Function of the Diaphragm in Health and Disease
Poole DC, Sexton WL, Farkas GA, Powers SK, Reid MB, Diaphragm structure and
function in health and disease, Med Sci Sports Exerc. 1997 Jun;29(6):738-54.
Department of Kinesiology, Kansas State University Manhattan 66506, USA.
The diaphragm is the primary muscle of inspiration, and as such
uncompromised function is essential to support the ventilatory and gas
exchange demands associated with physical activity. The normal healthy
diaphragm may fatigue during intense exercise, and diaphragm function is
compromised with aging and obesity. However, more insidiously, respiratory
diseases such as emphysema mechanically disadvantage the diaphragm,
sometimes leading to muscle failure and death. Based on metabolic
considerations, recent evidence suggests that specific regions of the
diaphragm may be or may become more susceptible to failure than others. This
paper reviews the regional differences in mechanical and metabolic activity
within the diaphragm and how such heterogeneities might influence diaphragm
function in health and disease. Our objective is to address five principal
areas: 1) Regional diaphragm structure and mechanics (GAF). 2) Regional
differences in blood flow within the diaphragm (WLS). 3) Structural and
functional interrelationships within the diaphragm microcirculation (DCP).
4) Nitric oxide and its vasoactive and contractile influences within the
diaphragm (MBR). 5) Metabolic and contractile protein plasticity in the
diaphragm (SKP). These topics have been incorporated into three discrete
sections: Functional Anatomy and Morphology, Physiology, and Plasticity in
Health and Disease. Where pertinent, limitations in our understanding of
diaphragm function are addressed along with potential avenues for future
Darnley GM, Gray AC, McClure SJ, Neary P, Petrie M, McMurray JJ, MacFarlane
NG, Effects of resistive breathing on exercise capacity and diaphragm function
in patients with ischaemic heart disease, Eur J Heart Fail. 1999 Aug;1(3):297-300.
Institute of Biomedical and Life Sciences, Glasgow University, Scotland, UK.
BACKGROUND: Muscle weakness has been suggested to result from the
deconditioning that accompanies decreased activity levels in chronic
cardiopulmonary diseases. The benefits of standard exercise programs on
exercise capacity and muscular strength in disease and health are well
documented and exercise capacity is a significant predictor of survival in
patients with chronic heart failure (CHF). Selective respiratory muscle
training has been shown to improve exercise tolerance in CHF and such
observations have been cited to support the suggestion that respiratory
muscle weakness contributes to a reduced exercise capacity (despite biopsies
showing the metabolic profile of a well trained muscle).
AIMS: This study aimed to determine the effects of selective inspiratory
muscle training on patients with chronic coronary artery disease to
establish if an improved exercise capacity can be obtained in patients that
are not limited in their daily activities.
METHODS: Nine male patients performed three exercise tests (with respiratory
and diaphragm function assessed before the third test) then undertook a
4-week program of inspiratory muscle training. Exercise tolerance,
respiratory and diaphragmatic function were re-assessed after training.
RESULTS: Exercise capacity improved from 812+/-42 to 864+/-49 s, P<0.05, and
velocity of diaphragm shortening increased (during quiet breathing from
12.8+/-1.6 to 19.4+/-1.1 mm s(-1), P<0.005, and sniffing from 71.9+/-9.4 to
110.0+/-12.3 mm s(-1), P<0.005). In addition, five from nine patients were
stopped by breathlessness before training; whereas only one patient was
stopped by breathlessness after training.
CONCLUSION: The major findings in this study were that a non-intensive
4-week training programmed of resistive breathing in patients with chronic
coronary artery disease led to an increase in exercise capacity and a
decrease in dyspnea when assessed by symptom limited exercise testing.
These changes were associated with significant increases in the velocity of
diaphragmatic excursions during quiet breathing and sniffing. Patients that
exhibited small diaphragmatic excursions during quiet breathing were most
likely to improve their exercise capacity after the training programmed.
However, the inspiratory muscle-training programmed was not associated with
any significant changes in respiratory mechanics when peak flow rate, forced
expiratory volume and forced vital capacity were measured. The resistive
breathing programmed used here resulted in a significant increase in the
velocity of diaphragm movement during quiet breathing and sniffing. In other
skeletal muscles, speed of contraction can be determined by the relative
proportion of fiber types and muscle length (Jones, Round, Skeletal Muscle
in Health and Disease. Manchester: University Press, 1990). The intensity of
the training programmed used here, however, is unlikely to significantly
alter muscle morphology or biochemistry. Short-term training studies have
shown that there can be increases in strength and velocity of shortening
that do not relate to changes in muscle biochemistry or morphology. These
changes are attributed to the neural adaptations that occur early in
training (Northridge et al., Br. Heart J. 1990; 64: 313-316). Independent of
the mechanisms involved, this small, uncontrolled study suggests that
inspiratory muscle training may improve exercise capacity, diaphragm
function and symptoms of breathlessness in patients with chronic coronary
artery disease even in the absence of heart failure.
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