Recent publications have suggested that intra-ocular pressure (IOP) may be an indirect assessment of intra-cranial pressure (ICP). Both IOP and ICP have similar physiologic pressure ranges and similar responses to changes in intra-abdominal, intra-thoracic and aortic pressure. Previous studies have demonstrated the relationships between retinal arterial pressure and aortic pressure, intra-ocular pressure and retinal venous pressure, intra-cranial pressure and retinal venous pressure. Power athletes routinely utilize the Valsalva maneuver during weightlifting. In fact there are reports of stroke, cerebral hemorrhage, subarachnoid hemorrhage, conjunctival, foveal and retinal hemorrhage, retinal detachment, hiatal hernia and pneumothorax associated with weightlifting. These events are thought to occur secondary to the extreme pressure elevations that occur in the intra-abdominal, intra-thoracic, intra-cranial, intra-ocular and vascular compartments. To date no human studies have examined the IOP changes that may occur with heavy resistance exercise. Therefore, we recruited power athletes (n = 11), who had participated in prior studies, from the local metropolitan area. The athletes had blood pressure status, drug screening and medical histories performed during previous investigations. Intra-ocular pressure was measured by noncontact tonometry at rest and during maximal isometric contraction. All subjects resting IOP were within normal ranges (mean 13 +/- 2.8 mmHg). Intra-ocular pressures were significantly (p < 0.0001) elevated in each subject during maximal contraction (mean 28 +/- 9.3 mmHg). One subject's IOP reached 46 mmHg during maximal contraction. Linear regression analysis demonstrated a significant linear relationship (r = 0.62, p < 0.0001) in the net change of IOP from rest to maximal contraction for each subject. This study demonstrates that IOP elevates to pathophysiologic levels during resistance exercise. The findings of conjunctival hemorrhages in two subjects further supports IOP being reflective of retinal venous pressure. The enormous pressures generated by power athletes during weightlifting leads to elevations in ICP which obstruct venous outflow leading to hemorrhage and elevations in IOP. The question remains as to whether these intermittent bursts of elevated IOP can lead to long-term pathological sequelae.
Recurrent and persistent CD consistently results from residual tumor. At repeated surgery the residual tumor can be found at or immediately contiguous to the site at which the tumor was found originally. Unappreciated dural invasion with growth of residual tumor within the cavernous sinus dura, which frequently occurs without residual tumor or dural invasion being evident on MR images or to the surgeon during surgery, is the basis of surgical failure in many patients with CD. Occult lateral dural invasion by tumor may also underlie recurrences of other types of pituitary adenomas.
Reports on the occurrence of left ventricular wall thickening in resistance-trained athletes have rejected the possibility for this physiological adaptation to occur without concomitant anabolic steroid abuse. Others have concluded short bursts of arterial hypertension that occur with maximal weight lifting are not sufficient to induce left ventricular wall thickening, and left ventricular wall thickness ≥13 mm should not be found in pure resistance-trained athletes. Therefore, we examined 4 elite resistance-trained athletes by two-dimensional echocardiography. In addition, we retrospectively examined the individual left ventricular dimensions of 13 bodybuilders from our previous echocardiographic studies. All 4 elite resistance-trained athletes had left ventricular wall thicknesses beyond 13 mm. One of the elite bodybuilders has the largest left ventricular wall thickness (16 mm) ever reported in a power athlete. Retrospectively, 43% of the drug-free bodybuilders and 100% of the steroid users had left ventricular wall thickness beyond the normal range of 11 mm. In addition, 1 drug-free subject and 3 steroid users were beyond the critical mark of 13 mm. No subjects demonstrated diastolic dysfunction. In contrast to previous reports, we have demonstrated that left ventricular wall thicknesses ≥13 mm can be found routinely in elite resistance-trained athletes. The use of anabolic steroids concomitant with intensive resistance exercise does appear to augment left ventricular size without dysfunction. Anabolic steroids may accelerate left ventricular wall thickening indirectly by increasing strength, thus augmenting the pressor response.
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