In a life-threatening situation, the heart beats faster and harder, invigorated by the fight-or-flight response, which instantaneously prepares a person to react or run. Now, a new study by researchers at Temple University School of Medicine (TUSM) shows that the uptick in heart muscle contractility that occurs under acute stress is driven by a flood of calcium into mitochondria–the cells’ energy-producing powerhouses.
Researchers have long known that calcium enters mitochondria in heart muscle cells, but the physiological role of that process was unclear. “The function of mitochondrial calcium uptake during stress generally was linked to the collapse of energy production and cell death,” explained John W. Elrod, PhD, Assistant Professor of Pharmacology and at the Center for Translational Medicine at TUSM, and senior investigator on the new study, which appears June 25 in the journal Cell Reports.
“We show, however, that in periods of acute stress, increased calcium uptake by mitochondria in the heart functions in ways that are good and bad: during the fight-or-flight response, it provides the necessary energetic support for the heart, but during a heart attack, it leads to the death of large numbers of heart cells,” Dr. Elrod said.
Timothy S. Luongo et al. The Mitochondrial Calcium Uniporter
Matches Energetic Supply with Cardiac Workload during Stress and
Modulates Permeability Transition. Cell Reports, June 2015 DOI: 10.1016/j.celrep.2015.06.017