Lose Fat in Less Time: Is Sprint Exercise a Leptin Signaling Mimetic in Human Skeletal Muscle?
We already know that sprint training and it’s counterparts like high intensity interval training (HIIT), and intense circuits like ‘tabata’ (20 seconds of high intensity work followed by 10 seconds rest continued for 4 minutes) and shown superior results in fat loss, resting metabolic rate, and cardiac output. Now, research is showing a hormonal connection to these superior training methods. At the end of this article is a free little tabata circuit you can try at home!
First a little background. The hormone leptin acts as an appetite suppressor. Obesity in some people is strongly correlated to leptin resistance (think of this like insulin and insulin resistance). The body no longer reacts to leptin and appetite is no longer suppressed. So this study suggests that sprinting kicks off the same cascade of signals as leptin. In other words it signals a drop in appetite. Just like exercise works in many of the same ways as insulin to clear blood sugar! How nice, it burns calories, raises metabolism, and serves as an appetite suppressant, that is a lot of bang for your exercise buck (psssst, guess what, it also saves you time, and time = money!). The Lab Rats are always excited when the bastards in white coats have their goggles on and needles out.
“Seriously, I was kidding about the 4 eyes comment”
In conclusion, this study shows that most of the signaling pathways activated by leptin in rodent skeletal muscle are also activated by sprint exercise in human skeletal muscle, despite a small reduction of leptin serum concentration after the sprint exercise. These findings imply that sprint exercise behave as a leptin mimetic and could be used to stimulate the leptin signaling pathways in human skeletal muscle. This opens the possibility of using sprint exercise to circumvent leptin resistance in obese humans and may lead to increased leptin sensitivity.We provide some evidence to support that the effects of sprint exercise on ERK, STAT3, STAT5, and SOCS3 are not mediated by changes in either serum leptin or IL-6 concentrations, while the expression of SOCS3 and the phosphorylation of STAT5 may have been induced by GH. Importantly, we showed that glucose ingestion 1 h prior to the sprint exercise abolishes or delays some of the exercise-elicited signaling responses, implying that the adaptative responses to sprint exercise training may be modulated by the postabsorp- tive state.
Note the fasting conditions that yielded the positive results. But, please don’t jump to conclusions on this yet and go out and sprint for an hour on an empty stomach. They used 75 grams of glucose (that’s a ton, enough for perhaps a 5 mile run) 1 hour before the run. And what we do know about glucose, is that it will raise insulin, which will blunt glycogen breakdown. It is therefore likely to suspect a similar reaction with leptin (sparing actions). Likewise, this was 1 30 second sprint. The human body has enough ATP and glucose floating around at ANY minute of the day to fuel such a short bout….however, NOT repeated bouts, a real sprint workout would have more like 10 of these sprints included (on the low end). So, you betcha, things would be much different if you were not using enough glucose to fuel a 5 mile run for one 30 second sprint (and if you faster than average that would be a little over 200 yards…but, if you did 10 of these, bwahahahahaha!). So don’t fret it is ok to eat before you sprint train. Some things are better than others, but 75gm of glucose would not be the option of choice.
More science jargon:
This study was designed to determine whether sprint exercise activates signaling cascades linked to leptin actions in human skeletal muscle and how this pattern of activation may be interfered by glucose ingestion. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before the Wingate test. Exercise elicited different patterns of JAK2, STAT3, STAT5, ERK1/2, p38 MAPK phosphorylation, and SOCS3 protein expression during the recovery period after glucose ingestion. Thirty minutes after the control sprint, STAT3 and ERK1/2 phosphorylation levels were augmented (both, P < 0.05). SOCS3 protein expression was increased 120 min after the control sprint but PTP1B protein expression was unaffected. Thirty and 120 min after the control sprint, STAT5 phosphorylation was augmented (P < 0.05). Glucose abolished the 30 min STAT3 and ERK1/2 phosphorylation and the 120 min SOCS3 protein expression increase while retarding the STAT5 phosphorylation response to sprint. Activation of these signaling cascades occurred despite a reduction of circulating leptin concentration after the sprint. Basal JAK2 and p38 MAPK phosphorylation levels were reduced and increased (both P < 0.05), respectively, by glucose ingestion prior to exercise. During recovery, JAK2 phosphorylation was unchanged and p38 MAPK phosphorylation was transiently reduced when the exercise was preceded by glucose ingestion. In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.
Drug companies have been working for years to mimic these sort of effects. Wait NO longer, pay NO money, and suffer NO side effects right NOW!
Don’t have a track? Don’t have time to drive to one? Try this tabata drill (one of my favorites):
1) Sprint in place for 20 seconds then rest for 10 seconds
2) High knees in place for 20 seconds then rest for 10 seconds
3) Butt kicks in placed then rest for 10 seconds
4) Speed Jumping Jacks in place then rest for 10 seconds…(then we are repeating the above)
5) Sprint in place for 20 seconds then rest for 10 seconds
6) High knees in place for 20 seconds then rest for 10 seconds
7) Butt kicks in placed then rest for 10 seconds
8) Speed Jumping Jacks in place then rest for 10 seconds
DONE! Now stop, rest and breath, now do it again;)