well
i guess not….asthma like ur condition cannot b treated by phsical therapy as u said,it’s an allergic condition and the only curative ttt is to stay away from the allergic factor.
u’ll lose nothing if u try

Well, as the lungs are a powerful muscle, I might give it a shot. I’ve never had personal experience, but I do take spiriva for my asthma, which is a muscle relaxer, and have had incredible results, so physical therapy might just do the trick.

Here is something which discussed therapy + asthma.

Some investigators have hypothesized that aggressive therapy with anti-inflammatory therapies to improve airway hyperreactivity (above and beyond their effects on conventional parameters of asthma control) may have additional long-term benefits.10

Concept of Airway Remodeling
The relation between the several types of airway inflammation (both early-phase and late-phase events) and the concept of airway remodeling, or the chronic nonreversible changes that may happen in the airways, remains a source of intense research.11 The natural history of airway remodeling is poorly understood, and although airway remodeling may occur in some patients with asthma, it may not be a universal finding. Clinically, airway remodeling may be defined as persistent airflow obstruction despite aggressive anti-inflammatory therapies, including inhaled corticosteroids (ICs) and systemic corticosteroids. Pathologically, airway remodeling appears to have a variety of features that include an increase in smooth muscle mass, mucus gland hyperplasia, persistence of chronic inflammatory cellular infiltrates, release of fibrogenic growth factors along with collagen deposition, and elastolysis (Figure 3). Many biopsy studies show these pathologic features from the airways of patients with chronic asthma. However, there are many unanswered questions, including whether features of remodeling are related to an inexorable progression of acute or chronic airway inflammation or whether remodeling is a phenomenon separate from inflammation altogether (Figure 4 and Figure 5).

Recent research has confirmed that the airway epithelium is an active regulator of local events, and the relation between the airway epithelium and the subepithelial mesenchyma is thought to be a key determinant in the concept of airway remodeling. A recent hypothesis by Holgate et al12 indicates that airway epithelium in asthma functions in an inappropriate “repair phenotype” in which the epithelial cells produce proinflammatory mediators as well as transforming growth factor-ß to perpetuate remodeling.

Exhaled Gases and Oxidative Stress
Asthma is characterized by specific biomarkers in expired air that reflect an altered airway redox chemistry, including lower levels of pH and increased reactive oxygen and nitrogen species during asthmatic exacerbations.13-18 Reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, and hydroxyl radicals cause inflammatory changes in the asthmatic airway. In support of this concept are the high levels of ROS and oxidatively modified proteins in airways of patients with asthma.14 High levels of ROS are produced in the lungs of asthmatic patients by activated inflammatory cells (ie, eosinophils, alveolar macrophages, and neutrophils).15 Increased ROS production of asthmatic patients’ neutrophils correlates with the severity of reactivity of airways in these patients, and severe asthma is associated with neutrophilic airway infiltrates. Concomitant with increased oxidants, antioxidant protection of the lower airways is decreased in asthmatic lungs.16,17

Another reactive species, nitric oxide (NO), is increased in the asthmatic airway.14 Nitric oxide is produced by nitric oxide synthase (NOS), all isoforms of which—constitutive (neuronal, or type I, and endothelial, or type III enzymes) and inducible (type II enzymes)—are present in the lung. Abnormalities of NOS I and NOS II genotype and expression are associated with asthma. Recent in vitro studies have suggested cytotoxic consequences associated with tyrosine nitration induced by reaction products of NO. Other investigators have measured products of arachidonic acid metabolism in exhaled breath condensate.18 Specifically, 8-isoprostane, a PGF2α analog that is formed by peroxidation of arachidonic acid, is increased in patients with asthma of different severities, and leukotriene E4-like immunoreactivity is increased in exhaled breath condensate of steroid-naïve patients with mild asthma with levels about threefold to fourfold higher than in healthy subjects.

For more info see:

Doing aerobics and running is good for asthmatics unless you have exercise induced asthma. Don’t do aerobics or exercises if you are having an asthma attack. Eating apples is scientifically known to build up lung capacity, even for people who don’t have asthma.

In Dr. Batmanheldi’s book, “Your not sick, your thirsty. Your body’s many cries for water”, the Dr. says asthma is an effect of dehydration. Our brains are about 80% water and our body is about 70%. The brain takes first priority over water consumption and when dehydrated, many symptoms can occur. Water drawn from sponges in the joints is arthritis. When our cells form a waxy substance around them to conserve water, that is cholesterol. When water is drawn upon from the postules in the lungs that help us breath due to dehydration, our lungs close up to conserve that water and we call it asthma.

Try drinking half your body weight in ounces of water daily to reduce your need for medications. Ex: 150 pounds = 75 ounces.