Both intensity (SPL) and duration of exposure, and repetitive exposure to unsafe levels of noise contribute to cochlear damage that results in hearing loss. The louder the noise is, the shorter the safe amount of exposure is. NIHL can be either permanent or temporary, called a threshold shift. Unsafe levels of noise can be as little as 70 dB (about twice as loud as normal conversation) if there is prolonged (24-hour) or continuous exposure. 125 dB (a loud rock concert is ~120 dB) is the pain level; sounds above this level cause instant and permanent ear damage. Noise and ageing are the primary causes of presbycusis, or age-related hearing loss, the most common kind of hearing loss in industrial society. The dangers of environmental and occupational noise exposure are widely recognized. Numerous national and international organizations have established standards for safe levels of exposure to noise in industry, the environment, military, transportation, agriculture, mining and other areas. Sound intensity or sound pressure level (SPL) is measured in decibels (dB). For reference:

An increase of 6 dB represents a doubling of the SPL, or energy of the sound wave, and therefore its propensity to cause ear damage. Because human ears hear logarithmically, not linearly, it takes an increase of 10 dB to produce a sound that is perceived to be twice as loud. Ear damage due to noise is proportional to sound intensity, not perceived loudness, so its misleading to rely on subjective perception of loudness as an indication of the risk to hearing, i.e.
Although a link between intensive exercise and exercise-induced arythmogenic right ventricular cardiomyopathy exists.No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athletes heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athletes heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athletes heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness. History
The athletes heart syndrome was first described in 1899 by Salomon Henschen. He compared the heart size of cross-country skiers to those who lived sedentary lives. He noticed that those who participated in competitive sports displayed symptoms of athletes heart syndrome. Henschen believed the symptoms were a normal adjustment to exercise, and felt concern was not needed.