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1 Unit of Cardiac Physiology, Univeristy of Manchester, Manchester, United Kingdom
2 School of Biological Sciences, University of Manchester, Manchester, United Kingdom
* To whom correspondence should be addressed. E-mail: trafford{at}man.ac.uk.
In mammals changes in photoperiod regulate a diverse array of physiological and behavioural processes, an example of which in the Siberian hamster (Phodopus sungorus) is the expression of bouts of daily torpor following prolonged exposure to short photoperiod. During torpor body temperature drops dramatically, yet unlike in non-hibernating or non-torpid species, the myocardium retains the ability to contract and is resistant to the development of arrhythmias. In the present study we sought to determine whether exposure to short photoperiod results in alterations to cardiac excitation contraction coupling, thus potentially enabling the heart to survive periods of low temperature during torpor. Experiments were performed on single ventricular myocytes freshly isolated from the hearts of Siberian hamsters that had either been exposed to 12 weeks of short day lengths (SD) or 12 weeks of long day lengths (LD). In SD acclimated animals the amplitude of the systolic Ca2+ transient was increased (e.g. from 142±17nmol.L-1 in LD to 229±31nmol.L-1 in SD at 4Hz, P<0.001). The increased Ca2+ transient amplitude in the SD acclimated animals was not associated with any change in the shape or duration of the action potential. However, sarcoplasmic reticulum Ca2+ content measured following current clamp stimulation was increased in the SD acclimated animals (at 4Hz, 110±5 versus 141±15µmol.L-1, P<0.05). We propose that short photoperiods re-programme the function of the cardiac sarcoplasmic reticulum resulting in an increased Ca2+ content and that this may be a necessary precursor for maintenance of cardiac function during winter torpor.
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