26 March 2009

Feast and Fast: the dichotomy of insulin and growth hormone

At its heart the human body is a machine. A very complicated machine to be sure, unknowable in completion given our current basis of knowledge, but it still obeys certain engineering concepts in the end. One of those concepts is that the operation of a machine is governed by its control system. When it comes to health, the hormonal system is the control system that governs just how well we feel. We stimulate it in various ways and it causes our bodies to react to those stimulus. Trying to pick apart these relationships is, in my opinion, the key to understanding how to obtain good health throughout our lives.

Today I'm going to write predominately about growth hormone and how it metabolizes fat. I got the idea primarily from the writings of Brad Pilon. I have not read his book; I worked from review articles in scientific journals.


The human body has two signaling systems:
  1. The nervous system, which primarily controls fast actions such as motion and thought.
  2. The endocrine (or hormonal) system, which primarily handles slower processes..
The characteristic time scale of the nervous system is milliseconds. It operates on the principle of action potentials: electrical impulses driven by the fast pumping of sodium and potassium ions. Hormones do not travel down specialized pathways, instead they use the circulatory system. In the endocrine system, the characteristic time is on the order of minutes or hours as hormones decay within the blood stream. From an evolutionary perspective, the endocrine system is much older, since even bacteria use a variety of signaling peptides to control their operation. The nervous system had to await the development of such advanced animals as the mighty squid.

When it comes to metabolism, the endocrine system is the one in control. There is a portion of the nervous system that controls the gut, the autonomic nervous system, but it acts largely independently of the brain. It controls aspects like opening sphincters, e.g. stomach emptying.

If the nervous system is a digital system, then the endocrine system is very much like an analogue circuit composed of resistors, capacitors, and inductors (in biological analogue circuits these are usually called push-pots). These elements can be formed into circuits that perform various functions (amplification, integration, differentiation, etc.). However, there are many, many elements that compose the endocrine system of the human body. If you were to draw a circuit diagram of the human body it would resemble not so much a Pentium CPU as a Gordian knot with its mass of interconnections.

Conceptually the hormone system is divided into the whole-body hormones (endocrine), local tissue hormones (paracrine), and single cell hormones (autocrine). I am mostly concerned with endocrine system since it is the one that affects multiple types of tissues such as fat, muscle, and vital organs. There are certain hormones related to digestion and metabolism that can be considered the premiere, most vital hormones to control such tasks.

Examples of top-tier hormones involved in the process of eating include:
  • Macronutrient metabolism hormones (insulin, growth hormone)
  • Sex hormones (testosterone, estrogen)
  • Appetite hormones (ghrelin, leptin)
  • Basal metabolism (thyroid)
  • Stress hormones (cortisol, epinephrine) (Jensen et al., 1987)
Many of these hormones interrelate with each other, either directly or through the mechanism of secondary, lower-tier hormones, in a very complicated system that is difficult to pick apart. Typically the hormonal system operates on the principle of negative feedback, so if production of one hormone surges, that will in turn generate feedback that will eventually damp it back to normal levels.

For people who are trying to lose fat, a reasonable objective is to tweak one or more hormonal levels to upset the existing equilibrium. A kilo here, a kilo there, and pretty soon you're talking about real weight loss. However, like any complex system, you have to feed it the proper inputs for it to function properly: Garbage in = garbage out.

The feast and fast cycle

Insulin is the primary regulator of carbohydrate and protein metabolism. (Human) growth hormone (abbreviated GH) is the primary regulator of fatty acid metabolism. Today, we're going to talk mostly about GH since most people already know a fair amount about insulin. If you don't, you can get started with my review of Gary Taubes' book, "Good Calories, Bad Calories."

So, to review, insulin is the hormone responsible for regulating the metabolism of glucose and most amino acids (exceptions are lysine and leucine) derived from the protein in your diet that are converted to glucose for the purpose of fuel (Gröschl et al., 2003). High levels of insulin also prevent your muscles from absorbing fatty acids in the blood: the body prefers to burn the low-energy density carbohydrates first and hold onto the superior fatty acids for lean times. A person with high levels of insulin in their blood is said to be in the feasted state.

The opposite to the feasted state is the fasted state. The hormone that characterizes the fasted state is growth hormone (review: Møller and Jørgensen, 2009). The general course of progressing from feasted to fasted goes something like this:
  1. You eat a meal with carbohydrates and protein. Digestion occurs over the course of several hours and insulin levels rise in response to the absorption of these macronutrients.
  2. Insulin sensitive tissues absorb glucose from the blood-stream. Glucagon, a second-tier hormone, causes the liver to break down the glycogen it stores into glucose, releasing it into the blood. This slows the rate at which insulin drops.
  3. Insulin continues to drop as the liver's supply of carbohydrate is reduced. Ghrelin (which I'll discuss later) is produced, which promotes appetite and the production of growth hormone. If the increase in appetite caused by ghrelin causes you to eat, you go back to stage 1. Otherwise, you make the transition into the fasted state as GH levels rise and blood sugar levels drop (Roth et al., 1963).
Growth hormone is basically the hormone that controls when your adipose (fat) tissues release fatty acids to be metabolized by the rest of your body. No growth hormone, no significant fat loss.
Figure 2. from Møller and Jørgensen (2009) on the interrelation of growth hormone, insulin growth factor, and insulin in the fed and fasted cycle.

However, this is not all growth hormone does. As the name suggests, GH, in conjunction with insulin-like growth factor, is involved in the growth of lean body mass: it increases the amount of protein in your muscles and vital organs, it increase the uptake of calcium by bones, etc. Growth hormone alone is insufficient to boost protein synthesis, however. I'll probably save the discussion of IGF-1 for another time (for further reading, start with Gibney, Healy, and Sönksen, 2007). In this context, growth hormone may be poorly named.

In addition to promoting fatty acid metabolism, GH shuts down the uptake of glucose into muscle tissue and stops the conversion of amino acids into glucose (Rabinowitz, Klassen, and Zieler, 1965). The fact that GH shuts down not just carbohydrate metabolism but also protein metabolism is critically important. It means that when one enters the fasted state, your muscle and organs are protected against being consumed to fuel your body (Nørrelund et al., 2006). This clearly illustrates the greatest failing of the high-carbohydrate, calorie-restricted "semi-starvation" diet that Taubes pans: if you maintain high insulin levels but insufficient calories, there's little to protect the protein in your muscles and vital organs from being consumed while your fat tissue goes untouched.

Furthermore, once a person becomes insulin resistant (and most obese individuals are), they become locked in a vicious cycle: insulin levels remain high for a long time after a meal, and stay high until the next meal, so the body never makes the transition from feasted to fasted and hence never burns any body fat. Let me reiterate: once you are obese, you will have a harder time losing body fat than a thinner individual. Unsurprisingly, growth hormone levels in obese people are depressed (Scacchi et al., 1999). The number one priority for losing weight then is improving insulin sensitivity. As an aside, this is a good reason to avoid supplementation with synthetic growth hormone: it may leave you with unnaturally elevated blood sugar for an extended period of time. Essentially growth hormone makes your tissues insulin resistant, but it normally only does so when blood glucose levels are depleted.

Body composition — whether you are lean or fat, i.e. the ratio of fat mass to lean body mass — is basically a function of the ratio of time you spend in the feasted state versus time you spend in the fasted state. Now, on the face of it, this statement is self-evident and rather useless. However, it's also very fundamental. In the natural situation, insulin and human growth hormone levels are reciprocal: GH is low when insulin is high, insulin is low when GH is high. A meta-analysis of GH found that high levels of growth hormone led to an increased basal metabolic rate of 141 [69-213] kcal/day (Liu et al., 2007). This corresponds to roughly a pound of fat per month.

What controls growth hormone levels?

So if growth hormone controls the release of fat from your fat tissues, what controls the release of growth hormone? Growth hormone is typically released in pulses from the pituitary gland. This pulsitile nature of growth hormone is similar to that of insulin in a healthy individual.

Figure 4 from Ho et al., 1988, showing the Fourier transform of GH secretion. Filled boxes are (24-hr) fasted subjects, open boxes are fed controls. Normally the horizontal axis of a Fourier transform is frequency but in this case it is period. This plot shows peaks at 110 min, 206 min, and 24 hr. The 24 hour cycle is likely caused by sleeping, the sources of the other peaks are less clear.

Growth hormone is primarily up-regulated by growth hormone releasing hormone (GHRH) and growth hormone releasing peptide, better known as ghreline. Growth hormone is primarily down-regulated by human growth inhibiting hormone (GHIH), typically known as somatostatin, and high blood glucose levels. I eagerly await the discovery of growth hormone releasing hormone releasing hormone (GHRHRH). Ok, I jest, low-levels of growth hormone and insulin stimulate GHRH.

Notice something interesting: ghrelin is an appetite controlling hormone. When you fast, GH production goes up and up and ghrelin goes down. When fasting, the hardest part is about six hours after your last meal when your insulin levels have dropped down and you have a strong appetite. However, if you get over this 'hump' you will find that your appetite largely goes away as the ghrelin circulating in your blood starts the secretion of GH. You will still get thirsty, but not ravenously hungry. I would generally recommend sleeping through this stage.

So what's the difference between controlling your body's overall insulin/GH levels very controlling your appetite to avoid binge eating? Can we actually separate the appetite hormones, leptin and ghrelin from the metabolism control hormones, insulin and growth hormone? As far as I can tell, appetite and blood sugar levels are basically the same thing. Trying to separate the two as wholly independent variables and then claiming that fat people simply lack self control when it comes to food is very very wrong. The science clearly shows that the two are deeply inter-related.
Figure 4. from Hartmann et al., 1992, showing the negative correlation between GH release and body-mass index in fasted subjects.

Production of growth hormone typically declines as we age. However, research has shown that growth hormone levels are more tightly correlated with visceral fat (belly fat) than age (Vahl et al, 1997). So do we get fat because we get old or do we get old because we get fat? Both answers appear to be correct, each to a degree. No one will live forever, but most of us would like to age gracefully. I'm about a decade younger than I was at this time one year ago.

Real-world means of increasing growth hormone levels

There are three basic ways to increase the amount of GH your body produces:
  1. Get adequate sleep. GH production spikes during sleep. Try not to eat before bedtime.
  2. Fast occasionally, for relatively short durations.
  3. Conduct intense exercise. Don't eat before or during your exercise.
'Intense' exercise in this context means you should exceed 75 % of your VO2 max lactate threshold (Pritzlaff et al., 1999). VO2 max Lactate threshold is the level at which the demands of your exercise exceeds your body's ability to breath in oxygen, causing the body to go anaerobic and produce lactic acid. Note that VO2 max lactate threshold is for your whole body, so you need to exercise your whole body or at least the biggest muscles (core, glutes, quads). You can do bicep curls until your arms fall off but since they're small muscles you won't get much of a GH boost from doing so. The best exercise for putting your whole body into the anaerobic threshold is probably sprint intervals.

Figure 1. from Pritzlaff et al., showing GH secretion pulses as a function of lactate threshold (LT) reached.

Of course, (2) and (3) can be combined. A word of warning, if you exercise hard at the end of a fast, be prepared for sore muscles (i.e. delayed onset muscle soreness) the next day.

A low-carbohydrate diet may have the advantage in this situation as the overall insulin pulse should be small and of shorter duration. The reason is fairly obvious: the body's tissues will be less insulin resistant and hence absorb glucose from the blood stream more readily. Hence one should enter the fasted state quicker after a low-carbohydrate diet than not. The more time you spend in the fasted state, the faster you're going to shed body fat.

The $64,000 dollar question is then, what effect does dietary fat have on growth hormone secretion? It appears that dietary fat intake increases the production of somatostatin from the gut, otherwise known as growth-hormone inhibiting hormone, although somatostatin down-regulates many many other hormones (Cappon et al., 1993). Anecdotal evidence from people who regularly fast is that fasting is easier to handle on a low-carbohydrate diet than a low-fat diet. I dug around for awhile on PubMed, but I wasn't able to find any research where subjects were fed diets of pure glucose and pure triglycerides and then their transition from feasted to fasted tested. It would be a good Master's thesis for someone if it really hasn't been done before. I did find tests that tested intravenously applied fatty acids in fasting but since somatostatin is produced by the digestive system their relevance isn't clear. The Hartman study from 1992 seems to be the best starting point for this line of research.

in alphabetical order:

Cappon JP, et al. "Acute effects of high fat and high glucose meals on the growth hormone response to exercise." J Clin Endocrinol Metab. 1993 Jun;76(6):1418-22.

Gibney J, Healy ML, Sönksen PH. "The growth hormone/insulin-like growth factor-I axis in exercise and sport." Endocr Rev. 2007 Oct;28(6):603-24.

Gröschl M, et al., "Endocrine responses to the oral ingestion of a physiological dose of essential amino acids in humans.", J Endocrinol. 2003 Nov;179(2):237-44.

Hartman ML, et al., "Augmented growth hormone (GH) secretory burst frequency and amplitude mediate enhanced GH secretion during a two-day fast in normal men." J Clin Endocrinol Metab. 1992 Apr;74(4):757-65.

Ho KY, et al. "Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man."J Clin Invest. 1988 Apr;81(4):968-75.

Jensen MD, et al., "Lipolysis during fasting. Decreased suppression by insulin and increased stimulation by epinephrine." J Clin Invest. 1987 Jan;79(1):207-13.

Liu H, et al. "Systematic review: the effects of growth hormone on athletic performance."
Ann Intern Med. 2008 May 20;148(10):747-58.

Pritzlaff CJ, et al. "Impact of acute exercise intensity on pulsatile growth hormone release in men." J Appl Physiol. 1999 Aug;87(2):498-504.

Møller N, Jørgensen JO, "Effects of Growth Hormone on Glucose, Lipid, and Protein Metabolism in Human Subjects." Endocr Rev. 2009 Mar 19.

Nørrelund H, et al., "The protein-retaining effects of growth hormone during fasting involve inhibition of muscle-protein breakdown." Diabetes. 2001 Jan;50(1):96-104.

Jesse Roth, et al., "Hypoglycemia: A Potent Stimulus to Secretion of Growth Hormone." Science 140(3570):987 - 988 (May 1963).

Scacchi M, Pincelli AI, Cavagnini F. "Growth hormone in obesity." Int J Obes Relat Metab Disord. 1999 Mar;23(3):260-71.

Vahl N, et al., "Abdominal adiposity rather than age and sex predicts mass and regularity of GH secretion in healthy adults." Am J Physiol. 1997 Jun;272(6 Pt 1):E1108-16.

David Rabinowitz, Gerald A. Klassen and Kenneth L. Zierler, "Effect of Human Growth Hormone on Muscle and Adipose Tissue Metabolism in the Forearm of Man." J. Clin. Invest. 44(1): 51-61 (1965).


E.D.M. said...

Do you have any guidelines for what a good plan using this data would look like? When to eat, when to fast, when to excercise and for how long...

Robert McLeod said...

Hmm... well I avoided giving specific criteria primarily because I think individuals should self-experiment to find what works best for them. When you're experimenting on yourself, going through the motions of theory -> hypothesis -> experiment, you've become an active participant. Too many people try to follow "the plan," see some gains and then they plateau. Rather than changing something else they get too anxious and end up crashing and burning.

Nonetheless, I can see the advantage of offering an example for use as a learning tool.

Looking at Figure 4. from Ho, we can hypothesize that fitting as many 'pulses' into a fast as possible could be a viable strategy. So we have the 24-hour period, that's sleep, so we have to include a sleep period in it. Then we need to fit in several 2-hour and 4-hour periods. Overall then, a 24-hour fast starting after dinner (say 7:00 pm) and finishing with dinner the next day would seem logical.

For an exercise component, there are three possible times: before bed-time, in the morning after awakening, and prior to dinner at the termination of the fast. Theoretically, a morning exercise period may be better for fat-burning and the last period, before the feast dinner, better for building muscle, given the insulin/insulin-like growth factor/growth hormone cycle. You might do this once, maybe twice a week.

In terms of exercise, any intense interval training should be fine. Try googling "Tabata sprints" for an example. You can do swim intervals, sprints, lift weights, do burpees (see YouTube), etc. it doesn't really matter just do what you find enjoyable. The things to keep in mind is you need about 10 minutes of 'warm-up' to get your blood flowing and the GH with it. Look at Figure 1. from Pritzlaff and the delay between starting exercise and GH secretion.

Møller cites a paper that shows your body needs to be quite warm to get a GH pulse out of exercise:

Wheldon A, Savine RL, Sonksen PH, Holt RI 2006 Exercising in
the cold inhibits growth hormone secretion by reducing the rise in
core body temperature. Growth Horm IGF Res 16:125–131

I would not exercise more than 30 minutes at high intensity. Realistically most people cannot train hard more than twice a week. Athletes can add more volume. I also do flexibility/range of motion work (typically yoga or dynamic stretching) and play/endurance (whitewater kayaking at the moment). Now that I have experience with it I much prefer to exercise fasted. I don't really 'bonk' anymore from low-blood sugar levels.

For advice on fasting itself, a little anxiety the first time is natural. Once you know you aren't going to die if you don't eat in the next half a day, it becomes much easier. I would avoid artificial sweeteners -- some can cause an insulin response -- and excessive caffeine. Stick to water, decaf coffee, and green tea, for example.

Stephan Guyenet said...


Nice post. I had an idea a while back, I can't remember if I've shared it with you or not. How someone reacts to a fast probably has a lot to do with their fasting insulin level. If you have hyperinsulinemia, it probably prevents energy mobilization during a fast and makes you feel like crap. So many people I know have to eat constantly or else they crash. That has to be pathological.

Robert McLeod said...


The correlation of GH production to visceral (belly) fat also seems to bear that out. I get a vague impression that ghrelin is also involved fairly heavily in this problem. Ghrelin would mesh in nicely with appetite disfunction/anxiety associated with this style of eating.

Recall our conversation about thin people with diabetes, but they still typically have central obesity? It seems that subcutaneous and interstitial muscular fat is fairly benign, but accumulate fat around the smooth muscle and organs in your torso and you're in trouble!

From the point of view seeing the endocrine system as a control system, it seems that since it is an analogue system it should have numerous metastable (i.e. local minima) states outside of its normal operating point. When you accumulate belly fat, for whatever reason, the system is perturbed to a new metastable equilibrium. A paleolithic man would never get there, but with the eatable food-like substances in our modern diet we can and do in record numbers. If that's the case then it will take a fairly strong stimulus to pop out of that local minima, over the gap, and back to the normal evolutionary state.

Anonymous said...

Good article buy one minor nitpick.

You state: "VO2 max is the level at which the demands of your exercise exceeds your body's ability to breath in oxygen, causing the body to go anaerobic and..'

This is NOT VO2 max. The VO2 max is the maximum amount of oxygen that can be taken up, transported and used by the body. What you just described is the anaerobic threshold. This generally occurs at a significantly lower percentage of maximum intensity than VO2 max.

I.e. in a Vo2 Max test one of the criteria is a HR withing 5 bpm of max. If an individual has a anaerobic threshold 80% of that they're a very gifted endurance athlete.

I don't mean this to be a pain, but I wanted to point it out, since I though the rest of this was very well composed.

VVilly said...

My Mom is a diabetic now for 20 years (type 2 and now completely injection dependent).
Recently her blood sugar has on average been very high. When it goes down to what is still considered high - 9-12 mmol/L, she experiences all the symptoms of low blood sugar. The pharmacist confirmed that it takes time to adjust to a lower blood sugar level after having elevated blood sugar for an extended time.

Alicia said...

Fascinating post. I'm pretty much chemistry illiterate, so I always appreciate thorough explanations like this.

The thing about dietary fat and somatostatin is tripping me up a bit. So many of the studies mentioned in _Good Calories, Bad Calories_ promoted fat loss through high fat diets, and it's been working for me recently as well.

I've actually been losing so fast I'm worried about getting loose skin, so maybe the somatostatin is a good thing.

Anyway, thanks for this post.

Jessica said...

What an awesome read! Thank you so much for writing such a thorough "intro" to the topic of growth hormone.

Robert McLeod said...


You are quite correct, I've fixed the post to replace VO2 max with lactate threshold.


The human body can repair a lot of damage but at some point, some damage is permanent. Regardless, I think any diabetic would be well served by a low-carbohydrate diet. You might want to show your mother the following blog:


Some Girl:

Somatostatin is simply a hormone that turns off numerous other hormones, including growth hormone. It's fairly logical that after a high fat meal your body should stop releasing fat stores and start absorbing them. What I don't know if how fast that process is compared to sugar and insulin. With a high-carbohydrate diet you also release glycogen from the liver, which extends the time your body stays in the feasted state after a meal.

In particular, for people who have a defective insulin metabolism, if the fat-burning pathway isn't similarly broken, then using it would seem to be a path back to good health.

Also, because of the protein preservation aspect, I think if you are restricting calories below maintenance levels, then low-carb is a smarter route.

Anonymous said...

Ray Peat, A Renowned Nutritional Counselor, seems to think that lactate production should be avoided rather then stimulated:


Quote : "Incidental stresses, such as strenuous exercise combined with fasting (e.g., running or working before eating breakfast) not only directly trigger the production of lactate and ammonia, they also are likely to increase the absorption of bacterial endotoxin from the intestine. Endotoxin is a ubiquitous and chronic stressor. It increases lactate and nitric oxide, poisoning mitochondrial respiration, precipitating the secretion of the adaptive stress hormones, which don't always fully repair the cellular damage."

Your comments ?

E.D.M. said...


Thank You. I am at the point where I need to change up what I am doing. Just discovered self-experimenting and it makes much more sense.

Robert McLeod said...


I would say that Peat is not adequately supporting his thesis statements. For example, the quote you provided isn't supported at all.

Similarly, he states, "Nervous and hormonal factors can cause lactate to accumulate, even without prior damage to the mitochondria (e.g., B. Levy, et al., 2003)." However, when I read that article it's about injecting rats with bacteria to make them go into septic shock. So I'm left scratching my head as to how that research supports that statement.

P.S. why did you capitalize, "A Renowned Nutritional Counselor?"

Albert said...

How does the following fit it. I copied it from a poster called Sheppard in an Immortality Institute forum


start post

People like De Vany and Di Pasquale have perpetrated this myth. The idea is that under normal conditions, insulin and GH are fairly antagonistic. Well then, increases in insulin after exercise must mean that growth hormone will go down. Not exactly:


I also find it funny that some of the same people that advocated carbohydrates post exercise to counteract increases in cortisol (similar logic as above) just a few years ago, now follow the same type of hormonal-centric thinking and want to fast after exercising.

I'm also skeptical about the GH and circadian rhythm thing, as this didn't show much difference in humans. I would have preferred different styles of exercise, though. And, I've never spent much time looking into it. And, also note that growth hormone response to exercise goes down in the chronic state, so I'm not sure any of this is worth worrying about.

end post


Bryce said...

Thank you for this excellent, succinct post. I'll be checking your blog out in the future in the hopes of finding anything even half as useful!

Some Girl,

I wouldn't worry about the Somatostatin. According to Brad Pilon, author of EatStopEat, a great book on fasting, the general message here is to avoid eating (especially fat) right before you work out, because it can mute the HGH response by releasing things like Somatostatin. I'd go so far as to say that waiting about 60 minutes after an intense workout would help maximize HGH output.

The rest of the time, eat your fat!


Robert McLeod said...


Yeah I almost always eat after serious exercise. Eating a little bit of pure protein before exercise isn't a bad idea either.

Al said...

Thanks for your time and work, Robert.

What, in your opinion, is specifically the reason(s) to forego black coffee and caffeine during a fast?

- Al

Robert McLeod said...


On the topic of black full-test coffee on a fast, caffeine can affect some of the hormones involved in fasting and lower blood sugars.

http://www.annals.org/cgi/content/full/119/8/799Personally, I feel pretty crummy if I drink caffeine while fasted. If you don't, you don't, but I'm not going to condone it.

Al said...

Thanks for your time, Robert.

- Al

kevin said...


I can't tell you how thrilled I am to have discovered this post. It articulates and explains some of the more prominent dietary and fitness-related "hunches" that I've slowly discovered--empirically, through my own body--over the past few years, noticing things like 1)the difference in fat loss from sprint intervals in the pool versus distance swims or 2) the difference in my mental clarity after 24 hours of fasting versus 2 minutes after eating a kingsize snickers, etc. Coming from a background in the arts, I have a hard time wading through the tsunami of scientific research out there and the even bigger (and uglier) tsunami of its coverage in the media. This post is so informative and so accessible, even to the less science-minded person. So, again, I'm thrilled. I can't help but wonder why this dichotomy--this fundamental facet of each and every human body--is not more widely publicized and known. How many lives and dollars could a proper understanding of the fast/feast cycle help save in the world at large? Don't feel compelled to comment on that question--I'm just thinking out loud. Thanks for the post and if you ever find yourself on the south shore of Lake Superior, stop by the Apostle Islands for some paddling!