Introduction A growing body of evidence demonstrates that minimal volume of high-intensity interval training and resistance training can serve as effective alternates to traditional time-consuming training, inducing similar or even superior physiological adaptations (Babraj et al., 2009). However, whether an acute minimal volume high-intensity interval exercise (HIE) and resistance exercise (RES) would affect QTc interval, an index of ventricular depolarization/repolarization, is not known. The purpose of this study was to examine QT interval before and after an acute HIE and RES bout. Methods Fifteen male adults (age: 24.2±2.4 years; BMI: 20.6±1.7) underwent: (1) HIE: all-out cycling exercise 30 sec × 4, interspersed with 4 min of rest; (2) RES: a circuit of nine resistance exercise involved the large muscle groups with ten repetitions, interval with 1 min of rest; and (3) CON: a control session of no exercise. QT interval (corrected by heart rate, QTc) was measured pre-exercise, immediately post-exercise, at 20-min intervals thereafter within 120 min, and 12h, 13h and 14h after exercise. The HIE, RES and CON sessions (total 14 min each) were carried out in random order at the same time of day and separated by at least 7 days. Results QTc increased (P<0.05) immediately after exercise in both groups (HIE: 411±6 vs. 462±6 ms; RES: 411±5 vs. 447±4 ms) and peak QTc occurred at this time point followed by a progressive recovery, but 120min recovery QTc data were significantly higher in HIE than RES (P<0.05). In the RES QTc had returned to baseline at 60 min after exercise but was still significantly elevated in HIE. For HIE, the QTc length returned to baseline by 12 h post exercise. Discussion Consistent with previous findings from traditional time-consuming exercise (Heffernan et al., 2008), an acute bout of HIE or RES significantly increases QTc length. Thus, during recovery from acute HIE or RES, there is prolongation of depolarization and repolarization of the ventricles. Given drugs that produce mild QT prolongation (i.e., 5–10ms) in healthy individuals have been found to induce much greater and clinically relevant prolongation in susceptible populations (Indik et al.2006), it is reasonable to speculate that risk of untoward cardiovascular events is increased following such exercise, especially in at-risk populations. In addition, our results also indicate that the magnitude of QTc responses to exercise was significantly higher in HIE than in RES. Thus, arrhythmia susceptibility within 12 h following HIE should be not ignored.