LAUSR

Chee et al. (2021) have recently claimed that supplementing older male adults (70 years; n = 7, 3 of whom were on statins medication) with a daily carnitine and protein formulation that also contained 44 g of sugars in conjunction with twiceweekly exercise training sessions at 50% VO2max over 25 weeks would increase their muscle total carnitine stores. Subsequently, the higher muscle total carnitine levels were hypothesised to (1) improve wholebody insulin sensitivity and (2) increase wholebody fat oxidation during a moderateintensity exercise undertaken after training. The reference was made against a similar age and medicated small group of male adults who received a similar drink formulation (but without carnitine) and exercise training. The authors acknowledged there was no basis for upholding the claim that carnitine supplementation would improve resting insulinstimulated wholebody or skeletal muscle glucose disposal. Furthermore, the authors could not show any significant mean group differences in energy expenditure, nor in the rates of plasma appearance or disappearance during two supposedly identical exercise tests— 1 h of exercise at 50% VO2max— undertaken before and after carnitine/placebo supplementation. Conversely, the authors upheld the claim that carnitine supplementation in older male adults would increase wholebody fat oxidation, predominantly in the form of intermyofibrillar lipids (IMCL). Nevertheless, the evidence called in to support the latter claim does not stand up to detailed scrutiny, is circumstantial at best or is missing, and may convey an unsubstantiated message to the public. In fact, the personal interpretation of the present commentator, which will be detailed later, is that carnitine supplementation in conjunction with biweekly training sessions for 25 weeks increased CHO oxidation rather than that of IMCL. Let us assume for a moment that the authors’ claim that a 20% rise in fat/IMCL oxidation would occur with carnitine supplementation and training is correct. Then, an extra ~40 (220– 180) J/kg lean body released from fat/IMCL would have contributed to the energy expenditure in the carnitine treated group during the 60 min exercise test at 50%VO2max. Also, assuming a total lean mass of 50 kg (table 1; Chee et al., 2021) and that 1 g of triacylglycerol generated 39.4 kJ through oxidation (authors’ conversion factor), then an additional (40 × 60 × 50)/39,400 or 3 g of fat/IMCL would have been burnt during each exercise session. However, an increase in fat oxidation in the treated group should have occurred earlier rather than exclusively during the exercise test undertaken at the end of the training. If we assume generously that the additional fat oxidation with carnitine loading started from the first week of training, then a total of 150 g of fat/IMCL (3 g fat × 2 sessions per week × 25 weeks) would have been oxidised over 25 weeks (or <1 g fat/daily on average). In line with these calculations, the data displayed in table 1 and figure 5d (Chee et al., 2021) show no change in any regional fat content across all subjects irrespective of group or time. Equally, this minute amount of fat, which could have certainly not been captured by a DEXA scan, would have also been easily masked by the effects on the wholebody composition by the additional 44 g of sugars that all subjects had to ingest daily for 25 weeks. Overall, the claim that total carnitine would increase fat oxidation by 20%, predominantly in muscle IMCL, during the exercise test would have been insignificant when translated to an absolute value. It is also worth remembering that the reported increase in fat oxidation during the exercise test was derived from data recorded from a male cohort where six out of fourteen were on statins medication, a drug wellknown to interfere with wholebody fat handling. The males in the treated group appeared to store primarily 22% more muscle total carnitine than in the control group, even before supplementation (figure 1a; 3rd vs 1st column; Chee et al., 2021). However, a control male with the lowest muscle total carnitine content (10 mmol/kg dm) of all males enrolled in the study may have contributed to the sizable difference between the groups at the baseline. At the end of the training, it was equally unexpected to notice a marked decline in muscle total carnitine once again in another control male (figure 1a, left panel; Chee et al., 2021). Given the small number of males in each group, these two control males were, therefore, most likely to have acted as leverage points to biasedly increase the mean difference between the treated group and control at 25 weeks, thereby raising the chance of declaring a falsepositive finding (figure 1b; Chee et al., 2021). The authors also state that the values of the carnitine forms reported in the study cover the main three forms of carnitine: free, shortand longchain acylcarnitine. However, as figure 1 (Chee et al.,