD; and Ali A. Ehsani, MD(Circulation 1992;86:494-503)

To investigate the mechanism of the age-related decline in exercise capacity, we measured

oxygen uptake, cardiac output, heart rate, and other cardiovascular responses to submaximal

and maximal treadmill exercise in healthy sedentary and endurance exercise-trained younger

and older men and women. We estimated fat-free mass in the same individuals from

measurements of body weight and density. Our findings provide evidence that the decline in

VO2max with age is related primarily to a lower maximal cardiac output. Although a slower

maximal heart rate accounts for a portion of this effect, a smaller stroke volume is of greater

importance. Differences in VO2max between 25- and 65-year-old sedentary subjects of the same

sex are approximately 40%. (10% per decade). After normalization of results to fat-free mass,

however, VO2max , maximal cardiac output, and stroke volume were an average of 24%, 17%,

and 8% lower, respectively, in older than in younger individuals.

Page 5: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

The smaller stroke volume observed in older subjects at maximal exercise was associated with a

higher mean blood pressure in women and sedentary men. For these groups, stroke work in the

older subjects was equal to or greater than that in younger individuals. Stroke volume and

cardiac output at maximal exercise were lower in women than in men, even after normalization

to weight. Normalization of results to fat-free mass eliminated the sex difference entirely in

sedentary subjects and substantially reduced it in trained individuals. Thus, the sex difference is

largely a result of the greater percentage of body fat in women. However, there were sex

differences in mechanisms by which exercise capacity was enhanced in conditioned versus

sedentary subjects. Training status had a larger effect on stroke volume and maximal cardiac

output but a smaller effect on maximal arteriovenous oxygen difference in men than in women.

Sex differences in the nature and magnitude of adaptations to training were particularly evident

in older subjects.

Page 6: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Exercise as Cardiovascular TherapyRoy J. Shephard, MD, PhD, DPE; Gary J. Balady, MDCirculation 1999;99;963-972

Possible Biological Mechanisms for Exercise-Induced Reductions in All-Cause and Cardiac MortalityCardiovascular influencesReduction of resting and exercise heart rateReduction of resting and exercise blood pressureReduction of myocardial oxygen demand at submaximal levels of physical activityExpansion of plasma volumeIncrease in myocardial contractilityIncrease in peripheral venous toneFavorable changes in fibrinolytic systemIncreased endothelium-dependent vasodilatationIncreased gene expression for nitric oxide synthaseEnhanced parasympathetic tonePossible increases in coronary blood flow, coronary collateral vessels, and myocardial capillary density

Page 7: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Metabolic influencesReduction of obesityEnhanced glucose toleranceImproved lipid profile

Lifestyle influencesDecreased likelihood of smokingPossible reduction of stressShort-term reduction of appetite

Page 8: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Does Exercise Reduce Inflammation? Physical Activity and C-Reactive ProteinAmong U.S. AdultsEarl S. FordEPIDEMIOLOGY September 2002, Vol. 13 No. 5

In conclusion, the results of this study showed that physical activity is inversely associated with

C-reactive protein concentrations, suggesting that physical activity may mitigate inflammation.

Research to delineate the exact mechanisms through which physical activity influences

the inflammatory process will help improve our understanding of some of the benefits of

physical activity.

Furthermore, additional research concerning the relation of the intensity, duration, and type of

physical activity with inflammation could yield additional insights into how physical activity

might influence inflammation.

Page 9: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

The anti-inflammatory effect of exercise: its role in diabetes and cardiovascular disease controlBente Klarlund Pedersen1Essays in Biochemistry volume 42 2006

Role of inflammation in the pathogenesis of atherosclerosis. Further, inflammation

has been suggested to be a key factor in insulin resistance

Recent findings demonstrate that physical activity induces an increase in the systemic levels of a

number of cytokines with anti-inflammatory properties

Given that skeletal muscle is the largest organ in the human body, the discovery that

contracting muscle is a cytokine producing organ opens a new paradigm: skeletal muscle is an

endocrine organ that by contraction stimulates the production and release of cytokines, which

can influence metabolism and modify cytokine production in tissue and organs

The evidence for a beneficial effect of physical training in patients with coronary heart disease is

strong. Few studies have examined the isolated effect of training on the prevention of diabetes

in patients with impaired glucose tolerance, but there is good evidence for a beneficial effect of

combined physical training and dietary modification

Page 10: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

The beneficial effect of training in patients with type 2 diabetes is very well documented, and

there is international consensus that physical training comprises one of the three cornerstones

of the treatment of diabetes together with diet and medicine.

The players in chronic low-grade inflammation and its link with chronic diseases

The local inflammatory response is accompanied by a systemic response known as the acute

phase response. This response includes the production of a large number of hepatocyte-derived

acute phase proteins, such as CRP and can be mimicked by the injection of cytokines. Chronic

low-grade systemic inflammation has been introduced as a term for conditions in which a 2- to

3-fold increase in the systemic concentrations of TNF-α, IL-1, IL-6, IL-1ra, sTNF-R and CRP is

reflected; TNF-α derives mainly from the adipose tissue

Page 11: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

The link between inflammation, insulin resistance and atherosclerosis

Ageing is associated with increased resting plasma levels of TNF- α, IL-6, IL-1ra, sTNF-R and CRP.

High levels of TNF-α are associated with dementia and atherosclerosis. Also, elevated levels of

circulating IL-6 are associated with several disorders. Increased levels of both TNF- α and IL-6

are observed in obese individuals, in smokers and in patients with type 2 diabetes mellitus.

Plasma concentrations of IL-6 have been shown to predict all-cause mortality as well as

cardiovascular mortality. Furthermore, plasma concentrations of IL-6 and TNF- α have been

shown to predict the risk of myocardial infarction in several studies, and the CRP level is shown

to be a stronger predictor of cardiovascular events than the low density lipoprotein cholesterol

level.

Page 12: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Mounting evidence suggests that TNF- α plays a direct role in the metabolic syndrome.

Accumulating data suggest that IL-6 enhances glucose uptake in myocytes. A number of studies

indicate that IL-6 enhances lipolysis as well as fat oxidation. IL-6 as a potent modulator of fat

metabolism in humans, increasing lipolysis as well as fat oxidation without causing

hypertriacylglycerolaemia.

The cytokine response to exercise differs from that elicited by severe infections. The fact that

the classical pro-inflammatory cytokines, TNF-α and IL-1, in general do not increase with

exercise indicates that the cytokine cascade induced by exercise markedly differs from the

cytokine cascade induced by infections. Typically, IL-6 is the first cytokine released into the

circulation during exercise. The level of circulating IL-6 increases in an exponential fashion (up to

100-fold) in response to exercise, and declines in the post-exercise period. A marked increase in

circulating levels of IL-6 after exercise without muscle damage has been a remarkably consistent

finding. Plasma IL-6 increases in an exponential fashion with exercise and is related to exercise

intensity, duration, the mass of muscle recruited and one’s endurance capacity.

Page 13: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Young healthy individuals performed 3 h of dynamic two-legged knee-extensor exercise at

50% of their individual maximal power output. This exercise induced an only moderate increase

in heart rate (from 113 to 122 beats·min−1), but induced a 16-fold increase in IL-6 mRNA, a 20-

fold increase in plasma IL-6 and a marked IL-6 release from working muscle. When the same

model was applied in elderly healthy untrained subjects, even higher amounts of IL-6 were

released from working muscle during exercise at the same relative intensity. The role of IL-6

released from contracting muscle during exercise is to act in a hormone-like manner to mobilize

extracellular substrates and/or augment substrate delivery during exercise. In addition, IL-6 has

important anti-inflammatory effects.

.

Page 14: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

The anti-inflammatory effects of acute exercise and regular training

Longitudinal studies show that regular training induces a reduction in CRP levels and suggest

that physical activity may suppress systemic low-grade inflammation. To study whether acute

exercise induces a true anti-inflammatory response, a model of ‘low grade inflammation’ was

established in which we injected a low dose of Escherichia coli endotoxin to healthy volunteers,

who had been randomized to either rest or exercise prior to endotoxin administration. In resting

subjects, endotoxin induced a 2- to 3-fold increase in circulating levels of TNF-α. In contrast,

when the subjects performed 3 h of ergometer cycling and received the endotoxin bolus at 2.5

h, the TNF-α response was totally blunted. The long-term effect of exercise on the progression

of disease may be ascribed to the anti-inflammatory response elicited by an acute bout of

exercise, which in part is mediated by muscle-derived IL-6. These anti-inflammatory effects of

exercise may offer protection against TNF-induced insulin resistance. It is suggested that muscle

contraction-induced factors, so-called myokines, may be involved in mediating the health

benefits of exercise and play important roles in the protection against diseases associated with

low-grade inflammation such as cardiovascular diseases and type 2 diabetes.

Page 15: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

http://www.arthritis.org/index.php

Regular, moderate exercise offers a whole host of benefits to people with arthritis. Mainly,

exercise reduces joint pain and stiffness, builds strong muscle around the joints, and increases

flexibility and endurance. It reduces inflammation from arthritis and related conditions and

reduces the risk of other chronic conditions. It also helps promote overall health and fitness by

giving you more energy, helping you sleep better, controlling your weight, decreasing

depression, and giving you more self-esteem. Furthermore, exercise can help stave off other

health problems such as osteoporosis and heart disease.

OA is characterized by the breakdown of cartilage – the part of a joint that cushions the ends of

the bones and allows easy movement. As cartilage deteriorates, bones begin to rub against one

another. This can cause stiffness and pain that make it difficult for you to use that joint.

Osteoarthritis can also damage ligaments, menisci and muscles. Over time OA may create a

need for joint replacements.

Page 16: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

There are two types of OA – primary and secondary. Primary osteoarthritis is generally

associated with aging and the "wear and tear" of life. The older you are, the more likely you are

to have some degree of primary osteoarthritis. However, not everyone gets it – not even the

very old. That’s because OA is a disease, and not part of the normal aging process. Secondary

osteoarthritis, in contrast, tends to develop relatively early in life, typically 10 or more years

after a specific cause, such as an injury or obesity. Other problems can occur inside the joint as

cartilage breakdown affects the joint components. Fragments of bone or cartilage may float in

joint fluid, causing irritation and pain. Spurs, or osteophytes, can develop on the ends of the

bones, damaging surrounding tissues and causing pain. Fluid inside the joint may not have

enough of a substance called hyaluronan, which may affect the joint’s ability to absorb shock.

And although inflammation is not a main symptom of osteoarthritis, it can occur in the joint

lining in response to the cartilage breakdown.

Page 17: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

What causes osteoarthritis?

Like other chronic conditions, osteoarthritis has no single, specific cause. Instead, there are

several factors involved in the disease, including heredity and lifestyle. The following factors

may contribute to osteoarthritis:

Genes: One possibility is that certain people may have a defect in the gene responsible for the

body’s production of collagen, the protein that makes up cartilage. This somewhat rare genetic

defect might lead to abnormally weak cartilage that wears down after just a few decades of

normal activity, causing osteoarthritis as early as age 20.

Other genetically based traits may result in slight defects in the way the bones and joints fit

together so that cartilage wears away faster than usual. The inherited trait known as joint laxity,

or double-jointedness, in which the joints bend farther than the usual angles, may also increase

the risk for osteoarthritis.

Page 18: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

What is Rheumatoid Arthritis?

Rheumatoid arthritis, or RA, is a form of inflammatory arthritis and an autoimmune disease. For

reasons no one fully understands, in rheumatoid arthritis, the immune system – which is

designed to protect our health by attacking foreign cells such as viruses and bacteria – instead

attacks the body’s own tissues, specifically the synovium, a thin membrane that lines the joints.

As a result of the attack, fluid builds up in the joints, causing pain in the joints and

inflammation that’s systemic – meaning it can occur throughout the body.

Rheumatoid arthritis is a chronic disease, meaning it can’t be cured. Most people with RA

experience intermittent bouts of intense disease activity, called flares. In some people the

disease is continuously active and gets worse over time. Others enjoy long periods of remission

– no disease activity or symptoms at all. Evidence shows that early diagnosis and aggressive

treatment to put the disease into remission is the best means of avoiding joint destruction,

organ damage and disability.

Page 19: Effects of detraining on cardiovascular responses to exercise: role of blood volume EDWARD F. COYLE, MAR1 K. HEMMERT, AND ANDREW R. COGGAN J. Appl. Physiol

Engaging in moderate physical activity on a regular basis helps decrease fatigue, strengthen

muscles and bones, increase flexibility and stamina, and improves your general sense of well-

being. When your symptoms are under control, work with your health-care team to develop a

full exercise program that includes stretching for joint flexibility and range of motion, strength

training for joint support and aerobic (cardiovascular) exercise for overall health, weight control,

muscle strength and energy level.