Nicole has a B.S. in Exercise Science, a Masters in Cell and Molecular Nutrition and is currently finishing up her PhD in Biochemistry and Molecular Nutrition. You can find her name tacked on to quite a bit of published research as well as various well respected texts.
Academics aside, she’s right in the heart of the physique game and has some compelling things to say. We’re hitting all of the hot topics of scientific physique enhancement and Nicole has brought some exciting information to the table. So listen up people, this is one interview you want to pay attention to. But you have to promise you won’t just look at the pictures…
Sure. I wake up around 6:30 am and head immediately to the gym down the street. Then it’s home to pick up my dog and walk her around Beacon Hill or let her run along the Charles River. Finally it is off to the lab around 9:30 am, and once I get there everyday is unique, which is part of what I love about it. An average day consists of experiments, research, writing and attending various seminars and meetings. I usually leave the lab around 7:30 pm and then meet with clients if necessary, take my dog to the park, and/or head back to the gym for cardio. I try to get to bed by 11 pm.
My first fitness competition was in the summer of ‘03 in Denver, where I won the Colorado State Fitness Championships. The following year, after moving to Boston, I won the Bev Francis Atlantic States in NYC. My final show to date was in Vegas for the 2004 USA Championships, where I placed 5th.
Competing was a wonderful experience! It was so fun to see what level you can take your body to when you really put your mind to it. There are some things that are best learned first hand, and that experience taught me so much about myself as well as training and nutrition in general. As far as competing again, I would love to, especially after being recently diagnosed with diabetes. I feel like it would be a whole new challenge and that I would again learn so much. But it won’t be for a while. My time constraints and career goals just won’t allow for it at this point.
I have spent the last 3 months trying to replace some of the muscle that I lost through my diagnosis last year. It’s amazing how quickly lean mass disappears in the absence of insulin!!
Starting about a month ago, I’ve shifted my focus to leaning out for summer. To do this (and this has worked tremendously well for me previously) I weight train 4 days on / one day off, and split the muscles into a 3-day split. But I have 6 different workouts: the first 3 days I hit the muscles with higher intensity and some power movements. These workouts are really built around the core exercises such as bench press, squats, deadlifts, etc, performing high sets and low reps for each movement.
The next 3 workouts I do higher volume and less rest. I start with some of the core exercises here as well, but just a couple sets and then bring in a lot more variety in the types of exercises, reps, and tempos that I choose (Mechanical Advantage Drop Sets, 1 + 1/3’s, etc). I like to use these workouts to incorporate some fun fitness specific exercises, such as one-arm push-ups, walking on my hands, press handstands, burpees, etc, especially when I’m prepping for a show. As for cardio, I do 10-15 minutes of high intensity interval training (HIIT) post-lifting after 3 of those 6 workouts. I try to do 30-45 min of a more steady state cardio at night 2-3x per week when I get the chance.
My nutrition definitely changes a bit throughout the year, primarily through the avenue of carbohydrate manipulation…more when I am trying to gain muscle, and less when I am leaning out. This seems to work really well for me. But of course, this last year has been really quite unique as I’ve tried to get a handle on my diabetes.
My fat intake is always between 25-35%. When my carbs are higher during muscle building phases I keep my fat intake at the lower end of the window, around 25%. As I decrease carb intake to lean out, I elevate protein intake just slightly, but I mostly substitute fat (increased to 35%).
For the most part, with a few exceptions including periodic carb-up days and the last few weeks of a competition lean-out when I gradually drop calories (though never under 1200 kcal per day).
This past year I have really cut back in order to fully focus on finishing up my PhD. I am no longer training through a gym, so I mostly do fitness consulting (designing nutrition and workout plans). As such, clients are more transient. I still work more regularly with quite a few fitness/figure/bodybuilding competitors though.
I work with both males and females, although the majority of my clientele tends to be female. And one to keep your eye out for is Dr. Angel Allison. She is currently preparing for the USA Figure Championships in July and is looking awesome!
I work in an energy metabolism laboratory, where we primarily study obesity and diabetes. I definitely want to continue diabetes and/or obesity research. Upon graduation later this year, I will be seeking a post-doctoral fellowship at a pharmaceutical company. I love doing research and really want to be at the heart of the drug discovery process.
Well, mTOR is certainly a hot topic. It seems like everyday there is something new coming out! And things just keep getting more and more complicated. It seems that now mTOR can help drive mitochondrial biogenesis (make more mitochondria) and increase the oxidative capacity of mitochondria. This means more fat burning potential!
Well I can’t say I know that much, but it will be very interesting to see if the human studies support some of the new animal data. So it seems that mVps34, which is very abundant in skeletal muscle, may be a key player in regulating muscle protein turnover following resistance exercise.
So basically, sitting upstream of mTOR, this lipid kinase allows mTOR to respond to intracellular nutrient status, namely amino acid depletion. As such, mVps34 is inhibited by amino acid starvation, and additionally inhibited by AMPK. It (mVps34) initially goes up about 3 hours after resistance training and stays up for quite awhile. I think the working hypothesis is that depletion of intracellular amino acid pools (as would occur with exercise), activate mVps34 and promote autophagy in an effort to replenish amino acid pools and maintain mTOR activation to drive protein synthesis. One last interesting tidbit is that its expression is higher in type I oxidative muscles…it will be interesting to see if there are any ramifications for this, and I for one am curious to find out if there are any gender differences in this protein. Time will tell!
Well I don’t think this is actually an AMPK issue because I am not sure that stimulants taken around a workout will alter exercise-induced AMPK activity. Caffeine doesn’t. What happens at rest and what happens during a workout are not necessarily comparable. AMPK is a cellular energy sensor, and as such it gets activated during exercise because ATP is being depleted. I suspect that being such a tightly regulated energy sensor, nutrition is really going to be superior to any supplemental agent in terms of modulating its activity during exercise. (Chronic AMPK activation (i.e. pharmaceuticals) and inhibition of hypertrophy is another issue). Indeed, it seems that AMPK activity may be tightly linked to glycogen storage. I just got back from a meeting where I heard this from Dr. Graham Hardie himself, a pioneer researcher in the AMPK field. Interestingly, skeletal muscle AMPK activity (even during exercise) is inhibited by high glycogen levels. Molecularly, the Hardie hypothesis is that a lot of cellular AMPK is actually bound to large glycogen molecules. Basically, under conditions where muscle glycogen levels are high, AMPK is more-or-less sequestered by glycogen and only able to phosphorylate glycogen synthase (GS, thereby inhibiting glycogen synthesis).
So with high glycogen levels, only non-bound AMPK can phosphorylate its other well-known targets. Thus, in a sequestering sort of way, glycogen inhibits traditional AMPK activity. When glycogen starts to be broken down, as occurs with exercise, more AMPK becomes non-bound and is free to act on other targets, such as those in pathways leading to increased glucose uptake and fatty acid oxidation. This leads to the suspicion that sipping on carbs before and/or during a workout could decrease AMPK activity during workouts or perhaps prevent any increases that may occur with a supplemental agent that actually activates AMPK. But the jury is still out on implications of this inhibition. ?
Well, the concern on AMPK and hypertrophy is that AMPK inhibits mTOR. But during exercise, AMPK gets activated as ATP gets depleted, (and yes, mTOR activity is suppressed), but this allows glucose to be taken up more readily, and fat to be oxidized at a greater rate. Good things when you are working out!
Exactly, it’s really what happens after exercise that matters in terms of hypertrophy. Post work-out AMPK activity declines as mTOR and mVps34 activity go up. Assuming proper nutrition follows training, insulin and amino acids will activate anabolic pathways. And you may have better workouts with some caffeine! Now if you are concerned about potential attenuation of insulin signaling with caffeine ingestion, well…a study hot off the press is demonstrating that co-ingestion of caffeine with PWO carbs actually increases glycogen re-synthesis. It seems that insulin-sensitizing exercise can override the insulin sensitivity impairments seen with caffeine ingestion in individuals at rest, at least in terms of glycogen re-synthesis. But again, this actually doesn’t have anything to do with AMPK because caffeine did not increase AMPK activity that occurred with exercise, nor did caffeine prevent the decrease in AMPK activity that occurred with carb ingestion following the exercise. And furthermore, Akt phosphorylation was slightly higher after PWO carb ingestion in the caffeine group suggesting that maybe this caffeine benefit could spill over to other anabolic pathways (i.e. mTOR) as well.
I agree with your point that I am extrapolating a bit, but I definitely think it’s similar and potentially relevant to weight training. For one thing, yes these were carb depleted trained men, but that only makes it more interesting that caffeine still had effects, as glycogen replenishing conditions were already more optimal, hence making it more difficult to see further benefit.
Clearly, the mechanism of this interaction between caffeine and exercise needs to be delineated. But if the mechanism is glycogen depletion, which is possible, then similar results could be predicted with weight training as well. But of course cardio and weight training produce distinct hormonal milieu, and so clearly more studies will need to be done to confirm these data in different populations and different physiological states, but in the mean time, I for one will continue to caffeinate my cardio and weight training.
Think of perilipin as the gatekeeper of stored triglyceride. I’m guessing that got your attention…
Well I am actually not sure what this lipid droplet protein means to physique-enhancement in a lean individual, but molecularly, perilipin acts as a barrier to prevent lipolysis in the basal state, but enhances lipolysis in the presence of stimulation such as that occurring with catecholamines. Upon catecholamine stimulation, perlilpin targets HSL (Hormone Sensitive Lipase) to the lipid droplet, thereby allowing triglyceride to be released and hydrolyzed. Interestingly, obese women have less perilipin and higher rates of lipolysis (obviously lipolysis does not equal fat oxidation!!).
When we look to the mice, the perilipin knockout mouse is lean and resistant to diet induced obesity, seemingly a good thing, right? Well, these mice become insulin resistant with time, probably due to the high concentration of free fatty acids floating around. Furthermore, TNFa (an inflammatory cytokine that promotes insulin resistance) decreases perilipin, thereby chronically increasing adipocyte lipolysis. This is not a good thing and interestingly, a recent study showed that metformin (a popular drug used to treat type 2 diabetes) prevents this decrease in perilipin seen with TNF? treatment, at least in cells. Finally, I know of one obscure paper that showed that a plant extract could decrease body weight in females in part by decreasing perilipin, but I am still skeptical. I’ll leave you with this…there are currently some really interesting studies being done to look at gene-diet interactions with relation to perilipin. We’ll have to wait and see I guess!
That wraps it up for part one of this interview. Make sure to check back next week for part two of Marc McDougal’s interview with Nicole Rogers.